Nephrology USMLE Practice Questions
Renal physiology, electrolytes, and kidney diseases.
5 free nephrology practice questions
Pick an answer and check it. After each question you get the same explanation StepGenie students see: the stem decoded clue by clue, the reasoning chain with its infographic, why every wrong option is wrong, and the trap the question was built around. Step 1 questions test mechanism; Step 2 CK questions ask for the next step.
A 31-year-old woman presents to a walk-in clinic with a 2-day history of dysuria, urinary frequency, urgency, and intense suprapubic pain. She recently returned from a short honeymoon trip to Prague. Vital signs are within normal limits, including a temperature of 36.5°C (97.7°F). Physical examination is notable for marked suprapubic tenderness. Costovertebral angle tenderness is absent, and pelvic examination is normal. Which of the following organisms is most likely to be isolated in this patient?
Correct answer · E
Staphylococcus saprophyticus
Decoding the stem
Step-by-step reasoning
Step 1 of 5
Dysuria, frequency, urgency, and suprapubic pain with normal vitals indicate acute uncomplicated cystitis (lower urinary tract infection).
Step 2 of 5
Absence of fever and costovertebral angle tenderness localizes infection to the bladder, not kidneys (rules out pyelonephritis).
Step 3 of 5
Patient is a young sexually active woman (honeymoon trip implies recent intercourse), a classic risk group for Staphylococcus saprophyticus UTIs.
Step 4 of 5
Among UTI pathogens, E. coli is most common overall, but among Gram-positive cocci, Staph saprophyticus is strongly associated with young sexually active females.
Step 5 of 5
Therefore, the most likely organism isolated from her urine culture is Staphylococcus saprophyticus.
Why not the others?
A. Streptococcus agalactiae
This option implies Group B Strep, associated with neonatal sepsis/meningitis and UTIs in pregnant or chronically ill adults, BUT this patient is a healthy, nonpregnant woman with classic uncomplicated cystitis and a stronger association with Staph saprophyticus.
B. Enterococcus faecalis
This option implies Enterococcal UTI, which is more common in hospitalized patients, those with catheters, or after antibiotic use, BUT this patient is an otherwise healthy outpatient with classic honeymoon cystitis.
C. Proteus mirabilis
This option implies a urease-positive, motile Gram-negative rod causing alkaline urine and often struvite stones, BUT there is no history of stones, flank pain, or recurrent infections; demographic and context more strongly fit Staph saprophyticus.
D. Klebsiella pneumoniae
This option implies a nosocomial or complicated UTI (often in diabetics, alcoholics, or hospitalized patients), BUT the vignette describes an otherwise healthy young woman with community-acquired honeymoon cystitis, classically linked to Staph saprophyticus.
Exam trap
Students may default to more common UTI organisms (e.g., Enterococcus, Klebsiella) by patterning on generic UTI, but the key demographic—young sexually active woman on honeymoon—specifically points to Staphylococcus saprophyticus as a classic exam association.
The bottom line
Staphylococcus saprophyticus causes acute cystitis in young sexually active women: dysuria, frequency, suprapubic pain, afebrile, no CVA tenderness.
A 32-year-old woman presents with a 2-month history of fatigue, muscle weakness, paresthesias, headache, and palpitations. Her pulse is 75/min and blood pressure is 152/94 mm Hg. Physical examination is unremarkable. Further evaluation reveals low serum renin activity. Lab Values: - Sodium: 144 mEq/L - Potassium: 2.9 mEq/L - Bicarbonate: 31 mEq/L - Creatinine: 0.7 mg/dL Which of the following is the most likely diagnosis?
Correct answer · C
Aldosteronoma
Decoding the stem
Step-by-step reasoning
- 1
Young patient with hypertension (152/94) and symptoms like headache/palpitations suggests a possible secondary, endocrine cause of HTN rather than simple essential hypertension.
