Assignment Level: Intermediate

Advanced MCQs for Nephrologists

Assess advanced clinical reasoning in IgA nephropathy pathology, Oxford MEST-C risk assessment, supportive care, rapidly progressive disease, and treatment decisions.

IgA Nephropathy — Advanced

Difficulty: Advanced

Test advanced clinical reasoning in IgA nephropathy pathology, Oxford MEST-C risk assessment, supportive care, rapidly progressive disease, and treatment decisions. This quiz contains 10 single-best-answer questions. Explanations are shown after quiz completion.

1 / 10

Which biopsy finding is most characteristic of IgA nephropathy on immunofluorescence microscopy?

Linear glomerular IgG deposition

Predominant mesangial IgA deposition

Full-house staining with C1q predominance

Purely subepithelial IgG4 deposits

IgA nephropathy is characterized by dominant or codominant mesangial deposition of IgA on immunofluorescence microscopy.

2 / 10

A patient with biopsy-proven IgA nephropathy has persistent proteinuria of 1.2 g/day despite optimized blood pressure control and maximized ACE inhibitor therapy. What is the most appropriate next principle of management?

Immediate cyclophosphamide for all patients

No follow-up because proteinuria is below 2 g/day

Further optimize supportive care and assess progression risk before disease-specific therapy

Long-term high-dose glucocorticoids without risk assessment

Supportive care remains foundational. Persistent proteinuria despite optimized care warrants reassessment of adherence, blood pressure, sodium intake, eGFR trajectory, and individualized consideration of disease-specific therapy.

3 / 10

Which histologic feature is included in the Oxford MEST-C classification of IgA nephropathy?

Linear IgG staining intensity

Anti-GBM antibody titer

Percentage of crescents only

Endocapillary hypercellularity

The Oxford classification includes mesangial hypercellularity, endocapillary hypercellularity, segmental sclerosis, tubular atrophy/interstitial fibrosis, and crescents (MEST-C).

4 / 10

A patient with IgA nephropathy presents with rapidly declining eGFR, hematuria, and crescents in 35% of glomeruli. Which concern is most important?

Benign isolated microscopic hematuria

Rapidly progressive IgA nephropathy requiring urgent assessment for aggressive therapy

Minimal-change disease

Alport syndrome

A rapid eGFR decline with extensive crescents suggests rapidly progressive IgA nephropathy, a high-risk presentation requiring urgent exclusion of alternative causes and consideration of immunosuppressive treatment.

5 / 10

Which clinical feature is associated with increased risk of progression in IgA nephropathy?

Transient hematuria that resolves completely

Normal blood pressure and stable eGFR

Persistent proteinuria and declining eGFR

Absence of proteinuria over repeated measurements

Persistent proteinuria, hypertension, reduced eGFR, and adverse histologic findings are associated with higher progression risk.

6 / 10

A patient with IgA nephropathy develops gross hematuria during an upper respiratory infection, followed by persistent microscopic hematuria. What pattern does this represent?

Post-streptococcal glomerulonephritis

Alport syndrome

Thin basement membrane disease exclusively

Synpharyngitic hematuria

IgA nephropathy classically causes synpharyngitic hematuria, occurring during or shortly after mucosal infection rather than after a prolonged latent period.

7 / 10

Which statement best describes the role of tonsillectomy in routine IgA nephropathy management?

It is mandatory for all biopsy-proven cases

It is not routine therapy and should not replace optimized nephroprotective care

It reliably prevents kidney failure in adults

It replaces renin–angiotensin system blockade

Tonsillectomy is not routine therapy for IgA nephropathy in most international practice settings and should not replace supportive kidney-protective treatment.

8 / 10

A patient with IgA nephropathy has nephrotic-range proteinuria, preserved eGFR, and biopsy showing minimal mesangial changes with diffuse foot-process effacement but no significant IgA deposits. Which alternative diagnosis should be considered?

