Nephrology — MCQs
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Milk-Alkali syndrome may be caused by ingestion of
Which condition can present both as nephritic syndrome and nephrotic syndrome?
Chronic kidney disease is defined as the presence of a diminished GFR for at least?
A 20-year-old smoker presents with hemoptysis and hematuria. What is the most likely diagnosis?
A 60-year-old male with a history of COPD and heart failure presented with shortness of breath and signs of right-sided heart failure. He was catheterized and initiated on treatment. After 8 days, he developed right flank pain, high-grade fever, and rigors. Examination revealed cloudy urine in the catheter and pain in the urethral region. Urine microscopy and culture were performed. Ultrasound of the abdomen showed pyelonephritis of the right kidney. Urine studies indicated increased WBCs. The isolated organism, when Gram stained, showed tiny deep pink colonies on MacConkey agar. Colonies grown on tellurite agar are provided. The organism is heat-resistant and can grow in 40% bile, 6.5% NaCl, and at pH 9.6. To which of the following drugs is this organism intrinsically resistant?
Hyperkalemia is caused by which of the following conditions?
What is the GFR (mL/min per 1.73m2) for a patient in stage IV of chronic kidney disease?
Which of the following is NOT a feature of Chronic Renal Failure?
A 42-year-old female presents with diazepam and alcohol overdose. She is comatose with a temperature of 34.5°C, BP of 100/80 mmHg, and creatinine of 2.4 mg/dL. Her AST is 500 IU/L and GGT is 35 IU/L. Urine dipstick showed 3+ for blood, but urine analysis was normal. Ultrasound abdomen was normal. What is the most likely diagnosis?
A 45-year-old patient on hemodialysis for one week has noted that his blood pressure is more difficult to control. He reports good compliance with his medications, which include erythropoietin, ferrous sulfate, vancomycin, and vitamin D. His blood pressure is 180/99 mm Hg. What is the most likely cause for the worsening control of his blood pressure?
Nephrology Indian Medical PG Practice Questions and MCQs
Question 401: Milk-Alkali syndrome may be caused by ingestion of
- A. Calcium carbonate (Correct Answer)
- B. Magnesium sulfate
- C. Aluminium trisilicate
- D. Aluminium hydroxide
Explanation: **Explanation:** **Milk-Alkali Syndrome (MAS)** is a clinical triad of **hypercalcemia, metabolic alkalosis, and acute kidney injury (AKI)**. It is caused by the excessive ingestion of calcium and absorbable alkali. [1] **Why Calcium Carbonate is correct:** Calcium carbonate is the most common culprit because it provides both a high concentration of elemental calcium and a source of alkali (carbonate). 1. **Hypercalcemia:** Excessive calcium intake leads to increased intestinal absorption, causing hypercalcemia. This induces renal vasoconstriction and a "calcium-sensing receptor" mediated diuresis, leading to volume depletion. 2. **Alkalosis:** The carbonate component acts as a buffer. Hypercalcemia also inhibits the parathyroid hormone (PTH), which increases bicarbonate reabsorption in the proximal tubule, further worsening alkalosis. [1] 3. **Renal Failure:** The combination of volume depletion and hypercalcemic vasoconstriction leads to AKI and potential nephrocalcinosis. **Why other options are incorrect:** * **Magnesium sulfate:** Used primarily as an osmotic laxative or for eclampsia; it does not contain calcium or significant absorbable alkali. * **Aluminium trisilicate & Aluminium hydroxide:** These are non-absorbable antacids. While they can cause phosphate depletion, they do not lead to hypercalcemia or the classic MAS triad. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Modern Etiology:** Historically caused by "Sippy’s diet" (milk and cream for peptic ulcers), it is now most commonly seen in women taking **calcium carbonate supplements for osteoporosis prevention**. * **PTH Levels:** In MAS, PTH is typically **suppressed** (unlike primary hyperparathyroidism). * **Lab Findings:** Hypercalcemia, hypocalciuria (due to alkalosis enhancing calcium reabsorption), and metabolic alkalosis. [1] * **Treatment:** Aggressive hydration with isotonic saline and discontinuation of the offending agents.
