Nephro MKSAP

Laxative abuse. is the most likely cause of this patient's normal anion gap metabolic acidosis. Normal anion gap metabolic acidosis can be caused by gastrointestinal bicarbonate loss, renal loss of bicarbonate, or the inability of the kidney to excrete acid. The normal physiologic response to systemic acidosis is an increase in urine acid excretion. Therefore, an initial diagnostic step in normal anion gap metabolic acidosis is to determine whether the kidney is appropriately excreting acid or whether impaired kidney acid excretion is the cause of the metabolic acidosis. Increased acid excretion by the kidney is reflected as a marked increase in urine ammonium. However, urine ammonium is difficult to measure directly. Because ammonium carries a positive charge, chloride is excreted into the urine in equal amounts with ammonium to maintain electrical neutrality. Therefore, the amount of chloride in the urine reflects the amount of ammonium present, and the urine anion gap can be used as an indicator of the ability of the kidney to excrete acid. The urine anion gap is calculated as follows:Urine Anion Gap = (Urine Sodium + Urine Potassium) - Urine Chloride. In the context of increased urinary ammonium excretion, therefore, the urine anion gap will be negative. The negative urine anion gap in this patient (-6 mEq/L [-6 mmol/L]) suggests a gastrointestinal cause of the normal anion gap metabolic acidosis, and laxative abuse is a possible, even likely explanation. In addition, the low urine potassium indicates appropriate renal compensation in context of laxative-induced hypokalemia.

A 24-year-old woman is evaluated for progressive muscle weakness of several months' duration. She provides no pertinent personal or family history and takes no medications. On physical examination, temperature is normal, blood pressure is 94/58 mm Hg, pulse rate is 98/min, and respiration rate is 16/min. BMI is 19. The remainder of the examination is normal. Laboratory studies: Serum electrolytes : Sodium 142 mEq/L (142 mmol/L) ,Potassium 2.8 mEq/L (2.8 mmol/L) ,Chloride 120 mEq/L (120 mmol/L) ,Bicarbonate 15 mEq/L (15 mmol/L) Urine electrolytes: Sodium 18 mEq/L (18 mmol/L) ,Potassium 8.0 mEq/L (8.0 mmol/L) ,Chloride 32 mEq/L (32 mmol/L) ,Urinalysis pH 5.0; no blood or protein Which of the following is the most likely cause of this patient's metabolic acidosis?

Measurement of the serum cystatin C level. Cystatin C may be preferable to creatinine to assess kidney function in individuals with higher muscle mass. An increase in muscle mass would be expected to result in an increase in serum creatinine level in the absence of change in kidney function. This muscular man with a BMI of 29 has increase in muscle mass. Because serum creatinine is derived from the metabolism of creatinine produced by muscle, a significant increase in muscle mass would be expected to increase serum creatinine. An elevation in serum creatinine could also occur with creatine supplements, which he is not taking. This patient has a normal urinalysis and no proteinuria, all of which indicate no evidence of underlying kidney disease. Cystatin C, which is cleared by the kidney, is produced by all nucleated cells; therefore, levels are less dependent on muscle mass. Cystatin C can also be used for more accurate glomerular filtration rate estimation in these patients as a component of the Chronic Kidney Disease Epidemiology Collaboration equation.

A 26-year-old man is evaluated during a follow-up visit after presenting to an urgent care clinic for back pain 1 week ago. Laboratory studies at that time were significant for a serum creatinine level of 1.4 mg/dL (123.8 µmol/L); other laboratory studies, including urinalysis, were normal. A urine albumin-creatinine ratio obtained in preparation for this visit is 10 mg/g. He is a personal trainer, and his daily exercise regimen includes weightlifting. He states that his back pain has resolved. He occasionally takes ibuprofen; the last use was 1 week ago. He takes no over-the-counter supplements. On physical examination today, vital signs are normal. BMI is 29. The patient is muscular, without signs of obesity. There is no muscle tenderness. Which of the following is the most appropriate management?

Secondary focal segmental glomerulosclerosis (FSGS). FSGS is the most common form of the nephrotic syndrome in black persons. In the United States, FSGS currently accounts for up to 40% of idiopathic (primary) nephrotic syndromes in adults. The pathogenesis of FSGS stems from podocyte injury due to immunologic, genetic, and/or hyperfiltration causes. A large and growing proportion of FSGS cases are considered secondary forms of FSGS due to hyperfiltration injury in the setting of relatively reduced renal mass. The overworking of the glomerulus in this setting leads to adaptive podocyte injury and segmental sclerosis. This hyperfiltration form of FSGS is classically seen in patients with obesity but also can manifest in patients with a history of premature birth or solitary kidney. This patient has two risk factors for the secondary form of FSGS: obesity and a history of premature birth. In addition, her presentation is more typical of a secondary FSGS lesion, with subnephrotic proteinuria and no associated clinical findings. Electron microscopy of her kidney biopsy would be expected to show only mild to moderate effacement of the podocyte's foot processes. An immunologic route to injury is considered the main pathogenic mechanism behind primary forms of FSGS, with leukocytes producing a soluble circulating factor that directly targets podocytes. In such cases, proteinuria tends to be heavy (nephrotic range) with associated hypoalbuminemia, and edema is usually present on physical examination. Electron microscopy of a kidney biopsy with primary FSGS will typically show extensive effacement of the podocyte's foot process.

A 27-year-old woman is evaluated for proteinuria identified on urinalysis performed for a life insurance examination. She reports no symptoms. History is significant for premature birth, a 2-year history of hypertriglyceridemia and prediabetes, and a 5-year history of obesity. The remainder of her medical history is unremarkable. Her only medication is gemfibrozil. On physical examination, vital signs are normal. BMI is 37. The remainder of the examination is unremarkable. Laboratory studies: Albumin 3.8 g/dL (38 g/L) ,Creatinine 1.0 mg/dL (88.4 µmol/L) ,Hemoglobin A1c 6.4% ,Urinalysis No blood; 3+ protein ,Urine protein-creatinine ratio 2100 mg/g Kidney ultrasound shows normal-appearing kidneys with no masses or hydronephrosis.Which of the following is the most likely diagnosis?

Multiple myeloma. This patient's acute kidney injury (AKI) is due to hypercalcemia from multiple myeloma. Classic symptoms of polyuria, polydipsia, and nocturia sometimes occur with elevated serum calcium levels of 11 mg/dL (2.8 mmol/L) or less. Other symptoms such as anorexia, nausea, abdominal pain, constipation, increased serum creatinine levels, and mild mental status changes are more likely to occur with levels >11 mg/dL (2.8 mmol/L). Kidney dysfunction is found in about 30% of patients diagnosed with multiple myeloma, often due to cast nephropathy (also termed myeloma kidney), a condition in which excess monoclonal free light chains precipitate in the distal tubules and incite tubulointerstitial damage. Hypercalcemia and exposure to nephrotoxic agents are other frequent causes of kidney dysfunction. Hypercalcemia can decrease glomerular filtration rate through renal vasoconstriction, the natriuretic effects of high serum calcium levels, and impaired renal concentrating ability. This patient has orthostatic hypotension, a bland urinalysis with hyaline casts, and a low urinary sodium, consistent with a prerenal AKI from hypovolemia. The constellation of hypercalcemia, normal anion gap metabolic acidosis, pancytopenia, and AKI suggests multiple myeloma as the etiology.

A 75-year-old woman is hospitalized for a 1-week history of dizziness, nausea, vomiting, increased urination, and decreased appetite. History is significant for hypertension treated with hydrochlorothiazide. She also takes calcium carbonate for bone health. On physical examination, blood pressure is 150/85 mm Hg supine and 122/70 mm Hg standing, pulse rate is 78/min supine and 100/min standing, and respiration rate is 18/min. There is no neck vein distention. Cardiac, pulmonary, and abdominal examinations are unremarkable. There is no lower extremity edema. Laboratory studies: Hematocrit 30% Leukocyte count 3000/μL (3.0 × 109/L) Platelet count 82,000/μL (82 × 109/L) Calcium 12.8 mg/dL (3.2 mmol/L) Creatinine 3.7 mg/dL (327.1 µmol/L) Electrolytes : Sodium 132 mEq/L (132 mmol/L) ,Potassium 4.9 mEq/L (4.9 mmol/L) ,Chloride 115 mEq/L (115 mmol/L) , Bicarbonate 17 mEq/L (17 mmol/L),Phosphorus 6.2 mg/dL (2.0 mmol/L) ,Urine sodium 15 mEq/L (15 mmol/L) ,Urinalysis Specific gravity 1.018; trace protein; few erythrocytes/hpf; occasional leukocytes/hpf; few granular casts; numerous hyaline casts. Which of the following is the most likely cause of this patient's hypercalcemia and acute kidney injury?

Surreptitious vomiting. Metabolic alkalosis is diagnosed by an elevation in serum bicarbonate concentration. This disorder is caused either by a loss of acid or administration or retention of bicarbonate. Conditions that contribute to the maintenance of metabolic alkalosis include volume contraction, ineffective arterial blood volume, hypokalemia, chloride depletion, and decreased glomerular filtration. Laboratory evaluation of metabolic alkalosis is based on urine chloride concentration. Metabolic alkalosis is considered saline responsive when associated with true hypovolemia and responds to correction of the volume deficit with isotonic saline. Saline-responsive metabolic alkalosis presents with a low urine chloride of <15 mEq/L (15 mmol/L); the most common causes are vomiting, nasogastric suction, and diuretic use. Hypokalemia occurs secondarily due to aldosterone elevation and cation loss as the kidney attempts to lose bicarbonate. Although these patients are usually hypovolemic or normovolemic (with normal or low blood pressures), patients with preexisting chronic hypertension may present with high to normal blood pressures.

A 28-year-old woman is evaluated in the emergency department for muscle cramps and weakness. She notes a weight loss of 15 kg (33 lb) over the past 3 months; baseline weight was 115 kg (254 lb). She reports no abdominal pain or diarrhea. She has a 1-year history of type 2 diabetes mellitus, for which she takes metformin. On physical examination, temperature is normal, blood pressure is 122/72 mm Hg, pulse rate is 100/min, and respiration rate is 18/min. BMI is 36. Muscle strength of the lower and upper extremities is 4/5. Other than weakness, neurologic examination is normal. Laboratory studies: Electrolytes : Sodium 138 mEq/L (138 mmol/L) ,Potassium 2.4 mEq/L (2.4 mmol/L) ,Chloride 92 mEq/L (92 mmol/L) ,Bicarbonate 34 mEq/L (34 mmol/L) Arterial blood gases : pH 7.50 ,PCO2 45 mm Hg (6.0 kPa) ,Urine sodium 40 mEq/L (40 mmol/L) ,Urine potassium 60 mEq/L (60 mmol/L) ,Urine chloride 5 mEq/L (5 mmol/L). Which of the following is the most likely diagnosis?