Minimal-change disease with incidental or limited IgA deposits

Anti-GBM disease

Diabetic nephropathy

Amyloidosis as the only possibility

Nephrotic syndrome with diffuse foot-process effacement and minimal structural injury should prompt consideration of minimal-change disease, even if limited IgA deposits are present.

9 / 10

Which therapy is primarily aimed at reducing intraglomerular pressure and proteinuria in IgA nephropathy?

Cyclophosphamide

Rituximab in every patient

Plasma exchange

ACE inhibitor or angiotensin receptor blocker

Renin–angiotensin system blockade lowers intraglomerular pressure and proteinuria and is a core component of supportive management.

10 / 10

Before considering systemic glucocorticoids in a high-risk IgA nephropathy patient, which assessment is particularly important?

Whether the patient has isolated microscopic hematuria only

Whether proteinuria has ever been measured

Infection risk, metabolic toxicity, eGFR, and whether supportive care has been optimized

Whether blood pressure is untreated

Systemic glucocorticoids carry substantial infection and metabolic risks. The decision should incorporate kidney risk, eGFR, comorbidities, infection risk, and optimization of supportive care.

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The average score is 100%

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Intermediate MCQs for Nephrologists

Assess emergency recognition and management of hyperkalemia, ECG toxicity, potassium redistribution, chronic treatment, and dialysis indications.

Hyperkalemia — Intermediate

Difficulty: Intermediate

Test your clinical reasoning in ECG toxicity, emergency treatment, potassium redistribution, medication causes, chronic treatment, and dialysis indications. This quiz contains 10 single-best-answer questions. Explanations are shown after quiz completion.

1 / 10

Which ECG finding is classically associated with early hyperkalemia?

Peaked T waves

U waves

Prolonged QT interval

Diffuse ST elevation

Tall, narrow, peaked T waves are a classic early ECG manifestation of hyperkalemia. Progressive toxicity can cause PR prolongation, QRS widening, and sine-wave morphology.

2 / 10

A patient has potassium 7.2 mmol/L with widened QRS complexes. Which treatment should be given immediately to stabilize the cardiac membrane?

Intravenous calcium gluconate

Oral sodium polystyrene sulfonate

Intravenous furosemide only

Insulin without glucose

Intravenous calcium stabilizes the cardiac membrane and is indicated for hyperkalemia with ECG changes. It does not lower serum potassium, so potassium-shifting and removal therapies are also required.

3 / 10

In a patient with severe hyperkalemia and no contraindication, what is the expected effect of intravenous insulin with glucose?

Redistribution of potassium into cells

Immediate removal of potassium from the body

Increased gastrointestinal potassium absorption

Inhibition of aldosterone secretion

Insulin stimulates Na+/K+-ATPase activity and shifts potassium intracellularly. Glucose is co-administered to reduce the risk of hypoglycemia.

4 / 10

Which medication most commonly causes hyperkalemia by reducing aldosterone-mediated potassium excretion?

Spironolactone

Amlodipine

Furosemide

Doxazosin

Spironolactone antagonizes the mineralocorticoid receptor, reducing distal sodium reabsorption and potassium secretion.

5 / 10

A patient with chronic kidney disease has persistent potassium 5.8 mmol/L without ECG changes despite dietary counseling. Which intervention can promote gastrointestinal potassium elimination?

A potassium-binding agent such as patiromer

Intravenous calcium gluconate alone

Sodium bicarbonate in every case

A thiazide-free diet

Patiromer binds potassium in the gastrointestinal tract and can support chronic hyperkalemia management. It is not a substitute for emergency membrane stabilization when ECG toxicity is present.

6 / 10

Which laboratory pattern most strongly suggests pseudohyperkalemia?

High serum potassium with normal plasma potassium and marked hemolysis

High serum and plasma potassium with ECG changes

Low serum potassium with thrombocytopenia

High urine potassium with severe hypokalemia

Pseudohyperkalemia is suspected when serum potassium is high but plasma potassium is normal, often due to hemolysis, difficult phlebotomy, thrombocytosis, or leukocytosis.