- 2
Lab findings show hypokalemia (K 2.9) and metabolic alkalosis (HCO3− 31), pointing toward increased mineralocorticoid activity (↑Na reabsorption, ↑K and H+ secretion).
- 3
Increased mineralocorticoid effect can result from primary hyperaldosteronism (adrenal) or secondary hyperaldosteronism (renin-driven, e.g., renal artery stenosis).
- 4
The crucial clue is low serum renin activity, meaning the kidney is not driving aldosterone; aldosterone secretion is autonomous and suppressing renin via negative feedback.
- 5
Autonomous aldosterone secretion with low renin, hypokalemia, metabolic alkalosis, and hypertension = primary hyperaldosteronism most commonly due to an aldosterone-producing adenoma (aldosteronoma).
Why not the others?
A. Renal artery stenosis
This option implies secondary hyperaldosteronism driven by renal ischemia → renin should be high, BUT this patient has low renin activity, arguing against this mechanism.
B. Cushing syndrome
This option implies excess cortisol, which can cause HTN and sometimes hypokalemia, BUT we’d expect central obesity, striae, glucose abnormalities; also renin is not characteristically low solely from cortisol excess in this stereotypical pattern.
D. Laxative abuse
This option implies GI potassium and bicarbonate loss, leading to hypokalemia but typically metabolic acidosis or mixed picture, and does not explain hypertension or low renin.
E. Pheochromocytoma
This option implies catecholamine-secreting tumor with episodic severe HTN, sweating, tremor, anxiety, and normal K+, BUT this patient has chronic HTN, hypokalemia, metabolic alkalosis, and low renin, favoring aldosterone excess instead.
Exam trap
Hypokalemia and hypertension may push you toward renal artery stenosis or Cushing, but careful attention to low renin and metabolic alkalosis specifically localizes the problem to primary aldosterone excess (aldosteronoma), not a renin-driven or cortisol-driven process.
The bottom line
Primary hyperaldosteronism (aldosteronoma): HTN, hypokalemic metabolic alkalosis, low renin, normal creatinine due to autonomous adrenal aldosterone secretion.
A 48-year-old man presents to the emergency department with sudden onset right flank pain that began 3 hours ago. He also reports gross hematuria. Over the past 2 weeks, he has developed progressive lower extremity swelling and a 4-kg (9-lb) weight gain. Physical examination reveals bilateral 2+ pitting edema of the lower extremities. Urinalysis shows 4+ protein, positive glucose, and multiple red blood cell and fatty casts. Abdominal CT demonstrates an enlarged right kidney with prominent collateral vessels and a filling defect in the right renal vein. Which of the following is the most likely underlying cause of this patient’s symptoms?
Correct answer · C
Loss of antithrombin III
Decoding the stem
Step-by-step reasoning
Step 1 of 6
Massive proteinuria (4+), edema, weight gain, and fatty casts define nephrotic syndrome.
Step 2 of 6
In nephrotic syndrome, large plasma proteins are lost in the urine, including antithrombin III.
Step 3 of 6
Loss of antithrombin III decreases natural anticoagulant activity, shifting hemostasis toward a hypercoagulable state.
Step 4 of 6
Hypercoagulability in nephrotic syndrome commonly leads to venous thromboses, especially renal vein thrombosis.
Step 5 of 6
Renal vein thrombosis presents with acute flank pain, hematuria, and imaging showing a renal vein filling defect and enlarged kidney.
Step 6 of 6
Therefore, this patient’s symptoms are best explained by loss of antithrombin III due to nephrotic-range protein loss.
Why not the others?
E. Antiphospholipid antibodies
This option implies antiphospholipid syndrome, which causes recurrent miscarriages and arterial/venous thromboses, BUT there is no history of autoimmune disease, miscarriages, or typical lab markers; nephrotic findings (heavy proteinuria, fatty casts) directly point to a renal protein-loss mechanism instead.
