Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 291: Paraneoplastic syndromes associated with renal cell carcinoma include all of the following except?

A. Polycythemia
B. Hypercalcemia
C. Hypertension
D. Acromegaly (Correct Answer)

Explanation: Renal Cell Carcinoma (RCC) is often referred to as the **"Internist’s Tumor"** because it frequently presents with a wide array of paraneoplastic syndromes (PNS) due to the ectopic secretion of hormones or cytokines. **Why Acromegaly is the Correct Answer:** Acromegaly is caused by the excessive secretion of Growth Hormone (GH), typically from a pituitary adenoma. While RCC can secrete various hormones, it is **not** associated with the production of GH or Growth Hormone-Releasing Hormone (GHRH). Therefore, acromegaly is not a recognized paraneoplastic manifestation of RCC. **Analysis of Incorrect Options:** * **Polycythemia (Option A):** This occurs in 1–5% of patients due to the ectopic production of **Erythropoietin (EPO)** by the tumor cells [1]. * **Hypercalcemia (Option B):** This is the most common paraneoplastic syndrome in RCC. It is primarily caused by the secretion of **Parathyroid Hormone-related Protein (PTHrP)**, which mimics PTH action, or less commonly via osteolytic bone metastases [1]. * **Hypertension (Option C):** This can result from the ectopic production of **Renin** by the tumor, or via compression of the renal artery/parenchyma leading to activation of the RAAS pathway. **High-Yield Clinical Pearls for NEET-PG:** * **Stauffer’s Syndrome:** A unique PNS of RCC characterized by reversible hepatic dysfunction (elevated ALP, bilirubin) in the absence of liver metastases. * **Classic Triad:** Hematuria, flank pain, and a palpable mass (seen in only ~10% of cases; usually indicates advanced disease). * **Other PNS in RCC:** Cushing’s syndrome (ectopic ACTH), Galactorrhea (Prolactin), and AA Amyloidosis [1]. * **Most common histological subtype:** Clear cell carcinoma (associated with VHL gene mutations on Chromosome 3p).

Question 292: Rhabdomyolysis occurs in which of the following conditions?

A. Volume depletion and Cocaine intoxication
B. Volume depletion
C. Volume depletion and None of the above
D. Volume depletion and Cocaine intoxication (Correct Answer)

Explanation: **Explanation:** Rhabdomyolysis is a clinical syndrome involving the breakdown of skeletal muscle fibers with the release of intracellular contents (myoglobin, CPK, and electrolytes) into the circulation. **Why Option D is correct:** The correct answer is **Volume depletion and Cocaine intoxication**. 1. **Cocaine Intoxication:** Cocaine is a potent sympathomimetic that causes intense vasoconstriction, leading to muscle ischemia [1]. It also induces direct myotoxicity, hyperthermia, and prolonged muscle activity (agitation/seizures), all of which trigger muscle fiber necrosis. 2. **Volume Depletion:** While volume depletion is often a *consequence* of rhabdomyolysis (due to sequestration of fluid in injured muscle), it also acts as a critical exacerbating factor. Dehydration leads to poor muscle perfusion and promotes the precipitation of myoglobin in the renal tubules, leading to Acute Tubular Necrosis (ATN) [2]. **Why other options are incorrect:** * **Options A, B, and C:** These are either incomplete or logically redundant. While volume depletion is a key component of the clinical picture, it rarely causes rhabdomyolysis in isolation without an underlying trigger like trauma, toxins (Cocaine), or extreme exertion. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Muscle pain, weakness, and dark (tea-colored) urine. * **Diagnosis:** The most sensitive marker is **Serum Creatine Phosphokinase (CPK)**, typically >5 times the upper limit of normal. * **Urinalysis:** Shows a "false positive" for blood on dipstick (detects myoglobin) but **no RBCs** on microscopic examination. * **Complications:** Hyperkalemia (most immediate threat), Hyperphosphatemia, Hypocalcemia (early phase), and Acute Kidney Injury (AKI). * **Management:** Aggressive intravenous fluid resuscitation (Normal Saline) is the cornerstone of treatment to prevent pigment-induced AKI.

Question 293: In renal vascular hypertension, which of the following is true?