7 / 10

A patient with diabetic kidney disease has hyperkalemia, normal-anion-gap metabolic acidosis, and low renin activity. Which disorder is most likely?

Type 4 renal tubular acidosis

Distal renal tubular acidosis

Proximal renal tubular acidosis

Respiratory acidosis

Type 4 RTA is associated with hypoaldosteronism or aldosterone resistance, impaired potassium excretion, and hyperchloremic metabolic acidosis.

8 / 10

After insulin and glucose for severe hyperkalemia, when is rebound hyperkalemia most likely to occur?

After the intracellular shift effect wears off if potassium removal was not achieved

Only after calcium administration

Before insulin has any effect

Never, because insulin removes potassium

Insulin redistributes potassium but does not eliminate it. Rebound can occur within hours unless potassium is removed through urine, the gastrointestinal tract, or dialysis.

9 / 10

A patient with life-threatening hyperkalemia has advanced kidney failure, pulmonary edema, and minimal urine output. Which definitive treatment is most appropriate?

Urgent hemodialysis

Oral calcium carbonate

Observation with repeat ECG tomorrow

Fluid restriction alone

Hemodialysis rapidly removes potassium and is indicated when severe hyperkalemia is refractory or accompanied by advanced kidney failure, oliguria, or other urgent dialysis indications.

10 / 10

Which dietary counseling point is most appropriate for a patient with recurrent hyperkalemia and CKD?

Review potassium sources and avoid indiscriminate substitution with processed foods containing potassium additives

Avoid all fruits and vegetables permanently

Increase potassium-containing salt substitutes

Use salt substitutes freely because they contain no sodium

Dietary counseling should identify high-potassium foods and potassium additives while preserving nutritional quality. Potassium-containing salt substitutes can worsen hyperkalemia.

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The average score is 0%

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Intermediate MCQs for Nephrologists

Assess your clinical reasoning in primary and mixed acid–base disorders, compensation, anion-gap interpretation, and renal tubular acidosis.

Acid–Base Disorders — Intermediate

Difficulty: Intermediate

Test your clinical reasoning in primary and mixed acid–base disorders, compensation, anion-gap interpretation, and renal tubular acidosis. This quiz contains 10 single-best-answer questions. Explanations are shown after quiz completion.

1 / 10

A 54-year-old patient has a serum bicarbonate of 16 mmol/L, chloride 116 mmol/L, and sodium 140 mmol/L after several days of profuse diarrhea. Which acid–base disorder best explains these findings?

High-anion-gap metabolic acidosis

Normal-anion-gap metabolic acidosis

Metabolic alkalosis

Respiratory acidosis

The anion gap is 140 − (116 + 16) = 8 mmol/L, which is normal. Gastrointestinal bicarbonate loss from diarrhea produces hyperchloremic, normal-anion-gap metabolic acidosis.

2 / 10

A patient with metabolic acidosis has a serum bicarbonate concentration of 12 mmol/L. Using Winter’s formula, which arterial PCO2 is most consistent with appropriate respiratory compensation?

12 mmHg

26 mmHg

40 mmHg

52 mmHg

Winter’s expected PCO2 is approximately 1.5 × HCO3− + 8 ± 2, or 26 ± 2 mmHg. A substantially higher value suggests concurrent respiratory acidosis.

3 / 10

A patient has sodium 140 mmol/L, chloride 100 mmol/L, and bicarbonate 10 mmol/L. Albumin is normal. What is the calculated serum anion gap?

10 mmol/L

20 mmol/L

30 mmol/L

50 mmol/L

The anion gap is Na − (Cl + HCO3−) = 140 − (100 + 10) = 30 mmol/L, indicating a high-anion-gap metabolic acidosis.

4 / 10

A patient with diabetic ketoacidosis has bicarbonate 10 mmol/L and PCO2 35 mmHg. What additional acid–base process is present?

Concurrent respiratory alkalosis

Concurrent respiratory acidosis

Concurrent metabolic alkalosis only

No additional process

Winter’s expected PCO2 is about 23 ± 2 mmHg. A measured PCO2 of 35 mmHg is too high, indicating inadequate ventilation and a concurrent respiratory acidosis.

