Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 281: Nephrotic syndrome is caused by all of the following systemic diseases EXCEPT?

A. Atherosclerosis (Correct Answer)
B. Diabetes Mellitus (DM)
C. Systemic Lupus Erythematosus (SLE)
D. Amyloidosis

Explanation: Atherosclerosis is a macrovascular disease characterized by the buildup of plaques in large and medium-sized arteries. While it can lead to **Renal Artery Stenosis (RAS)** and subsequent ischemic nephropathy or secondary hypertension, it does not cause **Nephrotic Syndrome** [1]. Nephrotic syndrome requires significant damage to the glomerular filtration barrier (podocytes and basement membrane), leading to massive proteinuria (>3.5g/day). Atherosclerosis primarily affects the arterial wall, not the glomerular capillary loops [1]. **2. Why the Other Options are Incorrect:** * **Diabetes Mellitus (DM):** The most common cause of secondary nephrotic syndrome worldwide. Hyperglycemia leads to non-enzymatic glycosylation, glomerular hyperfiltration, and Kimmelstiel-Wilson nodules, resulting in heavy proteinuria [3]. * **Systemic Lupus Erythematosus (SLE):** Lupus Nephritis (especially Class IV and V) involves immune complex deposition that disrupts the glomerular basement membrane, frequently presenting as nephrotic or nephritic-nephrotic syndrome. * **Amyloidosis:** Both primary (AL) and secondary (AA) amyloidosis involve the deposition of insoluble fibrillar proteins in the mesangium and capillary walls, making it a classic systemic cause of profound nephrotic syndrome [3]. **3. NEET-PG High-Yield Pearls:** * **Most common cause of Nephrotic Syndrome in adults:** Diabetes Mellitus (Secondary); Focal Segmental Glomerulosclerosis (Primary) [2]. * **Most common cause in children:** Minimal Change Disease [2]. * **Amyloidosis Clue:** Look for "Apple-green birefringence" under polarized light with Congo Red stain. * **SLE Clue:** "Wire-loop lesions" on light microscopy (Class IV). * **Atherosclerosis Clue:** Associated with "Hollenhorst plaques" in the retina or "Blue toe syndrome" after vascular procedures [1].

Question 282: Pulmonary-renal syndrome is seen in all, EXCEPT:

A. Goodpasture's syndrome
B. Antineutrophil cytoplasmic antibodies (ANCA)-associated small-vessel vasculitis
C. Lupus erythematosus, or cryoglobulinemia
D. Membranoproliferative glomerulonephritis (MPGN) (Correct Answer)

Explanation: **Explanation:** **Pulmonary-renal syndrome (PRS)** is a clinical entity characterized by the combination of **diffuse alveolar hemorrhage (DAH)** and **rapidly progressive glomerulonephritis (RPGN)**. [1] **Why MPGN is the correct answer:** Membranoproliferative glomerulonephritis (MPGN) is primarily a pattern of glomerular injury caused by immune complex deposition or complement dysregulation. While it causes nephrotic or nephritic syndromes, it is **not** typically associated with pulmonary hemorrhage. Therefore, it does not fall under the classic definition of PRS. **Analysis of other options:** * **Goodpasture’s Syndrome:** The classic PRS [3]. It is caused by anti-glomerular basement membrane (anti-GBM) antibodies that cross-react with the alveolar basement membrane (Type IV collagen) [2]. * **ANCA-associated Vasculitis:** Includes Granulomatosis with polyangiitis (GPA) and Microscopic polyangiitis (MPA) [3]. These are the most common causes of PRS, where small-vessel inflammation leads to both capillaritis in the lungs and crescentic GN in the kidneys [1]. * **SLE and Cryoglobulinemia:** Systemic Lupus Erythematosus (SLE) can cause PRS via immune-complex mediated small-vessel vasculitis. Cryoglobulinemia, though rarer, can also trigger systemic vasculitis involving both organs. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of PRS:** ANCA-associated vasculitis (specifically Microscopic Polyangiitis) [1]. * **Diagnostic Gold Standard:** Renal biopsy (shows crescents) and serology (Anti-GBM, ANCA, ANA) [2]. * **Iron Deficiency Anemia:** Often seen in PRS due to recurrent intrapulmonary bleeding (sequestration of iron in macrophages). * **Treatment:** High-dose corticosteroids and Cyclophosphamide (or Rituximab); Plasmapheresis is specifically indicated in Goodpasture’s to remove circulating antibodies.