Fabry disease. an X-linked recessive inborn error of glycosphingolipid metabolism caused by deficiency of α-galactosidase A. The enzyme deficiency leads to defective storage of sphingolipid and progressive endothelial accumulation, causing abnormalities in the skin, eye, kidney, heart, brain, and peripheral nervous system. Typically, the disease begins in childhood with episodes of pain and burning sensations in the hands and feet. These painful episodes can be brought on by exercise, fever, fatigue, or other stressors. In addition, young patients often develop angiokeratomas (violaceous papules with overlying scale), decreased perspiration, and corneal and lens opacities of the eyes. The disease is progressive, and symptoms of kidney, heart, and/or neurologic involvement usually occur between the ages of 30 and 45 years. As an X-linked disorder, males who inherit a mutation in the gene responsible for α-galactosidase always display the disease phenotype. Females, on the other hand, who inherit only one copy of a disease-causing mutation, can show a wide range of clinical manifestations, ranging from asymptomatic carriers to severe heart and kidney failure no different from a hemizygous male's phenotype. This variability is likely due to varying degrees of random inactivation of one copy of the X chromosome in each cell (lyonization). The most common finding of Fabry disease seen in heterozygous females is corneal dystrophy, which occurs in more than half of females. Fabry disease should be considered as a cause of chronic kidney disease of unknown etiology in young adulthood, especially when there is a family history of early end-stage kidney disease or cardiovascular-related death (via myocardial infarction or cerebrovascular accident). Diagnosis can be made via kidney biopsy but also noninvasively with measurement of leukocyte enzymatic activity and subsequent genetic confirmation. Screening for the disease is recommended for family members of affected patients. Enzyme replacement therapy with recombinant human α-galactosidase A is available.

A 29-year-old man is evaluated in the emergency department for a 3-week history of headaches. He reports a painful burning sensation in his toes and feet for the past few years, particularly after he exercises at the gym, and states that he does not sweat as much after exercise compared with his peers. He takes no medications. Family history is notable for the following: His maternal grandfather and maternal granduncle had similar burning sensations in their feet for years and died from strokes in their early 40s; and his mother has occasional burning sensations in her feet as well as corneal dystrophy. On physical examination, blood pressure is 160/95 mm Hg; other vital signs are normal. Numerous angiokeratomas over the sternal area are present. Reduced pain and temperature sensation in the lower extremities bilaterally is noted. Laboratory studies show a blood urea nitrogen level of 60 mg/dL (21.4 mmol/L) and a serum creatinine level of 4.1 mg/dL (362.4 µmol/L); urinalysis shows 2+ blood and 3+ protein. Kidney ultrasound shows increased echogenicity in bilateral kidneys. Which of the following is the most likely diagnosis?

Hepatitis C antibodies. This patient presents with glomerulonephritis (elevated serum creatinine level, hematuria, and subnephrotic proteinuria), which shows a membranoproliferative (MPGN) pattern on kidney biopsy. The new approach to MPGN lesions is a bifurcation based on the pattern of staining on immunofluorescence microscopy. The more common pattern, as seen in this patient, is immune-complex deposition with the presence of both immunoglobulin (IgG, IgM, and/or IgA) and complement (C1q and/or C3) on immunofluorescence, which infers that the classical pathway has been activated by an inciting cause or event that generally falls into one of three major categories: infectious, autoimmune, or malignancy associated. The most common is infectious, specifically infection with hepatitis C virus (HCV).

A 29-year-old man is hospitalized for lower extremity edema and fatigue that has progressed over the past 6 months. Laboratory studies document kidney failure. History is notable for obesity. He has a remote history of intravenous drug use and a 5-year history of multiple sex partners (men and women). He takes no medications. On physical examination, the patient is afebrile, and blood pressure is 148/94 mm Hg; other vital signs are normal. BMI is 38. There is no rash. There is pitting edema in the lower extremities to the ankles bilaterally. The remainder of the physical examination is unremarkable. Laboratory studies: C3 60 mg/dL (600 mg/L) ,C4 7.0 mg/dL (70 mg/L) ,Creatinine 2.8 mg/dL (247.5 µmol/L) ,Urinalysis 3+ blood; 3+protein ,Urine protein-creatinine ratio 2900 mg/g. Kidney biopsy shows membranoproliferative glomerulonephritis on light microscopy, with immunofluorescence microscopy showing 3+ staining for IgG, 1+ staining for IgM, 2+ staining for C1q, and 2+ staining for C3. Results of which of the following tests will most likely explain this patient's findings?

Discontinue mycophenolate mofetil and begin azathioprine. Fertility increases after kidney transplantation, although fertility rates remain lower and pregnancy complications are higher compared with the general population. Pregnancy planning for a kidney transplant recipient is essential to improve outcomes and includes adjusting medications and optimizing clinical status. Kidney transplant recipients should wait 1 to 2 years with a stable allograft before attempting conception. Other comorbid conditions (such as systemic lupus erythematosus) should also be stable prior to conception. Outcomes are improved with better allograft function (serum creatinine <1.5 mg/dL [132.6 µmol/L]) and stable immunosuppression. Mycophenolate mofetil (as well as sirolimus and everolimus) is teratogenic and needs to be replaced 3 to 6 months prior to conception with azathioprine, which is generally safer and well tolerated in pregnancy.

A 31-year-old woman seeks preconception counseling. She has end-stage kidney disease secondary to focal segmental glomerulosclerosis. She received a haploidentical kidney transplant from her brother 2 years ago. She had an acute rejection episode 18 months ago that was successfully treated with glucocorticoids, and kidney function has been stable since that time. She currently feels well and reports no symptoms. Current medications are mycophenolate mofetil, tacrolimus, and prednisone. On physical examination, vital signs are normal. The allograft is palpable in the right lower quadrant and is nontender. Laboratory studies show a serum creatinine level of 1.3 mg/dL (114.9 µmol/L). Which of the following is the most appropriate management?

Adynamic bone disease. The most likely bone pathology is adynamic bone disease in this patient with end-stage kidney disease and normal serum calcium and phosphorus and relatively suppressed parathyroid hormone (PTH) and alkaline phosphatase levels. Adynamic bone disease can occur in patients with chronic kidney disease (CKD) or those on dialysis. It is typically associated with significant vascular calcifications. The gold standard for the diagnosis of adynamic bone disease is bone biopsy; however, this is rarely performed. Adynamic bone disease has no specific markers, but a constellation of findings may suggest this diagnosis. Patients with adynamic bone disease may present with fracture or bone pain. The latter has been attributed to the inability to repair microdamage because of low turnover. Serum calcium may be normal or elevated because the bone is unable to take up calcium. High PTH and alkaline phosphatase would exclude adynamic bone disease; in this disorder, both are typically normal. Treatment is targeted at factors that allow PTH secretion to rise. This includes avoiding calcium-based binders, conservative use of vitamin D, and decreasing the dialysate calcium concentration. It is important to note that, as with the general population, patients with CKD may also develop osteoporosis, particularly if they received glucocorticoid therapy for the primary kidney disorder or for immunosuppression in the setting of a kidney transplant.

A 78-year-old woman is evaluated in the emergency department for severe pain in the left hip after a fall. History is significant for end-stage kidney disease as of 18 months ago, hypertension, and peripheral vascular disease. Medications are lisinopril, amlodipine, sevelamer, and epoetin alfa. She is also receiving morphine for the hip pain. On physical examination, blood pressure is 132/70 mm Hg, and pulse rate is 72/min; other vital signs are normal. The left lower extremity is externally rotated at the hip. Peripheral pulses are diminished. The remainder of the physical examination is noncontributory. Laboratory studies: Alkaline phosphatase 78 U/L ,Calcium 9.7 mg/dL (2.4 mmol/L) ,Phosphorus 4.2 mg/dL (1.4 mmol/L) ,Parathyroid hormone 62 pg/mL (62 ng/L) ,25-Hydroxyvitamin D 32 ng/mL (80 nmol/L). Radiographs of the hips show a left hip fracture and calcified arteries.Which of the following is the most likely diagnosis for the underlying bone disease?

Potassium citrate. In addition to increasing fluid intake, potassium citrate is appropriate to prevent future calcium oxalate stones in this patient. Patients with chronic diarrhea and malabsorption are at increased risk for forming calcium oxalate stones for three reasons. First, because of the diarrhea and concomitant metabolic acidosis, urine citrate, an inhibitor of crystallization, is often reduced. In addition, volume depletion from the diarrhea decreases urine volume and thus increases the concentration of calcium and oxalate in the urine. Finally, in malabsorption, especially fat malabsorption as occurs in chronic pancreatitis, enteric calcium binds to fat as opposed to oxalate, leaving oxalate free to be absorbed and excreted in the urine. Although treatment should be based on the metabolic evaluation in this patient, his low urine pH and low serum bicarbonate level suggest that he has metabolic acidosis. Decreased systemic pH lowers urine citrate excretion. Supplementation with citrate as a base equivalent will help correct the acidosis and increase urine citrate, bind urinary calcium, and decrease the formation of calcium oxalate stones.

A 38-year-old man is evaluated after passing his second kidney stone. History is significant for chronic pancreatitis secondary to a past history of alcohol abuse. He has three to four loose bowel movements each day. He reports no fever, flank pain, or dysuria. There is no family history of kidney disease, hyperparathyroidism, or nephrolithiasis. Current medications are pancreatic enzymes and multivitamins. Physical examination reveals a thin man. Vital signs and the remainder of the examination are unremarkable. Laboratory studies: Calcium 8.5 mg/dL (2.1 mmol/L) Creatinine 0.7 mg/dL (61.9 µmol/L) Electrolytes : Sodium 137 mEq/L (137 mmol/L) ,Potassium 3.5 mEq/L (3.5 mmol/L) ,Chloride 104 mEq/L (104 mmol/L) ,Bicarbonate 21 mEq/L (21 mmol/L) ,Urinalysis Specific gravity; pH 5.0; negative dipstick; positive for calcium oxalate crystals. In addition to increasing fluid intake, which of the following is the most appropriate management?

Type 1 (hypokalemic distal) renal tubular acidosis. The most likely cause of this patient's laboratory findings is type 1 (hypokalemic distal) renal tubular acidosis (RTA). It is due to a defect in urine acidification in the distal nephron and is most commonly caused by decreased activity of the proton pump in collecting duct intercalated-A cells. Because of the inability to excrete hydrogen ions, patients develop a metabolic acidosis with compensatory hyperchloremia, resulting in a normal anion gap, which is 8 mEq/L (8 mmol/L) in this patient, and the inability to acidify urine below a pH of 6.0, even in the context of an acidemia. The urine anion gap (using the equation: [Urine Sodium + Urine Potassium] - Urine Chloride) would be positive in this case, reflecting decreased acid excretion in the form of ammonium and chloride. The same defects also cause potassium wasting, and the increased proximal resorption of citrate that occurs with metabolic acidosis leads to hypocitraturia and increased risk of calcium phosphate kidney stones and nephrocalcinosis. This patient most likely has Sjögren syndrome (arthralgia, sicca, parotid gland enlargement) with concomitant interstitial nephritis (echogenicity seen on kidney ultrasound), one of the most common diseases associated with a distal RTA.