5 / 10

Which finding most strongly supports distal (type 1) renal tubular acidosis?

Urine pH below 5.0 during systemic acidosis

Persistent urine pH above 5.5 during systemic acidosis

Hyperkalemia with low renin

Marked glucosuria with normal serum glucose

In distal RTA, the collecting duct cannot adequately secrete hydrogen ions, so urine pH remains inappropriately high—usually above 5.5—even during systemic metabolic acidosis.

6 / 10

A patient with diabetic kidney disease has normal-anion-gap metabolic acidosis and persistent hyperkalemia. Which mechanism is most likely?

Excessive distal hydrogen secretion

Reduced aldosterone activity or resistance

Increased ammonium excretion

Primary respiratory alkalosis

Type 4 RTA results from hypoaldosteronism or aldosterone resistance, causing impaired potassium and acid excretion. Hyperkalemia is a characteristic clue.

7 / 10

A patient with vomiting has metabolic alkalosis, low urine chloride, and evidence of volume depletion. Which treatment is most appropriate initially?

Intravenous isotonic saline

Intravenous sodium bicarbonate

Acetazolamide as sole therapy

Immediate hemodialysis

Vomiting causes chloride and volume depletion, producing saline-responsive metabolic alkalosis. Isotonic saline restores effective volume and chloride delivery, allowing renal bicarbonate excretion.

8 / 10

In chronic respiratory acidosis, by approximately how much does serum bicarbonate increase for each 10-mmHg increase in PCO2 above 40 mmHg?

1 mmol/L

2 mmol/L

3.5–4 mmol/L

10 mmol/L

With chronic respiratory acidosis, renal compensation increases bicarbonate by approximately 3.5–4 mmol/L for every 10-mmHg increase in PCO2.

9 / 10

A patient with tinnitus and tachypnea has a high-anion-gap metabolic acidosis and a low PCO2. Which exposure most likely produces this mixed disorder?

Opioids

Salicylates

Thiazide diuretics

Pure methanol exposure

Salicylates stimulate the respiratory center, causing respiratory alkalosis, and later produce high-anion-gap metabolic acidosis.

10 / 10

A patient has sodium 138 mmol/L, chloride 100 mmol/L, bicarbonate 12 mmol/L, and albumin 2 g/dL. What is the best interpretation after albumin correction?

The anion gap is normal and no additional process is present

The measured gap is 26 mmol/L and is substantially elevated after correction

The patient has isolated metabolic alkalosis

Albumin has no meaningful effect on the anion gap

The measured anion gap is 26 mmol/L. Because the normal gap falls as albumin falls, correcting for albumin increases the estimated gap further, confirming significant high-anion-gap acidosis.

Your score is

The average score is 70%

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MCQs for Nephrologists

Acute Kidney Injury (AKI) MCQs for Nephrologists

1 / 10

1-A 68-year-old male with a history of alcoholic cirrhosis (MELD score 25), ascites, and spontaneous bacterial peritonitis is admitted with a serum creatinine (SCr) of 2.5 mg/dL, up from a baseline of 1.0 mg/dL three months ago. His mean arterial pressure is 75 mmHg, and his urine output is 400 mL in the past 24 hours. After a 1 L albumin 25% bolus, his SCr is 2.8 mg/dL. Which of the following is the most appropriate next step in management?

Administer furosemide to challenge for a diuretic response.

Initiate broad-spectrum antibiotics for presumed sepsis.

Start terlipressin and albumin infusion.

Place a transjugular intrahepatic portosystemic shunt (TIPS).

2 / 10

2- A 55-year-old female with a history of hypertension and type 2 diabetes undergoes coronary angiography with contrast. Her baseline SCr is 1.8 mg/dL. Two days later, her SCr is 2.4 mg/dL. Which of the following statements regarding the prevention of contrast-induced AKI (CI-AKI) is most accurate?