Question 402: Which condition can present both as nephritic syndrome and nephrotic syndrome?
- A. Minimal change disease
- B. Acute proliferative glomerulonephritis
- C. Rapidly progressive glomerulonephritis
- D. Membranoproliferative glomerulonephritis (Correct Answer)
Explanation: **Explanation:** **Membranoproliferative Glomerulonephritis (MPGN)** is the correct answer because it is a unique glomerular disease characterized by both basement membrane thickening (membranous feature) and mesangial cell proliferation (proliferative feature). This dual pathology allows it to present across a wide clinical spectrum. While it often presents with **nephrotic-range proteinuria**, the underlying inflammatory/proliferative process frequently causes **nephritic features** such as hematuria, hypertension, and azotemia. **Analysis of Options:** * **Minimal Change Disease (A):** This is the classic cause of "pure" nephrotic syndrome. It involves podocyte effacement without inflammation, meaning hematuria and hypertension are typically absent. * **Acute Proliferative Glomerulonephritis (B):** Also known as PSGN, this is the prototype for **nephritic syndrome**. While mild proteinuria can occur, it rarely reaches the massive levels required for nephrotic syndrome. * **Rapidly Progressive Glomerulonephritis (C):** This is an aggressive **nephritic** condition characterized by crescent formation and a rapid decline in GFR. It is not a primary cause of nephrotic syndrome. **NEET-PG High-Yield Pearls:** * **MPGN Morphology:** Look for "Tram-track" appearance or "double contouring" of the basement membrane on Silver stain due to mesangial interposition. * **Complement Levels:** MPGN is associated with **hypocomplementemia**. Type II MPGN (Dense Deposit Disease) is specifically linked to **C3 Nephritic Factor**. * **Other "Mixed" Presentations:** Besides MPGN, **Systemic Lupus Erythematosus (SLE)** and **Amyloidosis** (rarely) can also show overlapping nephritic-nephrotic features.
Question 403: Chronic kidney disease is defined as the presence of a diminished GFR for at least?
- A. 1 month
- B. 3 months (Correct Answer)
- C. 6 months
- D. 12 months
Explanation: **Explanation:** The definition of **Chronic Kidney Disease (CKD)** is based on the **KDIGO (Kidney Disease: Improving Global Outcomes)** guidelines. CKD is defined as abnormalities of kidney structure or function, present for **>3 months**, with implications for health [1]. **Why 3 months is correct:** The 3-month threshold is used to distinguish "chronic" disease from "acute" kidney injury (AKI) or transient conditions. A persistent reduction in the Glomerular Filtration Rate (GFR <60 mL/min/1.73 m²) or markers of kidney damage (such as albuminuria, electrolyte abnormalities, or structural changes on imaging) for at least 90 days indicates irreversible loss of nephrons or permanent structural damage [1]. **Why other options are incorrect:** * **1 month:** This duration falls under the category of **Acute Kidney Disease (AKD)**. AKD describes kidney damage or decreased GFR lasting less than 3 months but more than the 7-day window used for AKI. * **6 and 12 months:** While these durations certainly qualify as chronic, they are not the minimum diagnostic criteria. Waiting for 6–12 months would unnecessarily delay diagnosis and the initiation of Reno-protective therapies. **High-Yield Clinical Pearls for NEET-PG:** * **Markers of Kidney Damage:** Even if GFR is >60, a patient can be diagnosed with CKD if they have persistent **Albuminuria** (AER ≥30 mg/24h; ACR ≥30 mg/g). * **Staging:** CKD is staged from G1 to G5 based on GFR [1]. **Stage G3a** begins when GFR drops below 60 [1]. **Stage G5** (Kidney Failure) is GFR <15 [1]. * **Most Common Cause:** Globally and in India, **Diabetes Mellitus** is the leading cause of CKD, followed by Hypertension [1]. * **Small Kidneys:** On ultrasound, bilateral shrunken kidneys (<8–9 cm) are a hallmark of CKD, except in cases like Diabetes, Amyloidosis, and Polycystic Kidney Disease (PKD), where kidneys may be normal or enlarged.
