Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 481: Which of the following are features of Rhabdomyolysis?

A. Present with acute muscular weakness
B. Calf muscles commonly ruptured
C. Myoglobinuria (Correct Answer)
D. Acute renal failure is most common

Explanation: **Explanation:** **Rhabdomyolysis** is a clinical syndrome involving the breakdown of skeletal muscle fibers, leading to the release of intracellular contents (myoglobin, creatine kinase, and electrolytes) into the systemic circulation. **Why Myoglobinuria is the correct answer:** When muscle necrosis occurs, **myoglobin** is released. It is a small monomeric protein that is rapidly filtered by the glomerulus. When its concentration exceeds the protein-binding capacity of plasma, it spills into the urine (**myoglobinuria**), typically turning the urine a characteristic **"tea-colored" or "cola-colored."** On a dipstick, this will show a false-positive result for blood (orthotoluidine positive) despite the absence of RBCs on microscopy [2]. **Analysis of Incorrect Options:** * **A. Present with acute muscular weakness:** While weakness can occur, the classic clinical triad is **myalgia (muscle pain), weakness, and dark urine**. Myalgia is often the more prominent presenting symptom than isolated acute weakness. * **B. Calf muscles commonly ruptured:** Rhabdomyolysis involves muscle **necrosis/lysis**, not mechanical rupture. While any muscle group can be affected, it is often associated with crush injuries [1] or prolonged immobilization rather than spontaneous rupture of the calf. * **C. Acute renal failure is most common:** While Acute Kidney Injury (AKI) is a **serious and well-known complication** (occurring in ~15–40% of cases), it is not the "most common" feature. The most common features are biochemical elevations (e.g., elevated Creatine Kinase). **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Serum **Creatine Kinase (CK)** levels. A rise of 5 times the upper limit of normal (usually >5,000 U/L) is diagnostic. * **Electrolyte Abnormalities:** Hyperkalemia (most dangerous), Hyperphosphatemia, and **Hypocalcemia** (early phase due to deposition in necrotic muscle). * **Pathogenesis of AKI:** Caused by direct tubular toxicity of heme, intratubular cast formation, and renal vasoconstriction. * **Management:** Aggressive **intravenous hydration** (Normal Saline) is the cornerstone of treatment to prevent AKI.

Question 482: Which of the following is seen in nephrotic syndrome?

A. Low serum calcium
B. Raised AT-III
C. Low lipid (Correct Answer)
D. Platelet activation

Explanation: **Explanation:** Nephrotic syndrome is characterized by heavy proteinuria (>3.5 g/day), hypoalbuminemia, edema, and hyperlipidemia [1]. **Why Option C is Correct (Note: There is a discrepancy in the provided key):** In clinical practice, nephrotic syndrome is characterized by **Hyperlipidemia** (High lipids), not low lipids [1]. The liver compensates for low oncotic pressure (due to albumin loss) by increasing the synthesis of lipoproteins (VLDL, LDL). Additionally, there is decreased clearance of lipids due to reduced lipoprotein lipase activity. *If the question intended to identify a classic feature, "Hyperlipidemia" is the hallmark; if "Low lipid" is marked correct in your source, it is likely a typographical error in the question paper or key.* **Analysis of Other Options:** * **A. Low serum calcium:** Patients often have low **total** serum calcium because 40-50% of calcium is bound to albumin. As albumin is lost in urine, total calcium drops, though **ionized (active) calcium** usually remains normal. * **B. Raised AT-III:** This is incorrect. Nephrotic syndrome is a **hypercoagulable state** partly because Antithrombin III (AT-III), a natural anticoagulant, is a small protein lost in the urine [1]. Low AT-III levels increase the risk of Renal Vein Thrombosis. * **D. Platelet activation:** This is actually **seen** in nephrotic syndrome. Hypercoagulability is driven by increased platelet aggregation, loss of AT-III, and increased synthesis of clotting factors (Fibrinogen) by the liver. **NEET-PG High-Yield Pearls:** 1. **Most common cause:** Minimal Change Disease (Children), Membranous Nephropathy (Adults - though FSGS is rising) [2]. 2. **Hypercoagulability:** Loss of AT-III, Protein C, and S in urine; increased Fibrinogen. 3. **Infection Risk:** Loss of IgG and Complement factors (Factor B) leads to susceptibility to encapsulated organisms (e.g., *S. pneumoniae*). 4. **Urinary finding:** "Fatty casts" and "Maltese cross" appearance under polarized light due to lipiduria.

