STEP - Renal & Resp Stuffs

1) Presence of casts indicates that hematuria or pyuria is of what origin? 2) Bladder CA, kidney stones show what in urine? 3) Acute cystitis show what in urine?

1) glomerular or renal tubular origin 2) hematuria, NO casts 3) pyuria, NO casts

Granular casts in urine mean what?

Acute tubular necrosis; muddy brown in appearance

A 64-year-old man comes to the hospital due to generalized weakness and fatigue for the past several weeks. He has a history of uncontrolled hypertension and nonadherence to medical therapy. Blood pressure is 160/100 mm Hg, pulse is 90/min, and respirations are 22/min. Oxygen saturation is 95% on room air. Physical examination shows elevated jugular venous pressure, bilateral crackles, and 3+ pitting edema in both legs. Laboratory results are as follows: BUN: 82 mg/dL Creatinine: 4.8 mg/dL Which of the following additional findings are most likely present?

Advanced chronic kidney disease typically involves the accumulation of unmeasured acidic compounds in the blood; therefore, anion gap metabolic acidosis with respiratory compensation is expected. ↓ pH, ↓ bicarb, 20 anion gap, PaCO2 = 28

A previously healthy 45-year-old male undergoes an elective hernia repair under spinal anesthesia. Postoperatively, he complains of difficulty voiding. Bladder catheterization shows a post-void residual of 300cc of urine. This patient would most likely benefit from which of the following medications?

Contraction of the detrusor muscle is stimulated by muscarinic cholinergic agonists. Bethanechol, a muscarinic agonist, often improves bladder-emptying in patients with post-surgery urinary retention.

Waxy casts in urine mean what?

End stage renal disease or chronic kidney disease

A 21-year-old male presents to his physician after noticing that his urine had a "frothy" appearance. He also complains of easy fatigability and anorexia. His past medical history is significant only for an upper respiratory infection several weeks ago. Physical examination reveals symmetric pitting edema of the ankles. Which of the following is most likely decreased in this patient?

Frothy, foamy urine may be caused by proteinuria or bile salts in the urine. This patient's history of a recent upper respiratory infection and ankle edema on physical exam suggest a diagnosis of nephrotic syndrome with associated low serum albumin. Hypoalbuminemia → ↓ plasma oncotic pressure and causes interstitial edema formation due to net plasma filtration. Minimal change disease (MCD) is the most common cause of nephrosis in children.

RBC casts in urine mean what?

Glomerulonephritis or HTN emergency

Causes for metabolic alkalosis (HCO3 > 28 mEq/L) ↑↑ pH + ↑↑ HCO3

H+ loss or HCO3 excess Loop diuretics (loss of Cl) Vomiting (loss of Cl) Antacid use Primary Hyperaldosteronism (loss of H)

Causes for Respiratory alkalosis (PCO2 < 36 mm Hg) ↑↑ pH + ↓↓ CO2

Hyperventilation: Anxiety or panic attacks Hypoxemia (↑ altitude) Salicylates (early reaction) Tumors Pulmonary embolism

Causes for Respiratory acidosis (PCO2 > 44 mm Hg) ↓↓ pH + ↑↑ PCO2

Hypoventilation Airway obstruction acute lung disease chronic lung disease opioids, sedatives weak respiratory muscles

The glomerular filtration rate (GFR) can be estimated by the _____ or ______ clearance, while the renal plasma flow (RPF) is calculated using the para-aminohippuric acid clearance. The filtration fraction (FF = GFR / RPF) is the fraction of the RPF that is filtered across the glomerular capillaries into Bowman's space. It is usually equal to ______% in healthy individuals.

Inulin or creatinine clearance FF is usually = 20% in healthy people

Causes for met acidosis w/ ↑ anion gap (accumulation of unmeasured acidic compounds)

MUDPILES Methanol (formic acid) Uremia (CKD) DKA Propylene glycol Iron tablets or INH Lactic acidosis Ethylene glycol (oxalic acid) Salicylates (late reaction)

Fatty casts or "oval fat bodies" in urine mean what?

NephrOtic syndrome (proteins); "maltese cross sign"

A 55-year-old man comes to the hospital due to progressive fatigue and weakness. Medical history includes type 2 diabetes mellitus and obesity. Laboratory results are as follows: Sodium: 138 mEq/L Chloride: 110 mEq/L Bicarbonate: 18 mEq/L Which of the following is the most likely diagnosis?

Renal Tubular Acidosis Nonanion gap metabolic acidosis (NAGMA) results from the loss of bicarbonate (HCO3−) (usually from the kidneys or gastrointestinal tract), leading to a relative increase in H+. Common causes include renal tubular acidosis and severe diarrhea. NAGMA is also referred to as hyperchloremic acidosis because the decrease in serum HCO3− is compensated for by an increase in serum chloride to maintain electronegative balance.

A 55-year-old man is evaluated due to worsening fatigue and exertional shortness of breath. He has no chronic medical conditions and takes no medications. Physical examination shows facial puffiness and bilateral lower extremity edema. Urinalysis shows 3+ proteinuria. Which of the following tests would be most helpful for establishing a specific diagnosis

Serum protein electrophoresis→ Renal amyloidosis Renal amyloidosis typically presents with proteinuria and nephrotic syndrome. The diagnosis is confirmed by kidney biopsy showing apple-green birefringence with Congo red stain under polarized light. Serum protein electrophoresis demonstrating a monoclonal protein helps establish the diagnosis of immunoglobulin light chain (AL) amyloidosis.

A 57-year-old man comes to the emergency department due to the abrupt onset of severe right eye pain and ipsilateral headache. The patient also has severe nausea and describes seeing halos around objects. After initial treatment with the appropriate medication, the pain severity decreases. Urine output also slightly increases, and the urine pH becomes more alkaline. The medication used to treat this patient's eye condition predominantly acts on which of the following nephron segments?

This patient with abrupt-onset unilateral headache and eye pain with nausea and visual halos likely has acute angle-closure glaucoma, which is characterized by ↑ IOP caused by impaired drainage of aqueous humor. Aqueous humor production is promoted by carbonic anhydrase; carbonic anhydrase inhibitors (eg, acetazolamide) rapidly ↓ IOP in patients with glaucoma. Carbonic anhydrase is also present in the renal PCT, where it catalyzes reactions necessary for bicarbonate (HCO3) reabsorption. By inhibiting carbonic anhydrase, acetazolamide blocks reabsorption of HCO3− in the PCT; the resulting urinary loss of HCO3− leads to mild diuresis with ↑ urine pH and consequent mild metabolic acidosis. Acetazolamide is often used to help offset the metabolic alkalosis that is commonly caused by loop diuretics.

A 67-year-old man comes to the office due to generalized weakness, easy fatigability, anorexia, and intermittent nausea for the past several months. He also says that he is "itching and scratching a lot." Physical examination shows bilateral lower extremity pitting edema and skin excoriations. Laboratory results show a SCr level of 3.4 mg/dL and a BUN of 48 mg/dL. A renal biopsy is performed. Light microscopy of the tissue sample shows widespread narrowing of the renal arterioles with deposition of homogeneous, glassy material in the vessel walls that stains pink with periodic acid-Schiff (PAS) stain. This patient most likely has which of the following underlying conditions?

This patient's symptoms (eg, fatigue, weakness, itching) are most likely due to accumulation of uremia toxins secondary to progressive CKD. His renal biopsy shows deposition of eosinophilic hyaline material in the intima and media of small arteries and arterioles, which is characteristic of hyaline arteriolosclerosis. It is typically seen in patients with untreated or poorly controlled hypertension (HTN) or diabetes mellitus. Chronic/repetitive endothelial injury caused by hemodynamic stress or hyperglycemia causes leakage of plasma constituents across the vascular endothelium and stimulates smooth muscle cell (SMC) proliferation and excessive EC matrix production. Malignant HTN (extreme or rapidly developing hypertension) causes fibrinoid necrosis and hyperplastic arteriolosclerosis. Fibrinoid necrosis is characterized by localized destruction of the vascular wall with a circumferential ring of pink, amorphous material surrounding the lumen. Hyperplastic arteriolosclerosis consists of onion-like, concentric thickening of the walls of arterioles due to laminated layers of SMCs with intervening basement membrane reduplication (onion skinning). This patient's lack of concentric SMC thickening and absence of vascular necrosis are more suggestive of hyaline arteriolosclerosis.