A 40-year-old woman is evaluated for arthralgia, dry eyes, and dry mouth of several weeks' duration. She has been taking naproxen and acetaminophen daily for about 1 week. She has no pertinent personal or family history. On physical examination, vital signs are normal. Mucous membranes and conjunctivae are dry. Bilateral parotid gland enlargement is present. Laboratory studies: Creatinine 0.9 mg/dL (79.6 µmol/L) Electrolytes : Sodium 138 mEq/L (138 mmol/L) ,Potassium 3.1 mEq/L (3.1 mmol/L) ,Chloride 118 mEq/L (118 mmol/L) ,Bicarbonate 12 mEq/L (12 mmol/L) ,Glucose 74 mg/dL (4.1 mmol/L) ,Urinalysis pH 7.0; no blood, protein, glucose, erythrocytes, or leukocytes. Kidney ultrasound shows echogenic normal-sized kidneys.Which of the following is the most likely cause of the patient's laboratory findings?

Add hydrochlorothiazide. such as hydrochlorothiazide. Hypercalciuria is the most common metabolic risk factor for calcium oxalate stones. In patients with hypercalcemia, increased filtered calcium results in hypercalciuria. However, hypercalciuria is often idiopathic and commonly familial, occurring without associated hypercalcemia. Hypercalciuria due to hypercalcemia is treated by addressing the cause of increased serum calcium. In patients with other forms of hypercalciuria, thiazide diuretics reduce calcium excretion in the urine by inducing mild hypovolemia, triggering increased proximal sodium reabsorption and passive calcium reabsorption. This effect can be enhanced by the addition of sodium restriction.

A 42-year-old man is evaluated during a follow-up visit for kidney stones. He had his first stone 4 years ago. Despite increasing his water intake, he has had two additional episodes. Stone analysis has revealed only calcium oxalate. He is in otherwise good health. He has no history of urinary tract infections. There is no family history of kidney disease, hyperparathyroidism, or nephrolithiasis. The physical examination and vital signs are unremarkable. The patient weighs 80 kg (176 lb). Laboratory studies: Calcium 9.6 mg/dL (2.4 mmol/L), Creatinine 0.9 mg/dL (79.6 µmol/L) Electrolytes : Sodium 138 mEq/L (138 mmol/L) ,Potassium 4.1 mEq/L (4.1 mmol/L) ,Chloride 105 mEq/L (105 mmol/L) ,Bicarbonate 25 mEq/L (25 mmol/L) ,Urinalysis Specific gravity 1.008; pH 5.5; no blood, protein, leukocyte esterase, or nitrites 24-Hour Urine Studies: Volume 2945 mL pH 5.2 ,Calcium 320 mg/24 h (normal range, <320 mg/24 h) ,Citrate 790 mg/24 h (normal range, 300-1100 mg/24 h) ,Oxalate 32 mg/24 h (normal range, <40 mg/24 h) ,Sodium 140 mEq/24 h (normal range, 40-220 mEq/24 h) ,Uric acid 640 mg/24 h (normal range, <800 mg/24 h). Noncontrast helical CT scan shows a 4-mm stone in the lower pole of the left kidney and a 3-mm stone in the mid pole of the right kidney.Which of the following is the most appropriate next step to decrease this patient's stone recurrence?

No additional Management at this time. An ACE inhibitor and statin are appropriate for this patient with recently diagnosed primary membranous glomerulopathy. His kidney biopsy findings are consistent with the diagnosis, and the presence of anti-phospholipase A2 receptor (PLA2R) antibodies has been shown to approach 100% specificity for the primary form of this disease. Approximately one third of patients with primary membranous glomerulopathy experience a spontaneous remission of disease over the first 6 to 24 months without immunosuppression. Therefore, within the first 6 months of diagnosis, barring signs of severe complications of the nephrotic syndrome (such as kidney failure, anasarca, or deep vein thrombosis), the recommended strategy is to treat patients with primary membranous glomerulopathy conservatively with renin-angiotensin system blockers, cholesterol-lowering medications (if cholesterol is above goal), and diuretics (for edema). The patient is then monitored with examinations and laboratory studies to gauge for spontaneous remission. If proteinuria increases in 6 to 12 months, a course of immunosuppression should be considered for those with persistent nephrotic-range proteinuria. With the advent of serologic testing for anti-PLA2R antibodies, these titers can now be followed during the observation period alongside traditional clinical parameters, such as proteinuria. Falling anti-PLA2R titers are associated with remission, whereas persistently high titers are associated with ongoing disease activity.

A 44-year-old man is evaluated during a follow-up visit for membranous glomerulopathy, which was diagnosed last week on kidney biopsy. He has no other pertinent personal or family history. His only medication is furosemide. On physical examination, vital signs are normal. There is trace bilateral lower extremity edema to the ankles. The remainder of the examination is unremarkable. Laboratory studies performed before kidney biopsy: Albumin 3.0 g/dL (30 g/L) ,Total cholesterol 310 mg/dL (8.0 mmol/L) ,Creatinine 0.8 mg/dL (70.7 µmol/L) ,Antinuclear antibodies Negative ,Anti-phospholipase A2 receptor antibodies Titer: 1:80 ,Hepatitis B surface Ag and Ab antibodies Negative , Hepatitis C Ab antibodies Negative , HIV antibodies Negative ,24-Hour urine protein excretion 6500 mg/24 h. Ultrasound of the kidneys shows normal appearance with no evidence of thrombus in the renal veins. An ACE inhibitor and a statin are initiated. Which of the following is the most appropriate additional management?

Add Metolazone. Addition of the thiazide diuretic metolazone is the most appropriate treatment. Edema management in a patient with newly diagnosed nephrotic syndrome generally starts with a salt-restricted diet and an oral loop diuretic, with a goal weight loss of 1 to 2 kg (2.2-4.4 lb) per week. Loop diuretics should be uptitrated toward this weight loss goal until a maximal dose is achieved, with close monitoring of electrolytes. It is appropriate for blood urea nitrogen, serum creatinine, and serum urate to rise slightly (≤10%) with effective diuresis. When oral loop diuretics have been maximally uptitrated, and weight loss and edema control are insufficient, it is often necessary to add a second oral diuretic (a thiazide diuretic and/or potassium-sparing diuretic) that works distal to the loop of Henle, which in this case can be accomplished via the addition of metolazone in this patient taking maximal-dose furosemide.

A 45-year-old man is evaluated during a follow-up visit for membranous glomerulopathy diagnosed 3 weeks ago. He reports persistent lower extremity edema and no weight loss despite adhering to a low-salt diet and taking maximal-dose furosemide. He does not have shortness of breath or abdominal discomfort. Other medications are enalapril and simvastatin. On physical examination, vital signs are normal. The patient weighs 80 kg (176.4 lb), with a baseline weight of 75 kg (165.3 lb). There is no rash. Cardiac examination is normal, and there is no evidence of jugular venous distention. The lungs are clear on examination. There is pitting edema in the legs bilaterally to just below the patellae. Laboratory studies: Albumin 2.9 g/dL (29 g/L) ,Blood urea nitrogen Normal ,Creatinine 1.0 mg/dL (88.4 µmol/L) ,Electrolytes Normal ,Urinalysis No blood; 4+ protein ,Urine protein-creatinine ratio 6100 mg/g. Doppler ultrasound of the lower extremities performed 3 weeks ago showed no evidence of deep venous thrombosis. Which of the following is the most appropriate management?

Lifestyle modification. According to the American College of Cardiology/American Heart Association (ACC/AHA) blood pressure guideline, this patient has elevated blood pressure (BP), defined as systolic BP between 120-129 mm Hg and diastolic BP <80 mm Hg. Meta-analysis of observational studies has demonstrated that elevated BP and hypertension (systolic BP >130 mm Hg or diastolic BP >80 mm Hg) are associated with an increased risk of cardiovascular disease, end-stage kidney disease, subclinical atherosclerosis, and all-cause death. Nonpharmacologic therapy alone is especially useful for prevention of hypertension, including in adults with elevated BP, and for management of high BP in adults with milder forms of hypertension. Recommended lifestyle modifications include weight loss in adults with overweight or obesity; a heart-healthy diet that facilitates achieving a desirable weight; reduced sodium intake; high potassium intake (unless contraindicated by the presence of chronic kidney disease or use of drugs that reduce potassium excretion); increase in physical activity; and limiting alcohol consumption of standard drinks to no more than two (men) or one (women) per day.

A 46-year-old man is evaluated during a follow-up visit for elevated blood pressure. His average blood pressure with home blood pressure monitoring is 126/77 mm Hg. He has no other pertinent medical history and takes no medications. On physical examination, blood pressure is 128/78 mm Hg; other vital signs are normal. BMI is 28. The remainder of the examination is unremarkable. Which of the following is the most appropriate next step in management?

Calcium oxalate. This patient has classic symptoms of renal colic, including flank pain that radiates to the groin. Stone movement may result in pain migration to the genitalia. Nausea, vomiting, and dysuria may also be present. Microscopic hematuria is usually noted, although its absence does not exclude a stone. Patients with diarrhea who are volume depleted and have a metabolic acidosis are at increased risk for developing a kidney stone, particularly stones composed of calcium oxalate and uric acid. In this patient with Crohn disease and chronic diarrhea, the most likely composition of the stone is calcium oxalate because the chronic metabolic acidosis (suggested by the low serum bicarbonate concentration and relatively low urine pH) increases calcium loss from bone and decreases citrate excretion. Citrate is the major inhibitor of calcium crystallization in the urine. In addition, if there is concomitant fat malabsorption, a common occurrence in inflammatory bowel disease, calcium will bind to fat in the gut, allowing increased absorption of oxalate.

A 46-year-old man is evaluated in the emergency department for right flank pain that began 3 hours ago. He describes the pain as sharp and severe with radiation to the right testicle. History is significant for chronic diarrhea from Crohn disease; he has two to three loose bowel movements each day. He reports no nausea, vomiting, or abdominal pain. He has no dysuria. On physical examination, the patient appears uncomfortable. There is right costovertebral angle tenderness. Laboratory studies: Electrolytes : Sodium 138 mEq/L (138 mmol/L) ,Potassium 3.9 mEq/L (3.9 mmol/L) ,Chloride 106 mEq/L (106 mmol/L) ,Bicarbonate 21 mEq/L (21 mmol/L) ,Urinalysis Specific gravity 1.025; pH 5.5; moderate blood; no protein, leukocyte esterase, or nitrites. Kidney ultrasound shows a 6-mm stone at the right ureteral pelvic junction. Which of the following is the most likely composition of this patient's kidney stone?

Polydipsia. This patient has isovolemic hypotonic hyponatremia secondary to polydipsia. Isovolemia is documented by the presence of normal vital signs and physical examination findings. Hypotonicity is documented by the low calculated serum osmolality of 263 mOsm/kg H2O, using the following equation:Isovolemic hypotonic hyponatremia is secondary either to impaired dilution of urine or to water intake that exceeds the kidney's ability to excrete dilute urine. Urine osmolality distinguishes between these two entities. Urine osmolality <100 mOsm/kg H2O indicates excessive water intake, as seen with psychogenic polydipsia or poor solute intake. Because the kidney cannot excrete pure water, a minimal solute concentration of 50 mOsm/kg H2O is required. If solute intake is low while liquid intake remains high (as seen in beer potomania or chronic low food intake), water excretion is limited by available urinary solute.