Question 483: In chronic glomerulonephritis, what is the most significant urinary finding?

A. Albuminuria
B. Bacteriuria
C. Fixed specific gravity (Correct Answer)
D. Red blood cell casts

Explanation: **Explanation:** In Chronic Glomerulonephritis (CGN), the progressive destruction of nephrons leads to a loss of the kidney's ability to concentrate or dilute urine [2]. This physiological state is known as **Isosthenuria**. **1. Why "Fixed Specific Gravity" is correct:** As chronic renal damage progresses, the renal tubules lose their responsiveness to ADH and their ability to maintain the medullary osmotic gradient. Consequently, the kidney can no longer modify the glomerular filtrate. The urine specific gravity becomes "fixed" at approximately **1.010**, which is identical to the specific gravity of plasma [3]. This is a hallmark of end-stage renal disease and significant tubular dysfunction. **2. Analysis of Incorrect Options:** * **Albuminuria:** While common in CGN, it is non-specific [1]. It occurs in various conditions like nephrotic syndrome, diabetes, and acute glomerulonephritis. It does not necessarily indicate the "chronic" or "fixed" nature of the disease as accurately as isosthenuria. * **Bacteriuria:** This indicates a Urinary Tract Infection (UTI), not a primary glomerular disease. * **Red Blood Cell (RBC) Casts:** These are the hallmark of **Acute Glomerulonephritis** (Nephritic Syndrome). While they may be seen in acute exacerbations of CGN, they are often absent in the late, sclerotic stages of the disease. **Clinical Pearls for NEET-PG:** * **Isosthenuria:** Specific gravity fixed at 1.010 [3]. * **Broad Casts:** Also known as "Renal Failure Casts," these are highly characteristic of chronic renal failure/CGN as they form in dilated, atrophic tubules. * **Small, shrunken kidneys** on ultrasound are the classic imaging finding for CGN (except in Diabetes, Amyloidosis, and Polycystic Kidney Disease).

Question 484: All of the following conditions can lead to chronic renal failure (CRF) except?

A. Post-streptococcal glomerulonephritis (Correct Answer)
B. Membranoproliferative glomerulonephritis
C. Minimal change disease
D. Focal glomerulosclerosis

Explanation: **Explanation:** The correct answer is **A. Post-streptococcal glomerulonephritis (PSGN)**. [1] Chronic Renal Failure (CRF) or Chronic Kidney Disease (KD) results from irreversible damage to the nephrons over a period of months or years. [4] The key to answering this question lies in understanding the prognosis of different glomerular diseases. 1. **Why PSGN is the correct answer:** PSGN is a classic example of an **acute nephritic syndrome** that follows a Group A Beta-hemolytic Streptococcal infection. In the pediatric population (the most common age group), the prognosis is excellent, with >95% of patients achieving complete recovery without any long-term renal sequelae. It rarely, if ever, progresses to CRF. [1] 2. **Why the other options are wrong:** * **Membranoproliferative GN (MPGN):** This is a chronic, progressive disease. Most patients eventually develop end-stage renal disease (ESRD) over 10–15 years. [2] * **Focal Segmental Glomerulosclerosis (FSGS):** This is a leading cause of nephrotic syndrome in adults and is notorious for its poor response to steroids and high rate of progression to CRF. [1] * **Minimal Change Disease (MCD):** While MCD generally has a good prognosis and does not typically cause CRF, the question asks which "can" lead to CRF. In rare cases of "steroid-resistant" MCD or when it is a precursor to FSGS, progression can occur. However, compared to PSGN, it is less "benign" in terms of long-term histological transformation. *(Note: In some exam contexts, MCD is also considered benign; however, PSGN is the most definitive answer as it is an acute, self-limiting condition).* [1] **NEET-PG High-Yield Pearls:** * **Most common cause of CRF in India:** Diabetes Mellitus (followed by Hypertension). [4] * **PSGN Hallmark:** Low C3 complement levels that normalize within 6–8 weeks. * **Lumpy-Bumpy Appearance:** Immunofluorescence in PSGN shows granular IgG and C3 deposits. [3] * **Rule of thumb:** Acute Nephritic syndromes (like PSGN) usually resolve; Chronic Nephrotic syndromes (like FSGS/MPGN) often progress.