WBC in urine mean what?

Tubulointerstitial inflammation Acute pyelonephritis Transplant rejection

Benign prostatic hyperplasia leads to progressive bladder outlet obstruction. Over time, increased urinary pressures can cause ___________ and renal parenchymal atrophy with scarring. This can progress to chronic kidney disease.

hydronephrosis

Causes for metabolic acidosis w/ NORMAL anion gap (loss of HCO3)

HARDASS Hyperchloremia or Hyperalimentation Addison disease Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion

Therapy with _________ reduces the ability of the kidneys to concentrate urine primarily by antagonizing the action of vasopressin (antidiuretic hormone) in the collecting tubules and ducts. Nephrogenic diabetes insipidus caused by _______ usually resolves following discontinuation of the drug. However, impairment can be permanent following years of chronic use.

Lithium Antagonize ADH in the principle cells in the collecting duct

Hyaline casts in urine mean what?

Nonspecific finding, formed from Tamm-Horsfall mucoprotein secreted by renal tubular cells

A 5-year-old boy is brought to the office by his parents due to bed-wetting. The patient has stayed dry during the day since age 3 but has continued to wet the bed 4 or 5 nights a week. He urinates approximately 5 times during the day; the urinary stream is continuous and strong. Bowel movements occur daily and are soft. The patient is otherwise healthy and takes no daily medications. Height and weight are tracking along the 75th percentile. Vital signs and examination are normal. Urinalysis is unremarkable. This patient's bed-wetting is most likely caused by which of the following?

Primary nocturnal enuresis (ie, bed-wetting at age ≥5 without prior nighttime urinary continence) is caused primarily by a brain maturational delay in the development of bladder control.

A group of researchers is studying secondary hypertension in porcine models of renal artery stenosis. During an experiment, a clip is placed that constricts the right renal artery to 30% of its original cross-sectional area. A few days later, hemodynamic and biochemical measurements are recorded and compared to measurements obtained before clip placement. Which of the following changes is most likely to be seen in the experimental animals?

Unilateral renal artery stenosis causes hypoperfusion and activation of the renin-angiotensin-aldosterone system. Angiotensin II causes arteriolar vasoconstriction and increases aldosterone and antidiuretic hormone synthesis. The resultant hypertension helps reduce the decline in glomerular filtration rate in the affected kidney, but causes a pressure natriuresis with increased sodium excretion in the unaffected kidney.

A 76-year-old man comes to the office due to bilateral flank pain and nausea. The patient has not urinated for 24 hours. Medical history is significant for diet-controlled type 2 diabetes and degenerative arthritis of the knee. He occasionally takes naproxen for pain. Temperature is 36.9 C (98.4 F), blood pressure is 140/90 mm Hg, and pulse is 90/min. Cardiopulmonary examination reveals no abnormalities. Abdominal examination shows suprapubic fullness. Mild bilateral costovertebral angle tenderness is present. Laboratory results show a blood urea nitrogen level of 32 mg/dL and creatinine level of 2.6 mg/dL. Four weeks ago, laboratory studies were normal. Which of the following is the most likely cause of this patient's renal dysfunction?

Urethral compression Acute urinary retention is characterized by anuria and bladder distension and can result in hydronephrosis and acute kidney injury (ARF). A palpable, distended bladder is present on examination, and abdominal and flank pain may be present. The MCC of urinary retention is bladder outlet obstruction (urethral compression) due to BPH. Post renal azotemia: stones, BPH, neoplasm, congenital anomalies

A 73-year-old man comes to the office due to blood in his urine. He has noted bright red blood at the end of micturition on several occasions but has had no urinary frequency or pain with urination. The patient has a history of hypertension and chronic bronchitis. He has smoked a pack of cigarettes daily for 30 years. Temperature is 37 C (98.6 F). Abdominal, external genital, and rectal examinations are unremarkable. Urinalysis shows hematuria. Urine cytology is positive for malignant cells. Cystoscopy is planned for visualization and biopsy of suspected urinary tract cancer. Which of the following features would be most suggestive of a poor prognosis?

Urothelial (transitional cell) carcinoma is the most common type of bladder cancer. Tumor stage is the most important factor for determining prognosis and is based on the depth of invasion into the bladder wall and the degree of regional (eg, lymph nodes) and metastatic spread. Tumor invasion into the muscularis propria layer of the bladder wall carries an unfavorable prognosis.

__________ are vasopressin V2 receptor antagonists (ie, aquaretics) used to treat hyponatremia. _______ block the effects of antidiuretic hormone (vasopressin), increasing renal free water excretion without directly affecting excretion of sodium or potassium. Diuresis of free water with vaptans results in increased plasma osmolality, increased serum sodium, increased urine output, and lowered urine osmolality.

Vaptans (eg, tolvaptan)

A 65-year-old man comes to the office with a 2-day history of skin rash and low-grade fever. He has had no cough, shortness of breath, chest pain, vomiting, dysuria, or urinary frequency. The patient was recently diagnosed with acute gouty arthritis and has been taking indomethacin for the past 10 days. Temperature is 38.1 C (100.6 F), blood pressure is 130/90 mm Hg, and pulse is 86/min. Examination shows a diffuse, maculopapular skin rash. Mucosal surfaces are moist without any lesions. Cardiopulmonary examination shows no abnormities. There is no costovertebral angle tenderness. Serum creatinine is 2.3 mg/dL (baseline 1.1 mg/dL, 2 weeks ago). Urinalysis shows numerous white blood cells/hpf. Which of the following is the most likely cause of this patient's acute renal dysfunction?

This patient has a rash, fever, acute kidney injury, and pyuria following the introduction of indomethacin, which is consistent with acute interstitial nephritis (AIN). AIN is a common cause of renal dysfunction and is characterized by inflammatory infiltration of the renal interstitium, likely due to IgE- and T-cell-mediated HSN rxns. Up to 75% of AIN cases are due to medications, particularly nonsteroidal anti-inflammatory drugs (eg, indomethacin), antibiotics (eg, penicillins, rifampin), diuretics, and proton pump inhibitors. Clinical features of AIN resemble an allergic response and include fever, rash, and eosinophilia. Urinalysis typically demonstrates sterile pyuria; white blood cell casts, hematuria, and mild proteinuria may also be seen.

Chronic kidney disease (CKD) often causes hyperphosphatemia due to the impaired ability of the kidneys to excrete phosphorus. Hyperphosphatemia is thought to be the inciting event in the onset of CKD-related mineral bone disorder. Elevated blood phosphate triggers the release of ___________ from bone, which lowers calcitriol production and intestinal calcium absorption. Reduced circulating Ca, along with hyperphosphatemia, leads to secondary hyperparathyroidism. Dietary phosphorus restriction is recommended for patients with CKD. However, oral phosphate binders are usually needed if dietary restriction is not sufficient to lower phosphate levels. Phosphate binders can be calcium containing (eg, calcium carbonate/acetate) or non-calcium containing. ___________ is a nonabsorbable anion-exchange resin that binds intestinal phosphate to reduce systemic absorption. The resulting complex is eliminated in the feces.

FGF-23 Sevelamer

This patient with flank pain, low-grade fever, and hematuria has a _________. ___________ are most commonly caused by cardioembolic disease (ie, originating from the left atrium or ventricle). Atrial fibrillation, suggested by this patient's intermittent palpitations and history of sleep apnea, is the greatest risk factor, although emboli from mural thrombi (following myocardial infarction), prosthetic valves, or valvular vegetations (ie, endocarditis) are also implicated. Complete occlusion of the renal artery can occur more rarely due to direct arterial injury (eg, dissection, vasculitis) or hypercoagulable states (eg, antiphospholipid syndrome). The kidneys are predisposed to embolic infarctions due to their high perfusion rates and limited collateral circulation.