A 48-year-old woman is evaluated in the emergency department for a 1-day history of hearing voices. History is significant for bipolar disorder. Medications are lithium carbonate and quetiapine. On physical examination, the patient is disheveled and looks chronically ill. She is alert and oriented but appears anxious. Blood pressure is 138/78 mm Hg, and pulse rate is 80/min without orthostatic changes. There is no edema. The remainder of the examination is normal. Laboratory studies: Blood urea nitrogen 6 mg/dL (2.1 mmol/L) Creatinine 0.9 mg/dL (79.6 µmol/L) Electrolytes : Sodium 126 mEq/L (126 mmol/L) ,Potassium 3.5 mEq/L (3.5 mmol/L) ,Chloride 94 mEq/L (94 mmol/L) ,Bicarbonate 26 mEq/L (26 mmol/L) ,Glucose 156 mg/dL (8.7 mmol/L) ,Urine sodium 12 mEq/L (12 mmol/L) ,Urine osmolality 96 mOsm/kg H2O. Which of the following is the most likely cause of this patient's hyponatremia?

Intravenous calcium. In addition to administration of 0.9% saline and furosemide, intravenous calcium is appropriate treatment for this patient with hypermagnesemia. Because the kidney can efficiently eliminate magnesium, hypermagnesemia occurs infrequently and most commonly results from excessive intake in the setting of decreased kidney function. Numerous medications such as antacids and laxatives contain magnesium, and magnesium sulfate is the treatment of choice for prevention of eclampsia. Hypermagnesemia is usually not associated with significant symptoms until the level is >7.2 mg/dL (2.9 mmol/L). Symptoms include somnolence, headache, loss of deep tendon reflexes, bradycardia, hypotension, and hypocalcemia. At levels >12 mg/dL (4.9 mmol/L), flaccid paralysis, respiratory failure, and complete heart block can occur. Hypermagnesemia is usually self-limited. Magnesium-containing medications should be discontinued, and magnesium excretion can be enhanced with saline diuresis. In patients with hypotension and significant neuromuscular deficits, treatment is aimed at direct antagonism of the effects of hypermagnesemia, which is accomplished by intravenous administration of calcium. After this, efforts to lower the serum level should be instituted. If kidney function is adequate, a trial of 0.9% saline and furosemide will increase kidney excretion. Magnesium-containing agents should be limited or avoided in individuals with kidney disease.

A 48-year-old woman is evaluated in the emergency department for lower extremity weakness, nausea, and increased somnolence occurring during the past 24 hours. She had constipation for 3 days, for which she drank one bottle of milk of magnesia each night. History is significant for hypertension as well as stage G4 chronic kidney disease secondary to autosomal dominant polycystic kidney disease. Her only medication is lisinopril. On physical examination, temperature is 36.6 °C (97.9 °F), blood pressure is 94/54 mm Hg, pulse rate is 58/min, respiration rate is 16/min, and oxygen saturation is 92% breathing ambient air. Bilateral flank fullness is present. Deep tendon reflexes are diminished diffusely. Strength in the lower extremities is 3/5. Laboratory studies: Calcium 8.0 mg/dL (2 mmol/L) ,Creatinine 3.9 mg/dL (344.8 µmol/L) Electrolytes : Sodium 138 mEq/L (138 mmol/L) ,Potassium 3.7 mEq/L (3.7 mmol/L) ,Chloride 104 mEq/L (104 mmol/L) ,Bicarbonate 22 mEq/L (22 mmol/L) ,Magnesium 8.1 mg/dL (3.3 mmol/L) ,Phosphorus 4.4 mg/dL (1.4 mmol/L). In addition to administration of 0.9% saline and furosemide, which of the following is the most appropriate treatment?

5% dextrose in 0.9% saline. for this patient who most likely has alcoholic ketoacidosis. Alcoholic ketoacidosis occurs in patients with chronic ethanol abuse, frequently with associated liver disease, and develops following an episode of acute intoxication. This patient has an increased anion gap metabolic acidosis (with an anion gap of 31), and ketoacidosis due to acute ethanol intoxication is the most likely cause. The ethanol level may be low or normal at the time of presentation because ingested ethanol may have already been extensively metabolized. Decreased insulin secretion (as a result of starvation) and increased counter-regulatory hormones cause lipolysis and generation of ketones, such as acetoacetate, which result in the anion gap. The urine in this case shows ketones, although ketone test results may be falsely negative in some cases because the nitroprusside reagent in the ketone assay detects only acetoacetate and the ketone β-hydroxybutyrate may predominate. Treatment with dextrose will increase insulin and decrease glucagon secretion, while saline will repair any volume deficit; the combination will correct ketoacidosis. In patients with alcoholism, thiamine should be administered before any glucose-containing solutions to decrease the risk of precipitating Wernicke encephalopathy.

A 49-year-old man is evaluated in the emergency department for abdominal pain, vomiting, and nausea after binge drinking. History is significant for alcohol abuse, with numerous hospitalizations for intoxications and withdrawal. On physical examination, temperature is normal, blood pressure is 122/72 mm Hg sitting and 100/62 mm Hg standing, pulse rate is 100/min sitting and 118/min standing, respiration rate is 22/min, and oxygen saturation is 97% breathing ambient air. BMI is 18. Abdominal examination reveals diffuse abdominal tenderness to palpation; there is no rebound tenderness, ascites, or evidence of trauma. Neurologic examination is normal. There is no edema. Laboratory studies: Electrolytes : Sodium 137 mEq/L (137 mmol/L) ,Potassium 3.7 mEq/L (3.7 mmol/L) ,Chloride 96 mEq/L (96 mmol/L) ,Bicarbonate 10 mEq/L (10 mmol/L) ,Ethanol 10 mg/dL (2.2 mmol/L) ,Glucose 94 mg/dL (5.2 mmol/L) ,Lactate 0.8 mEq/L (0.8 mmol/L) Arterial blood gases : pH 7.26 ,PCO2 23 mm Hg (3.1 kPa) ,Urinalysis Specific gravity 1.020; pH 5.5; positive ketones; no blood or cells. Thiamine and B-complex vitamin are administered. Which of the following is the most appropriate treatment?

Hemodialysis. Intermittent hemodialysis (IHD) is the most efficient way to correct this patient's hyperkalemia in the setting of anuric-oliguric acute kidney injury (AKI). IHD, typically delivered 3 to 6 times a week for 3 to 5 hours per session, allows for rapid correction of electrolyte disturbances and rapid removal of drugs or toxins. This patient has severe hyperkalemia with electrocardiographic changes, which should be corrected urgently to prevent lethal cardiac arrhythmias. Calcium, insulin, and dextrose are only temporizing measures and will not result in potassium removal from the body. Only dialysis will result in potassium removal from the body.

A 79-year-old woman is evaluated for hyperkalemia. She was admitted to the surgical ICU after having an urgent partial colectomy for a ruptured diverticulum with peritonitis. She was treated with intravenous fluids, antibiotics, and vasopressor therapy. Today, postoperative day 1, she is oliguric with urine output <5 mL/h for the past 4 hours. She is now weaned off the vasopressor therapy. History is significant for hypertension and stage G4 chronic kidney disease. Outpatient medications are amlodipine, irbesartan, and furosemide. Current medications are morphine, propofol, cefotaxime, and metronidazole. On physical examination, the patient is intubated and mechanically ventilated. A urinary catheter is in place. Temperature is 38.9 °C (102.0 °F), blood pressure is 108/70 mm Hg, and pulse rate is 101/min. There is generalized anasarca. The abdomen is distended and quiet. Laboratory studies: Creatinine 3.6 mg/dL (318.2 µmol/L); baseline, 2.0 mg/dL (176.8 µmol/L) Electrolytes : Sodium 142 mEq/L (142 mmol/L) ,Potassium 7.1 mEq/L (7.1 mmol/L) ,Chloride 102 mEq/L (102 mmol/L) ,Total bicarbonate 17 mEq/L (17 mmol/L) ,Arterial pH 7.25 ,Urine sediment Brown granular casts. Electrocardiogram shows peaked T waves with a QRS of 140 ms. In addition to intravenous calcium, insulin, and dextrose, which of the following is the most appropriate treatment?

Reassess serum creatinine level in 1 week. Some medications (such as cimetidine, trimethoprim, cobicistat, dolutegravir, bictegravir, and rilpivirine) reduce proximal tubule secretion of creatinine, resulting in increases in serum creatinine that are nonprogressive. This patient has chronic kidney disease (CKD), long-standing hypertension, and HIV infection. His antiretroviral medication regimen was recently adjusted to a once-a-day dosing, with the integrase inhibitor raltegravir discontinued and dolutegravir started 3 weeks ago. Dolutegravir is known to interfere with creatinine secretion without affecting glomerular filtration rate. Slight increases in serum creatinine of 0.2 to 0.3 mg/dL (17.7-26.5 µmol/L) may occur. This is more pronounced in those with preexisting CKD, in which creatinine secretion may contribute proportionately more to creatinine clearance. In patients with HIV taking the integrase inhibitors dolutegravir or bictegravir, the non-nucleoside reverse transcriptase inhibitor rilpivirine, or the pharmacokinetic enhancer (CYP3A inhibitor) cobicistat, serum creatinine elevations are nonprogressive and will remain unchanged within 1 to 2 weeks of initiation. Therefore, in the absence of other signs of kidney disease (hematuria, pyuria, or increasing proteinuria), reassessment of the serum creatinine level in 1 week will confirm the drug's effect in this patient. Further increases in serum creatinine levels will require additional evaluation.

A 50-year-old man is evaluated during a routine follow-up visit. History is significant for chronic kidney disease, long-standing hypertension, and HIV infection. His antiretroviral regimen was recently adjusted to a once-a-day dosing, with the integrase inhibitor raltegravir discontinued and dolutegravir started 3 weeks ago. In addition to dolutegravir, current medications are abacavir, lamivudine, and lisinopril. Physical examination and vital signs are normal. Laboratory studies: Serum creatinine 1.5 mg/dL (132.6 µmol/L); baseline, 1.3 mg/dL (114.9 µmol/L) ,Urinalysis No blood, protein, or erythrocytes ,Urine albumin-creatinine ratio 100 mg/g (unchanged from baseline). Which of the following is the most appropriate next step in management?

Lead nephropathy. which causes a chronic tubulointerstitial disease after years of continuous or intermittent lead exposure. Lead nephropathy can occur in patients with occupational exposure to lead or exposure to lead in water, soil, paint, or food products. Chronic lead nephropathy is frequently associated with hyperuricemia, hypertension, and recurrent gouty attacks. This patient's lead exposure is likely due to lead-contaminated moonshine. Contamination occurs when lead-containing car radiators are used to condense the alcohol during the distilling process. The initial diagnostic test is measurement of blood lead levels, although lead levels may have normalized if exposure has been reduced or stopped.

A 50-year-old man is evaluated for worsening right toe pain of 3 days' duration. He went to an urgent clinic 6 months ago for similar pain and was diagnosed with gout and hypertension. He has consumed illegally distilled alcohol (moonshine) for years. He is a native of Illinois, and his occupation history includes farming, tractor mechanic, and the postal service. His only medications are losartan and a 7-day course of ibuprofen for his previous gout attack. He reinitiated ibuprofen 2 days ago. On physical examination, blood pressure is 148/84 mm Hg. The right great toe is red, swollen, warm, and tender to touch. There are no tophi. The remainder of the examination is unremarkable. Kidney ultrasound shows echogenic but normal-sized kidneys bilaterally and no calculi. Laboratory studies: Creatinine 2.0 mg/dL (176.8 µmol/L) ,Urate 9.0 mg/dL (0.53 mmol/L) ,Urinalysis Specific gravity 1.009; pH 5.0; 2+ protein; 3-5 leukocytes/hpf; occasional fine granular and waxy casts , Urine protein-creatinine ratio 1200 mg/g. Which of the following is the most likely diagnosis?

