Nephrology - Case Studies

A 65-year-old man with a history of smoking, hypertension, and peripheral vascular disease was admitted 3 days earlier for unstable angina. He underwent a cardiac catheterization and three- vessel coronary bypass grafting 48 hours prior to your call from the intern. His postoperative course was complicated by a subendocardial infarction but was otherwise unremarkable until yesterday when his urine output began to drop (150 cc in 24 hours). His serum creatinine was noted to be 3.5 mg/dL (1.2 mg/dL on admission). The patient is intubated and can give no history. Medications include digoxin, lasix, enalapril, IV nitroglycerin, atenolol, and perioperative cefazolin. For which type(s) of acute renal failure is this patient MOST at risk? (A) prerenal and intrarenal (B) intrarenal only (C) postrenal (D) not at risk for acute renal failure (E) cannot be determined from the information provided

(A) Acute renal failure can be classified as prerenal, intrarenal, or postrenal. The most common causes of prerenal ARF are diseases and disorders that (a) cause a decline in effective circulating volume, such as hemorrhage, GI losses, dehydration, excessive diuresis, burns, trauma, and peritonitis; (b) cause a change in systemic vascular resistance, such as sepsis, anesthesia, anaphylaxis; some medications such as ACE inhibitors and NSAIDs; and renal artery stenosis; or (c) cause a decline in cardiac output, such as CHF and shock. Intrarenal causes of ARF include diseases and disorders that cause acute tubular necrosis (ATN) (toxins such as aminoglycosides, contrast media, chemotherapy, massive hemolysis, rhabdomyolysis, hyperuricemia; or intrarenal vasoconstriction due to seizures, cocaine, and alcohol), AIN (some medications, such as penicillin, cephalosporins, sulfonamides, diuretics, NSAIDs, phenytoin, and allopurinol; some infections such as cytomegalovirus (CMV), histoplasmosis, Rocky Mountain Spotted Fever; and some diseases such as systemic lupus erythematosus (SLE), Sjogren's syndrome, and sarcoidosis), and glomerulonephritis (autoimmune disorders, malignant HTN, thrombotic thrombocytic purpura (TTP), and hemolytic uremic syndrome (HUS)). Postrenal causes are the least common etiology of ARF and include obstruction due to benign prostatic hypertrophy (BPH), mass, or bilateral renal calculi. This patient has several risk factors for developing ARF: recent cardiac arrest with a period of decreased effective circulating volume, recent administration of contrast dye during the cardiac catheterization and anesthesia during the bypass surgery, and he is on an ACE inhibitor and a diuretic. All of these place him at risk for either prerenal or intrarenal ARF, most likely ATN. Since he is at risk for both, the best way to determine the cause is to analyze the urine, specifically looking for cells and casts, the specifics of which will help determine the etiology. He is at negligible risk for postrenal ARF as he has no history of BPH. Bilateral obstructing renal calculi would be extremely rare and, though possible, a mass is unlikely to be causing his ARF given the preponderance of other risk factors. In ARF, the serum creatinine increases about 1 to 2 mg/dL/day. (McMillan, 2007; Watnick and Morrison, 2009, pp. 797-801)

Which of the following treatments for hyperkalemia works by redistributing potassium from the blood into the cell? (A) sodium polystyrene sulfonate po (B) insulin and D5W IV (C) low potassium diet (D) calcium gluconate IV (E) hemodialysis

(B) Hyperkalemia can be treated by three mechanisms: antagonizing the effect on the cell membrane, which can be achieved by infusing calcium gluconate 10 to 30 mL of 10% solution IV; redistributing potassium from the blood into the cell, which can be accomplished by infusing sodium bicarbonate 44 to 132 mEq IV or regular insulin along with glucose (5-10 g of glucose per unit of insulin); or removing it by giving sodium polystyrene sulfonate (Kayexalate) po or via retention enema or by initiating hemo- or peritoneal dialysis. Insulin acts to drive potassium into the cell but must be given with glucose to avoid significant hypoglycemia. (Cho et al., 2009, pp. 775-776)

The most serious consequence of rapid correction of hyponatremia is (A) brainstem herniation (B) central pontine myelinolysis (C) muscle cramps (D) hypernatremia (E) fluid overload

(B) Hyponatremia is defined as a serum sodium concentration of <130 mEq/L. Common causes include dehydration, diarrhea, vomiting, overuse of diuretics, syndrome of inappropriate ADH, postoperative state, hypothyroidism, congestive heart failure (CHF), liver disease, and pulmonary disease. Rapid correction of hyponatremia can result in severe brain damage, including central pontine myelinolysis. For this reason, the serum sodium concentration in those patients displaying neurological symptoms should be increased by no more than 1 to 2 mEq/L/h and no more than 25 to 30 mEq/L in the first 2 days. Once neurological symptoms improve, the rate of increase should be decreased to 0.5 to 1 mEq/L/h. (Cho et al, 2009, pp. 767-770)

Large numbers of epithelial cells on urine sediment indicate (A) UTI (B) acute tubular necrosis (C) sample contamination (D) vaginitis in women (E) prostatitis in men

(C) Squamous epithelial cells line the distal portion of the urethra in men and the entire urethra in women. They appear in the urine due to inadequate cleaning of the external urinary meatus prior to obtaining the sample and indicate that the sample is contaminated. In women, the source is usually vaginal/perineal. Uncircumcised men commonly have squamous epithelial cells in the urine sample. (McBride, 1998, p. 103)

Which of the following is diagnostic of nephrotic syndrome? (A) hypoalbuminemia, hypolipidemia, proteinuria >10 g/24 h (B) hypoalbuminemia, hyperlipidemia, proteinuria >1 g/24 h (C) hypoalbuminemia, hyperlipidemia, proteinuria >2 g/24 h (D) hypoalbuminemia, hyperlipidemia, proteinuria >3.5 g/24 h (E) normal albumin, hyperlipidemia, proteinuria >10 g/24 h

(D) Nephrotic syndrome is defined as proteinuria >3.5 g/24 h resulting in hypoalbuminemia (<3.0 g/dL), hyperlipidemia (total cholesterol >250 mg/dL), and edema, probably due to increased renal tubule permeability. Causes include diabetic nephropathy, HIV nephropathy, chronic hepatitis B and C, amyloidosis, systemic lupus erythematosus, constrictive pericarditis, Hodgkin's disease, minimal change disease, and many medications, including phenytoin and NSAIDs. (Watnick and Morrison, 2009, pp. 815-817)

A unilateral small kidney on ultrasound would suggest which of the following etiologies? (A) polycystic kidney disease (B) hypertensive nephrosclerosis (C) diabetic nephropathy (D) renal artery stenosis (E) malignancy

(D) Renal artery stenosis causes compromised blood flow to the kidney, resulting in atrophy. Frequently, the contralateral kidney will hypertrophy in an attempt to compensate for the declining GFR. Polycystic kidney disease results in enlarged kidneys due to growth of multiple cysts. Hypertensive nephrosclerosis and diabetic nephropathy affect both kidneys equally and would result in bilateral, not unilateral, cortical atrophy. Malignancy would not result in atrophy. (Watnick and Morrison, 2009, pp. 805, 810)

Which of the following complications are associated with Stage III kidney disease? (A) no notable complications (B) acid-base abnormalities (C) hypertension only (D) anemia, disorders of calcium and phosphorus metabolism (E) fluid and electrolyte abnormalities

(D) Stage III: GFR 30 to 59 mL/min; complications include anemia, HTN, malnutrition, disorders of calcium and phosphorous metabolism, reduced functioning and well-being, neuropathy; screen for and treat complications as appropriate, avoid nephrotoxins, control cardiovascular risk factors, adjust doses of renally excreted medications. (NKF-K/DOQI

How often should patients with diabetes mellitus be screened for microalbuminuria? (A) once a month (B) every 3 months (C) every 6 months (D) once a year (E) there is no specific timetable

(D) The American Diabetes Association (ADA) recommends checking urine for microalbumin 5 years after the diagnosis is made and once a year thereafter to screen for diabetic nephropathy in patients with type I diabetes mellitus. For patients with type II diabetes mellitus, the ADA recommends checking the urine at the time of the diagnosis and yearly thereafter. (American Diabetes Association, 2009, p. 533)