Question 404: A 20-year-old smoker presents with hemoptysis and hematuria. What is the most likely diagnosis?
- A. Goodpasture syndrome (Correct Answer)
- B. Nephrotic syndrome
- C. Guillain-Barré syndrome
- D. IgA Nephropathy
Explanation: ### Explanation **Correct Answer: A. Goodpasture syndrome** **Medical Concept:** Goodpasture syndrome (Anti-GBM disease) is characterized by the presence of circulating antibodies against the **alpha-3 chain of Type IV collagen**. This specific collagen is found in the basement membranes of both the **pulmonary alveoli** and the **renal glomeruli**. This leads to the classic clinical dyad of **Pulmonary Hemorrhage (Hemoptysis)** and **Rapidly Progressive Glomerulonephritis (Hematuria)** [2]. Smoking is a known risk factor that triggers pulmonary involvement by increasing alveolar capillary permeability, allowing antibodies to access the basement membrane. **Analysis of Incorrect Options:** * **B. Nephrotic syndrome:** Typically presents with heavy proteinuria (>3.5g/day), edema, and hypoalbuminemia, rather than hemoptysis and gross hematuria. * **C. Guillain-Barré syndrome:** An acute inflammatory demyelinating polyradiculoneuropathy presenting with ascending muscle weakness and areflexia; it has no primary renal or pulmonary hemorrhagic manifestations. * **D. IgA Nephropathy:** The most common cause of glomerulonephritis worldwide. While it presents with hematuria (often "synpharyngitic"), it does not typically cause pulmonary hemorrhage/hemoptysis [1]. **High-Yield NEET-PG Pearls:** * **Immunofluorescence (IF):** Shows **Linear IgG deposits** along the glomerular basement membrane (Pathognomonic). * **HLA Association:** Strongly associated with **HLA-DR2**. * **Treatment:** The triad of **Plasmapheresis** (to remove antibodies), Corticosteroids, and Cyclophosphamide [2]. * **Differential Diagnosis:** Always consider Granulomatosis with Polyangiitis (GPA), but GPA is usually associated with upper respiratory tract involvement (sinusitis) and c-ANCA positivity.
Question 405: A 60-year-old male with a history of COPD and heart failure presented with shortness of breath and signs of right-sided heart failure. He was catheterized and initiated on treatment. After 8 days, he developed right flank pain, high-grade fever, and rigors. Examination revealed cloudy urine in the catheter and pain in the urethral region. Urine microscopy and culture were performed. Ultrasound of the abdomen showed pyelonephritis of the right kidney. Urine studies indicated increased WBCs. The isolated organism, when Gram stained, showed tiny deep pink colonies on MacConkey agar. Colonies grown on tellurite agar are provided. The organism is heat-resistant and can grow in 40% bile, 6.5% NaCl, and at pH 9.6. To which of the following drugs is this organism intrinsically resistant?
- A. Cephalosporins (Correct Answer)
- B. Aminoglycosides
- C. Vancomycin
- D. Linezolid
Explanation: ***Cephalosporins*** - **Enterococcus** species have **intrinsic resistance** to cephalosporins due to their **low-affinity penicillin-binding proteins (PBPs)**, making these antibiotics ineffective against enterococci. - This resistance is **inherent** to the organism's structure and is not acquired through genetic mutations or plasmids. *Aminoglycosides* - Enterococci are **not intrinsically resistant** to aminoglycosides, though they show **low-level resistance** due to poor uptake. - **Synergistic combinations** with cell wall-active agents like ampicillin can overcome this resistance and achieve bactericidal effects. *Vancomycin* - **Vancomycin-sensitive enterococci (VSE)** are susceptible to vancomycin and it remains a first-line treatment for serious enterococcal infections. - **Vancomycin resistance (VRE)** is an **acquired resistance** mechanism, not intrinsic, involving van gene clusters that alter cell wall precursors. *Linezolid* - Enterococci are generally **susceptible** to linezolid, which inhibits **protein synthesis** by binding to the 50S ribosomal subunit. - Linezolid is often used as an **alternative therapy** for vancomycin-resistant enterococci (VRE) infections.