Question 485: Which of the following conditions is not associated with an increased anion gap?

A. Salicylate poisoning
B. Proximal RTA (Correct Answer)
C. Ethylene glycol poisoning
D. Lactic acidosis

Explanation: ### Explanation Metabolic acidosis is categorized based on the **Anion Gap (AG)**, calculated as $[Na^+] - ([Cl^-] + [HCO_3^-])$. The normal range is 8–12 mEq/L. **Why Proximal RTA is the correct answer:** Proximal Renal Tubular Acidosis (Type 2 RTA) is a **Normal Anion Gap Metabolic Acidosis (NAGMA)**, also known as hyperchloremic metabolic acidosis [1]. In this condition, the proximal tubule fails to reabsorb bicarbonate ($HCO_3^-$). To maintain electroneutrality as bicarbonate is lost, the kidneys retain Chloride ($Cl^-$). Since the increase in chloride offsets the decrease in bicarbonate, the anion gap remains unchanged. **Analysis of Incorrect Options (High Anion Gap Metabolic Acidosis - HAGMA):** * **Salicylate poisoning:** Aspirin overdose causes HAGMA due to the accumulation of salicylic acid and interference with the Krebs cycle, leading to organic acid buildup [1]. * **Ethylene glycol poisoning:** Metabolism of this antifreeze agent produces glycolic and oxalic acids, which contribute unmeasured anions to the blood. * **Lactic acidosis:** This is the most common cause of HAGMA, resulting from tissue hypoxia (Type A) or metabolic derangements (Type B), leading to the accumulation of lactate anions [1]. **NEET-PG High-Yield Pearls:** * **Mnemonic for HAGMA:** **MUDPILES** (Methanol, Uremia, DKA, Propylene glycol, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates). * **Mnemonic for NAGMA:** **USED CARP** (Ureterosigmoidostomy, Small bowel fistula, Extra chloride, Diarrhea, **RTA**, Pancreatic fistula). * **Key Distinction:** All RTAs (Type 1, 2, and 4) cause NAGMA [1]. If a question features RTA vs. toxins/shock, RTA is almost always the "normal gap" outlier.

Question 486: What type of RBC is typically seen in chronic renal failure?

A. Microcytic
B. Macrocytic
C. Normocytic (Correct Answer)
D. None of the above

Explanation: **Explanation:** The hallmark of anemia in Chronic Renal Failure (CRF) is a **Normocytic Normochromic Anemia**. **Why Normocytic is Correct:** The primary cause of anemia in CRF is the **deficiency of Erythropoietin (EPO)** [2]. EPO is a glycoprotein hormone produced by the peritubular interstitial cells of the kidney [2], [3]. As renal parenchyma is lost, EPO production decreases, leading to reduced stimulation of the bone marrow to produce red blood cells [2]. Since the defect lies in the *quantity* of cells produced rather than the *quality* of hemoglobin synthesis or cell division, the resulting RBCs are normal in size (normocytic) and color (normochromic). **Why other options are incorrect:** * **Microcytic:** This is typically seen in Iron Deficiency Anemia (IDA). While CRF patients may develop IDA due to chronic blood loss (hemodialysis or GI bleeds) or functional iron deficiency (hepcidin-mediated), the classic, primary presentation of renal anemia remains normocytic [1]. * **Macrocytic:** This is characteristic of Vitamin B12 or Folate deficiency. While malnutrition can occur in uremic patients, it is not the standard hematological profile of renal failure itself. **High-Yield Clinical Pearls for NEET-PG:** * **Target Hemoglobin:** In patients on EPO therapy for CRF, the target Hb is usually **10–11.5 g/dL**. Aiming for normal levels (>13 g/dL) increases the risk of stroke and cardiovascular events (CHOIR and CREATE trials). * **Burr Cells (Echinocytes):** These are small, spiked RBCs often seen on the peripheral smear of uremic patients. * **Resistance to EPO:** The most common cause of a poor response to exogenous EPO in CRF patients is **Iron Deficiency** [1]. Always check ferritin and TSAT levels before starting EPO.