A 32-year-old woman presents for a routine physical examination. She feels well with no specific complaints. On physical examination, her blood pressure is noted to be 154/92 mm Hg. You note slight fullness to the abdomen on palpation without tenderness or obvious mass. Routine labs are ordered, including a UA, with the following results: BUN 12 Creatinine 0.8 UA and sediment analysis: 2+ blood, trace protein, negative leukocyte esterase, negative nitrite; 10 to 20 red blood cells (RBCs) per high power field (HPF), no leukocytes, bacteria, or other cells; rare granular cast What is the most likely cause of the hematuria? (A) urinary tract infection (B) glomerulonephritis (C) renal calculi (D) urinary sample contamination (E) polycystic kidney disease

(E) Polycystic kidney disease (PKD) is an autosomal dominant disorder that affects approximately 500,000 patients in the United States, occurring in about 1 in 800 live births. Fifty percent of patients will reach ESRD by age 60, and PKD accounts for approximately 10% of hemodialysis patients. It is the most common hereditary disorder to result in ESRD. Family history is positive in 75% of cases, but genetic mutations can occur spontaneously, and patients can present without a family history. Signs and symptoms of PKD include abdominal fullness due to enlarged kidneys, abdominal pain due to bleeding into cysts, microscopic or gross hematuria, depending on the extent of the disease, and hypertension. Patients are often asymptomatic, and the first signs of the disease may be hypertension, microscopic hematuria, and mild proteinuria. Abdominal fullness and pain occur later in the disease, as the number and size of cysts increase. Ultrasound is the diagnostic test of choice to detect PKD: three or more cysts in patients younger than 30, three or more cysts in each kidney in patients 30 to 59 years of age, and five or more cysts in each kidney in patients older than 60 are the diagnostic criteria. Complications include pain, gross hematuria from a ruptured cyst, infected cysts, nephrolithiasis, HTN, and cerebral aneurysms (10% to 15% of patients have arterial aneurysms in the Circle of Willis). There is no effective treatment. Good control of blood pressure and a low protein diet may slow disease progression. There are two distinct genotypes of PKD—PKD1 and PKD2. The disease progresses more slowly in the latter. Urinary tract infection would not fit this patient scenario, as she has no dysuria, and UA is negative for leukocytes, leukocyte esterase, nitrites, and bacteria. Renal calculi would not cause abdominal fullness and hypertension and would be symptomatic on presentation. The urine sample is not contaminated as there are no squamous epithelial cells reported. In the absence of RBC casts and clinical signs and symptoms, this would not be glomerulonephritis. (Watnick and Morrison, 2009, pp. 824-825)

The organism responsible for most cases of peritonitis in patients on peritoneal dialysis is (A) Candida albicans (B) Escherichia coli (C) Streptococcus pneumoniae (D) Pseudomonas aeruginosa (E) Staphylococcus aureus

(E) S. aureus is the organism responsible for most cases of peritonitis in patients on peritoneal dialysis. Overall, gram-positive organisms are responsible for 50% of cases, and gram-negative organisms cause 15% of cases. Four percent of cases are polymicrobial in nature. Improper technique by the patient in making catheter connections during dialysis exchanges is the reason for bacterial inoculation in most cases. Abdominal pain, fever, and cloudy dialysis fluid are the presenting symptoms and signs. (Burkart, 2008)

hereditary nephritis causes hematuria, renal failure and deafness, +/- eye involvement with family h/o hematuria

Alport syndrome

When adjusting medication dosing for patients with CKD, which of the following factors is the LEAST important? (A) serum blood urea nitrogen (BUN) level (B) serum creatinine level (C) age (D) weight (E) gender

(A) Because many drugs are excreted in the urine, knowledge of the renal function is important when dosing medication, especially in patients with abnormal GFR. Drug toxicity or adverse side effects may occur if the drug is dosed improperly. Estimation of the creatinine clearance can help in making the proper drug adjustment for the degree of CKD. In a steady state (ie, stable creatinine), the Cockcroft-Gault equation can be used to estimate creatinine clearance. The formula is.. see image below... In female patients, the result is multiplied by 0.85 because of smaller muscle mass. Appropriate medication adjustments can be made based on the estimated creatinine clearance. The MDRD (modification of diet in renal disease) equation is the most accurate indicator of GFR, utilizing serum creatinine level, age, gender, and race, and it also eliminates the need for a 24-hour urine collection, which is cumbersome and inconvenient. The equation can be accessed online at www.kdoqi.org. The blood urea nitrogen is not a reliable index, because several factors may alter tubular reabsorption of, or generation of, urea. These include the patient's hydration status, protein intake, and degree of catabolic activity occurring. (Levey, 1998, p. 23; Watnick and Morrison, 2009, p. 796)

Which of the following is a potential complication of acute pyelonephritis? (A) perinephric abscess (B) renal vein thrombosis (C) allergic interstitial nephritis (D) struvite stones (E) hepatic failure

(A) Because pyelonephritis is an infectious disease, the most likely complication is a perinephric abscess, which occurs as the result of inadequate therapy. Since it is not vascular in origin, renal vein thrombosis would not occur. Allergic interstitial nephritis is caused by an antigen-antibody reaction, which does not occur with acute pyelonephritis. Struvite stones are due to chronic infection with urease-producing organisms, such as Proteus and Pseudomonas, not to an acute infection. Hepatic failure can be a complication of acute renal failure, but not acute pyelonephritis. (Stoller et al., 2009, p. 830)

Which of the following urinary findings is suggestive of acute glomerulonephritis? (A) red cells and red cell casts (B) white cells and white cell casts (C) renal tubular epithelial cells (D) oval fat bodies (E) hyaline casts

(A) Casts in the urine indicate a pathologic process, with the exception of the presence of the rare hyaline cast (1 to 2/HPF). The acute inflammatory process of glomerulonephritis is characterized by red cells and red cell casts in the urine. White cells and white cell casts occur with an allergic or infectious process, such as acute interstitial nephritis or pyelonephritis, respectively. Renal tubular epithelial cells indicate damage to the renal tubules, as with acute tubular necrosis. Oval fat bodies result from renal tubular cells that have absorbed fats or monocytes and macrophages that have ingested fats. (Post and Rose, 2008)

Assuming that a patient has maintained a normal baseline creatinine of 1.0 mg/dL with a normal glomerular filtration rate (GFR) of 100 mL/min, which of the following indicates a more significant change in the GFR? (A) increase in creatinine from 1.0 to 2.0 mg/dL (B) increase in creatinine from 2.0 to 4.0 mg/dL (C) increase in creatinine from 4.0 to 8.0 mg/dL (D) increase in creatinine from 8.0 to 16.0 mg/dL

(A) GFR describes the amount of blood passing through the kidneys per minute. There is an inverse relationship between GFR and serum creatinine. In a patient with normal renal function, doubling of the serum creatinine represents a loss of approximately 50% of GFR. Using this information, the loss of GFR can be estimated from changes in the serum creatinine. For example, assume normal creatinine levels of 1.0 mg/dL and normal GFR of 100 mL/min. A doubling of the serum creatinine from 1.0 mg/dL to 2.0 mg/dL represents an approximate reduction in GFR from 100 mL/min to 50 mL/min (50% of GFR has been lost). Each additional doubling of the creatinine decreases the remaining GFR by approximately one half. When renal function is severely impaired, large increases in the creatinine (ie, from 8.0 to 16.0 mg/dL) represent only small decreases in GFR (from about 12 to 6 mL/min). This example emphasizes the importance of detecting increases in serum creatinine early. However, serum creatinine level does not become abnormal until ~25% of renal function is lost. Therefore, other methods of estimating GFR are more useful in detecting early decreases in GFR. (Levey, 1999; Stevens and Perrone, 2008)

Which of the following is most useful in diagnosing renal artery stenosis? (A) magnetic resonance angiography (MRA) (B) computed tomography (CT) scanning (C) captopril renal scan (D) renal artery biopsy (E) intravenous pyelogram (IVP)