Renal infarct Renal infarctions are most commonly caused by cardioembolic disease; atrial fibrillation is the greatest risk factor. Clinical features include flank pain, nausea, vomiting, low-grade fever, and hypertension (due to renin release from hypoxic tissue). Gross pathology demonstrates sharply demarcated, yellow-white, wedge-shaped areas with surrounding hyperemia.

A 48-year-old woman comes to the emergency department due to worsening headache, blurred vision, and nausea for the past several days. She also has had ↓ urine output. Medical history is significant for systemic sclerosis. Blood pressure is 190/110 mm Hg and pulse is 96/min. Physical examination shows diffuse skin thickening involving the hands, face, and anterior chest. There are no focal neurologic deficits, but a flame-shaped retinal hemorrhage is present. Laboratory studies reveal ↑ BUN & SCr, which were within normal limits during a recent office visit. Urine microscopy shows no sediment. A primary injury to which of the following structures is the most likely cause of this patient's acute kidney injury?

Small Renal Vessels Scleroderma renal crisis (SRC) is a life-threatening complication of systemic sclerosis characterized by acute renal failure and severe hypertension. SRC is caused by immune-mediated injury to small renal vessels that leads to reduced renal perfusion due to vascular narrowing and obliteration.

A 64-year-old man comes to the office due to generalized edema, fatigue, and dyspnea on exertion for 2 months. The patient has a 25-year history of poorly controlled rheumatoid arthritis. Temperature is 36.9 C (98.4 F), blood pressure is 108/70 mm Hg, and pulse is 90/min. The patient is thin and appears chronically ill but is in no acute distress. There is no lymphadenopathy. Breath sounds are decreased at the lung bases. Musculoskeletal examination shows severe deformities of the hands and feet related to rheumatoid arthritis. There is pitting edema of both legs up to the knees. Peripheral pulses are normal. Urinalysis shows 4+ protein but is otherwise normal. A renal biopsy is performed. Which of the following histologic abnormalities is most likely to be seen in this patient's glomeruli?

AA amyloidosis results from excessive serum amyloid A produced in rheumatoid arthritis and other chronic inflammatory conditions. Renal disease, the most common manifestation, presents as nephrotic syndrome. Light microscopy shows amorphous pink deposits with apple-green birefringence on Congo red stain under polarized light.

A 30-year-old woman is evaluated for almost daily headaches and intermittent blurry vision. Medical history includes obesity but no other chronic conditions. Physical examination shows bilateral symmetric papilledema. There are no other focal neurological deficits. Brain imaging is normal, and blood cell counts and serum chemistry studies are within normal limits. Lumbar puncture reveals an elevated opening pressure, and idiopathic intracranial hypertension is diagnosed. Weight loss is advised, and the patient is prescribed acetazolamide therapy. Which of the following changes are most likely to occur in this patient over the next several days due to the medication?

Acetazolamide is a carbonic anhydrase inhibitor (weak diuretic). The drug also ↓ ICP and improves symptoms in patients with idiopathic intracranial hypertension. This effect is independent of the kidneys & is due to a ↓ rate of CSF production by the choroid plexus. Carbonic anhydrase inhibitors block reabsorption of sodium bicarbonate in the PCT, leading to ↑ excretion of HCO3-. This alkalinizes the urine (↑ pH) while ↓ blood pH → mild metabolic acidosis. Compensatory response: ventilation is ↑ to facilitate CO2 removal and ↓ blood PaCO2 (compensatory respiratory alkalosis). The overall diuretic effect is weak because most of the Na+ blocked from reabsorption in the PCT is reabsorbed distally. ↑ distal reabsorption of Na+ stimulates ↑ K+ excretion, leading to ↑ urine K and mild hypokalemia. Because paracellular calcium (Ca2+) reabsorption is coupled to Na+ reabsorption in the PCT, urinary Ca2+ excretion is slightly ↑ (total serum Ca2+ is slightly reduced). Answer: PaCO2 ↓, Total serum Ca ↓, Urine K ↑, urine pH ↑

A 73-year-old man comes to the emergency department with unstable angina. He undergoes coronary angiography via the femoral approach. A stent is placed in the right coronary artery, and the patient is discharged. He returns to the emergency department 2 days later with blue discoloration of his right toe. He has pain and mild tingling in the affected toe. Medical history is significant for hyperlipidemia and coronary artery disease. On physical examination, the right toe appears cyanotic, and there is livedo reticularis affecting the right thigh. Peripheral pulses in the lower extremities are bilaterally palpable. Serum creatinine is 2.8 mg/dL (preoperatively it was 1.0 mg/dL). Which of the following histopathologic findings would most likely be seen on biopsy of this patient's kidney?

Cholesterol clefts in the arterial lumen Invasive vascular procedures can be complicated by atheroembolic disease, which may involve the kidneys, GIT, CNS, and the skin. Light microscopy shows a partially or completely obstructed arterial lumen with needle-shaped cholesterol clefts within the atheromatous embolus. Atheroemboli only partially occlude the renal vessels, therefore acute tubular necrosis (ATN) does not typically occur early in the disease process. Complete vessel occlusion with resultant ATN can occur later (weeks to months) due to an endothelial inflammatory response. However, as opposed to toxin-induced ATN (eg, aminoglycosides), which causes diffuse, extensive proximal tubular injury, ischemic ATN typically causes patchy necrosis of the proximal tubules.

A 70-year-old man is brought to the hospital by his son for evaluation of worsening fatigue. The patient has not seen a physician in the past 15 years. He takes naproxen occasionally for knee arthritis. PE of the prostate shows no abnormalities. Laboratory results are as follows: Hemoglobin 10.5 g/dL Leukocytes 7,100/mm3 Platelets 150,000/mm3 Sodium 135 mEq/L Potassium 5.1 mEq/L BUN 45 mg/dL Creatinine3.0 mg/dL Urine sediment is unremarkable. Ultrasound examination shows bilateral small kidneys and no hydronephrosis. Kidney biopsy shows intimal thickening and luminal narrowing of the renal arterioles with evidence of glomerular sclerosis. Which of the following is most likely responsible for this patient's kidney disease?

Chronic hypertension can result in hypertensive nephrosclerosis, which is characterized by compensatory medial hypertrophy and fibrointimal proliferation; endothelial damage from elevated systemic pressure also leads to hyaline arteriolosclerosis. The narrowed arteriolar lumens cause a progressive decrease in renal blood flow, resulting in glomerular ischemia and fibrosis (glomerulosclerosis).

A researcher is studying the effect of various manipulations on kidney blood flow and glomerular filtration. What is most likely to both ↓ renal plasma flow and ↑ the filtration fraction?

Constriction of the EFFERENT arteriole ↑ capillary hydrostatic pressure or the Bowman's space oncotic pressure will ↑ GFR ↑ in capillary oncotic pressure or Bowman's space hydrostatic pressure will ↓ GFR. The filtration fraction (FF) can be calculated by dividing the GFR by the renal plasma flow (RPF). Increases in GFR or decreases in RPF will increase the FF.

A __________ anomaly is caused by abnormal extrinsic forces on a developing fetus. Talipes equinovarus (clubfoot) is an anomaly in which the foot is plantarflexed and pointed inward due to restricted in utero movement.

Deformation Risk factors include any condition that restricts fetal movement, such as breech presentation, uterine fibroids, or multiple gestation.

A 36-year-old woman with end-stage renal disease secondary to type 1 diabetes mellitus comes to the office for routine examination. The patient's medical history includes hypertension, diabetic retinopathy, and neuropathy. Hemodialysis was started 2 months ago along with an erythropoiesis-stimulating agent. She takes daily long- and short-acting insulin, lisinopril, and calcitriol. Her hemoglobin has increased from 7.4 g/dL to 10.2 g/dL over the past 2 months. Which of the following complications is most likely to be seen with the agent used to treat this patient's anemia?

Erythropoiesis-stimulating agents (ESAs) can substantially improve anemia symptoms, avoiding the need for blood transfusions in chronic kidney disease and dialysis patients. However, ESAs are associated with increased risk for hypertension and thromboembolic events.