Rosuvastatin. A statin is appropriate to treat dyslipidemia in this patient with stage G4 chronic kidney disease (CKD). Guidelines from the Kidney Disease: Improving Global Outcomes (KDIGO) group provide a grade 1A recommendation to treat adults aged ≥50 years with an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2, but not treated with chronic dialysis or kidney transplantation (GFR categories G3a-G5), with a statin or statin/ezetimibe combination. This recommendation largely emanates from results of the Study of Heart and Renal Protection (SHARP) trial, which included 9270 participants with CKD (mean eGFR, 27 mL/min/1.73 m2) who received simvastatin 20 mg plus ezetimibe 10 mg daily or placebo and were followed for 5 years. Statin plus ezetimibe therapy led to a significant 17% reduction in the relative hazard of the primary outcome of major atherosclerotic events (coronary death, myocardial infarction, nonhemorrhagic stroke, or any revascularization) compared with placebo (HR, 0.83; 95% CI, 0.74-0.94), driven by significant reductions in nonhemorrhagic stroke and coronary revascularization. It should be noted that simvastatin plus ezetimibe did not reduce the risk of progression to end-stage kidney disease. In addition, the 2018 American College of Cardiology/American Heart Association Guideline on the Management of Blood Cholesterol indicates that it is reasonable to initiate a moderate-intensity statin with or without ezetimibe in adults 40 to 75 years of age with CKD, an LDL cholesterol level of 70 to 189 mg/dL (1.7 to 4.8 mmol/L), and a 10-year atherosclerotic cardiovascular disease risk of ≥7.5%. The guideline recommends against initiating statin therapy in patients on dialysis, but it may be reasonable to continue statins in patients who are beginning dialysis therapy for advanced kidney disease.

A 51-year-old man is evaluated during a routine follow-up visit for stage G4 chronic kidney disease and hypertension. He is asymptomatic. Medications are valsartan, amlodipine, and furosemide. On physical examination, blood pressure is 140/70 mm Hg, and pulse rate is 70/min. BMI is 32. The remainder of the physical examination is noncontributory. Laboratory studies: HDL cholesterol 32 mg/dL (0.83 mmol/L) ,LDL cholesterol 119 mg/dL (3.08 mmol/L) ,Total cholesterol 208 mg/dL (5.39 mmol/L) ,Triglycerides 289 mg/dL (3.27 mmol/L). Which of the following is the most appropriate management for this patient's dyslipidemia?

Kidney biopsy. This patient with sepsis has developed AKI that has continued to worsen despite discontinuation of antibiotics 4 days ago. His urinalysis is notable for hematuria, pyuria, and proteinuria. The differential diagnosis includes ischemic or toxic acute tubular necrosis in the setting of hypotension, acute interstitial nephritis (AIN) from antibiotics or a proton pump inhibitor, and infection-associated glomerulonephritis. Given multiple potential contributing factors, a kidney biopsy is necessary to differentiate.

A 51-year-old man is evaluated in the hospital for acute kidney injury. He was admitted 14 days ago with sepsis and community-acquired pneumonia requiring mechanical ventilation. He was treated empirically with ceftriaxone and azithromycin; additional medications included omeprazole, insulin, and subcutaneous heparin. On hospital day 3, blood cultures were positive for Streptococcus pneumoniae, and ceftriaxone was continued. Hospital course was complicated by the ICU stay, with mechanical ventilation and pneumothorax requiring thoracostomy tube placement. On admission, his serum creatinine level was 1.0 mg/dL (88.4 µmol/L), increasing to 1.9 mg/dL (168 µmol/L) on hospital day 10; omeprazole and ceftriaxone were discontinued, and he was transferred to the floor. Today, hospital day 14, he is oliguric. History is significant for hypertension and diabetes mellitus. Outpatient medications are losartan and metformin. On hospital day 14, the patient is on 4-L oxygen by nasal cannula. A right-sided thoracostomy tube is in place. Temperature is 36.1 °C (97.0 °F), blood pressure is 145/78 mm Hg, pulse rate is 92/min, and respiration rate is 12/min. There are coarse rhonchi in the left lower lung field. The remainder of the examination is normal. Current (hospital day 14) laboratory studies: Creatinine 2.7 mg/dL (238.7 µmol/L) ,Fractional excretion of sodium 3% ,Urinalysis 2+ blood; 2+ protein; 5-10 erythrocytes/hpf; 5-10 leukocytes/hpf; 3-5 granular casts/hpf ,Urine protein-creatinine ratio 1100 mg/g. Kidney ultrasound is normal and without hydronephrosis. Which of the following is the most appropriate next step in management?

Hypomagnesemia. Symptoms of hypokalemia include weakness or paralysis; decreased gastrointestinal motility or ileus with nausea; and cardiac arrhythmias. This patient has symptomatic hypokalemia, presenting with lower extremity weakness and nausea. Hypokalemia can be caused by renal losses or nonrenal losses. In this case, the urine potassium is inappropriately high, pointing toward renal potassium wasting. Renal losses of potassium can occur with renal tubular acidosis; renal excretion of non-reabsorbable anions such as bicarbonate, hippurate, and ketones; drugs such as aminoglycosides or cisplatinum; Gitelman and Bartter syndromes; or hypomagnesemia. Hypomagnesemia is common, occurring in up to 12% of hospitalized patients. Chronic alcohol abuse results in excessive urinary excretion of magnesium and appears to reflect a reversible alcohol-induced tubular dysfunction. Intracellular magnesium is necessary to modulate the excretion of potassium through the potassium channel in the cortical collecting tubule. Hypomagnesemia results in loss of potassium through this channel. Importantly, the hypokalemia will be refractory to therapy until magnesium is repleted. Target levels for magnesium replacement are at least 2 mg/dL (0.83 mmol/L).

A 52-year-old woman is evaluated in the emergency department for a 2-day history of lower extremity weakness and nausea. She reports no diarrhea. History is significant for hypertension treated with amlodipine. She has a history of alcohol abuse. On physical examination, vital signs are normal. On neurologic examination, lower extremity strength is 4/5. The remainder of the examination is unremarkable. Laboratory studies: Albumin 3.0 g/dL (30 g/L) Calcium 8.4 mg/dL (2.1 mmol/L) ,Creatinine 0.7 mg/dL (61.9 µmol/L) Electrolytes : Sodium 136 mEq/L (136 mmol/L) ,Potassium 2.1 mEq/L (2.1 mmol/L) ,Chloride 104 mEq/L (104 mmol/L) ,Bicarbonate 26 mEq/L (26 mmol/L) ,Magnesium 1.4 mg/dL (0.58 mmol/L) ,Urine potassium 30 mEq/L (30 mmol/L). Which of the following is the most likely cause of this patient's hypokalemia?

Tunneled internal jugular central venous catheter. In patients with osteomyelitis, 6 weeks of antimicrobial therapy after surgical débridement is the preferred treatment course, and for most patients this requires long-term reliable venous access. However, this patient's advanced degree of kidney disease, relatively young age, and type 2 diabetes mellitus put her at high risk for progressing to end-stage kidney disease, and the upper extremity veins should be protected for future hemodialysis access creation. The American Society of Nephrology recommends nephrology consultation first before placing peripherally inserted central catheter (PICC) lines in patients with stage G3 to G5 CKD. PICCs are long catheters that are inserted peripherally and terminate in the central veins. PICCs are popular because of their ease of insertion and use. However, a national, population-based analysis revealed that PICCs placed before or after hemodialysis initiation were independently associated with lower likelihoods of transition to any working fistula or graft. PICC lines can lead to significant vein trauma and venous stenosis in the veins that may be used for arteriovenous fistula creation. This could impair blood flow through the fistula, impair maturation, and even lead to primary nonfunctioning of the hemodialysis access. Although central lines are associated with central venous stenosis, a central line is a better alternative than a PICC for long-term parenteral antibiotics because central lines are not inserted into a peripheral vein, which would be used for the creation of a hemodialysis site.

A 52-year-old woman is hospitalized for a toe ulcer and foot pain occurring for 1 month. History is significant for stage G4 chronic kidney disease (estimated glomerular filtration rate , 22 mL/min/1.73 m2) and type 2 diabetes mellitus. Medications are lisinopril, sevelamer, sodium bicarbonate, insulin glargine, and insulin aspart. On physical examination, vital signs are normal. A foul-smelling toe ulcer is present. Probe-to-bone test is positive. A plain radiograph shows changes compatible with osteomyelitis. The patient undergoes wound débridement and bone biopsy. Bone cultures are pending, and empiric antibiotic therapy is to be administered. Which of the following is the most appropriate venous access strategy?

Heparin. The most likely cause of this patient's elevated serum potassium level is heparin. Hypoaldosteronism caused by heparin, inhibitors of the renin-angiotensin system, type 4 renal tubular acidosis, or primary adrenal disease can cause hyperkalemia. Both unfractionated and low-molecular-weight heparin use is associated with a decrease in aldosterone synthesis. This occurs more frequently in patients with chronic kidney disease or diabetes mellitus, or in those taking an ACE inhibitor or angiotensin receptor blocker.

A 52-year-old woman was hospitalized 3 days ago for laparoscopic resection of the sigmoid colon secondary to recurrent diverticulitis. Diet has been advanced to a full diet. She has a 20-year history of hypertension, stage G3 chronic kidney disease, and migraine headaches. Medications are amlodipine, heparin, topiramate, and as-needed intravenous morphine. On physical examination, vital signs are normal. Mild incisional tenderness is present. The remainder of the physical examination is unremarkable. Laboratory studies: On Admission VS Today Creatinine 1.6 mg/dL (141.4 µmol/L) 1.9 mg/dL (168 µmol/L) Electrolytes : Sodium 140 mEq/L (140 mmol/L) 138 mEq/L (138 mmol/L) Potassium 4.9 mEq/L (4.9 mmol/L) 5.6 mEq/L (5.6 mmol/L) Chloride 102 mEq/L (102 mmol/L) 110 mEq/L (110 mmol/L) Bicarbonate 25 mEq/L (25 mmol/L) 20 mEq/L (20 mmol/L) Glucose 116 mg/dL (6.4 mmol/L) 128 mg/dL (7.1 mmol/L) Urine output during the past 24 hours is 1400 mL.Which of the following is the most likely cause of this patient's elevated serum potassium?

Light chain cast nephropathy. In multiple myeloma, acute kidney injury from light chain cast nephropathy is the most common type of kidney disease. Cast nephropathy is characterized by intratubular obstruction with light chain casts that can result in acute tubular injury. A clinical clue to the diagnosis is the presence of an elevated urine protein-creatinine ratio, with minimal proteinuria detected by dipstick urinalysis (dipstick urinalysis detects albumin but not light chains). Other supporting findings are the presence of anemia and hypercalcemia (when calcium measurement is corrected for albumin).