(A) Magnetic resonance angiography, enhanced with gadolinium, is 99% to 100% sensitive and 71% to 96% specific for diagnosing renal artery stenosis (RAS). This study has largely replaced the captopril renal scan and contrast-enhanced arteriography in diagnosing RAS. The principle behind the captopril renal scan is that ACE inhibitors lower GFR. In a kidney with already- compromised blood flow due to RAS, administration of the ACE inhibitor further decreases GFR in the affected kidney despite maintenance of adequate plasma volume. GFR in the contralateral kidney remains normal. Subsequent injection of a radionuclide reveals delayed uptake in the compromised kidney. Although arteriography provides the most definitive diagnosis, it carries its own risks of contrast-induced injury and bleeding. MRA is a low-risk procedure due to its noninvasive nature. Renal artery biopsy would not yield this diagnosis. IVP is utilized to visualize the anatomical structure of the urinary tract in situations such as urinary tract trauma and outflow obstruction, although increasingly it too is being replaced by noninvasive testing, such as ultrasound, CT scanning, and MRI. It remains a useful test to pinpoint the location of a calculus in the urinary tract. (DuBose and Santos, 2008, pp. 892-893; Watnick and Morrison, 2009, p. 810)

Which of the following signals a good prognosis for recovery from acute renal failure (ARF)? (A) maintenance of normal urine output as creatinine increases (B) low blood urea nitrogen level (C) the etiology of the ARF is sepsis (D) the etiology of the ARF is pregnancy (E) aggressive use of furosemide to stimulate urine output

(A) Maintenance of normal urine output as the serum creatinine level increases, so-called nonoliguric ARF, has a better prognosis for recovery than oliguric ARF. Oliguria is defined as urine output <500 mL/24 h. Anuria is absence of urine output. A low BUN level does not indicate the degree of renal damage because the blood urea nitrogen level can be affected by other factors, such as an elevated rate of catabolism, dietary protein intake, and gastrointestinal bleeding. Poor outcome is associated with ARF, due to sepsis and pregnancy. Administration of furosemide has not been shown to favorably affect the outcome of ARF. (McMillan, 2007)

Your 65-year-old patient with a history of tobacco abuse was recently diagnosed with stage III lung cancer. He has not started treatment yet and presents to his oncologist with complaints of nausea, anorexia, and increasing fatigue over the last several days. He has been eating less than usual but has been able to maintain a normal fluid intake. His wife reports that he has been more forgetful and confused than usual. His medical history includes hypertension, for which he has been taking 25 mg of hydrochlorothiazide for 12 years, and gastroesophageal reflux disease (GERD), for which he takes omeprazole. He has no history of significant side effects from his medications. You order labs, and the calcium level is elevated at 11.9 mg/dL. What is the most likely etiology of his hypercalcemia? (A) malignancy (B) hyperparathyroidism (C) thiazide diuretic use (D) dehydration (E) vitamin D toxicity

(A) Primary hyperparathyroidism and malignancy account for 90% of all cases of hypercalcemia. Ten to twenty percent of patients with cancer develop hypercalcemia, most commonly because of breast, lung, kidney, head and neck carcinomas, and multiple myeloma and lymphoma. Given this patient's history of lung cancer, this is the most likely etiology of his hypercalcemia. Although it is possible that the patient's symptoms could be due to hyperparathyroidism, this is a relatively rare disorder, affecting only about 0.1% of the population, making malignancy a much more likely etiology. He is taking a low dose of hydrochlorothiazide, which has been stable for years; therefore, this is unlikely to be causing excessive fluid losses and dehydration with hemoconcentration. However, this medication could be exacerbating the hypercalcemia. He is not taking vitamin D, so there is nothing to suggest vitamin D toxicity. (Cho et al., 2009, pp. 778-780; Fitzgerald, 2009, pp. 1007-1009; Rugo, 2009, pp. 1483-1484)

Which of the following statements about postinfectious glomerulonephritis is TRUE? (A) It is most commonly due to an immunologic reaction to a streptococcal antigen. (B) It is a process that will inevitably result in renal failure. (C) It occurs in 50% of people with a history of streptococcal pharyngitis. (D) It is a disease that results only from infection with Streptococcus. (E) Treatment of the streptococcal infection with antibiotics will prevent its development.

(A) Renal biopsies done on patients with postinfectious glomerulonephritis (GN) show deposition of immune complexes and proliferation of inflammatory cells. The most common cause of postinfectious GN is Group A beta-hemolytic Streptococci, but other organisms, such as Staphylococcus aureus, can cause it as well. Antibiotic treatment for the underlying infection has no impact on the development of postinfectious GN because the kidney has already been exposed to the microbial antigen before treatment was initiated. About 25% of those infected with nephritogenic strains will develop postinfectious GN, but not all people are infected with these strains. Most patients recover spontaneously, and progression to renal failure is extremely rare. (Watnick and Morrison, 2009, pp. 802, 811-812)

Which of the following best describes the pathophysiologic mechanism of distal renal tubular acidosis? (A) a defect in the ability of the distal renal tubule to excrete hydrogen ion (B) a defect in the ability of the distal renal tubule to reabsorb bicarbonate (C) a defect in the ability of the proximal renal tubule to excrete hydrogen ion (D) a defect in the ability of the proximal renal tubule to reabsorb bicarbonate (E) inadequate aldosterone production

(A) Renal tubular acidosis is classified into sub-types: Type I is characterized by an inability of the distal renal tubule to excrete hydrogen ion. Type II is characterized by overexcretion of HCO3- into the urine. Type III is no longer used, as it is considered a subtype of Type I, where there is a distal acidification defect and a proximal bicarbonate leak. Type IV is caused by either aldosterone deficiency or an inability of the distal tubule to respond to aldosterone. (Cho et al., 2009, p. 788)

Which of the following types of renal calculi is associated with an infectious cause? (A) struvite (B) uric acid (C) calcium oxalate (D) cystine (E) calcium phosphate

(A) Struvite stones form when urea-splitting organisms, such as Proteus, Klebsiella, Pseudomonas, and Staphylococcus, are present in the urinary tract. Ammonia is formed when urease breaks down urea. This results in an alkaline urine, which decreases the solubility of struvite, favoring the production of stones. Calcium stones result from hyperabsorption of calcium in the intestine, impaired renal tubular reabsorption of calcium, primary hyperparathyroidism, intestinal hyperabsorption of oxalate, and hypocitraturia. Uric acid stones are due to hyperuricosuria or a urinary pH <5.5, which causes uric acid to dissociate. They are also the only radiolucent calculi. Cystinuria, an inborn error of metabolism, results in cystine stones. (Stoller et al., 2009, pp. 833-837)

Based upon the following laboratory values, what is the patient's estimated serum osmolality? Na 132mEq/L Glucose 167mg/dL BUN 15mg/dL (A) 279 mOsm/kg (B) 285 mOsm/kg (C) 292 mOsm/kg (D) 301 mOsm/kg (E) 315 mOsm/kg

(A) The following formula can be used to estimate serum osmolality when an actual lab value is not available: <Equation in picture> Utilizing this formula, the estimated serum osmolality would be <Equation in picture> Normal serum osmolality is 285 to 295 mOsm/kg. Serum osmolality is the measure of the total concentration of solutes in the blood. It is helpful to be able to estimate serum osmolality for various reasons, including to help determine the cause of serum sodium abnormalities and to determine whether inactive metabolites, such as methanol, ethylene glycol, and salicylates, may be present in the blood. A low serum osmolality in the presence of hyponatremia suggests volume overload. (Cho et al., 2009, pp. 766-767)

What is the most likely etiology of the acid-base disturbance in the patient scenario above? (A) diarrhea (B) hypokalemia (C) vomiting (D) acute renal failure (E) alcohol (EtOH) intoxication

(A) This patient has been having significant diarrhea for several days, which is the most likely cause of the metabolic acidosis. (Cho et al, 2009, pp. 787-788)

Prolonged, heavy use of nonsteroidal anti-inflammatory drugs (NSAIDs) causes which type of kidney damage? (A) glomerular (B) tubulointerstitial (C) autoimmune (D) macrovascular

(B) Analgesic nephropathy results from ingestion of at least 1 g of analgesics per day for at least 3 years. NSAIDs are also one of the most common causes of acute interstitial nephritis. The pathophysiologic mechanism of injury appears to be tubulointerstitial inflammation and papillary necrosis. (Watnick and Morrison, 2009, p. 822)