Question 487: The captopril test is used as a diagnostic test for?

A. Renovascular hypertension (Correct Answer)
B. Postural hypotension
C. Acute congestive heart failure
D. Myocardial infarction

Explanation: The **Captopril Test** (specifically the Captopril Renography or Captopril-enhanced DTPA/MAG3 scan) is a classic diagnostic tool for **Renovascular Hypertension (RVH)**, most commonly caused by renal artery stenosis [1], [2]. **1. Why Renovascular Hypertension is correct:** In renal artery stenosis, the affected kidney experiences decreased perfusion pressure [1]. To maintain the Glomerular Filtration Rate (GFR), the kidney activates the Renin-Angiotensin-Aldosterone System (RAAS). Angiotensin II causes **vasoconstriction of the efferent arteriole**, which maintains intraglomerular pressure. When Captopril (an ACE inhibitor) is administered, it blocks the formation of Angiotensin II. This leads to **efferent arteriolar vasodilation**, causing a sharp drop in intraglomerular pressure and a significant **reduction in GFR** in the stenotic kidney. This functional drop is captured via radionuclide imaging (MAG3), confirming the diagnosis [2]. **2. Why other options are incorrect:** * **Postural Hypotension:** Diagnosed via the "Tilt Table Test" or by measuring blood pressure changes upon standing. * **Acute Congestive Heart Failure:** Diagnosed clinically and via NT-proBNP levels and Echocardiography. While ACE inhibitors are used for treatment, they are not used as a diagnostic "test." * **Myocardial Infarction:** Diagnosed via ECG changes and cardiac biomarkers (Troponin I/T) [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Renal Angiography remains the gold standard for RVH. * **Screening:** Duplex Doppler or CT/MR Angiography are now more commonly used than the Captopril test in modern practice [1], [4]. * **Clinical Clue:** Suspect RVH if a patient develops an acute rise in serum creatinine (>30%) after starting an ACE inhibitor or ARB. * **Physical Sign:** A continuous abdominal bruit is highly suggestive of renal artery stenosis [1].

Question 488: What is the typical blood flow rate used in a hemodialysis machine?

A. 100-200 ml/min
B. 300-500 ml/min (Correct Answer)
C. 700-800 ml/min
D. >1000 ml/min

Explanation: **Explanation:** In hemodialysis, the **Blood Flow Rate (Qb)** is a critical determinant of solute clearance (Kt/V). To achieve adequate removal of urea and creatinine within a standard 3-to-4-hour session, a flow rate of **300–500 ml/min** is required [1]. This range is optimized to maximize the concentration gradient across the dialyzer membrane while remaining within the physiological limits of a well-functioning arteriovenous fistula (AVF) or graft. **Analysis of Options:** * **Option A (100-200 ml/min):** This rate is too slow for efficient adult dialysis. It is typically only used during the initiation of the very first dialysis session to prevent **Dialysis Disequilibrium Syndrome (DDS)** or in pediatric cases. * **Option C & D (700-1000+ ml/min):** These rates are physiologically unsustainable for most vascular accesses. High flow rates exceeding 600 ml/min significantly increase the risk of high-output cardiac failure and can cause excessive turbulence, leading to hemolysis or access stenosis. **NEET-PG High-Yield Pearls:** 1. **Dialysate Flow Rate (Qd):** Usually maintained at **500–800 ml/min** (typically 1.5 to 2 times the blood flow rate) to maintain a steep diffusion gradient. 2. **Vascular Access:** The "Gold Standard" is the **Brescia-Cimino fistula** (Radio-cephalic) [1]. 3. **Rule of 6s:** A mature fistula should have a diameter >6mm, be <6mm deep, and have a flow of >600ml/min. 4. **Dialysis Disequilibrium Syndrome:** Caused by rapid removal of urea from the blood, leading to cerebral edema. Prevented by using lower blood flow rates (Option A) in the initial session.