A 30-year-old man is admitted to the intensive care unit after his wife found him unconscious at home. She says that he has lost a significant amount of weight recently despite no significant change in dietary habits. Laboratory studies show a serum pH of 7.1 and positive serum ketones. His mucus membranes are extremely dry. Treatment is initiated, and the patient's condition improves. However, he now has fever, headache, and eye pain. Examination of the nasal cavity shows a black necrotic eschar adherent to the inferior turbinate. Which of the following procedures would most likely reveal the pathogen responsible for this patient's infection?

Facial pain, HA, and nasal eschar in a patient with likely DKA (pH 7.1, positive ketones, and dry mucous membranes in a young patient with recent unintended weight loss) are suggestive of mucormycosis, caused by Mucor or Rhizopus. Mucosal (histo) biopsy is necessary for diagnosis. The fungi appear as ribbon-like broad nonseptate hyphae with right-angle branching. Tissue invasion is seen along blood vessels; vascular thrombosis and tissue necrosis can occur. A black necrotic eschar in the nasal cavity is characteristic. Management includes amphotericin B and surgical debridement.

A 42-year-old man comes to the office due to a 2-week history of reddish-brown urine, fatigue, joint pain, and a lower extremity rash. The patient has no medical history, and family history is unremarkable. He has had multiple sexual partners and only uses protection intermittently. Temperature is 37.7 C (99.9 F), blood pressure is 146/94 mm Hg, and pulse is 75/min. Palpable purpura and pitting edema are present in bilateral lower extremities. Laboratory results are as follows: Serum chemistry: SCr: 3.2 mg/dL Liver Fx studies: AST: 78 U/L ALT: 96 U/L Immuno studies: C3 & C4: ↓ UA: Protein: 3+ WBC: 2-3 RBC: many/hpf Casts: several Which of the following immunologic mechanisms is most likely responsible for this patient's renal injury?

Immune glomerular injury results from IC or neutrophil activation. IC formation in the kidney typically produces renal-limited disease (except anti-GBM/Goodpasture's disease). Preformed circulating IC deposition is usually associated with small vessel vasculitis and hypocomplementemia. This patient's AKI/ARF (eg, ↑ SCr), proteinuria, HTN, and glomerular hematuria (eg, red cell casts) are indicative of glomerulonephritis (GN). GN is commonly a manifestation of small vessel vasculitis (SVV), which usually has associated systemic symptoms (eg, fever, fatigue). GN due to SVV is immune-mediated by 3 possible mechanisms: 1) Ab vs Ag in the glomerulus w/ IC formation in the kidney 2. Preformed circulating IC vs endogenous or exogenous Ag, w/ subsequent deposition in the kidneys 3. Ab vs neutrophil Ag → neutrophil activation w/o significant IC deposition Several features of this patient's presentation suggest GN/SVV due to HCV (exogenous Ag). Evidence for HCV infection includes multiple sexual partners and ↑ aminotransferases. HCV-infected patients often produce cryoglobulins vs exogenous HCV-Ag that form circulating ICs → activate complement, causing hypocomplementemia. These circulating ICs can deposit in small vessels ("cryoglobulinemic vasculitis") affecting the kidney (eg, membranoproliferative GN), skin (eg, palpable purpura), and joints (eg, arthralgias).

A 60-year-old woman is being evaluated for abnormal renal function. She is found to have a serum creatinine of 2.2 mg/dL on routine laboratory monitoring; her creatinine level a year ago was 1.2 mg/dL. The patient has a history of nonischemic cardiomyopathy and systolic heart failure and has been on a stable medical regimen for the past 2 years. She has no dyspnea, fever, rash, or lower extremity swelling but has been taking ibuprofen for 2 weeks due to left knee osteoarthritis. UA reveals no abnormalities Ibuprofen is discontinued, and her kidney function returns to normal in a week. Which of the following best explains this patient's transient deterioration in renal function?

Impaired afferent arteriolar vasodilation Patients with intravascular volume depletion (eg, congestive heart failure, diarrhea, excessive diuresis) and chronic kidney disease depend on renal prostaglandin production to dilate the afferent glomerular arteriole and maintain the glomerular filtration rate. Nonsteroidal anti-inflammatory drugs inhibit prostaglandin synthesis, which can cause prerenal azotemia in at-risk patients.

A 75-year-old man comes to the office for follow-up of HTN. In recent weeks, his BP has consistently been 160-165/85-90 mm Hg. Medical history includes a right carotid endarterectomy for recurrent transient ischemic attacks, MI 2 years ago, and coronary artery bypass surgery for unstable angina 1 year ago. The patient currently takes metoprolol, clopidogrel, amlodipine, and rosuvastatin. He quit smoking 20 years ago and does not drink alcohol. The patient is compliant with his medical therapy and office visits. Ramipril is added to his medication regimen. One week later, SCr is 2.1 mg/dL, up from a baseline of 1.1 mg/dL. Assuming the patient's baseline urinalysis is normal, a repeat urinalysis at this time would most likely reveal which of the following?

In renal artery stenosis, ↑ production of AGII causes ↑ systemic BP (to increase renal perfusion) and preferential constriction of the glomerular efferent arteriole (to increase glomerular filtration). Patients with bilateral renal artery stenosis are dependent on this response to maintain renal function; initiation of ACE inhibitors or angiotensin II receptor blockers can precipitate ARF. However, urinalysis is typically unremarkable (ie, no hematuria, proteinuria, or casts).

A 62-year-old man is brought to the emergency department by ambulance following a motor vehicle collision. The patient is obtunded but responds to painful stimuli. Blood pressure is 160/90 mm Hg, pulse is 50/min, and respirations are 10/min. Brain imaging reveals diffuse axonal injury and cerebral edema but no intracranial hematoma. Intravenous mannitol is administered to treat elevated intracranial pressure. Thirty minutes later, the patient has worsening tachypnea and hypoxemia. Chest x-ray shows new bilateral interstitial infiltrates. Which of the following is the most likely cause of this patient's respiratory distress?

Intracranial pressure can be temporarily reduced with intravenous mannitol, an osmotically active agent that increases plasma oncotic pressure, causing water from the interstitial space to be drawn into the vascular compartment. In some patients (eg, history of heart failure, low left ventricular reserve function), rapidly increased intravascular volume can cause pulmonary edema by abruptly increasing pulmonary capillary hydrostatic pressure.

A 44-year-old man comes to the hospital due to acute onset of central chest pain radiating to the left arm. He used cocaine a few hours ago. Blood pressure is 160/100 mm Hg, pulse is 98/min, and respirations are 18/min. On examination, the patient appears anxious and diaphoretic. Electrocardiogram shows ST-segment elevation in the anterior leads. Laboratory studies reveal an elevated cardiac troponin level and a serum potassium concentration of 3.1 mEq/L. Which of the following is the most likely cause of this patient's hypokalemia?

Low serum potassium is a common medical condition that can result from several mechanisms, including decreased oral intake, renal or gastrointestinal loss, or increased entry into cells. This patient with a cocaine-induced myocardial infarction most likely developed acute hypokalemia due to stress-related beta-adrenergic hyperactivity, which causes potassium to shift intracellularly. Severe physiologic stress (eg, myocardial infarction, head injury) results in significant endogenous catecholamine (eg, norepinephrine, epinephrine) release. Epinephrine activates the beta-2 receptor, leading to increased activity of the sodium-potassium ATPase pump and the sodium-potassium-2-chloride cotransporter, both of which transport potassium intracellularly. Adrenergic activity also stimulates the release of insulin, which further promotes intracellular potassium shifting. Although cocaine does not directly stimulate beta-2 receptors, it does increase catecholamine release, likely worsening hypokalemia. Similar intracellular shifts can be seen with beta-agonist medications (eg, albuterol, dobutamine) and sympathomimetics (eg, pseudoephedrine). Patients with other sources of potassium loss (eg, diuretics, diarrhea) are at increased risk.

A 72-year-old woman is evaluated due to a month of fatigue and shortness of breath on exertion. The patient has also had lower back pain but no fever or cough. She takes valsartan for hypertension. Temperature is 37.2 C (99 F), blood pressure is 130/80 mm Hg, pulse is 84/min, and respirations are 14/min. On physical examination, the conjunctivae are pale. The remainder of the examination is normal. Laboratory results are as follows: Hb: 8.2 g/dL SCr: 2.1 mg/dL Ca: 11.2 mg/dL Total protein: 8.5 g/dL Albumin: 3.7 g/dL X-rays of the lower back demonstrate multiple areas of radiolucency in the L4 and L5 vertebrae. Serum protein electrophoresis reveals a monoclonal gamma globulin spike. Further studies are most likely to show which of the following?