A 72-year-old man is transported via ambulance to the emergency department with severe chest pain and shortness of breath. Electrocardiogram (ECG) reveals ST-segment elevation in leads II, III, and aVF. While in the emergency department, he loses consciousness and is found to be in ventricular fibrillation. Resuscitation is successful, and a pulse is restored within 3 minutes. He is taken to the cardiac catheterization laboratory, where he undergoes two-vessel stenting. Two days later, his creatinine has increased from a baseline of 1.1 to 2.2 mg/dL. The next day, the creatinine is 3.9 mg/dL. Fractional excretion of sodium is ordered. You would expect this to be (A) <1 (B) >1 (C) unchanged from baseline (D) undetectable (E) equal to the serum creatinine level

(B) Intrinsic ARF results in alterations in the kidneys' ability to respond to changes in hemostasis. When the integrity of the kidneys remains intact, sodium is conserved when GFR declines in an attempt to reestablish volume and perfusion, resulting in a fractional excretion of sodium (FENa) of <1. However, when the glomeruli are injured, the kidneys lose the ability to reabsorb sodium as the GFR decreases, and the FENa will be >1. The etiology of this patient's renal failure is most likely contrast-induced acute tubular necrosis following an ischemic episode, which is intrinsic ARF. (Cho et al., 2009, p. 798)

A 73-year-old man with type II diabetes mellitus was diagnosed with CKD 4 years ago. At this time, his creatinine is 1.9 mg/dL, with an estimated GFR of 72 mL/min. What stage of kidney disease has this patient reached? (A) Stage I (B) Stage II (C) Stage III (D) Stage IV (E) Stage V

(B) Kidney disease is characterized by five stages, based upon GFR. Specific complications are associated with each stage, and specific treatments are recommended based upon the complication. Stage >I: GFR 90 mL/min; patient has a history of previous kidney damage; no specific complications; avoid nephrotoxins, control cardiovascular risk factors. Stage II: GFR 60 to 89 mL/min; no specific complications; evaluate rate of decline in GFR, avoid nephrotoxins, control cardiovascular risk factors. Stage III: GFR 30 to 59 mL/min; complications include anemia, HTN, malnutrition, disorders of calcium and phosphorous metabolism, reduced functioning and well-being, neuropathy; screen for and treat complications as appropriate, avoid nephrotoxins, control cardiovascular risk factors, adjust doses of renally excreted medications. Stage IV: GFR 15 to 29 mL/min; complications include all of those in stage III, in addition to fluid, electrolyte, acid-base abnormalities; screen for and treat complications as appropriate, begin planning for ESRD with transplant or dialysis, avoid nephrotoxins, control cardiovascular risk factors, adjust doses of renally excreted medications. Stage V: GFR <15 mL/min; initiate dialysis or transplant when appropriate. (NKF-K/DOQI Guidelines, 2002, pp. 26, 45-66; Watnick and Morrison, 2009, pp. 803-810)

A 66-year-old man with a medical history of aortic stenosis is admitted to the hospital with increasing shortness of breath. Physical examination reveals a regular pulse of 120 beats/min, blood pressure of 95/50 mm Hg, and a respiratory rate of 32 breaths/min. The estimated jugular venous pressure (JVP) is greater than 15 cm, rales are heard halfway up the lung fields bilaterally, and a holosystolic murmur is heard at the apex. There is a tender enlarged liver with hepatojugular reflux and 2+ pretibial and pedal edema. Plain film of the chest reveals cardiomegaly and pulmonary edema. ECG is suggestive of left ventricular hypertrophy. Admission laboratory studies include the following: Na 128mEq/L K 3.6mEq/L Chloride 93mEq/L Glucose 75mg/dL BUN 45mg/dL Bicarbonate 27mEq/L Creatinine 1.0mg/dL Urine Na 12mEq/L What type of hyponatremia does this patient most likely have? (A) hypovolemic hypotonic (B) hypervolemic hypotonic (C) hypovolemic isotonic (D) hypervolemic hypertonic (E) hypovolemic hypertonic

(B) Most often, hyponatremia is due to excessive water retention rather than a true sodium deficiency. The first step in evaluating hyponatremia is to determine serum osmolality. Knowing whether the serum is isotonic (normal osmolality), hypotonic (low osmolality), or hypertonic (high osmolality) can help determine the etiology of the hyponatremia, and therefore, treatment. The most common causes of isotonic hyponatremia are hyperproteinemia and hyperlipidemia. The most common causes of hypertonic hyponatremia are hyperglycemia, presence of radiocontrast agents, and the presence of inactive metabolites, that is, mannitol, sorbitol, glycerol, and maltose. Treatment is aimed at correcting the underlying disorder. Most commonly, hyponatremia occurs in the setting of low osmolality (hypotonic). To further evaluate the etiology of the hyponatremia, it must be determined if the patient is hypovolemic, euvolemic, or hypervolemic. Hypovolemic hyponatremia is usually due either to extrarenal or intrarenal sodium losses. Extrarenal losses occur from dehydration, diarrhea, and vomiting. Urinary sodium measures <10 mEq/L (normal, >20 mEq/L), as the kidneys are avidly retaining sodium in an attempt to restore volume. Treatment is directed at restoring volume. Intrarenal sodium losses occur from the use of diuretics and ACE inhibitors, nephropathies, and mineralocorticoid deficiency. Urinary sodium measures >20 mEq/L. Treatment is directed at reversing the underlying cause. The most common causes of euvolemic hyponatremia are SIADH, postoperative hyponatremia, hypothyroidism, psychogenic polydipsia, and endurance exercise. In these cases, electrolyte-free water is retained, which results in a true physiologic hyponatremia. Treatment is directed at correcting the underlying abnormality and replacing sodium losses. Hypervolemic hyponatremia is caused by congestive heart failure, liver disease, nephrotic syndrome, and advanced CKD in general, anything that causes fluid retention. Treatment is directed at treating the underlying disease, restricting water intake, and facilitating excretion of water. The first step in characterizing this patient's hyponatremia is to determine the serum osmolality, which is 276 mOsm/kg. This is low, so we know that this is hypotonic. Second, we have to determine the volume status. Urinary sodium is 12 mEq, which does not indicate either intrarenal or extrarenal losses of sodium and is not consistent with hypovolemia. Given the elevated JVP, extensive edema, and hepatojugular reflux, this patient is presenting with a clinical picture of fluid overload, or hypervolemia. This patient has hypervolemic hypotonic hyponatremia due to CHF. (Cho et al, 2009, pp. 767-771)

A renal ultrasound would be most beneficial for diagnosing which of the following? (A) nephrotic syndrome (B) polycystic kidney disease (C) glomerulonephritis (D) acute tubular necrosis (E) lupus nephritis

(B) Renal ultrasound is useful for assessing kidney size and thickness of the cortex, and for the presence of masses, cysts, obstruction, and hydronephrosis. Intrinsic disease is best assessed by establishing the clinical context, analyzing the urine for protein, cells, and casts, and possibly by doing a biopsy. Loss of cortical thickness is a nonspecific finding, and ultrasound does not establish an etiology. (Bazari, 2008, pp. 810-811; Watnick and Morrison, 2009, p. 805)

When initially screening for CKD, which of the following would be ordered? (A) 24-hour urine collection (B) blood pressure measurement, serum creatinine level, spot urine protein measurement (C) renal ultrasound (D) abdominal CT scan (E) renal angiogram

(B) Screening for the presence of chronic kidney disease involves checking a serum creatinine level, checking blood pressure for the presence of hypertension, checking urinary protein for evidence of glomerular injury, and obtaining a history to check for the presence of risk factors, such as hypertension, diabetes mellitus, autoimmune disease, infection, or family history. Initial screening would not include a 24-hour urine collection. This is a cumbersome, inconvenient, more expensive test than the spot urinary protein reading and would not provide additional information. Renal ultrasound and abdominal CT scan would not be indicated in the initial stages of the work-up. These would be done only after laboratory studies were done and only if indicated. (NKF-K/DOQI Guidelines, 2002, p. 31)

The most common cause of nephrotic syndrome in children is (A) post-streptococcal glomerulonephritis (B) minimal change disease (C) diabetes mellitus (D) NSAIDs (E) polycystic kidney disease