Question 283: Gross hematuria, 3 days following an upper respiratory tract infection in a young female is likely due to?

A. Post-streptococcal glomerulonephritis
B. IgA nephropathy (Correct Answer)
C. Minimal change disease
D. Membranous glomerulonephritis

Explanation: ### Explanation The clinical presentation of gross hematuria occurring shortly after an upper respiratory tract infection (URTI) in a young patient is a classic hallmark of **IgA Nephropathy (Berger’s Disease)** [1]. #### Why IgA Nephropathy is Correct The key differentiator here is the **latent period**. In IgA nephropathy, hematuria occurs **synpharyngitically** (simultaneously or within 1–3 days of the infection) [1]. The underlying mechanism involves the overproduction of galactose-deficient IgA1 in response to mucosal triggers (like a URTI), which forms immune complexes that deposit in the glomerular mesangium, causing immediate inflammation [1], [2]. #### Why Other Options are Incorrect * **Post-streptococcal glomerulonephritis (PSGN):** While it also presents with hematuria after a sore throat, the latent period is much longer (**1–3 weeks**) [1]. It is a Type III hypersensitivity reaction that requires time for antibody formation and immune complex deposition. * **Minimal Change Disease (MCD):** This typically presents as **Nephrotic Syndrome** (massive proteinuria, edema) rather than gross hematuria [1]. It is not typically triggered by an infection in this immediate temporal fashion. * **Membranous Glomerulonephritis:** This is a common cause of nephrotic syndrome in adults. It presents with insidious onset of edema and heavy proteinuria, not acute gross hematuria following a URTI [2]. #### NEET-PG High-Yield Pearls * **IgA Nephropathy** is the most common primary glomerulonephritis worldwide. * **The "Rule of Days vs. Weeks":** Hematuria within **days** of URTI = IgA Nephropathy; Hematuria after **weeks** of URTI = PSGN [1]. * **Diagnosis:** Confirmed by **Immunofluorescence**, showing granular IgA and C3 deposits in the **mesangium** [2]. * **Prognosis:** Associated with Henoch-Schönlein Purpura (HSP), which is considered the systemic version of the same pathology. High risk of progression is linked to persistent hypertension and heavy proteinuria.

Question 284: All of the following indicate Chronic Renal Failure (CRF) with respect to Acute Renal Failure (ARF), except-

A. Anemia (Correct Answer)
B. Small kidneys
C. Creatinine > 7 mg%
D. Constrictive pericarditis

Explanation: **Explanation:** The distinction between Acute Kidney Injury (AKI/ARF) and Chronic Kidney Disease (CKD/CRF) is a high-yield topic in NEET-PG [1]. The correct answer is **Anemia** because it is a common feature of **both** conditions, making it an unreliable differentiator [1]. 1. **Why Anemia is the correct answer:** While anemia is a hallmark of CKD (due to decreased Erythropoietin production), it is also frequently seen in ARF [1]. In acute settings, anemia can occur due to hemodilution, hemolysis (e.g., HUS), or acute blood loss. Therefore, its presence does not specifically point toward chronicity. 2. **Analysis of Incorrect Options:** * **Small Kidneys:** This is the most reliable sign of CRF. Chronic inflammation leads to fibrosis and parenchymal thinning (except in Diabetes, Amyloidosis, and Polycystic Kidney Disease). * **Creatinine > 7 mg%:** While high, the absolute value of creatinine does not differentiate ARF from CRF [1]. However, in the context of this specific question's logic, a very high, stable creatinine without acute symptoms often suggests the body has adapted to chronic failure. * **Constrictive Pericarditis:** This is a sequela of chronic uremic serositis. While acute uremic pericarditis can occur in ARF, "constrictive" changes imply a chronic, fibro-calcific process over time. **Clinical Pearls for NEET-PG:** * **Best indicator of CRF:** Bilateral small kidneys on Ultrasound (< 9 cm). * **Exceptions (Large kidneys in CRF):** "SHAPE" – **S**cleroderma, **H**IV nephropathy, **A**myloidosis, **P**olycystic kidney disease, **E**ndocrinopathy (Diabetes). * **Other signs of CRF:** Renal Osteodystrophy (secondary hyperparathyroidism) and Broad Waxy Casts on urinalysis.

Question 285: Which of the following is NOT true about Alport syndrome?