A 54-year-old woman is evaluated for a 4-week history of dyspnea on exertion, malaise, fatigue, and anorexia. History is significant for hypertension, gout, and osteoarthritis. Medications are losartan, hydrochlorothiazide, allopurinol, naproxen, and aspirin. On physical examination, blood pressure is 148/84 mm Hg, and pulse rate is 98/min; other vital signs are normal. Conjunctivae are pale. There is 2+ edema of the ankles. Laboratory studies: Hemoglobin 8.0 g/dL (80 g/L) ,Albumin 3.0 g/dL (30 g/L) ,Calcium 9.8 mg/dL (2.5 mmol/L) ,Creatinine 2.2 mg/dL (194.5 µmol/L); 3 weeks ago: 1.2 mg/dL (106.1 µmol/L) Total protein 8.4 g/dL (84 g/L) ,Urate 7.0 g/dL (0.41 mmol/L) ,Urinalysis 1+ protein; 2-5 granular casts/hpf; 1-2 erythrocytes/hpf ,Urine protein-creatinine ratio 6100 mg/g. Chest radiograph is normal. Which of the following is the most likely diagnosis?

D-lactic acidosis. D-lactic acidosis is an unusual cause of lactic acidosis that presents with an increased anion gap metabolic acidosis in patients with short-bowel syndrome, mostly in the context of small-bowel resection or jejunoileal bypass. D-lactate may accumulate when excess carbohydrates reach the colon and are metabolized to D-lactate by bacteria. Therefore, it is sometimes manifested after a large carbohydrate load. D-lactate is the stereoisomer of L-lactate, the isomer usually responsible for lactic acidosis. The conventional lactate assay measures the L-lactate isomer, and therefore lactic acid levels in this case are normal. Characteristic symptoms include intermittent confusion, slurred speech, and ataxia. The diagnosis should therefore be considered in a patient with characteristic neurologic findings who presents with an increased anion gap metabolic acidosis, normal lactate level, negative ketones, and short-bowel syndrome or other forms of malabsorption; it is confirmed by measuring a D-lactate level.

A 54-year-old woman is evaluated in the emergency department for ataxia, confusion, and slurred speech occurring for several days. History is significant for antiphospholipid antibody syndrome with superior mesenteric artery embolus 1 year ago that required resection of a large segment of the small bowel. Her only medication is warfarin. There is no history of over-the-counter medication use. On physical examination, blood pressure is 106/65 mm Hg, pulse rate is 95/min, and respiration rate is 20/min. The patient is confused, and her speech is slurred. She also has an unsteady, wide-based gait. Laboratory studies: Blood urea nitrogen 14 mg/dL (5.0 mmol/L) Electrolytes : Sodium 141 mEq/L (141 mmol/L) ,Potassium 3.8 mEq/L (3.8 mmol/L) ,Chloride 105 mEq/L (105 mmol/L) ,Bicarbonate 16 mEq/L (16 mmol/L) ,Glucose 99 mg/dL (5.5 mmol/L) ,Lactate 0.8 mEq/L (0.8 mmol/L) ,Osmolality 298 mOsm/kg H2O Arterial blood gases : pH 7.31 ,PCO2 33 mm Hg (4.4 kPa) ,Urinalysis No protein, ketones, cells, or crystals. Noncontrast CT of the head is normal. Which of the following is the most likely diagnosis?

Schedule a kidney biopsy. Clinical and laboratory features are often insufficient for definitive diagnosis of kidney disease. Kidney biopsy may therefore be essential for diagnosis and management. Indications include glomerular hematuria, severely increased albuminuria, acute or chronic kidney disease of unclear cause, and kidney transplant dysfunction or monitoring. In this case, the patient has an elevated serum creatinine without clear cause. Although further serologic testing may be done to guide diagnosis, a kidney biopsy will provide definitive diagnosis.

A 55-year-old man is evaluated for an increase in his serum creatinine level. History is significant for hypertension treated with lisinopril for 3 years. He reports no changes or additions to his medication regimen during the past year. On physical examination, the patient is afebrile, blood pressure is 145/92 mm Hg, and pulse rate is 84/min. There is no rash, alopecia, or joint abnormalities. The remainder of the examination is unremarkable. Laboratory studies: Complete blood count Normal ,Creatinine First specimen, 1.3 mg/dL (114.9 µmol/L); repeat specimen, 1.5 mg/dL (132.6 µmol/L); baseline 6 months ago, 0.9 mg/dL (79.6 µmol/L) ,Estimated glomerular filtration rate (eGFR) , using the Chronic Kidney Disease Epidemiology (CKD-EPI) Collaboration creatinine formula >60 mL/min/1.73 m2 ,Urinalysis Trace protein. Ultrasound reveals normal-sized kidneys with increased echogenicity, and no hydronephrosis or abnormalities of the collecting system are seen. Which of the following is the most appropriate management?

Sevelamer. Sevelamer is the most appropriate treatment for this patient with secondary hyperparathyroidism and hyperphosphatemia associated with stage G4 chronic kidney disease (CKD). Increased plasma parathyroid hormone (PTH) occurring as a result of CKD is referred to as secondary hyperparathyroidism. Increased PTH levels result in reduced calcium excretion and increased phosphorus excretion by the kidneys. Early in CKD, the PTH-induced increase in renal phosphorus excretion enables normal serum phosphorus levels despite reduced renal excretory capacity. However, as CKD progresses, the kidney is unable to compensate for the increased phosphorus, and phosphorus levels rise. This results in a vicious cycle as phosphorus stimulates PTH production. Initial treatment of secondary hyperparathyroidism in CKD stages G3 through G5 is correction of serum calcium, phosphorus, and vitamin D levels. Current Kidney Disease: Improving Global Outcomes (KDIGO) guidelines recommend that elevated phosphorus levels should be lowered toward the normal range, not into the normal range, because there is an absence of data showing that efforts to maintain phosphorus in the normal range are of benefit to CKD stage G3a to G4. Thus, treatment should be aimed at overt hyperphosphatemia, and decisions to start phosphate-lowering treatment should be based solely on progressively or persistently elevated serum phosphorus levels. KDIGO guidelines also recommend avoiding hypercalcemia. In this patient, treatment of hyperphosphatemia with a phosphate binder and a low phosphorus diet is indicated. Sevelamer is a non-calcium-containing binder that might improve bone turnover, limit vascular calcification, and reduce all-cause mortality, compared with calcium-containing binders, although these potential benefits have not been consistently proven.

A 56-year-old man is evaluated during a follow-up visit for diabetic nephropathy. He has a 15-year history of type 2 diabetes mellitus. Medications are insulin detemir, insulin aspart, lisinopril, furosemide, and atorvastatin. On physical examination, blood pressure is 129/76 mm Hg; other vital signs are normal. The remainder of the examination is unremarkable. Laboratory studies: Calcium 9.5 mg/dL (2.4 mmol/L) ,Phosphorus 7.2 mg/dL (2.3 mmol/L) ,Intact parathyroid hormone 385 pg/mL (385 ng/L) ,25-Hydroxyvitamin D 32 ng/mL (80 nmol/L) ,Estimated glomerular filtration rate 25 mL/min/1.73 m2. Which of the following is the most appropriate treatment?

Osmotic diuresis. Urea osmotic diuresis is the most likely cause of this patient's hypernatremia. This patient is recovering from acute kidney injury and is having a urea diuresis, with an elevated urine osmolality of 420 mOsm/kg H2O. In osmotic diuresis, urine osmolality is usually between 300 and 600 mOsm/kg H2O. The majority of the osmolality of the urine is made up of nonelectrolytes. This loss of electrolyte-free water is causing her serum sodium level to increase. The two major nonelectrolytes found in urine are urea and glucose. Her glucose is only 136 mg/dL (7.5 mmol/L), below the threshold for glucose appearing in the urine; therefore, the likely cause is excretion of urea. This can be confirmed by measuring urea in the urine.

A 56-year-old woman is evaluated for hypernatremia. She was admitted to the ICU 6 days ago for pyelonephritis and septic shock requiring intubation, administration of fluids, norepinephrine, and cefepime. She developed nonoliguric acute kidney injury. She has been weaned off the norepinephrine, and she has been extubated. Her serum sodium level has increased from 142 mEq/L (142 mmol/L) to 148 mEq/L (148 mmol/L) over the past 72 hours. Physical examination and vital signs are normal. Urine output is 2.5 L over the past 24 hours. Laboratory studies: Blood urea nitrogen 74 mg/dL (26.4 mmol/L) ,Creatinine 2.8 mg/dL (247.5 µmol/L) Electrolytes : Sodium 148 mEq/L (148 mmol/L) ,Potassium 3.7 mEq/L (3.7 mmol/L) ,Chloride 112 mEq/L (112 mmol/L) ,Bicarbonate 26 mEq/L (26 mmol/L) ,Glucose 136 mg/dL (7.5 mmol/L) ,Urine osmolality 420 mOsm/kg H2O. Which of the following is the most likely cause of this patient's hypernatremia?

Kidney transplant evaluation. is the most appropriate management for this patient with stage G4 chronic kidney disease (CKD). Referral to a kidney transplant center is indicated when the estimated glomerular filtration rate (eGFR) is <30 mL/min/1.73 m2. Kidney transplantation is the preferred treatment for patients with end-stage kidney disease, because it improves life expectancy and quality of life. It also provides a significant cost savings to the health care system compared with maintaining a patient on dialysis. Early referral allows adequate time to identify suitable living donors. If no living donor is available, early listing is essential to begin the waiting process for a deceased-donor kidney. Patients undergo an extensive health screening to identify potential issues that may affect the safety and/or outcome of the transplant. In the potential recipient, these include active malignancy, coronary ischemia, or active infections. An adequate social support system and financial resources also are important to ensure medication adherence and long-term survival of the transplanted allograft.

A 60-year-old woman is evaluated for fatigue and weakness. She reports no nausea or vomiting. History is significant for hypertension, stage G4 chronic kidney disease, and type 2 diabetes mellitus. Medications are labetalol, amlodipine, insulin glargine, insulin lispro, and sodium bicarbonate. On physical examination, blood pressure is 140/90 mm Hg; other vital signs are normal. A mature radiocephalic arteriovenous fistula (AVF) with a strong thrill and bruit is noted. There are no lung crackles. Trace pedal edema is present. Laboratory studies show normal serum bicarbonate and potassium levels, a blood urea nitrogen level of 50 mg/dL (17.8 mmol/L), and an estimated glomerular filtration rate of 18 mL/min/1.73 m2. Which of the following is the most appropriate management?

Vancomycin. The most common cause of hospital-acquired AKI is acute tubular necrosis (ATN), which represents damage and destruction of the renal tubular epithelial cells and is most commonly caused by ischemia or toxins. A careful evaluation of hemodynamics, volume status, medications, and physical findings of associated illness can help determine the cause of ATN. Most reported cases of vancomycin toxicity are due to acute interstitial nephritis; however, ATN has been reported. ATN is supported by the rapid rise in serum creatinine, fractional excretion of sodium >2%, and urine microscopy with numerous renal tubular epithelial cells and granular casts. Risk factors associated with vancomycin nephrotoxicity include chronic kidney disease, prolonged therapy, vancomycin doses ≥4 g/d, vancomycin trough concentrations >15 mg/L, and concomitant use of loop diuretics. Early recognition and prompt discontinuation of the drug are essential for renal recovery.