MM is associated with ↑ bone resorption due to the production of tumor-related cytokines (TNFα). This results in ↑↑ SCa levels, which ↓ PTH production. ↓ PTH → ↓ renal Ca reabsorption (hypercalciuria), and, in combination with renal insufficiency → ↓↓ 1,25-dihydroxy vitamin D synthesis.

A 64-year-old man who recently moved to the area comes to the office for a new patient evaluation. He has chronic low back pain, resulting from an injury 8 years ago, for which he uses several over-the-counter analgesics. Most recently, the patient has been taking naproxen daily. He has no other joint pain, fever, rash, urinary symptoms, or other medical conditions. Blood pressure is 135/70 mm Hg and pulse is 78/min. Examination shows trace lower extremity edema. Neurologic and musculoskeletal examinations reveal no abnormalities. Laboratory results show blood counts within normal limits, blood urea nitrogen of 12 mg/dL, and serum creatinine of 2.0 mg/dL. Urinalysis reveals 1+ protein and 3-4 white blood cells/hpf. Renal ultrasound demonstrates bilateral shrunken and irregular kidneys with a few papillary calcifications. Which of the following is the most likely cause of this patient's renal dysfunction?

NSAIDs concentrate in the renal medulla along the medullary osmotic gradient, with higher levels in the papillae. These drugs uncouple oxidative phosphorylation and increase oxidative stress, resulting in damage to tubular and vascular endothelial cells. Prolonged use results in chronic interstitial nephritis visualized as patchy interstitial inflammation with subsequent tubular atrophy and fibrosis, papillary necrosis, and scarring. Grossly, the kidneys appear shrunken with irregular contours and distortion of the caliceal architecture. NSAIDs also ↓ PG synthesis → renal vasoconstriction which further ↑ risk of ischemic papillary necrosis. Analgesic nephropathy is a form of CKD caused by prolonged, heavy intake of NSAIDs or acetaminophen. Pathologic characteristics include chronic interstitial nephritis and papillary necrosis.

A 6-week-old term boy is brought to the office due to increased fussiness and poor weight gain. The patient has several wet diapers per day. His anterior fontanelle is flat and mucous membranes are dry. Laboratory results include the following: Na: 148 mEq/L K: 3.5 mEq/L ADH: ↑ Urinalysis shows a specific gravity of 1.002. Which of the following is the most appropriate treatment for this patient's condition?

Patient suffers from Nephrogenic DI Tx w/ frequent water supplementation and, paradoxically, thiazide administration (eg, hydrochlorothiazide). Thiazides appear to ↓ renal water losses in NDI by inducing a mild volume depletion or diuresis that ↑ Na and water reabsorption in the PCT. This ↓ the total amount of water delivered to the collecting ducts, allowing for better retention of supplemental water. Nephrogenic diabetes insipidus is characterized by polyuria, dilute urine (low urine specific gravity), hypernatremia, and high antidiuretic hormone. Treatment includes thiazide diuretics and replacement of water losses.

A 56-year-old man with type 2 diabetes mellitus, hypertension, and chronic kidney disease is found to have a persistently elevated serum potassium level. He takes lisinopril. Blood pressure is 130/90 mm Hg. Physical examination shows no abnormalities. The patient is prescribed patiromer therapy. Which of the following best describes the mechanism of action of this medication?

Patiromer is a nonabsorbable cation exchange resin that binds colonic potassium in exchange for calcium, trapping potassium within the resin where it is then excreted in the feces. It is often used for treatment of chronic hyperkalemia. However, onset of action takes several hours, so it is not recommended as monotherapy in acute hyperkalemia. Adverse effects include gastrointestinal disturbance (eg, diarrhea), hypokalemia, hypercalcemia (due to luminal exchange of calcium), and hypomagnesemia (due to off-target binding of other positive ions). Patiromer may also bind certain medications (eg, ciprofloxacin, levothyroxine)

A 45-year-old woman comes to the office due to polyuria and nocturia. She has no fever, dysuria, or abdominal pain. The patient has no significant medical problems and takes no medications. Her temperature is 36.7 C (98 F), blood pressure is 120/80 mm Hg, and pulse is 76/min. The patient's mucous membranes appear dry. The remainder of her physical examination is normal. Her urine output and osmolality remain unchanged with water deprivation for several hours, but after administration of desmopressin, urine output decreases and urine osmolality increases. Renal clearance of which of the following substances would decrease the most after this patient's injection?

Polyuria that resolves with the administration of desmopressin (DDAVP, synthetic analogue of vasopressin) is likely secondary to deficient vasopressin secretion (central DI). Vasopressin produces a V2 receptor-mediated ↑↑ in H2O permeability within the cortical and medullary collecting ducts. As water leaves the tubular fluid, urea concentration greatly increases in these tubular segments. Although the cortical collecting duct is impermeable to urea, vasopressin activates urea transporters in the medullary collecting duct, increasing urea reabsorption and decreasing renal urea clearance. This passive reabsorption of urea into the medullary interstitium in the presence of ADH significantly increases the medullary osmotic gradient, allowing the production of maximally concentrated urine.

A 24-year-old woman with a medical history of bronchial asthma comes to the office due to shortness of breath and wheezing for the past 2-3 days. She developed a cold 4 days ago and is not feeling well. The patient has a nebulizer at home and used multiple doses of albuterol with little response prior to arriving. She takes no other medications. The patient is diaphoretic and in moderate respiratory distress. Respiratory examination shows bilateral wheezing, diffusely decreased breath sounds, and increased use of accessory muscles of respiration. Laboratory results reveal a serum potassium of 3 mEq/L. Which of the following mechanisms is the most likely cause of this patient's hypokalemia?

Potassium is primarily stored intracellularly (~98% of total body stores) through the action of the Na-K-ATPase pump. Beta-adrenergic activity increases the activity of the Na-K-ATPase pump; therefore, both endogenous catecholamines and therapeutic beta-2 agonists (eg, albuterol, dobutamine) can cause transient hypokalemia due to increased transport of potassium intracellularly.

A 1-hour-old boy is in the neonatal intensive care unit due to tachypnea and hypoxia. The infant was born at 39 weeks gestation via cesarean delivery due to recurrent variable decelerations. The pregnancy was complicated by lack of prenatal care. The infant weighs 3.2 kg (7 lb 1 oz). Physical examination shows a flattened nose and bilateral club feet. Breath sounds are markedly diminished bilaterally. The infant is intubated and mechanically ventilated, but oxygen levels do not improve. He dies an hour later. Which of the following is most likely to be found during autopsy of this infant?

Renal agenesis This is likely Potter sequence, which is characterized by pulmonary hypoplasia, flat facies, and lower limb deformity (eg, club foot). Potter sequence is caused by a urinary tract anomaly → ↓ fetal urine output. It is classically associated with bilateral renal agenesis but can occur secondary to other etiologies, including posterior urethral valves or fetal exposure to ACE inhibitors. Because fetal urine is the main component of amniotic fluid, ↓ fetal urine output can lead to low or absent amniotic fluid levels (ie, severe oligohydramnios). Inadequate amniotic fluid levels allow for ↑ external compression of the fetal face (flat facies) and extremities (eg, club foot). In addition, the umbilical cord is often compressed such that fetal heart rate abnormalities (eg, recurrent decelerations) are common during labor. Amniotic fluid also provides the fluid and growth factors needed for fetal lung development. Therefore, neonates with Potter sequence have pulmonary hypoplasia due to the lack of normal alveolar distension by aspirated amniotic fluid. Both lungs are affected, and respiratory failure (ie, hypoxia) is the most common cause of death in affected infants.