A. X-linked
B. Autosomal dominant (Correct Answer)
C. Nerve deafness
D. Glomerulonephritis

Explanation: **Explanation:** Alport Syndrome is a hereditary type IV collagen disease characterized by the triad of **progressive glomerulonephritis, sensorineural hearing loss, and ocular abnormalities.** [1] **Why "Autosomal Dominant" is the correct answer (the false statement):** The most common inheritance pattern of Alport Syndrome is **X-linked Dominant (approx. 85%)**, caused by mutations in the *COL4A5* gene. While an Autosomal Recessive form exists (due to *COL4A3* or *COL4A4* mutations), the **Autosomal Dominant form is extremely rare.** In the context of standard medical examinations like NEET-PG, Alport is classically taught and tested as an X-linked condition. **Analysis of other options:** * **X-linked:** This is the most common mode of inheritance (85% of cases), making it a true statement. [1] * **Nerve deafness:** Bilateral high-frequency sensorineural hearing loss is a hallmark feature, typically manifesting in late childhood or adolescence. * **Glomerulonephritis:** The disease is fundamentally a basement membrane disorder. It presents with persistent microscopic hematuria, progressing to proteinuria and eventually End-Stage Renal Disease (ESRD). [1] **High-Yield Clinical Pearls for NEET-PG:** * **Pathophysiology:** Defect in **Type IV Collagen** (the "Basket-weave" appearance on Electron Microscopy). [1] * **Ocular Sign:** **Anterior Lenticonus** (pathognomonic) – a conical protrusion of the lens surface. * **Dot-and-fleck retinopathy:** Yellowish-white granules in the perimacular region. * **Diagnosis:** Skin biopsy can sometimes be used for diagnosis because the α5(IV) chain is also expressed in the skin. * **Post-Transplant Complication:** Patients may develop **Anti-GBM disease** (Goodpasture-like syndrome) after a kidney transplant because the host immune system recognizes the "normal

Question 286: What is the most common cause of death in Autosomal Dominant Polycystic Kidney Disease (ADPKD)?

A. Renal failure
B. Ruptured berry aneurysm
C. Cardiovascular disease (Correct Answer)
D. Sepsis

Explanation: **Explanation:** **1. Why Cardiovascular Disease is Correct:** While ADPKD is primarily a renal disorder, the most common cause of mortality is **Cardiovascular Disease (CVD)**, accounting for nearly 50% of deaths. The underlying mechanism is multifactorial: chronic hypertension (the most common complication of ADPKD), left ventricular hypertrophy (LVH), and accelerated atherosclerosis. Hypertension in ADPKD occurs early—often before any decline in GFR—due to intrarenal ischemia caused by expanding cysts, which triggers the **Renin-Angiotensin-Aldosterone System (RAAS)**. **2. Analysis of Incorrect Options:** * **Renal Failure (Option A):** Although ADPKD is a leading cause of End-Stage Renal Disease (ESRD), patients on dialysis or post-transplant are more likely to die from cardiovascular complications than from uremia itself. Mutations in the PKD1 gene account for 85% of cases and PKD2 for about 15%; ESRD occurs in approximately 50% of patients with PKD1 [1]. * **Ruptured Berry Aneurysm (Option B):** This is a high-yield association (occurring in ~10% of patients), but it is **not** the most common cause of death. It is a significant cause of sudden neurological death, but its overall incidence is much lower than CVD. * **Sepsis (Option C):** While cyst infections and urinary tract infections are common morbidities, they are rarely the primary cause of death in the modern antibiotic era. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common extra-renal manifestation:** Hepatic cysts (usually asymptomatic). * **Most common initial symptom:** Flank pain or hematuria [1]. * **Genetics:** PKD1 (Chromosome 16) is more common and severe; PKD2 (Chromosome 4) has a slower progression [1]. * **Treatment Tip:** **Tolvaptan** (V2 receptor antagonist) is used to slow cyst growth and disease progression. * **Screening:** Ultrasound is the initial screening modality of choice for family members.

Question 287: An 80-year-old person has developed a posterior circulation (PCA) territory stroke. On ambulatory Holter, he is found to be having atrial fibrillation. What calculation should be used to evaluate for renal insufficiency of the patient?