A 61-year-old woman is evaluated in the ICU for acute kidney injury. She was discharged from the hospital 10 days ago following elective cholecystectomy. Seven days ago she was readmitted to the hospital with sepsis. A CT scan of the abdomen with intravenous contrast did not show any abdominal pathology but confirmed pneumonia. She was treated with intravenous fluids, norepinephrine infusion, vancomycin, and cefepime. The norepinephrine was stopped yesterday. History is significant for hypertension and stage G3a chronic kidney disease. Her baseline serum creatinine is 1.4 mg/dL (123.8 µmol/L). On admission the serum creatinine was 1.9 mg/dL (168 µmol/L) and returned to baseline by hospital day 2; it is 3.1 mg/dL (274 µmol/L) today. Outpatient medications are lisinopril and chlorthalidone. On physical examination, temperature is 37.6 °C (99.7 °F), blood pressure is 140/82 mm Hg, pulse rate is 103/min, and respiration rate is 20/min. Examination of the lungs reveals bilateral crackles. There is 1+ pedal edema of the extremities. The remainder of the physical examination is noncontributory. Current laboratory studies: Serum creatinine 3.1 mg/dL (274 µmol/L) ,Vancomycin trough 25 mg/L ,Fractional excretion of sodium 2.5% ,Urinalysis Specific gravity 1.012; pH 5.5; no blood; 1+ protein; trace leukocyte esterase; no nitrites; no glucose; 2-4 leukocytes/hpf; 5-10 renal tubular epithelial cells/hpf; 5-10 coarse granular casts/hpf. Kidney ultrasound reveals normal-sized kidneys and no hydronephrosis.

Begin Lisinopril. The most appropriate next step in management is to begin lisinopril. The patient most likely has atherosclerotic renovascular disease, given his age, diminished pulses, and resistant hypertension despite treatment with four antihypertensive medications, including a diuretic. Most patients with renovascular disease have atherosclerosis (>90%). In this patient, medical therapy should be optimized to include treatment of underlying cardiovascular risk factors such as hypercholesterolemia and addition of an ACE inhibitor or angiotensin receptor blocker (ARB) for blood pressure control. Kidney function should be checked 2 weeks after the addition of an ACE inhibitor or ARB to ensure that the serum creatinine does not increase, and the ACE inhibitor or ARB can be continued if there is not a >25% rise in the serum creatinine from baseline.

A 65-year-old man is seen in the hospital for preoperative evaluation prior to an umbilical hernia repair. Medical history is significant for hypertension, hyperlipidemia, and chronic kidney disease. Medications are metoprolol, amlodipine, furosemide, hydralazine, simvastatin, and aspirin. On physical examination, average blood pressure is 150/96 mm Hg, and pulse rate is 54/min; other vital signs are normal. BMI is 26. Cardiac examination reveals no murmurs, gallops, or rubs. The lungs are clear. The abdomen is nontender, with a bruit heard over the umbilical region. Lower extremity pulses are diminished. The remainder of the examination is unremarkable. Laboratory studies: Creatinine 1.7 mg/dL (150.3 µmol/L); 3 months ago: 1.8 mg/dL (159.1 µmol/L) ,HDL cholesterol 46 mg/dL (1.2 mmol/L) ,LDL cholesterol 100 mg/dL (2.6 mmol/L) ,Total cholesterol 180 mg/dL (4.7 mmol/L) ,Urine albumin-creatinine ratio 300 mg/g. Abdominal ultrasound with Doppler reveals 75% ostial right renal artery stenosis; there is no aortic aneurysm.Which of the following is the most appropriate next step in management?

Age- and sex-appropriate cancer screening. The initial step in the management of newly diagnosed membranous glomerulopathy is to evaluate for secondary forms of the disease, which account for approximately 25% of cases. Some of this evaluation is often done in the prebiopsy screening laboratory tests (for example, screening for hepatitis B and C viruses, lupus, and syphilis). Secondary forms of membranous glomerulopathy correlate with age. Cancer screening is particularly important in evaluating for secondary forms of membranous glomerulopathy in patients over the age of 65 years. Up to 25% of such patients will have a malignancy discovered within 1 year of diagnosis, essentially accounting for all forms of secondary membranous glomerulopathy in this age group. This 68-year-old woman with newly diagnosed membranous glomerulopathy has a 50-pack-year history of smoking. She should be sent for age- and sex-appropriate cancer screening, which would include cervical cytology and human papillomavirus testing, mammography, colonoscopy, and low-dose chest CT.

A 68-year-old woman is evaluated during a follow-up visit for a 3-week history of the nephrotic syndrome. She otherwise has been well and reports no additional symptoms. She has a 50-pack-year history of cigarette smoking with ongoing tobacco use. On physical examination, vital signs are normal. Pitting edema to the ankles is present. The remainder of the examination is unremarkable. Laboratory studies: Albumin 2.9 g/dL (29 g/L) ,C3 Normal ,C4 Normal ,Creatinine Normal, Rapid plasma reagin Normal ,Antinuclear antibodies Negative ,Hepatitis B antibodies Negative ,Hepatitis C antibodies Negative ,24-Hour urine protein excretion 10,000 mg/24 h. Kidney ultrasound shows normal-appearing kidneys with no evidence of thrombus in the renal veins. Lower extremity Doppler ultrasound shows no evidence of deep venous thrombosis. Kidney biopsy shows membranous glomerulopathy with negative staining for the phospholipase A2 receptor (PLA2R) on immunofluorescence. Which of the following is the most appropriate management?

Staphylococcus aureus. Staphylococcus aureus is the most likely cause of this patient's infection-related glomerulonephritis (IRGN). This patient has acute kidney injury in the setting of cellulitis, with active urine sediment and low serum complement levels. The biopsy shows a proliferative glomerulonephritis on light microscopy with immunofluorescence of C3 and IgA and subepithelial hump-like deposits on electron microscopy, confirming a diagnosis of IRGN. In the developed world, the epidemiology of IRGN has drastically shifted over the past few decades, moving away from streptococcal-associated glomerulonephritides to infections caused primarily by S. aureus and, at a significantly lower rate, gram-negative bacteria. In this patient with cellulitis and IRGN occurring at the time of infection, S. aureus is the most likely culprit pathogen.

A 71-year-old man is evaluated in the hospital for an elevated serum creatinine level. He was hospitalized 2 days ago for a 4-day history of progressive right lower leg cellulitis. History is also significant for type 2 diabetes mellitus with prior episodes of cellulitis. Medications are basal and prandial insulin. On physical examination, temperature is 38.9 °C (102.0 °F), blood pressure is 150/100 mm Hg, pulse rate is 100/min, and respiration rate is 20/min. A well-defined area of tender erythema and edema is present over the right foot and leg to just below the knee. The remainder of the examination is unremarkable. Laboratory studies: Leukocyte count 13,500/µL (13.5 × 109/L) ,C3 50 mg/dL (500 mg/L) ,C4 12 mg/dL (120 mg/L) ,Creatinine On admission: 2.4 mg/dL (212.2 µmol/L); baseline: 1.1 mg/dL (97.2 µmol/L) Urinalysis 3+ blood; 3+ protein ,Urine protein-creatinine ratio 4100 mg/g. Kidney biopsy shows endocapillary proliferation on light microscopy, co-dominant granular staining for C3 and IgA on immunofluorescence microscopy, and subepithelial hump-like deposits on electron microscopy.Which of the following is the most likely cause of this patient's kidney disease?

Examination of the urine sediment. for cells and casts. This patient has developed oliguric acute kidney injury (AKI). He has multiple risk factors for AKI, including type 2 diabetes mellitus, recent coronary arteriography, hypotension, and cardiac surgery. The main consideration is whether the AKI is due to renal hypoperfusion (prerenal AKI) or whether the AKI is due to acute tubular necrosis (ATN). In the setting of diuretics, the fractional excretion of urea (FEUrea) is more accurate than the fractional excretion of sodium because urea excretion is not promoted by diuretics and is still retained in volume-depleted states. FEUrea is calculated using the equation:FEUrea = (UUrea × PCreatinine)/(UCreatinine × PUrea) × 100%. FEUrea <35% is suggestive of a prerenal state. The presence of granular casts and/or renal epithelial cells has strong predictive value for ATN. Urine microscopy can also help differentiate other causes of AKI, such as acute interstitial nephritis and glomerulonephritis.

A 72-year-old man is evaluated in the hospital after developing acute kidney injury 2 days following coronary artery bypass grafting. He is currently on mechanical ventilation and requires vasopressors for hypotension. He underwent coronary angiography 12 hours prior to surgery. The serum creatinine has increased from 0.8 mg/dL (70.7 µmol/L) at baseline to 2.2 mg/dL (194.5 µmol/L), and urine output has decreased to 350 mL/24 h. History is significant for type 2 diabetes mellitus and coronary artery disease. Current medications are intravenous furosemide, insulin, propofol, fentanyl, and norepinephrine. On physical examination, the patient is intubated and mechanically ventilated. A urinary catheter is in place. Temperature is 37.9 °C (100.2 °F), blood pressure is 98/60 mm Hg, pulse rate is 105/min, respiration rate is 28/min, and oxygen saturation is 96% on 30% FIO2. There is no rash. Decreased breath sounds are heard in the lung bases. The remainder of the examination is noncontributory. Which of the following is the most appropriate test to perform next?

Increase Furosemide. Increasing the furosemide dose is the most appropriate treatment in this patient with cardiorenal syndrome type 1 (CRS1). CRS is a disorder of the heart and kidneys in which acute or long-term dysfunction in one organ induces acute or long-term dysfunction in the other. CRS is characterized by the triad of concomitant decreased kidney function, diuretic-resistant heart failure with congestion, and worsening kidney function during heart failure therapy. CRS1 is defined as a worsening kidney function in patients with acute worsening of cardiac function (decompensated heart failure, acute coronary syndrome, cardiogenic shock). Management is challenging because treatment directed toward improving cardiac function can worsen kidney function. For this patient, an increase to his loop diuretic dose to a sufficient dose to induce a diuresis is appropriate. Among patients with decompensated heart failure, the best outcomes may occur with aggressive fluid removal even if associated with mild to moderate worsening of kidney function. An elevated blood urea nitrogen (BUN)-creatinine ratio should not discourage the use of diuretic therapy in patients with evidence of congestion. The decline in his kidney function with relative increase in BUN-creatinine ratio reflects the CRS1 physiology, rather than volume depletion due to diuresis.