A. Factor V Leiden
This option implies an inherited activated protein C resistance thrombophilia, which causes DVT/PE, BUT the stem emphasizes new-onset nephrotic syndrome as the key change before thrombosis, indicating an acquired hypercoagulability (antithrombin loss) rather than a lifelong genetic disorder.
B. Increased lipoprotein synthesis
This option implies hyperlipidemia of nephrotic syndrome, which explains fatty casts, BUT hyperlipidemia itself does not directly cause an acute renal vein thrombosis; the specific prothrombotic mechanism is loss of antithrombin III.
D. Malignant erythropoietin production
This option implies erythrocytosis from EPO-producing tumors (e.g., renal cell carcinoma), which can enlarge the kidney, BUT the vignette shows nephrotic-range proteinuria, edema, and a clear venous filling defect without polycythemia or mass lesion typical of RCC.
Exam trap
The vivid renal vein thrombosis imaging can tempt you to pick any generic thrombophilia (e.g., Factor V Leiden). The key is to link the new nephrotic syndrome (massive proteinuria, edema, fatty casts) to its classic complication: urinary loss of antithrombin III causing a hypercoagulable state and renal vein thrombosis.
The bottom line
Nephrotic syndrome (heavy proteinuria, edema) causes urinary loss of antithrombin III, predisposing to renal vein thrombosis with flank pain and hematuria.
A 61-year-old man presents with 2 weeks of decreased urine output and malaise following an emergency coronary catheterization with stent placement for unstable angina. His medical history is significant for type 2 diabetes mellitus and osteoarthritis of the hips. Before hospitalization, he was taking insulin and naproxen; after the coronary intervention, aspirin, clopidogrel, and metoprolol were added. His temperature is 38°C (100.4°F), pulse is 93/min, and blood pressure is 125/85 mm Hg. Physical examination reveals mottled, reticulated, purplish discoloration of the feet. Renal biopsy shows intravascular spindle-shaped vacuoles. Labs: - Hemoglobin: 14 g/dL - Leukocyte count: 16,400/mm3 - Segmented neutrophils: 56% - Eosinophils: 11% - Lymphocytes: 31% - Monocytes: 2% - Platelet count: 260,000/mm3 - Erythrocyte sedimentation rate: 68 mm/h - Blood urea nitrogen: 25 mg/dL - Creatinine: 4.2 mg/dL Which of the following is the most likely cause of this patient's symptoms?
Correct answer · E
Cholesterol embolization
Decoding the stem
Step-by-step reasoning
- 1
Patient had recent coronary catheterization which can mechanically disrupt atherosclerotic plaques in large arteries (aorta, renal arteries).
- 2
Disrupted plaques release cholesterol crystals into the bloodstream → embolize to small- and medium-sized arteries in kidney, skin, and other organs.
- 3
In the kidney, cholesterol emboli lodge in arterioles, causing ischemia and subacute acute kidney injury (rising creatinine over days–weeks).
- 4
In the skin, small-vessel occlusion leads to livedo reticularis and purplish, mottled discoloration of the distal extremities.
- 5
Cholesterol crystals trigger an inflammatory reaction with eosinophilia and elevated ESR, reflecting systemic inflammation.
- 6
On biopsy, cholesterol is dissolved during processing, leaving intravascular spindle-shaped/needle-shaped clefts, the classic pathologic sign.
- 7
Together—post-catheterization, AKI, livedo reticularis, eosinophilia, and cholesterol clefts—confirm cholesterol embolization as the cause.
Why not the others?
A. Contrast-induced nephropathy
This option implies direct tubular toxicity/ischemia causing AKI within 24–72 hours of contrast, BUT this patient’s decline is over 2 weeks and is accompanied by livedo reticularis, eosinophilia, and biopsy cholesterol clefts—findings not seen in contrast nephropathy.