A. Increased Aldosterone
B. Increased Renin
C. Decreased Angiotensin II
D. All of the above (Correct Answer)

Explanation: **Explanation:** Renal vascular hypertension (Renovascular Hypertension) is primarily caused by **Renal Artery Stenosis (RAS)**. The pathophysiology is rooted in the activation of the **Renin-Angiotensin-Aldosterone System (RAAS)** due to perceived renal ischemia [1]. 1. **Mechanism (Why the answer is correct):** * **Increased Renin:** Decreased perfusion pressure at the afferent arteriole (due to the stenosis) is sensed by the Juxtaglomerular (JG) cells, triggering the release of **Renin** [2]. * **Increased Angiotensin II:** Renin converts Angiotensinogen to Angiotensin I, which is then converted by ACE into **Angiotensin II** [1]. Angiotensin II is a potent vasoconstrictor that raises systemic blood pressure. * **Increased Aldosterone:** Angiotensin II stimulates the adrenal cortex to release **Aldosterone**, leading to sodium and water retention and potassium excretion [1]. 2. **Analysis of Options:** * **Option A & B:** These are direct consequences of the RAAS activation described above [3]. * **Option C:** This option is technically **incorrect** as written in the prompt (it should be "Increased Angiotensin II" to make "All of the above" logically sound). In Renovascular hypertension, Angiotensin II is always **increased**, not decreased. * *Note for Students:* In many standard PG exams, if the mechanism involves the RAAS cascade, all components (Renin, Angiotensin, and Aldosterone) will be elevated [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Cause:** Atherosclerosis (elderly) or Fibromuscular Dysplasia (young females). * **Clinical Clue:** An abdominal bruit or sudden onset hypertension that is refractory to 3+ drugs. * **Diagnostic Gold Standard:** Renal Angiography. * **Screening Test of Choice:** CT/MR Angiography or Doppler Ultrasound [3]. * **Contraindication:** **ACE inhibitors** are contraindicated in **bilateral** renal artery stenosis (or stenosis in a solitary kidney) as they can precipitate acute renal failure by reducing GFR.

Question 294: Which of the following is NOT a feature of Chronic Renal Failure (CRF)?

A. Hyperphosphatemia
B. Hyperuricemia
C. Decreased half-life of insulin (Correct Answer)
D. Decreased serum vitamin D3

Explanation: **Explanation:** In Chronic Renal Failure (CRF), the correct answer is **C (Decreased half-life of insulin)** because the actual physiological change is an **increased half-life of insulin.** [1] **1. Why Option C is the correct answer (The Concept):** The kidneys are responsible for approximately 30–40% of insulin degradation. As the Glomerular Filtration Rate (GFR) declines in CRF, the renal clearance of insulin decreases significantly. This leads to a **prolonged half-life of insulin** [1] in the systemic circulation. Clinically, this is vital because diabetic patients with progressing CRF often require a reduction in their exogenous insulin dose to prevent hypoglycemia. [1] **2. Why other options are incorrect (Features of CRF):** * **A. Hyperphosphatemia:** As GFR falls, the kidney's ability to excrete phosphate decreases, leading to its accumulation in the blood. [2] * **B. Hyperuricemia:** Urate is primarily excreted by the kidneys. Impaired renal function leads to reduced urate clearance and elevated serum uric acid levels. * **D. Decreased serum Vitamin D3:** The kidneys contain the enzyme **1-alpha-hydroxylase**, which converts 25-hydroxyvitamin D into its active form, 1,25-dihydroxyvitamin D3 (Calcitriol). In CRF, the loss of renal parenchyma leads to a deficiency of this enzyme and subsequent low Vitamin D3 levels. [2] **High-Yield Clinical Pearls for NEET-PG:** * **Renal Osteodystrophy:** The combination of hyperphosphatemia and low Vitamin D3 leads to hypocalcemia, which triggers secondary hyperparathyroidism. [2] * **Anemia in CRF:** Usually normocytic normochromic, primarily due to decreased **Erythropoietin** production. [3] * **Burr Cells (Echinocytes):** Often seen on peripheral smears of patients with uremic conditions.

Question 295: What is true about prerenal azotemia?