Question 406: Hyperkalemia is caused by which of the following conditions?
- A. Gordon's syndrome (Correct Answer)
- B. Liddle's syndrome
- C. Bater's syndrome
- D. Vomiting
Explanation: **Explanation:** **Gordon's Syndrome (Pseudohypoaldosteronism Type II)** is the correct answer. It is a rare genetic disorder characterized by **hyperkalemia**, hypertension, and metabolic acidosis. The underlying pathophysiology involves a "gain-of-function" mutation in WNK kinases, leading to overactivity of the **Na-Cl cotransporter (NCC)** in the distal convoluted tubule. This increased sodium reabsorption limits sodium delivery to the distal collecting duct, thereby reducing potassium secretion (via ROMK channels), resulting in hyperkalemia despite normal renal function and aldosterone levels [1]. **Analysis of Incorrect Options:** * **Liddle’s Syndrome:** This is a "gain-of-function" mutation of the ENaC channels. It causes hypertension and metabolic alkalosis, but it leads to **hypokalemia** due to excessive sodium reabsorption coupled with increased potassium secretion. * **Bartter’s Syndrome:** This involves defects in the thick ascending limb (NKCC2/ROMK). It mimics loop diuretic use, leading to salt wasting, activation of the RAAS, and significant **hypokalemia**. * **Vomiting:** Gastric juice is rich in H+ and Cl-. Loss of gastric acid leads to metabolic alkalosis [1]. The resulting bicarbonaturia increases distal delivery of sodium, which promotes potassium excretion, causing **hypokalemia** [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Gordon’s Syndrome** is often called "Inverse Gitelman’s" because it affects the same transporter (NCC) but in the opposite direction. * **Treatment of Gordon’s:** Thiazide diuretics are highly effective as they directly inhibit the overactive NCC transporter. * **Mnemonic:** Remember that most tubular "syndromes" (Bartter, Gitelman, Liddle) cause **hypokalemia**; Gordon’s is the notable exception causing **hyperkalemia**.
Question 407: What is the GFR (mL/min per 1.73m2) for a patient in stage IV of chronic kidney disease?
- A. 60 - 89
- B. 30 - 59
- C. 15 - 29 (Correct Answer)
- D. < 15
Explanation: **Explanation:** Chronic Kidney Disease (CKD) is defined by the presence of kidney damage or a decreased Glomerular Filtration Rate (GFR) of less than 60 mL/min/1.73m² for a duration of 3 months or more. The KDIGO (Kidney Disease: Improving Global Outcomes) classification stages CKD based on GFR levels: * **Stage I:** GFR ≥ 90 (Kidney damage with normal or high GFR) * **Stage II:** GFR 60–89 (Mildly decreased GFR) * **Stage III:** GFR 30–59 (Moderately decreased GFR; often subdivided into IIIa: 45–59 and IIIb: 30–44) * **Stage IV: GFR 15–29 (Severely decreased GFR)** * **Stage V:** GFR < 15 (Kidney failure; often referred to as End-Stage Renal Disease or ESRD) **Analysis of Options:** * **Option A (60–89):** Represents Stage II CKD. * **Option B (30–59):** Represents Stage III CKD. * **Option C (15–29):** **Correct.** This range signifies Stage IV, where patients often begin showing significant clinical symptoms and require preparation for renal replacement therapy (RRT). * **Option D (< 15):** Represents Stage V CKD, requiring dialysis or transplantation. **High-Yield Clinical Pearls for NEET-PG:** 1. **Stage IV Management:** This is the critical window for creating vascular access (AV fistula) in anticipation of hemodialysis. 2. **Most Common Cause:** Diabetes Mellitus is the leading cause of CKD worldwide, followed by Hypertension. 3. **Formulae:** The **MDRD** and **CKD-EPI** equations are preferred over Cockcroft-Gault for staging because they are adjusted for body surface area (1.73m²). 4. **Anemia in CKD:** Usually begins in Stage III due to decreased Erythropoietin production.