Question 489: Which of the following is false about adult polycystic kidney disease?

A. Autosomal dominant inheritance
B. Associated with mitral valve prolapse
C. The most common cause of death is rupture of a berry aneurysm (Correct Answer)
D. Cysts can be found in the liver, lungs, and pancreas

Explanation: **Explanation:** Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common hereditary kidney disease [1]. While it is associated with significant extra-renal manifestations, the statement regarding the cause of death in Option C is incorrect, making it the right answer for this "false statement" question. **1. Why Option C is the correct answer (False statement):** While **Berry aneurysms** (specifically in the Circle of Willis) occur in about 5-10% of ADPKD patients, their rupture is **not** the leading cause of death. The most common cause of death in ADPKD patients is **cardiovascular disease** (including myocardial infarction and heart failure), followed by complications of end-stage renal disease (ESRD) and infections. **2. Analysis of Incorrect Options (True statements):** * **Option A:** ADPKD follows an **autosomal dominant** pattern, primarily involving mutations in the **PKD1** (85%, Chromosome 16) or **PKD2** (15%, Chromosome 4) genes [1]. * **Option B:** Cardiac valvular abnormalities are common; **Mitral Valve Prolapse (MVP)** is the most frequent, followed by aortic root dilatation. * **Option C:** ADPKD is a systemic disorder. **Liver cysts** are the most common extra-renal manifestation. Cysts can also occur in the pancreas, seminal vesicles, and arachnoid membrane. (Note: Lung cysts are rare but documented). **High-Yield Clinical Pearls for NEET-PG:** * **PKD1 vs. PKD2:** PKD1 mutations lead to earlier onset of ESRD (mean age ~54) compared to PKD2 (~74) [1]. * **Diagnosis:** Ultrasonography is the first-line screening tool (Revised Ravine Criteria). * **Treatment:** **Tolvaptan** (V2 receptor antagonist) is used to slow disease progression by reducing cyst growth. * **Associated condition:** Diverticulosis of the colon is more common in ADPKD patients on dialysis.

Question 490: Alport syndrome is inherited as:

A. X-linked (Correct Answer)
B. Co-dominant
C. Autosomal dominant
D. Autosomal recessive

Explanation: **Explanation:** Alport Syndrome is a hereditary nephritis caused by mutations in the genes encoding **Type IV collagen**, which is a critical structural component of the glomerular basement membrane (GBM), cochlea, and lens [1]. **1. Why X-linked is Correct:** The most common mode of inheritance (approximately **85% of cases**) is **X-linked Dominant**, caused by a mutation in the **COL4A5** gene. Because it is X-linked, males are typically more severely affected, often progressing to end-stage renal disease (ESRD), while females (carriers) may present only with isolated hematuria. **2. Analysis of Incorrect Options:** * **Autosomal Recessive (D) & Autosomal Dominant (C):** While these forms do exist (due to mutations in *COL4A3* or *COL4A4*), they are significantly less common (approx. 15%). In the context of competitive exams like NEET-PG, if a single best answer is required, X-linked is the standard choice as it represents the vast majority of cases. * **Co-dominant (B):** This pattern is not associated with the inheritance of Type IV collagen disorders. **3. Clinical Pearls for NEET-PG:** * **Classic Triad:** Hereditary nephritis (hematuria/ESRD), Sensorineural hearing loss (high frequency), and Ocular defects. * **Pathognomonic Ocular Sign:** **Anterior Lenticonus** (conical protrusion of the lens). * **Electron Microscopy (High Yield):** Shows characteristic **"Basket-weave appearance"** due to irregular thinning and thickening of the GBM. * **Key Association:** Patients may develop Anti-GBM disease (Goodpasture-like syndrome) after receiving a kidney transplant [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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