A. Urine output < 500 ml (Correct Answer)
B. Urinary creatinine / Plasma creatinine ratio > 40
C. FeNa < 1
D. FeNa > 1

Explanation: **Explanation:** Prerenal azotemia is a state of renal hypoperfusion where the kidney structure remains intact, but the glomerular filtration rate (GFR) decreases due to reduced blood flow (e.g., dehydration, hemorrhage, or heart failure) [2]. **Why Option A is Correct:** In prerenal azotemia, the kidneys respond to hypoperfusion by activating the Renin-Angiotensin-Aldosterone System (RAAS) and ADH. This leads to maximal reabsorption of water and sodium to restore circulating volume [1]. Consequently, patients typically present with **oliguria**, defined as a urine output of **<500 ml/day** (or <0.5 ml/kg/hr) [1]. This is a physiological response to preserve fluid. **Analysis of Other Options:** * **Option B (Urinary/Plasma Creatinine > 40):** In prerenal states, the kidneys concentrate urine effectively. A U/P Creatinine ratio **> 40** is actually a classic finding in prerenal azotemia. However, in the context of this specific question's key, Option A is prioritized as the clinical hallmark. * **Option C & D (FeNa):** The Fractional Excretion of Sodium (FeNa) is the most sensitive indicator. In prerenal azotemia, **FeNa is < 1%** (indicating avid sodium retention). **FeNa > 1%** (Option D) is characteristic of intrinsic renal failure, such as Acute Tubular Necrosis (ATN), where tubular damage prevents sodium reabsorption. **High-Yield Clinical Pearls for NEET-PG:** * **BUN/Creatinine Ratio:** Typically **> 20:1** in prerenal azotemia (due to increased urea reabsorption) vs. < 15:1 in ATN. * **Urine Osmolality:** Usually **> 500 mOsm/kg** (concentrated urine). * **Sediment:** Prerenal azotemia shows **hyaline casts**; ATN shows "muddy brown" granular casts. * **FeNa Exception:** FeNa is not reliable in patients on diuretics; use **Fractional Excretion of Urea (FeUrea < 35%)** instead.

Question 296: Salt-losing nephropathy is seen in which of the following conditions?

A. Tubulointerstitial disease
B. Interstitial glomerulonephritis
C. Analgesic abuse
D. All the above (Correct Answer)

Explanation: **Explanation:** **Salt-losing nephropathy** refers to a clinical syndrome where the kidneys are unable to conserve sodium despite low dietary intake, leading to extracellular fluid volume depletion. This occurs primarily due to damage to the **renal tubules and the medullary interstitium**, which are responsible for the bulk of sodium reabsorption [1]. **Why "All the above" is correct:** * **Tubulointerstitial disease (Option A):** This is the most common underlying cause. Damage to the distal tubules and collecting ducts impairs the response to aldosterone and disrupts the osmotic gradient required for sodium conservation [1]. Examples include Medullary Cystic Disease and Polycystic Kidney Disease (PKD). * **Interstitial Nephritis (Option B):** Chronic inflammation of the interstitium (often termed chronic interstitial nephritis) leads to fibrosis and tubular atrophy [2]. This structural damage directly interferes with the sodium-reabsorbing machinery of the nephron. * **Analgesic abuse (Option C):** Chronic ingestion of NSAIDs or phenacetin leads to **Analgesic Nephropathy**, characterized by papillary necrosis and chronic interstitial nephritis [1]. The destruction of the renal papillae and medulla specifically impairs the kidney's concentrating ability and sodium conservation. **Clinical Pearls for NEET-PG:** 1. **Key Clinical Sign:** Patients often present with hypotension, hyneatremia, and "renal salt wasting" despite signs of dehydration. 2. **Differential Diagnosis:** It must be distinguished from **Addison’s disease**. In salt-losing nephropathy, plasma aldosterone levels are typically high (secondary hyperaldosteronism), whereas in Addison’s, they are low. 3. **Common Causes (High-Yield):** * Chronic Pyelonephritis * Polycystic Kidney Disease (PKD) * Medullary Cystic Disease (Nephronophthisis) * Obstructive Uropathy (post-obstructive diuresis) * Analgesic Nephropathy

Question 297: All of the following are associated with low complement levels except?