Question 408: Which of the following is NOT a feature of Chronic Renal Failure?
- A. Impotence
- B. Restless legs
- C. Isothenuria
- D. All of the above (Correct Answer)
Explanation: Chronic Kidney Disease (CKD) or Chronic Renal Failure is a multisystem disorder resulting from a progressive decline in GFR [1]. The correct answer is **D (All of the above)** because all three listed features are classic manifestations of advanced renal failure. 1. **Impotence (Sexual Dysfunction):** This is highly prevalent in CKD patients due to multifactorial causes, including decreased testosterone levels, autonomic neuropathy, atherosclerosis, and side effects of antihypertensive medications. Hyperprolactinemia (due to decreased renal clearance) also contributes to erectile dysfunction and loss of libido [1]. 2. **Restless Legs Syndrome (RLS):** This is a common neuropsychiatric manifestation of uremia [1]. It is characterized by an irresistible urge to move the legs, usually associated with paresthesias. It often improves with dialysis or renal transplantation. 3. **Isosthenuria:** This refers to the kidney's inability to concentrate or dilute urine, resulting in a fixed urinary specific gravity (typically **1.010**, similar to plasma). This occurs due to the loss of the medullary osmotic gradient and tubular resistance to ADH. **Why other options are incorrect:** Since A, B, and C are all well-documented clinical features of Chronic Renal Failure, they cannot be excluded. Therefore, "All of the above" is the only logical choice. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest sign of CKD:** Isosthenuria (loss of concentrating capacity) often manifests as nocturia. * **Most common cause of death in CKD:** Cardiovascular disease (not renal failure itself). * **Hematology:** Normocytic normochromic anemia due to Erythropoietin deficiency is a hallmark [1]. * **Skin:** "Uremic frost" (urea crystals on skin) and "Half-and-half nails" (Lindsay’s nails) are classic signs.
Question 409: A 42-year-old female presents with diazepam and alcohol overdose. She is comatose with a temperature of 34.5°C, BP of 100/80 mmHg, and creatinine of 2.4 mg/dL. Her AST is 500 IU/L and GGT is 35 IU/L. Urine dipstick showed 3+ for blood, but urine analysis was normal. Ultrasound abdomen was normal. What is the most likely diagnosis?
- A. Hypothermia
- B. Alcoholic hallucinosis
- C. Rhabdomyolysis (Correct Answer)
- D. Acute interstitial nephritis
Explanation: ### **Explanation** The correct answer is **Rhabdomyolysis**. **1. Why Rhabdomyolysis is correct:** The clinical scenario presents a classic triad of findings diagnostic of rhabdomyolysis: * **The Trigger:** Prolonged immobilization (coma due to diazepam/alcohol overdose) leads to muscle compression and ischemia [1]. * **The "Heme-Pigment" Paradox:** The urine dipstick is **3+ for blood**, but microscopy shows **no RBCs**. This occurs because the dipstick cannot distinguish between hemoglobin and **myoglobin** [3]. * **Biochemical Markers:** Elevated **AST** (found in both liver and muscle) with a **normal GGT** (specific to liver/biliary tract) points toward a muscle source. The elevated creatinine (2.4 mg/dL) indicates **Acute Kidney Injury (AKI)**, a common complication caused by myoglobin-induced tubular toxicity [3]. **2. Why other options are incorrect:** * **Hypothermia:** While the patient is hypothermic (34.5°C), this is a secondary finding due to environmental exposure or CNS depression; it does not explain the heme-positive urine or elevated AST. * **Alcoholic Hallucinosis:** This is a withdrawal phenomenon occurring 12–24 hours after cessation [2]. This patient is currently comatose (intoxicated), not in withdrawal. * **Acute Interstitial Nephritis (AIN):** AIN typically presents with fever, rash, and eosinophiluria. It would not cause a positive heme dipstick in the absence of RBCs [3]. **3. NEET-PG Clinical Pearls:** * **Gold Standard Diagnosis:** The most sensitive marker for rhabdomyolysis is an elevated **Serum Creatine Kinase (CK)**, typically >5 times the upper limit of normal. * **Electrolyte Abnormalities:** Look for **Hyperkalemia, Hyperphosphatemia, and Hypocalcemia** (early phase). * **Management:** The mainstay of treatment is **aggressive fluid resuscitation** (Isotonic Saline) to maintain urine output and prevent pigment-induced AKI [3]. * **High-Yield Tip:** If AST > ALT and GGT is normal, always consider a muscle source (Rhabdomyolysis or Myositis) rather than liver pathology.