(B) The most common cause of nephrotic syndrome in children is minimal change disease. Diffuse injury to the capillaries is the underlying cause, resulting in significant proteinuria, edema, hypoalbuminemia, and hyperlipidemia. It accounts for 65% of cases of nephrotic syndrome in children; however, 10% of adults with nephrotic syndrome have minimal change disease. Treatment is with corticosteroids for 2 to 4 weeks, dietary sodium restriction, and sometimes diuretics to reduce the edema. Relapse and lack of response to corticosteroids can occur. If the latter occurs, renal biopsy is indicated to rule out other causes of the nephrotic syndrome, such as focal glomerulosclerosis and membranoproliferative glomerulonephritis. (Appel, 2008, p. 868; Kumar et al., 2007, pp. 549-550)

A 65-year-old woman with diabetes mellitus and peripheral vascular disease is about to undergo a diagnostic radiographic procedure involving the use of intravenous (IV) contrast dye. Her serum creatinine is 1.9 mg/dL. An appropriate action prior to the procedure would be to (A) start an ACE inhibitor (B) administer a 1,000 cc bolus of normal saline and acetylcysteine po (C) administer a 1,000 cc bolus of normal saline only (D) administer an intravenous diuretic (E) no specific preprocedure treatment is needed

(B) This patient has CKD with an elevated creatinine level of 1.9 mg/dL. Her kidney function can worsen if exposed to any nephrotoxins, including contrast dye and some medications, such as aminoglycosides, amphotericin B, NSAIDs, cisplatin, and cyclosporine. The mechanism of injury from contrast dye is thought to be due to renal vasoconstriction, possibly mediated by alterations in the amount of nitric oxide and/or endothelin present, which results in ischemia. In addition, there are also direct toxic effects of the contrast agents on the renal cells. A byproduct of the renal injury is oxygen-free radicals, which are important modulators of renal perfusion and GFR. Maintaining adequate hydration protects the glomeruli in the presence of vasoconstriction, therefore, providing a preprocedure fluid bolus of 1 L is appropriate. In addition, acetylcysteine has been found to have a potentially protective effect as well. N-Acetylcysteine is a precursor for glutathione synthesis. It improves endothelin-dependent vasomotor function in the coronary and peripheral circulation and is also a potent antioxidant that may result in scavenging of free radicals. Therefore, it improves renal hemodynamics and prevents direct oxidative tissue damage. The recommended dose of acetylcysteine is 600 mg po every 12 hours twice before and after a dye load. Contrast nephropathy is the third-leading cause of new ARF in the hospitalized population, with the injury usually occurring 24 to 48 hours after the study. Administering a diuretic and/or ACE inhibitor may worsen the risk of nephropathy. (Briguori et al., 2002; Watnick and Morrison, 2009, pp. 799-801)

Your 65-year-old patient with a history of tobacco abuse was recently diagnosed with stage III lung cancer. He has not started treatment yet and presents to his oncologist with complaints of nausea, anorexia, and increasing fatigue over the last several days. He has been eating less than usual but has been able to maintain a normal fluid intake. His wife reports that he has been more forgetful and confused than usual. His medical history includes hypertension, for which he has been taking 25 mg of hydrochlorothiazide for 12 years, and GERD, for which he takes omeprazole. He has no history of significant side effects from his medications. You order labs, and the calcium level is elevated at 11.9 mg/dL. How would you treat this patient's hypercalcemia? (A) increase thiazide diuretic dose (B) bisphosphonate (C) does not need to be treated (D) encourage fluid intake (E) initiate hemodialysis

(B) When hypercalcemia becomes symptomatic, it must be treated to prevent neurologic and muscular dysfunction. Principles of treatment include establishing euvolemia since hypercalcemia can result in volume depletion. Since excretion of sodium is accompanied by excretion of calcium, intravenous saline (0.45% or 0.9%), followed by IV furosemide, will replete volume and promote natriuresis. Once calcium levels have normalized, the treatment of choice is bisphosphonates for hypercalcemia associated with malignancy. IV administration of zoledronic acid 4 mg over 15 minutes normalizes serum calcium levels in less than 3 days in 80% to 100% of patients. Doses can be repeated as necessary. (Cho et al., 2009, pp. 779-780)

11. Which of the following best describes the mechanism of action of angiotensin-converting enzyme (ACE) inhibitors in controlling blood pressure and preventing or slowing kidney damage? (A) They result in systemic vasodilation. (B) They increase renal tubular excretion of sodium. (C) They result in dilation of the efferent arteriole, reducing glomerular pressure. (D) They block the angiotensin II receptor on the cell membrane. (E) They reduce production of angiotensinogen, the precursor to angiotensin I.

(C) ACE inhibitors prevent the conversion of angiotensin I to angiotensin II, thereby interrupting the renin-angiotensin-aldosterone system, which regulates blood pressure. The glomerular efferent arteriole dilates, given the decreased stimulus from angiotensin II to constrict. This lowers pressure in the glomerulus by lowering resistance to outflow. This effectively results in a decrease in GFR, resulting in increased serum creatinine and potassium levels. However, these changes are not necessarily indications to discontinue the ACE inhibitor. Usually, the creatinine increases 0.2 to 0.4 mg/dL and then levels out. Monitoring serum creatinine and potassium levels is indicated. If only mild increases occur and stabilize, or if there are no changes, the ACE inhibitor can, and should, be continued so that the patient derives the beneficial effect of the decline in pressure within the glomerulus, which will slow down the progression of CKD. (Benowitz, 2007, pp. 175-176)

Glucose will spill into the urine when the serum glucose reaches what level? (A) >126 mg/dL (B) 150 to 175 mg/dL (C) 180 to 200 mg/dL (D) >250 mg/dL (E) >400 mg/dL

(C) Because glucosuria does not occur until serum glucose levels are ≥180 mg/dL, urine testing is not considered an adequate screening tool for diagnosing diabetes mellitus. (Delmez and Windus, 2001, p. 1347)

Complications associated with hyperkalemia include (A) hyperventilation (B) nausea and vomiting (C) ventricular arrhythmias (D) diarrhea (E) seizures

(C) Hyperkalemia is defined as serum potassium level greater than 5.0 mEq/L. ECG changes (tall, peaked T waves and shortening of the QT interval) start to occur at 5.5 mEq/L. At serum levels of ≥6.5 mEq/L, the QRS will widen, the PR interval will be prolonged, and then the P wave will disappear. Nodal and ventricular arrhythmias can start to occur. A sine wave pattern precedes asystole at a serum level of ~10 mEq/L. (McMillan, 2007)

What is the most common complication of hemodialysis? (A) hypokalemia (B) hyperglycemia (C) hypotension (D) infection (E) anemia

(C) Hypokalemia can occur rarely as a complication of hemodialysis (HD) if excessive potassium is removed during the treatment. Hyperglycemia can result from peritoneal dialysis, since the dialysate contains dextrose. Infection occurs rarely, given meticulous maintenance of sterile technique. Anemia is a result of CKD and can be worsened by hemodialysis if significant bleeding occurs due to heparin administered during HD. However, hypotension remains the most common complication due to excessive removal of volume during treatment. (Tolkoff-Rubin, 2008, p. 938)

What is the most common electrolyte abnormality seen in hospitalized patients? (A) hypokalemia (B) hyperkalemia (C) hyponatremia (D) hypernatremia (E) hypomagnesemia

(C) Hyponatremia affects approximately 20% of hospitalized patients and is the most common electrolyte abnormality found in this population. The incidence of hypokalemia is less well- documented but has been estimated by one source to be approximately 13%. (Fukagawa et al., 2008, p. 758; Lederer et al., 2007)

The earliest sign of chronic kidney disease (CKD) is (A) microscopic hematuria (B) hypertension (HTN) (C) proteinuria (D) abnormal creatinine (E) hyperkalemia

(C) Injury to the nephron results in excessive protein leak and decreased protein reabsorption from the tubules. This occurs long before the creatinine becomes abnormal and 5 to 10 years before overt proteinuria, detectable by routine dipstick, develops. Persistent proteinuria eventually will result in an abnormal creatinine but, in the case of CKD, years later. Therefore, proteinuria, best assessed by the protein-to-creatinine ratio from a urine specimen, is considered the earliest marker of CKD. Microscopic hematuria can result from many processes, some transient, including infection, malignancy, calculi, acute glomerulonephritis, and IgA nephropathy, and is not, in and of itself, an indicator of permanent kidney damage. Hypertension, if not the cause of the CKD, can occur early in the course of CKD, but proteinuria usually occurs before hypertension develops. Chronic hyperkalemia develops later in the course of CKD, generally when glomerular filtration rate is <30 mL/min. (NKF-K/DOQI Guidelines, 2002, pp. 48-49)