Oral N-acetylcysteine (NAC) is a proven and effective prophylactic agent

Prophylactic renal replacement therapy is indicated in high-risk patients.

sodium bicarbonate is not superior to Intravenous isotonic saline to for prevention

The risk of CI-AKI is independent of the volume of contrast administered.

3 / 10

3- A 42-year-old male is admitted to the ICU with septic shock. His SCr has increased from 0.9 mg/dL to 2.1 mg/dL in 24 hours, and his urine output is 0.4 mL/kg/h for the past 12 hours. A urine sample is sent for biomarker analysis. Which of the following biomarker profiles would be most consistent with intrinsic AKI due to acute tubular necrosis (ATN)?

Low urine NGAL, low urine KIM-1

High urine NGAL, high urine KIM-1

High urine NGAL, low urine KIM-1

Low urine NGAL, high urine KIM-1

4 / 10

4- A 72-year-old female with acute decompensated heart failure (ADHF) develops worsening renal function (SCr increase from 2.0 to 3.0 mg/dL). Her central venous pressure (CVP) is 18 mmHg. Which of the following interventions is most likely to improve her renal function?

Increase the dose of her ACE inhibitor

Administer a bolus of intravenous normal saline

Initiate aggressive diuresis with a loop diuretic infusion

Start a dobutamine infusion.

5 / 10

5- A 60-year-old male with a history of CKD stage 3 (eGFR 45 mL/min/1.73m2) is scheduled for a non-urgent CT scan with contrast. Which of the following is the most appropriate strategy to minimize the risk of CI-AKI?

Administer oral hydration with water for 12 hours pre-procedure.

Start an infusion of 0.9% saline at 1 mL/kg/h for 6-12 hours pre-procedure and continue for 6-12 hours post-procedure

Administer a single dose of furosemide immediately before contrast administration.

No specific measures are needed as his eGFR is >30 mL/min/1.73m2.

6 / 10

6. A 35-year-old female with lupus nephritis is admitted with AKI (SCr 3.5 mg/dL). A kidney biopsy shows diffuse proliferative glomerulonephritis with cellular crescents in 60% of glomeruli. Which of the following is the most appropriate initial treatment?

High-dose oral prednisone.

Intravenous cyclophosphamide and pulse methylprednisolone.

Mycophenolate mofetil and rituximab.

Plasmapheresis and intravenous immunoglobulins (IVIG).

7 / 10

7. A 58-year-old male with AKI is on continuous renal replacement therapy (CRRT). His pre-filter ionized calcium is 1.25 mmol/L, and his post-filter ionized calcium is 0.25 mmol/L. He is receiving a standard citrate-based replacement fluid. Which of the following complications is he at highest risk for?

Metabolic acidosis

Metabolic alkalosis

Hypercalcemia

Hypocalcemia

8 / 10

8. A 45-year-old patient with a history of rhabdomyolysis develops AKI with a peak SCr of 5.0 mg/dL. His urine output improves, and his SCr starts to decline. During the recovery phase of AKI, which of the following electrolyte abnormalities is most likely to occur?

Hyperkalemia

Hypocalcemia

Hyperphosphatemia

Hypokalemia

9 / 10

9. A 65-year-old male with a history of prostate cancer treated with radiation therapy presents with a SCr of 4.0 mg/dL. A renal ultrasound shows bilateral hydronephrosis. Which of the following is the most appropriate initial management?

Immediate initiation of hemodialysis.

Placement of bilateral percutaneous nephrostomy tubes

Administration of a fluid challenge.

A trial of tamsulosin

10 / 10

10. A 28-year-old pregnant woman at 32 weeks gestation presents with a blood pressure of 160/110 mmHg, proteinuria (3+), and a SCr of 1.5 mg/dL. Her platelet count is 80,000/mm3, and her liver enzymes are elevated. Which of the following is the most definitive treatment for her AKI?

Labetalol infusion.

Magnesium sulfate infusion.

Delivery of the fetus

Plasma exchange.

Your score is

The average score is 46%

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Assignment Level: Intermediate

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