Question 410: A 45-year-old patient on hemodialysis for one week has noted that his blood pressure is more difficult to control. He reports good compliance with his medications, which include erythropoietin, ferrous sulfate, vancomycin, and vitamin D. His blood pressure is 180/99 mm Hg. What is the most likely cause for the worsening control of his blood pressure?
- A. Erythropoietin (Correct Answer)
- B. Ferrous sulfate
- C. Vancomycin
- D. Vitamin D
Explanation: **Explanation:** The correct answer is **Erythropoietin (EPO)**. Hypertension is a well-documented side effect of Erythropoiesis-Stimulating Agents (ESAs) like recombinant human erythropoietin, occurring in approximately 20-30% of patients on dialysis. **Why Erythropoietin causes Hypertension:** The underlying pathophysiology is multifactorial: 1. **Increased Peripheral Resistance:** EPO causes direct vasoconstriction of peripheral blood vessels. 2. **Increased Blood Viscosity:** As the hematocrit rises, the viscosity of the blood increases, leading to higher systemic vascular resistance. 3. **Endothelin Release:** EPO stimulates the release of endothelin-1 (a potent vasoconstrictor) and may decrease the production of nitric oxide (a vasodilator). 4. **Reversal of Anemic Vasodilation:** Chronic anemia causes compensatory peripheral vasodilation; as EPO corrects the anemia, this vasodilation is reversed, leading to a rise in blood pressure [2]. **Why other options are incorrect:** * **Ferrous sulfate:** Iron supplementation is used to support EPO therapy but does not have a direct hemodynamic effect on blood pressure. * **Vancomycin:** While it can cause "Red Man Syndrome" (hypotension due to histamine release) if infused too rapidly, it does not cause hypertension. * **Vitamin D:** Active Vitamin D (Calcitriol) analogs are used in CKD to manage secondary hyperparathyroidism and are not typically associated with acute worsening of hypertension [1]. **NEET-PG High-Yield Pearls:** * **Monitoring:** Blood pressure must be closely monitored when initiating EPO; a rapid rise in hemoglobin (>1 g/dL over 2 weeks) increases the risk of hypertensive crisis and seizures. * **Target Hb:** In CKD patients, the target Hemoglobin is generally **10–11.5 g/dL**. Targeting higher levels (>13 g/dL) is associated with increased cardiovascular risks and stroke. * **Route:** Subcutaneous administration of EPO is often preferred over intravenous as it allows for lower dosing and more gradual rises in hematocrit.
Practice by Chapter
Acute Kidney Injury
Practice Questions
Chronic Kidney Disease
Practice Questions
Glomerular Diseases
Practice Questions
Tubulointerstitial Diseases
Practice Questions
Nephrotic and Nephritic Syndromes
Practice Questions
Urinary Tract Infections
Practice Questions
Renal Replacement Therapy
Practice Questions
Fluid and Electrolyte Disorders
Practice Questions
Acid-Base Disorders
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Kidney in Systemic Diseases
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Kidney Stones and Obstructive Uropathy
Practice Questions
Hypertension in Kidney Disease
Practice Questions
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