A 43-year-old woman with borderline personality disorder is brought to the emergency department after taking an undetermined number of pills. She is lethargic but arousable. She refuses to answer questions. BP is 110/60 mm Hg and HR is 120/min and regular. Laboratory results are as follows: Serum chemistry: Sodium 139 mEq/L Potassium 3.3 mEq/L Chloride 98 mEq/L Bicarbonate 13 mEq/L Arterial blood gases on room air: pH 7.46 PaCO2: 19 mm Hg PaO2: 96 mm Hg Oxygen saturation 99% Which of the following best describes this patient's acid-base disturbance?

Salicylate poisoning causes mixed primary respiratory alkalosis and primary anion gap metabolic acidosis. Mixed acid-base disturbances can be recognized by inappropriate secondary compensation for one of the primary disturbances, indicating that an additional primary disturbance must be present. Early: Respiratory alkalosis (hyperventilation) Late: Met acidosis w/ ↑ anion gap OD: Tinnitus, AMS, hyperventilation, alkalosis, N/V, ↑T

A healthy 32-year-old man enrolls in a clinical study investigating potassium handling by the kidney. During the study period, he is given oral potassium supplements and potassium levels in the serum and urine are closely monitored. Compared to the amount of potassium delivered to the glomerular capillaries, the percentage of potassium remaining in this individual's tubular fluid is most likely to vary by which of the following amounts?

Several segments of the nephron are involved in the management of potassium (K+). However, most handle K+ at a relatively fixed rate that is independent of potassium load and do not play a significant role in the regulation of K+ excretion in the urine. These segments include the following: 1) Bowman's capsule: K+ is freely filtered across the glomerular membrane, the amount of K+ within Bowman's space is equal to that in the glomerular capillaries (ie, 100%) 2) PCT: Approximately 65% of the filtered K+ load is reabsorbed in the PCT, leaving ~35% of the total filtered load. 3) Ascending limb of the loop of Henle: Further resorbs about 25%-30% of the filtered K+ load through the action of the Na+/K+/2Cl- cotransporter → only 5-10% of K+ remaining in the tubular fluid after this segment Because this is a stable process, even in hyperkalemic states, patients will reabsorb the majority of filtered K+ in the PCT & ascending loop. Potassium regulation is therefore primarily mediated by the principal and α-intercalated cells of the late distal and cortical collecting tubules. Hypokalemia stimulates reabsorption of K+ via apically located H+/K+-ATPases on α-intercalated cells and can cause the amount of K+ in the collecting tubule to approach 1% of the filtered load. Conversely, an ↑ K+ load → principal cells to secrete K+ through apical K+ channels. High dietary K+ intake can cause the amount of K+ in the collecting tubules to actually exceed the filtered load (ie, >100%). Excessive K+ intake → ↑ K+ excretion through the following mechanisms: 1) High extracellular K+ levels directly stimulate basolateral Na+/K+ pumps on principal cells, increasing K+ secretion into the tubular fluid. 2) Elevated K+ levels also increase aldosterone secretion, which further enhances activity of principal cell Na+/K+ pumps and also increases their apical permeability to Na+ and K+ (leading to K+ loss in the tubular fluid).

A 52-year-old woman is evaluated due to 2 weeks of fever, fatigue, nonproductive cough, and dyspnea, which began shortly after visiting her family in Ohio. She also lost 1.5 kg (3.3 lb) over the same period. The patient has a history of rheumatoid arthritis and has been taking adalimumab for the past 6 months. She had negative tuberculosis skin testing prior to beginning the drug. Temperature is 38 C (100.4 F), blood pressure is 130/70 mm Hg, pulse is 92/min, and respirations are 18/min. Physical examination reveals bilateral lung crackles, mild generalized lymphadenopathy, and hepatosplenomegaly. Chest x-ray shows bilateral nodular densities and hilar lymphadenopathy. Urine testing is positive for a fungal antigen. Which of the following pathogenic processes is most important during the development of this patient's infection?

TNF-α inhibitors are associated with impairments to the cell-mediated immune response → ↑ risk of infx with intracellular bacteria and granulomatous fungi (Histoplasma capsulatum). Histoplasma replicates within the intracellular space of macrophages and can spread from the lungs to the lymph nodes and the RES (liver, spleen, bone marrow).

A 65-year-old man comes to the emergency department due to severe lower abdominal pain and nausea. He also has not been able to urinate for the past 24 hours. The patient has a history of hypertension and benign prostatic hyperplasia. On examination, a large mass is palpable in the suprapubic area. Multiple attempts at urethral catheterization are unsuccessful, and an ultrasound-guided midline suprapubic cystostomy is planned. Besides the bladder wall, which of the following structures is most likely to be penetrated by the trocar and cannula during the procedure?

The bladder is extraperitoneal. In the event of a suprapubic cystostomy, the trocar and cannula will pierce the layers of the abdominal (aponeurosis) wall but will not enter the peritoneum.

A 45-year-old man with a history of end-stage renal disease undergoes renal allograft transplantation. The donor kidney and proximal ureter are transplanted in the right iliac fossa, with implantation of the ureter into the patient's bladder. Six days following surgery, the donor kidney appears to be functioning well, but the patient develops fever and right lower quadrant abdominal pain. Imaging studies reveal a large pelvic fluid collection. Exploratory laparotomy is performed and discovers urinary leakage, with significant ischemia and necrosis of the transplanted ureter immediately adjacent to the site of implantation into the bladder. The proximal portion of the ureter appears normal. The healthy segment of this patient's transplanted ureter is most likely receiving blood from which of the following arteries?

The blood supply to the proximal ureter comes from branches of the renal artery. At the distal ureter, arterial blood supply arises from the superior vesical artery. In between, the arterial supply to the ureter is anastomotic and highly variable, with possible afferent branches from the gonadal, common and internal iliac, aorta, and uterine arteries. In a kidney transplant operation, the native kidneys are typically left in place, and the donor kidney is placed retroperitoneally in the right iliac fossa. Blood supply is established by anastomosing the donor renal artery with the recipient's external iliac artery. The proximal 1/3 of the donor ureter is preserved and used to establish continuity from the collecting system of the kidney to the recipient's bladder. Although the transplanted ureter will continue to receive blood through the donor's renal artery, the most distal portion may be susceptible to ischemia due to lack of anastomotic connections. Distal ureteral ischemia is a recognized complication of renal transplant and causes leakage of urine 5-10 days following transplant.

An 8-year-old boy is brought to the office due to acute facial puffiness. His mother reports that for the preceding 24 hours he has been easily fatigued and has had dark urine. The patient was treated for a skin infection 3 weeks ago but has no chronic medical conditions. Temperature is 36.1 C (97 F) and blood pressure is 140/94 mm Hg. Physical examination shows periorbital edema and mild pitting edema along the ankles. The remainder of the examination shows no abnormalities.

The fluorescent areas on the slide most likely indicate the presence of which of the following substances? This pediatric patient with nephritic syndrome (eg, periorbital edema, hematuria, hypertension) following a recent skin infection most likely has (PSGN), the most common cause of pediatric nephritic syndrome. This typically occurs after exposure to strains of group A Streptococcus that produce nephritogenic antigens that can activate the alternate complement pathway. These combine with antibodies to form immune complexes, which deposit on the glomerular basement membrane (GBM) and induce complement activation and inflammation. These immune complexes are visible on immunofluorescence microscopy as granular deposits of IgG, IgM, and C3 on the GBM and mesangium. Because these particular immune complexes tend to activate complement via the alternate pathway, the deposits rarely contain C1q or C4 (classic complement pathway components)

A 60-year-old woman comes to the office with intermittent flatulence, crampy abdominal pain, and watery diarrhea. Her symptoms started 2 months ago after she recovered from an episode of acute gastroenteritis associated with nausea, vomiting, and diarrhea. The patient's symptoms are worse after drinking "too much milk." She usually has 1 or 2 glasses of wine every evening with dinner. Physical examination is unremarkable. Initial laboratory evaluation, including serum chemistries, blood counts, stool cultures, and studies for ova and parasites, is negative. Which of the following is most likely decreased in this patient?