A. NIHSS score
B. ABCD2 score
C. CHADS2-Vasc score
D. Cockcroft-Gault formula (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Cockcroft-Gault formula** The patient has suffered an embolic stroke due to **Atrial Fibrillation (AF)**. In clinical practice, the management of AF requires anticoagulation (e.g., Warfarin or Direct Oral Anticoagulants like Dabigatran, Rivaroxaban). Most **Direct Oral Anticoagulants (DOACs)** require precise dose adjustments or are contraindicated based on renal function. The **Cockcroft-Gault formula** is the gold-standard method specifically used in clinical trials for DOACs to estimate **Creatinine Clearance (CrCl)** and determine appropriate dosing. **Analysis of Incorrect Options:** * **A. NIHSS score:** This is a tool used to quantify the neurological deficit and severity of an acute stroke. It does not assess renal function. * **B. ABCD2 score:** This is used to predict the risk of a stroke in the days following a Transient Ischemic Attack (TIA). * **C. CHA₂DS₂-VASc score:** This is a clinical prediction rule for estimating the **risk of stroke** in patients with non-valvular atrial fibrillation to determine if anticoagulation is necessary. It does not measure renal insufficiency. **Clinical Pearls for NEET-PG:** * **Cockcroft-Gault Formula:** $CrCl = \frac{(140 - \text{age}) \times \text{weight (kg)}}{72 \times \text{Serum Creatinine (mg/dL)}} \times (0.85 \text{ if female})$. * **High-Yield:** While MDRD and CKD-EPI are preferred for staging Chronic Kidney Disease (CKD), **Cockcroft-Gault** remains the standard for **drug dosing** (especially DOACs and Aminoglycosides) [1]. Serum creatinine is the most widely used compound for indirectly assessing GFR in clinical practice [1]. * **PCA Stroke Presentation:** Look for "The 3 Ds": Diplopia, Dizziness, and Dysarthria, or contralateral homonymous hemianopia with macular sparing.

Question 288: Which of the following is NOT used in the management of hypernatremia?

A. 5% dextrose in water
B. 0.9% saline in 5% dextrose
C. Nil by mouth (Correct Answer)
D. Indomethacin

Explanation: ### Explanation Hypernatremia is defined as a serum sodium concentration >145 mEq/L and always represents a **relative deficit of water** compared to sodium. The management goal is to replace the water deficit and address the underlying cause. **Why "Nil by mouth" is the correct answer:** "Nil by mouth" (NPO) is contraindicated in hypernatremia. In fact, the safest and most effective way to treat hypernatremia in a conscious patient is the **oral administration of plain water**. Restricting oral intake would exacerbate the water deficit and worsen the hypernatremic state. **Analysis of other options:** * **5% Dextrose in water (D5W):** This is the intravenous fluid of choice for correcting a pure water deficit [1]. Once the dextrose is metabolized, it provides "free water" to dilute the extracellular sodium [1]. * **0.9% Saline in 5% Dextrose:** While isotonic saline (0.9%) is usually avoided in hypernatremia, it is used in patients with **hypovolemic hypernatremia** who are hemodynamically unstable (shock) to restore circulatory volume before switching to hypotonic fluids. * **Indomethacin:** This is a specific treatment for **Nephrogenic Diabetes Insipidus (NDI)**. It inhibits prostaglandin synthesis; since prostaglandins antagonize the action of ADH, indomethacin enhances water reabsorption in the collecting ducts. **Clinical Pearls for NEET-PG:** * **Rate of Correction:** Do not exceed a reduction of **10–12 mEq/L in 24 hours** (or 0.5 mEq/L/hr) to prevent **Cerebral Edema**. * **Formula for Free Water Deficit:** $Water\ Deficit = Total\ Body\ Water \times \left(\frac{Current\ Na^+}{140} - 1 ight)$. * **Drug of Choice for Central DI:** Desmopressin (dDAVP). * **Drug of Choice for Lithium-induced NDI:** Amiloride (blocks lithium entry into ENaC channels).

Question 289: Which of the following is an absolute indication for hemodialysis in chronic kidney disease?