A 16-year-old girl is referred for a sports physical. Her blood pressure is 170/92 mm Hg. Urinalysis (UA) reveals 2+ protein. The girl's mother reports multiple episodes of urinary tract infections (UTIs) throughout childhood that were never investigated. The most likely diagnosis is (A) obstructive uropathy (B) orthostatic proteinuria (C) chronic reflux nephropathy (D) nephrotic syndrome (E) exercise-induced proteinuria

(C) Retrograde flow of urine from the bladder damages the renal interstitium, causing inflammation and fibrosis. If untreated, irreversible damage to the kidneys will occur. Because this is a tubulointerstitial process, the urinalysis will be negative for protein in the early stages of damage. Most damage is done before age 5, but if undetected, glomerular damage will occur and protein will appear in the urine eventually. Hypertension develops as the GFR decreases. (Watnick and Morrison, 2009, p. 822)

Abnormal urinary protein excretion is defined as (A) >30 mg/24 h (B) >150 mg/24 h (C) >300 mg/24 h (D) >1 g/24 h (E) >3.5 g/24 h

(C) The normal glomerulus filters a small amount of low-molecular-weight proteins, which are reabsorbed in the tubules, generally at a rate of <150 mg/24 h. However, up to 300 mg/24 h can be accepted as normal. High-molecular-weight proteins, such as albumin, are not filtered by the normal kidney, and therefore, albumin's appearance in the urine at >30 mg/24 h is considered abnormal. Standard urine dipsticks will react in the presence of all proteins, including glycoproteins, gamma-globulins, Tamm-Horsfall mucoproteins, Bence-Jones proteins, and albumin. However, they generally cannot detect protein until it reaches an excretion level of >200 to 300 mg/24 h. This will produce a urine dipstick reading of 1+ (equivalent to about 30 mg of protein in that sample). Contamination of the urine specimen with blood, semen, pus, vaginal discharge, and mucous can result in false-positive readings. Specific reagent strips designed to detect microalbuminemia, defined as 30 to 300 mg/24 h, have been developed and are the preferred strips to use when testing for early signs of diabetic nephropathy. Expressed another way, a protein level of >300 mg/24 h or a microalbumin level of >30 mg/24 h is defined as abnormal. A random spot urinary albumin-to-creatinine ratio is also a good screening test for early nephropathy, with normal results defined as 17 to 250 mg/g in men and 25 to 355 mg/g in women. (Graff, 1983, pp. 27-30; NKF-K/DOQI Guidelines, 2002, p. 21; Watnick and Morrison, 2009, pp. 794-795)

A 17-year-old boy high school wrestler is brought into the emergency department after he collapsed at a wrestling match. He spent time fully clothed in a hot sauna prior to the match to try to "make weight." Labs are ordered, and results come back as follows: Na 162mEq/L K 3.8mEq/L Chloride 121mEq/L Carbon dioxide 29mEq/L Weight 70kg Glucose 108mg/dL BUN 30mg/dL Creatinine 2.0mg/dL Urine Na <10mEq/L Urine osmolality 428mOsm/kg Which IV fluid regimen would most effectively treat this patient's hypernatremia? (A) quarter normal (hypotonic) saline (B) half-normal saline (C) isotonic (normal) saline (D) dextrose 5% in water (E) lactated Ringer's

(C) The patient presents with a combination of inadequate fluid intake and excessive losses due to perspiration, resulting in hypovolemia and hypernatremia. The most common causes of hypernatremia are inadequate fluid intake resulting in hemoconcentration and diabetes insipidus (DI), resulting in excessive renal fluid losses. Normal urine osmolality is 500 to 850 mOsm/kg but can range from 50 to 1,200 mOsm/kg depending on the patient's fluid intake. Urine osmolality >400 mOsm/kg indicates that the renal fluid-conserving mechanism is intact, as the kidneys are working to preserve volume. A lower urine osmolality would be consistent with DI, characterized by a lack of response to anti-diuretic hormone (ADH), resulting in excessive urinary losses of water with worsening hypernatremia. Treatment is directed at the cause. If the patient is dehydrated, restoring fluid volume is the goal. If the patient has DI, treating the underlying disease will lower the serum sodium level. For this dehydrated patient, the treatment would be to administer isotonic (normal) saline, which contains 0.9% sodium, because of the large free water deficit. Quarter-normal saline contains 0.25% sodium, half-normal saline contains 0.45% sodium, and lactated Ringer's solution is similar to half-normal saline in its sodium content. Dextrose 5% in water (D5W) contains no electrolytes. Isotonic saline is the appropriate choice because it treats not only the volume deficit but the serum osmolality as well. Its osmolality (308 mOsm/kg) is often lower than the plasma osmolality because of the hypovolemic state and, therefore, helps restore normal serum osmolality. Once serum osmolality becomes more normal, the isotonic saline can be replaced by D5W to replace the remaining free water deficit. If the free water deficit were less dramatic, initial IV fluid treatment could be half- normal saline, followed by D5W. (Cho et al., 2009, pp. 771-772; Graff, 1983, p. 19)

Which of the following diuretics results in potassium wasting? (A) triamterene (B) amiloride (C) hydrochlorothiazide (D) spironolactone (E) eplerenone

(C) The thiazide diuretics, including hydrochlorothiazide, block sodium reabsorption in the terminal portion of the loop of Henle and the proximal portion of the distal convoluted tubule. This leads to loss of both sodium and potassium in the urine. Triamterene, amiloride, spironolactone, and eplerenone are potassium-sparing diuretics. Triamterene and amiloride act to reduce potassium secretion in the distal tubule. Spironolactone and eplerenone are aldosterone receptor blockers. (Ives, 2007, p. 246)

A 32-year-old construction worker presents to the emergency department after being involved in an accident at a job site. His left thigh was pinned under a 100-lb cement block. He is in moderate pain on presentation, and there is swelling and a large ecchymosis over the entire anterior thigh. Urine is rust-colored. Urine dip is positive for blood and protein, negative for glucose, ketones, nitrite, and leukocyte esterase. Urine sediment is negative for cells, organisms, and casts. What is the most likely cause of the positive urine dip for blood? (A) hemoglobin due to hematoma formation (B) contamination of the urine sample (C) myoglobin due to rhabdomyolysis (D) red cell casts due to glomerulonephritis (E) UTI

(C) Urine reagent strips are suffused with an indicator dye that changes color when oxidized by peroxidase in hemoglobin, indicating the presence of blood in the urine. However, myoglobin also has peroxidase activity, and therefore, the indicator for blood on the dipstick will turn positive in the presence of myoglobin without hemoglobin. Myoglobin can appear in the urine as the result of rhabdomyolysis due to crush injuries, surgery, ischemia, hyperthermia, significant exercise, seizures, electric shock, illicit drug use, and muscle-wasting diseases. A positive urine dip for blood, with a negative urinary sediment for red cells, mandates a workup for diseases/injuries resulting in myoglobinuria. (Graff, 1983, p. 52; McBride, 1998, p. 68)

You have just received labs back on a 42-year-old woman with severe vomiting and no oral intake in the last 3 days. You note a metabolic alkalosis, based on her arterial blood gases. You also note that compensatory changes are present. Which of the following best represents these changes? (Normal PCO2 = 35-45 mm Hg, normal HCO3 = 24-31 mEq/L) (A) PCO2 = 32 mm Hg (B) PCO2 = 38 mm Hg (C) PCO2 = 47 mm Hg (D) HCO3 = 38 mEq/L (E) HCO3 = 24 mEq/L