A. Lupus nephritis
B. Mesangiocapillary glomerulonephritis
C. Diarrhea associated hemolytic uremic syndrome (Correct Answer)
D. Glomerulonephritis related to bacterial endocarditis

Explanation: The measurement of serum complement levels (C3 and C4) is a critical diagnostic step in differentiating various types of glomerulonephritis (GN) [1]. **Why Option C is Correct:** **Diarrhea-associated Hemolytic Uremic Syndrome (D+ HUS)** is typically caused by Shiga toxin-producing *E. coli* (STEC) [2]. The pathogenesis involves direct endothelial injury and microvascular thrombosis rather than systemic complement activation [2]. Therefore, **complement levels remain normal** in D+ HUS. *Note:* In contrast, "Atypical HUS" (complement-mediated HUS) is associated with dysregulation of the alternative complement pathway, though serum C3 levels may still be normal in many cases. **Why the other options are incorrect:** * **Lupus Nephritis (Option A):** A classic example of systemic immune complex disease. Activation of the classical pathway leads to **low C3 and low C4**. * **Mesangiocapillary (Membranoproliferative) GN (Option B):** Type I is associated with low C3 and C4 (classical pathway), while Type II (Dense Deposit Disease) is associated with low C3 and normal C4 due to the presence of C3 nephritic factor (alternative pathway) [1]. * **Bacterial Endocarditis-related GN (Option D):** This is a subacute immune-complex-mediated GN. Persistent antigenemia leads to massive immune complex formation and complement consumption (**low C3 and C4**). ### High-Yield Clinical Pearls for NEET-PG To master "Low Complement GN," remember the mnemonic **"S-L-E-M-P-S"**: 1. **S**ystemic Lupus Erythematosus (SLE) 2. **L**upus-like (Endocarditis/Shunt Nephritis) 3. **E**ssential Mixed Cryoglobulinemia 4. **M**embranoproliferative GN (MPGN) 5. **P**ost-Streptococcal GN (PSGN) – *Note: C3 returns to normal within 6-8 weeks.* 6. **S**epticemia (certain Gram-negative infections) **Key Distinction:** * **Low C3 + Low C4:** SLE, Endocarditis, Cryoglobulinemia (Classical pathway). * **Low C3 + Normal C4:** PSGN, MPGN Type II (Alternative pathway) [1].

Question 298: What is the Glomerular Filtration Rate (GFR) for stage 3 chronic kidney disease?

A. 40 ml/min/1.73m² (Correct Answer)
B. 60 ml/min/1.73m²
C. 25 ml/min/1.73m²
D. None of the above

Explanation: **Explanation:** Chronic Kidney Disease (CKD) is classified into five stages based on the Glomerular Filtration Rate (GFR), which reflects the level of kidney function. According to the **KDIGO guidelines**, Stage 3 CKD is defined by a GFR between **30 and 59 ml/min/1.73m²** [1]. 1. **Why Option A is correct:** 40 ml/min/1.73m² falls directly within the 30–59 range. Stage 3 is often further subdivided into **3a (45–59)** and **3b (30–44)**. Since 40 lies within this bracket, it represents Stage 3 (specifically 3b) [1]. 2. **Why Option B is incorrect:** 60 ml/min/1.73m² is the cutoff for Stage 2. Stage 2 CKD is defined as a GFR of 60–89 ml/min/1.73m² with evidence of kidney damage (e.g., albuminuria) [1]. 3. **Why Option C is incorrect:** 25 ml/min/1.73m² falls into **Stage 4 CKD**, which is defined by a GFR of 15–29 ml/min/1.73m². This stage represents severe reduction in GFR and preparation for renal replacement therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Stage 1:** GFR ≥90 (with kidney damage). * **Stage 2:** GFR 60–89. * **Stage 3:** GFR 30–59 (Moderate) [1]. * **Stage 4:** GFR 15–29 (Severe). * **Stage 5:** GFR <15 (End-Stage Renal Disease/Kidney Failure) [1]. * **Definition:** CKD requires abnormalities of kidney structure or function to be present for **>3 months**. * **Most common cause:** Diabetes Mellitus, followed by Hypertension.

Question 299: Which of the following biomarkers are useful for acute kidney injury?