A 72-year-old man is hospitalized for a 1-week history of worsening shortness of breath; he also has worsening lower extremity edema despite an increase in his furosemide dose 2 days ago. History is significant for hypertension, stage G3a chronic kidney disease, and heart failure with a preserved ejection fraction. Outpatient medications are amlodipine, lisinopril, furosemide, and low-dose aspirin. On physical examination, blood pressure is 112/60 mm Hg, and pulse rate is 97/min. BMI is 28. Cardiac examination reveals an elevated jugular venous pressure and an S4. Breath sounds are diminished at the lung bases. There is 2+ pitting edema of the lower legs. Laboratory studies: Blood urea nitrogen 64 mg/dL (22.8 mmol/L); 2 weeks ago, 40 mg/dL (14.3 mmol/L) ,Creatinine 2.3 mg/dL (203.3 µmol/L); 2 weeks ago, 1.9 mg/dL (168 µmol/L) ,Sodium 130 mEq/L (130 mmol/L); 2 weeks ago, 133 mEq/L (133 mmol/L) ,Urinalysis Specific gravity 1.009; 1+ protein; few hyaline casts. Chest radiograph shows bibasilar effusions and vascular congestion. Which of the following is the most appropriate treatment?

Make no changes to antihypertensive medications. According to target blood pressure goals recommended by the American College of Physicians and the American Academy of Family Physicians, this 72-year-old woman's blood pressure is at target, and no changes are necessary. This guideline recommends that antihypertensive drugs be initiated in patients ≥60 years old if blood pressure is >150/90 mm Hg, with a goal of reducing systolic blood pressure to <150 mm Hg to reduce the risk for mortality, stroke, and cardiac events. The guideline further recommends that physicians consider initiating or intensifying pharmacologic treatment in patients ≥60 years of age with a history of stroke or transient ischemic attack to achieve a target systolic blood pressure <140 mm Hg to reduce the risk for recurrent stroke. The guideline also recommends considering the initiation or intensification of pharmacologic treatment in some patients ≥60 years of age at high cardiovascular risk, based on individualized assessment, to achieve a target systolic blood pressure <140 mm Hg to reduce the risk for stroke or cardiac events. These recommendations are based on evidence that demonstrates the greatest absolute benefit of antihypertensive therapy is seen in patients with the highest blood pressure and cardiovascular risk.

A 72-year-old woman is evaluated during a routine visit. History is significant for hypertension treated with amlodipine and losartan. She has no other medical problems. She remains physically active and routinely plays tennis and golf. On physical examination, blood pressure is 142/84 mm Hg, and pulse rate is 72/min; other vital signs are normal. BMI is 24. The remainder of the examination is unremarkable. Laboratory studies show a serum creatinine level of 0.8 mg/dL (70.7 µmol/L) and a serum potassium level of 4.0 mEq/L (4.0 mmol/L). According to the target blood pressure goals recommended by the American College of Physicians and the American Academy of Family Physicians, which of the following would be an appropriate management?

Anti-glomerular basement membrane antibody. The most appropriate diagnostic test to perform next is anti-glomerular basement membrane (GBM) antibodies. This patient presents with a rapidly progressive glomerulonephritis (RPGN), an acute and steep rise in serum creatinine accompanied by hematuria and proteinuria. The differential diagnosis for RPGN is divided histologically into three patterns on immunofluorescence microscopy of the kidney biopsy: pauci-immune staining (for example, ANCA-associated glomerulonephritis), linear staining (for example, anti-GBM antibody disease), and granular staining (for example, lupus nephritis). The patient's positive antimyeloperoxidase (MPO) antibodies predict that she will have pauci-immune staining on the biopsy, but the linear staining on her biopsy is more consistent with anti-GBM antibody disease. Therefore, testing for anti-GBM antibodies is required to confirm this diagnosis, although treatment for her condition should not be delayed while awaiting results. One in three patients with anti-GBM antibody disease will have positive ANCA serologies, usually MPO antibodies (or p-ANCA in older assays). This combined seropositivity is most commonly seen in the subset of anti-GBM patients who are older women, as in this case. Diagnosing anti-GBM antibody disease could affect treatment decisions in this case, particularly whether to pursue plasmapheresis, which is indicated for all cases of anti-GBM antibody disease. For ANCA-associated glomerulonephritis, plasmapheresis is reserved for those with alveolar hemorrhage and/or severe kidney failure (defined as requiring dialysis or a serum creatinine >5.8 mg/dL [512.7 µmol/L]).

A 73-year-old woman is hospitalized for an elevated serum creatinine level that has been unresponsive to intravenous fluids. She was evaluated in the emergency department 2 days ago for weakness, myalgia, arthralgia, and cough and admitted to the hospital. She has no other medical history and takes no medications. On physical examination, the patient is afebrile. Blood pressure is 155/95 mm Hg, pulse rate is 70/min, and oxygen saturation is 98% breathing 2 L of oxygen per minute by nasal cannula. Cardiac examination is normal, without evidence of jugular venous distention. Dullness to percussion and diminished breath sounds are present at the posterior lung bases bilaterally. There is pitting lower extremity edema. Laboratory studies: Hemoglobin 9.9 g/dL (99 g/L) Creatinine Baseline 6 months ago: 0.7 mg/dL (61.9 µmol/L); Emergency department: 4.1 mg/dL (362.4 µmol/L); Hospital day 1: 4.3 mg/dL (380.1 µmol/L) Antinuclear antibodies Negative ,Antimyeloperoxidase antibodies Positive ,Antiproteinase 3 antibodies Negative ,Urinalysis 3+ blood; 2+ protein. Chest radiograph shows diffuse infiltrates at the lung bases bilaterally. Kidney biopsy shows necrotizing and crescentic glomerulonephritis with linear staining for IgG on immunofluorescence. Which of the following is the most appropriate diagnostic test to perform in this patient?

Pyroglutamic acidosis. Pyroglutamic acidosis, which presents with mental status changes and an increased anion gap, occurs in selected patients receiving therapeutic doses of acetaminophen on a chronic basis. Susceptible patients are those with critical illness, poor nutrition, liver disease, or chronic kidney disease, as well as those on a strict vegetarian diet. In this context, acetaminophen leads to depletion of glutathione, altering the γ-glutamyl cycle to overproduce pyroglutamic acid (also known as 5-oxoproline). Diagnosis can be confirmed by measuring urine levels of pyroglutamic acid.

A 79-year-old woman is evaluated in the emergency department for worsening confusion over the past 5 days. She also reports lower back pain for the past 3 months. History is significant for hypertension and coronary artery disease with stenting of the left anterior descending artery 2 years ago. Daily medications are metoprolol, hydrochlorothiazide, atorvastatin, low-dose aspirin, and acetaminophen. Her husband confirms that the patient takes all medications as directed. On physical examination, temperature is normal, blood pressure is 128/76 mm Hg, pulse rate is 72/min, respiration rate is 20/min, and oxygen saturation is 95% on ambient air. BMI is 19. There is no abdominal pain. The patient is weak, confused to time and place, and sleepy but easily arousable. The remainder of the neurologic examination is normal. Laboratory studies: Blood urea nitrogen 35 mg/dL (12.5 mmol/L) Creatinine 1.4 mg/dL (123.8 µmol/L) Electrolytes : Sodium 138 mEq/L (138 mmol/L) ,Potassium 4.8 mEq/L (4.8 mmol/L) ,Chloride 102 mEq/L (102 mmol/L) ,Bicarbonate 14 mEq/L (14 mmol/L), Lactate 0.7 mEq/L (0.7 mmol/L) Arterial blood gases : pH 7.31 ,PCO2 29 mm Hg (3.9 kPa) ,Urinalysis Specific gravity 1.025; no protein, ketones, cells, or crystals Which of the following is the most likely diagnosis?

Intra-abdominal pressure (IAP) measurement. This patient's findings are consistent with abdominal compartment syndrome, which occurs in the setting of abdominal surgery, large volume fluid resuscitation, and multiple transfusions. It can manifest as a distended abdomen, ascites, and sodium-avid acute kidney injury (AKI). The increased IAP causes direct compression of renal parenchyma and vasculature, resulting in oliguria and decreased glomerular filtration rate. The diagnosis of abdominal compartment syndrome is made by an IAP measurement >20 mm Hg and new organ dysfunction. Indirect measurement of IAP can be with intragastric, intracolonic, intravesical (bladder), or inferior vena cava catheters. Management includes supportive therapy, abdominal compartment decompression, and correction of positive fluid balance.

An 18-year-old man is evaluated in the ICU for oliguric acute kidney injury. Eighteen hours ago he underwent hepatectomy for a giant fibrolamellar hepatic carcinoma. During the procedure he developed coagulopathy and hepatic bleeding and required resuscitation with eight units of packed red blood cells, multiple units of fresh frozen plasma, and several liters of crystalloid fluids. He is receiving cefepime, gentamicin, propofol, and fentanyl. Urine output has decreased to 10 mL/h since ICU admission 14 hours ago. On physical examination, the patient is mechanically ventilated. Blood pressure is 120/70 mm Hg, pulse rate is 115/min, and respiration rate is 12/min. Breath sounds are decreased bilaterally. The abdomen is distended and tense with intact midline incision and wall edema. The remainder of the examination is noncontributory. Laboratory studies: Hemoglobin 10 g/dL (100 g/L) ,Creatine kinase 1250 U/L ,Creatinine 1.7 mg/dL (150.3 µmol/L); on admission: 0.9 mg/dL (79.6 µmol/L) ,Potassium 5.2 mEq/L (5.2 mmol/L) ,Urine sodium <20 mEq/L (20 mmol/L) ,Urinalysis Specific gravity 1.030; pH 5.5; 4+ blood; trace protein; too numerous to count erythrocytes; few hyaline casts. Kidney ultrasound reveals normal-sized kidneys and no hydronephrosis; a large volume of ascites is noted. Which of the following is the most appropriate diagnostic test to perform next?

Kidney biopsy. A kidney biopsy is the most appropriate next step for this patient who has the nephrotic syndrome most likely caused by minimal change glomerulopathy (MCG). MCG is the cause of the nephrotic syndrome in 10% to 15% of adults, with a significantly higher incidence in elderly patients (≥65 years of age) and very elderly patients (≥80 years of age). Most cases are idiopathic, but secondary causes must be considered in adults, including medications such as NSAIDs. Adults with MCG present with acute kidney injury (AKI) in up to 25% of cases. Factors associated with AKI include older age, male sex, hypertension, low serum albumin levels, and heavier proteinuria. The differential diagnosis for the nephrotic syndrome with AKI is limited to only a few entities: MCG with acute tubular necrosis or allergic interstitial nephritis, membranous glomerulopathy with bilateral renal vein thrombosis, amyloidosis with cast nephropathy, and collapsing focal segmental glomerulosclerosis. A kidney biopsy is therefore required to make the correct diagnosis.

An 81-year-old man is hospitalized for an acute onset of edema in his legs and abdomen. History is significant for chronic back pain, for which he takes daily ibuprofen. He has no other symptoms. On physical examination, vital signs are normal. There is no rash. Cardiac examination is without extra sounds or murmurs, and the estimated central venous pressure is normal. The lungs are clear on examination. Ascites is noted. There is 3-mm pitting edema of the extremities to the mid thigh. Laboratory studies: Albumin 2.1 g/dL (21 g/L) ,Creatinine 2.9 mg/dL (256.4 µmol/L) ,Electrolytes Normal ,Urinalysis No blood; 4+ protein , Urine protein-creatinine ratio 7200 mg/g , 24-Hour urine output 1.5 L. Doppler ultrasound of the kidneys is unremarkable.Which of the following is the most appropriate next step in management?