(C) With any acid-base disorder, the body tries to compensate to restore pH to normal. By definition, an alkalosis is characterized by a pH of >7.45. This patient has sustained losses of acid (HCl, NaCl, KCl) through vomiting. In addition, volume contraction results in a decrease in GFR, which causes avid sodium and bicarbonate reabsorption, further worsening the alkalosis. The body has two ways to increase serum levels of acid to try to decrease the pH to normal: the lungs slow the respiratory rate to retain CO2 and/or the kidneys reabsorb chloride and hydrogen ion [H+] and increase excretion of bicarbonate (HCO3). The lungs can respond more quickly (within minutes) and, therefore, PCO2 will rise before serum HCO3 will drop (over hours to days). Normal PCO2 levels are 35 to 45 mm Hg. This patient's PCO2 is 47 mm Hg, which indicates that her respiratory rate is slowing, and she is retaining CO2. Levels of 32 mm Hg and 38 mm Hg are low and normal, respectively, and, therefore, would not be appropriate compensation for the alkalosis. Normal serum bicarbonate levels are 24 to 31 mEq/L. An HCO3 level of 38 mEq/L would not be appropriate compensation, as this would increase the pH. A HCO3 level of 24 mEq/L is at the lower end of normal. Given that this patient's symptoms have been present for 3 days, one would expect the HCO3 level to be lower at this time as the kidneys have had time to adjust and increase excretion of HCO3. (Cho et al, 2009, pp. 790-792)

Which of the following statements about anemia associated with CKD is TRUE? (A) Iron and folic acid by mouth are the most effective treatments. (B) Transfusion of packed red blood cells monthly is the most effective treatment. (C) IM erythropoietin given monthly is the most effective treatment. (D) It is due to the inability of the kidney to transform erythropoietin into its physiologically (E) It occurs early in the course of CKD.

(D) Anemia associated with CKD is the result of inadequate erythropoietin synthesis by the kidneys. This hormone signals the bone marrow to synthesize red blood cells. A deficiency will result in anemia. In the absence of erythropoietin, iron would not be of use since red blood cell synthesis is inadequate. Folic acid would also not be of use and does not play a role in the etiology of this type of anemia. Transfusion is a tempering measure only, used to increase oxygen-carrying capacity in the case of symptomatic ischemia. Anemia due to erythropoietin deficiency generally does not occur until the GFR decreases to <60 mL/min, or approximately 50% of normal. Intramuscular administration of erythropoietin is the only effective treatment to induce red blood cell production. Depending on the formulation used, this can be given once a week or once every 2 weeks. Oral iron supplementation is needed to produce adequate hemoglobin for the increased de novo red cell production. (Guyton and Hall, 2006, p. 376; NKF-K/DOQI Guidelines, 2002, p. 51)

A 17-year-old boy high school wrestler is brought into the emergency department after he collapsed at a wrestling match. He spent time fully clothed in a hot sauna prior to the match to try to "make weight." Labs are ordered, and results come back as follows: Na 162mEq/L K 3.8mEq/L Chloride 121mEq/L Carbon dioxide 29mEq/L Weight 70kg Glucose 108mg/dL BUN 30mg/dL Creatinine 2.0mg/dL Urine Na <10mEq/L Urine osmolality 428mOsm/kg What is this patient's estimated free water deficit? (A) 2.1 L (B) 3.3 L (C) 5.1 L (D) 6.6 L (E) 7.2 L

(D) Approximately 60% of body weight is water: 20% of body weight is in the extracellular spaces and 40% in the intracellular spaces. Free water deficit can be calculated by using the following formula: Utilizing this formula, the patient's water deficit is approximately 6.6 L. (Cho et al., 2009, pp. 766, 772)

Most UTIs are caused by (A) Gram-positive bacteria (B) Pseudomonas aeruginosa (C) Staphylococcus aureus (D) Escherichia coli (E) Candida albicans

(D) Eighty-five percent of uncomplicated UTIs are caused by E. coli. Other common etiologic agents are the gram-negative bacteria Proteus, Klebsiella, and Enterobacter. (Norrby, 2008, pp. 2138-2139)

Hyperphosphatemia is associated with stage III CKD. Which of the following is the appropriate treatment for mild hyperphosphatemia in this patient population? (A) magnesium oxide 250 to 500 mg po tid (B) calcium carbonate 0.5 to 1.5 g po qd on an empty stomach (C) calcium carbonate 0.5 to 1.5 g po tid on an empty stomach (D) calcium carbonate 0.5 to 1.5 g po tid with meals (E) no treatment indicated for mild hyperphosphatemia

(D) Hyperphosphatemia develops in patients with CKD because of impaired renal excretion as GFR declines. Consequently, this results in downregulation of some phosphate transporters, a decrease in vitamin D production due to inhibition of an enzyme system that activates vitamin D, and an increase in PTH production. Also, as synthesis of 1,25-(OH)2D declines in the kidney, calcium absorption decreases further. Excess phosphorus complexes with calcium in the blood, decreasing ionized calcium levels, which results in hypocalcemia. As a result, PTH is further stimulated in an attempt to increase serum calcium levels. This eventually results in secondary hyperparathyroidism, renal osteodystrophy as calcium is drawn out of the bones to maintain a normal serum level, and extraosseous calcification of soft tissues due to calcium-phosphorus complexes. Treatment should be initiated early to prevent these long-term complications. Calcium carbonate binds phosphorous in the intestine before it can be absorbed and decreases serum levels. This must be taken with meals to bind dietary phosphorous. A synthetic phosphate binder, sevelamer hydrochloride, can also be utilized. The most effective regimen is 0.5 to 1.5 g po taken at the start of each meal. (Cho et al., 2009, p. 782; Guyton, 2006, p. 344; Lederer et al., 2007)

A 46-year-old man with a history of EtOH abuse is brought to the emergency department in the morning by his wife. She has noted that he has developed tremors in both arms, and he seems mildly confused to her. He complains of feeling weak, with some cramping in the legs. On physical examination, his blood pressure is noted to be 162/95 mm Hg, and his heart rate is 108 beats/min. There is no asterixis. Which of the following electrolyte disorders are you likely to find in this patient? (A) hypercalcemia (B) hypocalcemia (C) hypermagnesemia (D) hypomagnesemia (E) hyperphosphatemia

(D) Hypomagnesemia is a common finding in the patient who abuses alcohol. Other leading causes include diarrhea, diuretics, aminoglycosides, and amphotericin B. The etiology of hypomagnesemia in the patient with a history of alcohol abuse is thought to be a combination of malabsorption and inadequate dietary intake, possibly with alcohol exerting an antagonistic effect on absorption. Signs and symptoms are those of neuromuscular and central nervous system hyperirritability, including weakness and muscle cramps, tremors, nystagmus, a positive Babinski response, confusion, and disorientation. Hypertension, tachycardia, and ventricular arrhythmias may develop. (Fukagawa et al, 2008, pp. 774-775)

Which of the following patients would require the LONGEST antibiotic treatment course for a UTI? (A) a 32-year-old woman with a history of one UTI 3 years ago (B) a 79-year-old woman with a history of renal calculi but no previous history of UTI (C) an 8-year-old girl with no previous history of UTI (D) a 42-year-old man with no significant past medical history (E) a 41-year-old woman with history of cervical diaphragm use for birth control

(D) Men and pregnant women require the longest course of treatment for UTI—generally 7 to 10 days. Some advocate single-dose treatment of an uncomplicated UTI, although in practice, this is rare. Most are treated for 3 to 5 days with trimethoprim-sulfamethoxazole (TMP-SMZ) or a fluoroquinolone. Treatment with ampicillin, amoxicillin, and first-generation cephalosporins alone is infrequent given the widespread incidence of resistant organisms, as well as their decreased effectiveness in eliminating vaginal and periurethral colonization compared with TMP-SMZ. Remote history of UTI, history of renal calculi, and UTI in young girls are not indications to prolong antibiotic treatment course. Young, sexually active women are at higher risk for developing UTIs because of the risk of bacterial contamination into an anatomically short urethra, and those who use a diaphragm or spermicides are at highest risk. However, using these types of birth control does not indicate a need for a prolonged antibiotic course. (Bastani, 2001, pp. 1369-1370)

In patients with known chronic kidney disease, which of the following is an absolute indication to initiate dialysis? (A) proteinuria >3 g/24 h (B) GFR <10 mL/min (C) hyperkalemia >5.0 mEq/L (D) seizures (E) hyperphosphatemia >6.5 mg/dL