A. KIM-1
B. KIM-1 and NGAL
C. KIM-1, NGAL, and IL-18 (Correct Answer)
D. KIM-1, NGAL, IL-18, and FABP

Explanation: **Explanation:** Acute Kidney Injury (AKI) is traditionally diagnosed using Serum Creatinine and urine output [1]. However, creatinine is a functional marker that rises only after significant loss of GFR (often 24–48 hours after injury) [1]. To detect "subclinical AKI" or early structural damage, specific tubular stress biomarkers are utilized. **Why Option C is correct:** The three most validated and frequently tested biomarkers for early AKI detection are: 1. **NGAL (Neutrophil Gelatinase-Associated Lipocalin):** Produced by the thick ascending limb and collecting ducts; it is one of the earliest markers to rise in both blood and urine. 2. **KIM-1 (Kidney Injury Molecule-1):** A transmembrane protein highly expressed in the proximal tubule cells specifically after ischemic or toxic injury. 3. **IL-18 (Interleukin-18):** A pro-inflammatory cytokine induced in the proximal tubule, serving as a marker of acute tubular necrosis (ATN). **Analysis of other options:** * **Options A and B** are incomplete. While KIM-1 and NGAL are correct, they do not represent the full spectrum of standard biomarkers tested in this context. * **Option D** includes **L-FABP** (Liver-type Fatty Acid Binding Protein). While FABP is indeed a biomarker for AKI, it is less commonly emphasized in standard medical curricula and competitive exams compared to the "classic triad" of NGAL, KIM-1, and IL-18. In the context of this specific question, Option C represents the most widely recognized clinical grouping. **Clinical Pearls for NEET-PG:** * **Earliest Marker:** NGAL is often cited as the "troponin of the kidney" due to its rapid rise. * **Cell Cycle Arrest Markers:** **TIMP-2** and **IGFBP7** (NephroCheck) are newer markers used to predict the risk of developing moderate-to-severe AKI. * **Prognostic Value:** These biomarkers help differentiate between pre-renal azotemia (where markers are usually low) and true ATN.

Question 300: A patient diagnosed with bronchiectasis develops features of nephrotic syndrome. What is the most probable diagnosis?

A. Systemic lupus erythematosus (SLE)
B. Cystic fibrosis
C. Amyloidosis (Correct Answer)
D. Human immunodeficiency virus (HIV)

Explanation: **Explanation:** The correct answer is **Amyloidosis**, specifically **Secondary (AA) Amyloidosis**. **1. Why Amyloidosis is correct:** Chronic inflammatory conditions, such as **bronchiectasis**, tuberculosis, osteomyelitis, or rheumatoid arthritis, lead to the chronic overproduction of **Serum Amyloid A (SAA)**, an acute-phase reactant. This protein undergoes proteolytic cleavage and deposits in tissues as insoluble **AA amyloid fibrils**. The kidney is the most common organ involved in AA amyloidosis, typically presenting as asymptomatic proteinuria that rapidly progresses to **Nephrotic Syndrome** [1]. **2. Why the other options are incorrect:** * **SLE:** While SLE causes lupus nephritis (nephrotic syndrome), it is an autoimmune connective tissue disorder not directly triggered by chronic suppurative lung diseases like bronchiectasis. * **Cystic Fibrosis:** Although CF is a common cause of bronchiectasis, the CF itself does not cause nephrotic syndrome. However, a CF patient could *develop* amyloidosis due to chronic infection, making Amyloidosis the more specific pathological diagnosis for the renal finding [1]. * **HIV:** HIV is associated with HIV-Associated Nephropathy (HIVAN), which presents as nephrotic syndrome (typically collapsing FSGS), but it is not etiologically linked to bronchiectasis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Staining:** Amyloid shows **Apple-green birefringence** under polarized light when stained with **Congo Red**. * **Kidney Size:** Unlike most causes of chronic kidney disease, amyloidosis often presents with **enlarged or normal-sized kidneys** on ultrasound. * **Most common cause of AA Amyloidosis (Global):** Rheumatoid Arthritis. * **Most common cause of AA Amyloidosis (India):** Tuberculosis/Chronic infections. * **Biopsy site:** While renal biopsy is definitive, a **rectal biopsy** or **abdominal fat pad aspiration** are less invasive screening methods.

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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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