The patient is lactose intolerant; due to lactase non-persistence, prevalent in Asian & African populations. Lactase deficiency → incomplete hydrolysis of lactose into the glucose and galactose. The fermentation of undigested lactose by gut bacteria → ↑ production of short-chain FA (eg, acetate, butyrate, propionate) → acidifies the stool (↓ stool pH). During this process, H gas is produced → ↑ breath H content. ↑ amounts of undigested lactose in the bowel → ↑ stool osmolality, which attracts excess water in the bowel lumen, causing osmotic diarrhea.

A 2-week-old boy is brought to the clinic by his parents for evaluation of his umbilicus. The parents report that since the umbilical cord stump separated 2 days ago, there has been drainage from the umbilicus that increases when the patient cries. He is exclusively breastfed and continues to have normal wet diapers and stool output. The patient was born at term, and the pregnancy and delivery were uncomplicated. Vital signs are normal. Physical examination of the abdomen shows clear to pale yellow fluid leaking from the umbilical stump site with mucosal tissue at the base of the umbilicus. Samples are obtained for complete blood count. Laboratory results are as follows: Hemoglobin 14g/dL Platelets 240,000/mm3 Leukocytes 11,000/mm3 Neutrophils60% Lymphocytes32% Which of the following is the most likely cause of this patient's umbilical findings?

The urachus is a remnant of the allantois that extends from the bladder to the umbilicus. Failed obliteration of the allantois lumen can result in a patent urachus, which presents with urinary drainage from the umbilicus in the neonate.

A 27-year-old nursing assistant with a history of major depression and bulimia is brought to the emergency department after a suicide attempt. She claims to have ingested several diuretic pills 18 hours ago. The patient complains of frequent, large-volume urinations that started shortly after she ingested the pills. She has also been very thirsty but she denies nausea, vomiting, or diarrhea. Her temperature is 36.7 C (98 F), blood pressure is 96/60 mm Hg, pulse is 110/min, and respirations are 14/min. Physical examination shows dry oral mucosa and reduced skin turgor. Laboratory results are as follows: Sodium 122 mEq/L Potassium 2.8 mEq/L Chloride 84 mEq/L Bicarbonate 28 mEq/L Blood urea nitrogen 22 mg/dL Creatinine 1.4 mg/dL Calcium 11.4 mg/dL Albumin 3.9 g/dL Which of the following medications did this patient most likely ingest?

Thiazide and loop diuretics cause significant volume depletion, activating the renin-angiotensin-aldosterone system, which can lead to hypokalemia and metabolic alkalosis. Thiazide diuretics: hyponatremia and hypercalcemia Loop diuretics: hypocalcemia

A 28-year-old man is hospitalized following a motor vehicle collision complicated by severe hemorrhage. Over the next 8 hours his urine output is markedly decreased. Laboratory results reveal elevated blood urea nitrogen. The patient is given aggressive intravenous fluid hydration. After 24 hours of therapy, urine output is increased and blood urea nitrogen declines toward normal. Which of the following additional laboratory abnormalities suggests that this patient's initial oliguria is a compensation for volume contraction?

This patient developed symptoms of acute renal failure (ARF) (eg, low urine output, high blood urea nitrogen) after a massive hemorrhage. ARF can be classified according to 1 of 3 etiologies: Prerenal: Caused by decreased renal perfusion; the nephrons remain intact and tubular function is preserved. Etiologies include volume loss (eg, hemorrhage), low-output states (eg, myocardial infarction, congestive heart failure), or systemic vasodilation (eg, sepsis). Intrinsic: Caused by tubular epithelial or glomerular damage; resorptive capacity is lost. Etiologies include acute tubular necrosis (due to renal ischemia or nephrotoxins) or glomerular diseases (eg, glomerulonephritis, nephrotic syndrome). Postrenal: Caused by urinary tract obstruction with normal nephron capacity. Etiologies include bilateral calculi, enlarged prostate, or a renal tumor in an individual with a sole functional kidney. This patient with severe blood loss was at risk for prerenal and intrinsic renal failure; however, his rapid improvement with hydration suggests a prerenal (hypovolemic) etiology. His laboratory results reflect intact renal tubular function, with compensatory mechanisms to restore blood volume. Increased tubular sodium reabsorption results in low urine sodium (<20 mEq/L) and low fractional excretion of sodium (FENa), whereas increased water reabsorption leads to high urine osmolarity. Urea reabsorption also increases to help concentrate the urine, resulting in increased serum levels of urea; creatinine continues to be excreted, resulting in the characteristic BUN/creatinine ratio >20. In contrast, intrinsic ARF reflects tubular epithelium damage and loss of renal reabsorptive capacity. Water, sodium, and urea are excreted in the urine, leading to lower urine osmolarity, higher urinary sodium, higher urinary FENa, and a normal serum BUN/creatinine ratio.

A 1 week-old boy is evaluated in the hospital. The patient has been admitted due to urosepsis and is receiving antibiotic therapy. The mother received no prenatal care; the neonate was born at term via spontaneous vaginal delivery. Vital signs are normal. Examination shows lower abdominal distension with normal bowel sounds. The penis and scrotum appear normal. Renal ultrasonography and voiding cystourethrography reveal a diffusely thickened bladder wall with bilateral vesicoureteral reflux and hydronephrosis. Which of the following is the most likely cause of this patient's findings?

This patient has a diffusely thickened bladder wall with bilateral vesicoureteral reflux and hydronephrosis, findings consistent with bladder outlet obstruction. In newborn boys, the MCC is posterior urethral valves (PUVs). In utero, the urethra normally begins as a solid structure that canalizes to form its characteristic tubular structure. PUVs are likely due to incomplete canalization and are defined by a persistent urogenital membrane that obstructs the posterior urethra. The bladder outlet obstruction, which may be partial or complete, causes increased pressure in the proximal urinary tract, leading to the following: 1) Bladder distension with an increased contractile force required to overcome the obstruction, resulting in detrusor muscle hypertrophy and bladder wall thickening 2) Bilateral secondary vesicoureteral reflux due to higher pressure in the bladder relative to the ureters and hydronephrosis due to retrograde urine flow Diagnosis is often made via prenatal ultrasound, which may show oligohydramnios if the obstruction is severe. PUVs diagnosed after birth often present with lower abdominal distension, weak urinary stream (if the obstruction is partial), or urinary tract infection (UTI) due to urinary stasis and reflux.

A 45-year-old man comes to the emergency department due to urinary incontinence. He was diagnosed with multiple sclerosis a year ago after he developed transient acute vision loss in his right eye. A few weeks ago, he began having difficulty with his balance and had several episodes of urinary incontinence. The patient's walking has improved since, but he continues to urinate involuntarily. He has noticed increasing urinary frequency and cannot control the urge to urinate. His vital signs are normal. On examination, the patient has mild spastic paraparesis with increased reflexes in the lower extremities; bilateral Babinski sign; and a thoracic sensory level to pain, temperature, and vibration. An MRI of the spine reveals a new demyelinating lesion in the mid-thoracic spinal cord. Which of the following abnormalities will most likely be found on this patient's urodynamic studies?

This patient has urinary frequency and urge incontinence in the setting of an overactive or spastic bladder due to the presence of an upper motor neuron lesion in the spinal cord. Patients with multiple sclerosis often develop a spastic bladder a few weeks after developing an acute lesion of the spinal cord. Urodynamic studies show little or no residual urine after emptying as bladder contractility is normal but distensibility is poor. The bladder does not distend/relax properly due to loss of descending inhibitory control from the upper motor neuron.

A 58-year-old woman comes to the emergency department due to cramping mid-abdominal pain. Imaging shows a small bowel obstruction. Vital signs and laboratory studies, including complete blood count and comprehensive metabolic panel, are within normal limits. The patient is admitted to the hospital for nonsurgical management. Oral intake is withheld to promote bowel rest, and an isotonic saline infusion is administered for hydration. She has no vomiting or diarrhea and after 2 days the abdominal pain improves. Total administration of sodium chloride infusion was approximately 6 L. Which of the following changes have most likely occurred in this patient since the onset of her hospitalization? Blood pH? Serum bicarb? Serum Cl? Urine Na?