(D) The development of seizures due to uremia is an absolute indication to begin hemodialysis. The waste products of urea metabolism must be removed to abort the seizure activity. Proteinuria is never an indication to begin hemodialysis. Proteinuria is a sign of kidney damage, poses no immediate threat to life (although the underlying process causing it might), and hemodialysis will not correct it. Calculations of GFR are used to assess kidney function, predict when complications of CKD and ESRD (end-stage renal disease) will occur, and guide treatment plan but not to indicate when to initiate hemodialysis. Rather, the decision to initiate renal replacement therapy is a clinical one, based upon clinical assessment of functioning and physical manifestations of ESRD. A potassium level of >5.0 mEq/L does not represent an immediate threat to the patient and can be treated medically. Cardiac abnormalities associated with hyperkalemia generally occur at levels >6.5 mEq/L, and conservative measures to correct hyperkalemia generally are initiated when the serum level is >5.5 mEq/L, although this varies with practice. Hyperphosphatemia is best treated with phosphate binders, such as calcium carbonate and calcium acetate, and a low phosphorus diet. (Watnick and Morrison, 2009, pp. 800-801)

You are asked to see a diabetic patient with retinopathy and hypertension. On examination, the patient's blood pressure is noted to be 180/90 mm Hg. Urinalysis shows microalbumin of 300 mg/dL. Labs: blood urea nitrogen 22 mg/dL, creatinine 1.5 mg/dL. Which of the following classes of antihypertensive medications would be best to prescribe in this setting? (A) calcium channel blocker (B) loop diuretic (C) alpha blocker (D) thiazide diuretic (E) ACE inhibitor

(E) ACE inhibitors are the drug of choice in this setting. Control of systemic blood pressure can reduce renal vascular damage. In diabetic patients, ACE inhibitors are especially beneficial because of the added effect of reducing intraglomerular pressure and decreasing proteinuria. Current target blood pressure in patients with diabetic nephropathy is <130/80 mm Hg. Calcium channel blockers and diuretics do not offer renoprotective benefits but may be used to control hypertension. (American Diabetes Association, 2009, p. S28; JNC 7 Report, 2003; NKF- K/DOQI Guidelines, 2002, pp. 79-80; Watnick and Morrison, 2009, p. 819)

In which of the following settings would the use of an ACE inhibitor be contraindicated? (A) diabetic nephropathy (B) hypertensive nephrosclerosis (C) lupus nephritis (D) polycystic kidney disease (E) significant renal artery stenosis

(E) Among other mechanisms of action, ACE inhibitors interfere with vasoconstriction of the efferent arteriole, thereby decreasing pressure within the glomerulus. If significant blockage is present in the renal artery, blood flow to the glomerulus is already compromised, resulting in lowered glomerular pressure. If pressure within the glomerulus is lowered further because of the vasodilating effect of the ACE inhibitor on the efferent arteriole, blood flow is further compromised. Ischemia and acute renal failure can result. (Benowitz, 2007, pp. 175-176)

Which type/class of medications is useful to treat renal calculi due to hypercalciuria? (A) calcium channel blockers (B) colchicine (C) allopurinol (D) potassium citrate (E) thiazide diuretics

(E) In patients with hypercalciuria, thiazide diuretics can lower urinary calcium levels, reducing the risk of nephrolithiasis. An episode of nephrolithiasis mandates a metabolic workup, including blood work to check serum levels of creatinine, parathyroid hormone (PTH), calcium, phosphorus, and uric acid, and a 24-hour urine collection to measure pH, total volume, sodium, calcium, phosphorus, oxalate, citrate, cystine, and uric acid. (Stoller et al., 2009, pp. 834-835)

Which of the following is MOST indicative of UTI? (A) positive nitrite on dipstick (B) positive leukocyte esterase on dipstick (C) 2 to 3 white blood cells (WBCs) per high power field (HPF) on urine dipstick (D) urine culture revealing 10,000 to 20,000 colonies of Lactobacillus (E) positive nitrite and leukocyte esterase on dipstick

(E) Nitrite is formed when organisms that produce nitrate reductase, that is, Escherichia coli, Klebsiella, Proteus, and Enterobacter, are present in the urine. The enzyme reduces nitrate to nitrite. However, the urine has to be present in the bladder at least 4 hours for this to occur. Leukocyte esterase is produced by various WBCs, including polymorphonuclear neutrophils, monocytes, eosinophils, and basophils. The enzyme can appear in the urine with the presence of any of these WBCs and not just as the result of bacterial infection, although UTI is the most common cause of positive leukocyte esterase in the urine. Other causes are vaginal and perineal contamination. The combination of urinary nitrite and leukocyte esterase has a sensitivity and specificity of 85% and 75%, respectively, and therefore, provides more information than either alone. WBCs can occur in the urine as the result of infection, an inflammatory process, such as interstitial nephritis, or vaginal or perineal contamination, and levels <3 to 5 WBCs/HPF are not considered indicative of infection. Infection is strongly indicated when WBCs reach 4 to 6/HPF. Urine culture is considered positive for infection at >100,000 colonies. (Bastani, 2001, p. 1367; McBride, 1998, pp. 70-71)

Which of the following statements about urinary tract infections (UTIs) in patients with chronic indwelling catheters is true? (A) Leukocytes in the urine are always indicative of an acute UTI. (B) The most likely etiologic agent is Escherichia coli. (C) All positive findings of WBCs in the urine should be treated with antibiotics. (D) All positive findings of bacteriuria should be treated with antibiotics. (E) The etiology is likely to be polymicrobial.

(E) Patients with indwelling catheters are at risk for UTIs due to multiple organisms, including Pseudomonas aeruginosa, Acinetobacter baumannii, Serratia marcescens, Stenotrophomonas maltophilia, Proteus mirabilis, and Escherichia coli, which accounts for less than 50% of cases. Asymptomatic leukocyturia or bacteriuria need not be treated since this can result in increased incidence of antibiotic resistance. The patient should be observed for any signs or symptoms of UTI. If treatment is indicated, the best antibiotic choice is a beta-lactam/beta- lactamase inhibitor combination, possibly including vancomycin. (Bonomo and Johnson, 2004, p. 349; Norrby, 2008, p. 2139)

A 22-year-old woman presents to the emergency department after spending a week in Cancun for spring break. She noted onset of significant diarrhea about 3 days ago, accompanied by mild nausea but no vomiting. She hoped it would resolve on its own, but she is starting to feel worse with weakness and lightheadedness. You order labs with the following results: Na 138mEq/L K 2.2mEq/L Chloride 119mEq/L Bicarb 8mEq/L pH 7.32 PCO2 16mmHg BUN 68mg/dL Creatinine 2.0 mg/dL What is the nature of the acid-base disturbance? (A) respiratory acidosis (B) respiratory alkalosis (C) metabolic alkalosis (D) high anion gap metabolic acidosis (E) nonanion gap metabolic acidosis

(E) This patient's pH is acidemic, with a low HCO3, suggesting a metabolic acidosis. The PCO2 of 16 mm Hg represents appropriate pulmonary compensation for the acidosis, as the respiratory rate increases to expire more CO2. When evaluating a metabolic acidosis, the anion gap should be calculated to help determine the etiology. Calculation of the anion gap is done as follows: Na2+ − (Cl2- + HCO3). A normal anion gap is 8 to 12 mEq/L. This patient's anion gap is 138 − (119 + 8) = 138 − 127 = 11, which is normal. Causes of a normal anion gap metabolic acidosis include diseases/disorders that cause a loss of HCO3, including diarrhea, losses from an ileostomy, and carbonic anhydrase inhibitors. Disorders that cause losses of chloride, such as renal tubular acidosis, also cause a nonanion gap metabolic acidosis. (Cho et al, 2009, pp. 784- 788)

mc idiopathic nephropathy WW esp Asia and south american. Presents with hematuria following and upper respiratory infection

IgA nephropathy

What is the most common cause of kidney disease in North America? a. IgA nephropathy b. HTN c. Membranous nephropathy d. Renovascular nephropathy e. Diabetic nephropathy

The correct answer is E. The most common cause of kidney disease in North America is diabetic nephropathy, Choice (E). The most common cause of kidney disease worldwide is IgA nephropathy, Choice (A). Hypertension, Choice (B), is the second most common cause of kidney disease, right after diabetic nephropathy.