A. Metabolic acidosis
B. Uremic pericarditis (Correct Answer)
C. Uremic lung
D. Hyperkalemia

Explanation: In nephrology, the decision to initiate renal replacement therapy (RRT) is based on clinical symptoms rather than a specific GFR cutoff. The indications for urgent hemodialysis are often remembered by the mnemonic **AEIOU**. ### **Why Uremic Pericarditis is the Correct Answer** **Uremic Pericarditis** is considered an **absolute and urgent indication** for dialysis. It signifies severe uremic toxicity and carries a high risk of progression to cardiac tamponade or hemorrhagic pericardial effusion. Unlike other metabolic disturbances, uremic serositis (pericarditis or pleuritis) does not respond to medical management and requires immediate RRT to clear the middle-molecule toxins responsible for the inflammation. ### **Analysis of Incorrect Options** * **A. Metabolic Acidosis:** This is a *relative* indication. It only becomes an absolute indication if it is **refractory** to medical management (e.g., sodium bicarbonate) or if the pH is severely low (usually <7.1) [1]. * **C. Uremic Lung:** This refers to pulmonary edema due to fluid overload [1]. While a common reason for dialysis, it is an absolute indication only if it is **refractory to diuretics**. * **D. Hyperkalemia:** Similar to acidosis, hyperkalemia is an indication for dialysis only when it is **refractory to medical therapy** (insulin-dextrose, calcium gluconate, and potassium binders) or associated with life-threatening ECG changes. ### **Clinical Pearls for NEET-PG** * **AEIOU Mnemonic:** **A**cidosis (refractory), **E**lectrolytes (refractory Hyperkalemia), **I**ngestion (toxins like Salicylates, Lithium, Methanol), **O**verload (refractory pulmonary edema), and **U**remia (Pericarditis, Encephalopathy, or Neuropathy) [1]. * **Uremic Encephalopathy** (manifesting as asterixis or seizures) is another absolute indication [1]. * **Note:** Uremic pericarditis is typically "non-hemorrhagic" but can become hemorrhagic if anticoagulants (like Heparin) are used during dialysis; hence, **heparin-free dialysis** is preferred in these patients.

Question 290: Features of rhabdomyolysis include all of the following, EXCEPT?

A. Acute muscular weakness
B. Myoglobinuria
C. Hemoglobinuria (Correct Answer)
D. Acute Renal Failure

Explanation: ### Explanation **Rhabdomyolysis** is a clinical syndrome resulting from the breakdown of skeletal muscle fibers, leading to the release of intracellular contents (myoglobin, creatine kinase, and electrolytes) into the systemic circulation. **Why Hemoglobinuria is the Correct Answer:** Hemoglobinuria refers to the presence of free hemoglobin in the urine, typically resulting from **intravascular hemolysis** (RBC breakdown). In rhabdomyolysis, the pigment released is **myoglobin**, not hemoglobin. While both cause a "false positive" for blood on a urine dipstick (due to the peroxidase activity of the heme group), microscopic examination in rhabdomyolysis reveals an absence of RBCs, and the specific pigment is myoglobin (**Myoglobinuria**) [1]. **Analysis of Other Options:** * **A. Acute muscular weakness:** This is a hallmark clinical feature. The classic triad of rhabdomyolysis includes muscle pain, weakness, and dark (tea-colored) urine. * **B. Myoglobinuria:** As muscle cells disintegrate, myoglobin is filtered by the glomerulus. Its presence in the urine is a diagnostic feature and causes the characteristic dark discoloration. * **D. Acute Renal Failure (AKI):** This is a major complication. Myoglobin causes AKI through three mechanisms: direct tubular toxicity, cast formation (obstructing tubules), and induced renal vasoconstriction [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnostic:** Serum **Creatine Kinase (CK)** levels. A level >5 times the upper limit of normal (usually >5000 U/L) is highly suggestive. * **Electrolyte Abnormalities:** Hyperkalemia (most dangerous), Hyperphosphatemia, Hyperuricemia, and **Early Hypocalcemia** (due to calcium deposition in damaged muscle). * **Treatment:** Aggressive fluid resuscitation with Normal Saline is the most critical intervention to prevent AKI. * **Dipstick Paradox:** A positive dipstick for "blood" but **zero RBCs** on microscopy is a classic exam clue for myoglobinuria [1].

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Acute Kidney Injury

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Chronic Kidney Disease

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Glomerular Diseases

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Tubulointerstitial Diseases

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Nephrotic and Nephritic Syndromes

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Urinary Tract Infections

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Renal Replacement Therapy

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Fluid and Electrolyte Disorders

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Acid-Base Disorders

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Kidney in Systemic Diseases

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Kidney Stones and Obstructive Uropathy

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Hypertension in Kidney Disease

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Nephrology — MCQs

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