This patient likely has nonanion gap metabolic acidosis (NAGMA) due to infusion of excess normal saline. Excess sodium chloride increases serum chloride (Cl−) to cause hyperchloremia. Because Cl− and bicarbonate (HCO3−) are the predominant anions in the body, the increased serum Cl− causes intracellular shifting of HCO3− to maintain electronegative balance. This "loss" of HCO3− (reduced serum HCO3−) decreases blood pH. Infusion of excess normal saline also increases intravascular volume, which the kidneys respond to by increasing sodium (Na+) excretion, resulting in increased urine Na+. Other causes of NAGMA usually involve loss of HCO3− from the kidneys (eg, renal tubular acidosis) or gastrointestinal tract (eg, severe diarrhea). With these etiologies, serum Cl− is increased to compensate for the loss of HCO3−. Because of the inverse relationship between Cl− and HCO3−, NAGMA of any etiology is also referred to as hyperchloremic acidosis.

A 68-year-old man is evaluated in the hospital due to a pleural effusion. He has a history of base of tongue squamous cell carcinoma with involvement of multiple left anterior cervical lymph nodes. Two days ago, the patient underwent surgery to remove the tumor and the anterior cervical lymph nodes. Today, he has increasing shortness of breath, and chest x-ray reveals a large left pleural effusion. Which of the following was most likely injured during this patient's surgical procedure?

This patient with a pleural effusion 2 days after cervical lymph node removal most likely has a chylothorax due to intraoperative injury of the thoracic duct. It is most commonly injured during thoracic procedures (eg, esophagectomy) but can be injured in neck procedures as well (eg, cervical lymph node removal). Injury can result in leakage of lymph into either the neck or the thorax because a transected duct may retract into the chest

A 65-year-old hospitalized man is evaluated for decreased urine output and increased serum creatinine. The patient was admitted for 3-vessel coronary artery disease and underwent coronary artery bypass grafting surgery yesterday. Other medical conditions include type 2 diabetes mellitus and hypertension. He received a dose of intravenous vancomycin prior to the surgery for prophylaxis of surgical infection. The patient has also been receiving 100 mL/hour of intravenous normal saline for the past 24 hours. He is afebrile. Blood pressure is 130/80 mm Hg and pulse is 80/min. Examination shows bibasilar crackles. The abdomen is soft. Urine output over the past 6 hours is 100 mL. Laboratory results are as follows: Day of admission Today BUN 20 mg/dL 35 mg/dL SCr 1.3 mg/dL 2.5 mg/dL Urine sediment microscopy shows muddy brown casts. Which of the following is the most likely cause of this patient's current condition?

This patient with acute kidney injury (ARF) has muddy brown casts on urine microscopy; in the setting of recent major surgery this presentation suggests acute tubular necrosis (ATN) due to intraoperative renal ischemia. Surgeries complicated by significant blood loss or those requiring the use of cardiopulmonary bypass (eg, coronary artery bypass grafting) or aortic clamping can cause renal hypoperfusion. The risk is increased in the elderly and those with a history of chronic kidney disease, diabetes, or congestive heart failure. ATN is characterized by the presence of muddy brown granular casts composed of sloughed renal tubular epithelial cells. Patients have ↑ SCr, BUN:Cr <20:1 (indicating intrinsic renal pathology), and oliguria (low urine output). Histologically, flattened tubular epithelial cells with cellular necrosis and loss of the brush border are seen.

A 64-year-old man comes to the office due to persistent back pain, constipation, and easy fatigability for the last several months. Blood pressure is 115/75 mm Hg and pulse is 88/min. The patient has dry mucous membranes. Laboratory results are as follows: Hemoglobin: 8.6 g/dL MCV: 92 fL BUN: 68 mg/dL SCr: 3.8 mg/dL Total protein: 8.9 g/dL Albumin: 3.5 g/dL Renal biopsy is performed and light microscopy shows atrophic tubules, many of which contain large, obstructing, waxy casts that stain intensely with eosin. Which of the following is the most likely diagnosis in this patient?

This patient with back pain, fatigue, normocytic anemia, renal failure, and a gamma gap (serum total protein minus serum albumin ≥4 g/dL) likely has multiple myeloma (MM). MM is a lymphoproliferative disorder characterized by monoclonal plasma cell proliferation and production of monoclonal Ig . It should be suspected in elderly patients with any combination of hypercalcemia (causes constipation), normocytic anemia (causes fatigue), bone pain (often in the back and ribs due to lytic lesions), elevated gamma gap (due to the presence of large amounts of monoclonal proteins), or renal failure. Renal failure in MM is often caused by light chain cast nephropathy. Free light chains (Bence Jones proteins) are filtered by the glomerulus in small amounts and then reabsorbed in the tubules. When levels exceed reabsorptive capacity, light chains precipitate with Tamm-Horsfall protein and form casts that cause tubular obstruction and epithelial injury, leading to impaired renal function. On light microscopy, numerous large, glassy eosinophilic casts are seen. Deposition of light chain fragments in the glomerular mesangium and capillary loops can also cause renal failure in MM (amyloid light-chain amyloidosis).

A 34-year-old woman comes to the hospital with a 4-day history of abdominal cramps, nausea, and watery diarrhea. Today she developed dizziness on standing. Her child has had similar symptoms recently. The patient has no prior medical conditions and takes no medications on a regular basis. Blood pressure is 124/82 mm Hg while supine and 100/70 on standing; pulse is 98/min. Examination shows dry mucous membranes. The abdomen is soft and nontender. Laboratory results are as follows: Serum chemistry Sodium: 144 mEq/L BUN: 50 mg/dL SCr: 1.8 mg/dL Urinalysis Protein negative Red blood cells 0/hpf White blood cells 0-1/hpf Microscopy: few hyaline casts Urine sodium: 8 mEq/L Which of the following changes are most likely to be seen in this patient?

This patient with gastroenteritis has evidence of hypovolemia (dry mucous membranes, orthostatic dizziness/hypotension) and acute kidney injury. Decreased extracellular fluid volume stimulates compensatory mechanisms directed at maintaining systemic blood pressure and tissue oxygenation. This is largely driven by the sympathetic nervous system and the kidneys: 1) Activation of the renin-angiotensin-aldosterone system (RAAS) leads to elevated levels of angiotensin II (ATII), a potent vasoconstrictor that stimulates the release of aldosterone and endothelin 1. These increase sodium and water reabsorption and systemic vascular resistance to help maintain blood pressure. 2) Vasopressin (antidiuretic hormone) is released by the posterior pituitary in response to increased serum osmolarity and decreased systemic pressure; it increases urea and free water reabsorption by the renal collecting duct. 3) Increased sympathetic activity results in release of circulating norepinephrine and other catecholamines, which increases systemic vasoconstriction, renal sodium and water reabsorption, and heart rate. These neurohumoral mechanisms promote volume expansion and increase blood pressure, helping to maintain tissue perfusion. Laboratory studies characteristically reflect sodium, water, and urea reabsorption by the kidney, including low urine sodium (<20 mEq/L), low fractional excretion of sodium (<1%), and elevated blood urea nitrogen to creatinine ratio (>20:1). Urinary sediment is typically bland or may show hyaline casts (which suggest increased urine concentration).

A 35-year-old man who works as a nurse at a local hospital is brought to the emergency department due to confusion and lethargy. His temperature is 36.7 C (98 F), blood pressure is 86/48 mm Hg, pulse is 120/min, and respirations are 12/min. Arterial blood gas results show pH 7.54, PaCO2 49 mm Hg, and PaO2 85 mm Hg. Which of the following laboratory studies would be the most useful in determining the cause of this patient's acid-base abnormality?

This patient's arterial pH >7.45 is consistent with alkalemia. The PaCO2 is elevated (>40 mm Hg), indicating a respiratory acidosis, which does not explain the alkalemia. Therefore, primary metabolic alkalosis with respiratory compensation is most likely present. When the etiology of metabolic alkalosis is unknown, assessment of volume status and measurement of urine chloride can be helpful. Because low Cl- impairs renal excretion of HCO3-, total body chloride depletion often plays an important role in the pathogenesis of metabolic alkalosis. Etiologies of metabolic alkalosis that involve temporary chloride depletion (hypovolemia) will demonstrate low urine chloride and are amenable to treatment with Cl- repletion (saline responsive).