B. Renal papillary necrosis
This option implies medullary ischemia due to factors like sickle cell disease, diabetes, or chronic analgesic use, with gross hematuria and sloughed papillae, BUT this patient has skin ischemia (livedo), eosinophilia, and characteristic vascular biopsy changes instead of papillary sloughing.
C. Allergic interstitial nephritis
This option implies a drug-induced hypersensitivity (e.g., from NSAIDs, penicillins) causing AKI, eosinophilia, and often rash, BUT it does not cause livedo reticularis or intravascular spindle-shaped vacuoles; biopsy would show interstitial inflammatory infiltrates, not cholesterol clefts.
D. Analgesic nephropathy
This option implies chronic NSAID overuse leading to chronic interstitial nephritis and papillary necrosis, BUT this patient has an acute/subacute decline after a vascular procedure and biopsy shows cholesterol clefts, not chronic scarring or papillary necrosis.
F. Eosinophilic granulomatosis with polyangiitis
This option implies a small-vessel vasculitis with asthma, allergic rhinitis, and sinus disease plus eosinophilia, BUT the patient lacks respiratory/allergic features; timing after catheterization and biopsy cholesterol clefts indicate emboli, not ANCA-associated vasculitis.
G. Polyarteritis nodosa
This option implies necrotizing medium-vessel vasculitis often associated with hepatitis B, causing systemic symptoms, neuropathy, and mesenteric ischemia, BUT there is no hepatitis history or classic neuropathy/GI ischemia, and biopsy shows cholesterol clefts rather than transmural necrotizing arteritis of varying ages.
Exam trap
The presence of eosinophilia and recent new medications may push you toward allergic interstitial nephritis, but the key association is post-catheterization plus livedo and biopsy clefts pointing specifically to cholesterol embolization.
The bottom line
Cholesterol atheroembolism after vascular procedure → acute kidney injury, livedo reticularis, eosinophilia, ↑ESR; biopsy shows cholesterol clefts (spindle-shaped vacuoles).
A 63-year-old woman comes to the physician for a routine health maintenance visit. She reports intermittent fatigue, pruritic skin, and a gradual decrease in urine output over the past 2 years. Her medical history is significant for hypertension and type 2 diabetes mellitus complicated by diabetic nephropathy. Current medications include insulin, furosemide, amlodipine, a multivitamin, and recently initiated erythropoietin prescribed by her nephrologist. She adheres to a diet low in salt, protein, potassium, and phosphorus. Temperature is 37°C (98.6°F), pulse is 80/min, and blood pressure is 145/87 mm Hg. Physical examination reveals 1+ bilateral ankle edema. Lab Values: - Hemoglobin: 9.8 g/dL - Glucose: 98 mg/dL - Albumin: 4 g/dL - Sodium: 145 mEq/L - Chloride: 100 mEq/L - Potassium: 5.1 mEq/L - Blood urea nitrogen: 46 mg/dL - Creatinine: 3.1 mg/dL Which of the following complications is the most common cause of death in patients receiving long-term treatment for this patient's renal condition?
Correct answer · G
Cardiovascular disease
Decoding the stem
Step-by-step reasoning
- 1
Patient has long-standing diabetes with nephropathy, reduced urine output, elevated BUN/creatinine, uremic symptoms, and EPO therapy → advanced chronic kidney disease/ESRD.
- 2
ESRD patients are typically on or being prepared for long-term dialysis or transplant; question asks about complications in patients receiving long-term treatment for this renal condition.
- 3
ESRD causes hypertension, volume overload, dyslipidemia, chronic inflammation, vascular calcification, and anemia, all of which increase cardiac workload and damage vessels.
- 4
These changes accelerate atherosclerosis, promote left ventricular hypertrophy, and predispose to arrhythmias and heart failure.
- 5
Epidemiologic data show that in ESRD patients on long-term dialysis, the most common cause of death is cardiovascular disease (MI, sudden cardiac death, heart failure), not infection or malignancy.
Why not the others?
A. Malignancy
This option implies cancer-related mortality. ESRD patients do have a slightly increased cancer risk, BUT epidemiologically cardiovascular events far exceed malignancy as a cause of death.
B. Malnutrition
This option implies protein-calorie malnutrition and cachexia. While malnutrition can occur in ESRD (especially on restricted diets), it is not the leading cause of death; cardiovascular events are more common.
C. Discontinuation of treatment
This suggests death from stopping dialysis or therapy. Some patients do withdraw from dialysis, BUT population data show cardiovascular disease still accounts for the largest share of mortality.
D. Infection
ESRD and dialysis increase infection risk (e.g., catheter-related sepsis), BUT in large cohorts, cardiovascular disease remains the predominant cause of death, surpassing infections.
E. Anemia
Anemia of CKD causes fatigue and contributes to LVH, BUT it is treated (as in this patient with erythropoietin) and is not usually the direct cause of death; it instead feeds into cardiovascular mortality.
F. Gastrointestinal bleeding
Uremia can cause platelet dysfunction and GI bleeding, BUT this is far less common as a terminal event than myocardial infarction, heart failure, or arrhythmia in ESRD patients.
H. Cerebrovascular disease
Stroke risk is increased in ESRD, BUT overall, ischemic heart disease and other cardiac deaths occur more frequently than fatal strokes in this population.
Exam trap
ESRD is associated with many serious complications (infection, anemia, malnutrition), so it is tempting to pick these. However, population-level outcomes data show cardiovascular disease is by far the leading cause of death in dialysis and advanced CKD patients; knowing the epidemiology is key.
The bottom line
End-stage renal disease on dialysis most commonly leads to death from cardiovascular disease due to accelerated atherosclerosis, LVH, and arrhythmias.
Source: StepGenie question bank. Questions are written by StepGenie, not taken from NBME or USMLE materials, and are chosen for this page by how students actually performed on them (first-attempt accuracy on StepGenie). Selection last refreshed September 5, 2026.
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Nephrology — Frequently Asked Questions
How do you distinguish prerenal from intrinsic acute kidney injury?
Use the fractional excretion of sodium and the urine sediment together. Prerenal injury shows avid sodium retention with a fractional excretion below one percent, a high BUN to creatinine ratio, and bland sediment. Acute tubular necrosis shows a fractional excretion above two percent with muddy brown granular casts, because damaged tubules can no longer reabsorb sodium.
What is the systematic way to solve an acid-base question?
Check the pH to name the primary disorder, then confirm whether the primary change is respiratory or metabolic from the pCO2 and bicarbonate. Calculate the anion gap on every metabolic acidosis. Then check whether compensation matches the expected degree, because compensation that falls short or overshoots reveals a second, mixed disorder hiding in the vignette.
Which urinary casts point to which diagnosis?
Red blood cell casts indicate glomerulonephritis. White blood cell casts indicate interstitial nephritis or pyelonephritis. Muddy brown granular casts indicate acute tubular necrosis. Fatty casts and oval fat bodies accompany nephrotic syndrome. Hyaline casts are non-specific and can appear in concentrated urine from a healthy person, so they rarely drive the answer.
How do you separate nephritic from nephrotic syndrome?
Nephritic syndrome is an inflammatory picture with hematuria, red blood cell casts, hypertension and a moderate degree of proteinuria. Nephrotic syndrome is defined by heavy proteinuria with hypoalbuminemia, edema and hyperlipidemia, and the urine shows fatty casts rather than red cell casts. The distinction narrows the differential before you consider a specific disease.
Are the nephrology practice questions on this page free?
Yes. The 5 questions above come from StepGenie's question bank and can be answered here without an account, with the full explanation shown after each one. From the link under the set you can try three more Nephrology questions in the dashboard preview, also without an account; a free account is what lets you choose the system and keep going.