Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 61: Which of the following statements is true regarding specific nephrological conditions?

A. Henoch-Schönlein purpura (HSP) is associated with IgG deposition.
B. Hemolytic Uremic Syndrome (HUS) causes thrombocytopenia.
C. Inulin clearance is the best measure of Glomerular Filtration Rate (GFR). (Correct Answer)
D. Post-Streptococcal Glomerulonephritis (PSGN) is associated with increased complement levels.

Explanation: ### Explanation **1. Why Option C is Correct:** Inulin is a fructose polymer that serves as the **gold standard** for measuring Glomerular Filtration Rate (GFR). It is the ideal marker because it is freely filtered by the glomerulus and is **neither reabsorbed nor secreted** by the renal tubules. Therefore, the amount of inulin excreted in the urine per unit of time is exactly equal to the amount filtered, providing a precise measurement of GFR. **2. Why the Other Options are Incorrect:** * **Option A:** Henoch-Schönlein purpura (HSP), now known as IgA Vasculitis, is characterized by the systemic deposition of **IgA-dominant** immune complexes, not IgG. It typically presents with the tetrad of palpable purpura, arthritis, abdominal pain, and renal involvement. * **Option B:** While HUS does cause thrombocytopenia, the question asks for the *most* true statement regarding nephrological principles. However, in the context of standardized exams, Option C is the definitive physiological fact. (Note: HUS is characterized by the triad of Microangiopathic Hemolytic Anemia, Thrombocytopenia, and Acute Kidney Injury). * **Option D:** PSGN is a **hypocomplementemic** state. It is associated with **decreased** levels of C3 and CH50 due to the activation of the alternative complement pathway. Complement levels typically return to normal within 6–8 weeks. **3. NEET-PG High-Yield Clinical Pearls:** * **GFR Markers:** While Inulin is the "Gold Standard," **Creatinine clearance** is the most common "Clinical Method" (though it slightly overestimates GFR due to tubular secretion). * **PSGN:** The most common cause of acute nephritic syndrome in children. Look for "lumpy-bumpy" appearance (IgG and C3) on immunofluorescence. * **HUS:** Most commonly caused by Shiga toxin-producing *E. coli* (O157:H7). It is the most common cause of acquired AKI in children.

Question 62: An adolescent male presents with hypokalemia, metabolic alkalosis, hypercalciuria, and nephrocalcinosis. His blood pressure is normal. What is the likely diagnosis?

A. Bartter syndrome (Correct Answer)
B. Gitelman syndrome
C. Liddle syndrome
D. Renal tubular acidosis

Explanation: **Explanation:** The clinical presentation of **hypokalemia**, **metabolic alkalosis**, and **normal blood pressure** narrows the differential diagnosis to salt-wasting tubulopathies. The presence of **hypercalciuria** and **nephrocalcinosis** is the pathognomonic feature that confirms **Bartter syndrome**. 1. **Bartter Syndrome (Correct):** This condition results from a defect in the thick ascending limb of the Loop of Henle (mimicking chronic loop diuretic use). The failure of the Na-K-2Cl cotransporter leads to salt wasting, secondary hyperaldosteronism (causing hypokalemia and alkalosis), and a failure to reabsorb calcium. This excess urinary calcium (hypercalciuria) leads to nephrocalcinosis. 2. **Gitelman Syndrome:** Often confused with Bartter, it mimics thiazide diuretic use (defect in the distal convoluted tubule). Crucially, Gitelman presents with **hypocalciuria** (low urine calcium) and hypomagnesemia. It typically presents later in childhood and does not cause nephrocalcinosis. 3. **Liddle Syndrome:** While it causes hypokalemia and alkalosis, it presents with **hypertension** (due to ENaC overactivity) and low renin/aldosterone levels. 4. **Renal Tubular Acidosis (RTA):** Distal RTA (Type 1) can cause hypokalemia and nephrocalcinosis, but it results in **metabolic acidosis**, not alkalosis. **High-Yield Clinical Pearls for NEET-PG:** * **Bartter vs. Gitelman:** Look at urine calcium. Bartter = High Calcium (Loop diuretic-like); Gitelman = Low Calcium (Thiazide-like). * **Bartter Syndrome:** Often associated with polyhydramnios in utero and failure to thrive in infancy. * **Liddle Syndrome:** "Pseudo-hyperaldosteronism"—presents like Conn’s syndrome but with low aldosterone. Treatment is Amiloride, not Spironolactone.

Question 63: What is the definition of hypertension in children?

A. Average systolic blood pressure (SBP) and/or diastolic BP that is >=95th percentile for age, sex, and height on >=2 occasions
B. Average systolic blood pressure (SBP) and/or diastolic BP that is >=95th percentile for age, sex, and height on >=3 occasions (Correct Answer)
C. Average systolic blood pressure (SBP) and/or diastolic BP that is >=90th percentile for age, sex, and height on >=2 occasions
D. Average systolic blood pressure (SBP) and/or diastolic BP that is >=90th percentile for age, sex, and height on >=3 occasions

Explanation: In pediatric medicine, blood pressure (BP) is not defined by a fixed cut-off (like 140/90 mmHg in adults) but is relative to a child’s growth parameters. **1. Why Option B is Correct:** According to the **AAP (American Academy of Pediatrics)** and **NHBPEP** guidelines, hypertension in children (aged 1–13 years) is defined as an average systolic and/or diastolic blood pressure **≥95th percentile** for age, sex, and height, measured on at least **three separate occasions**. The requirement for three separate visits is crucial to rule out "White Coat Hypertension" and transient elevations due to stress or activity, ensuring a stable diagnosis before initiating long-term management. **2. Why Other Options are Incorrect:** * **Options A & C:** These are incorrect because a diagnosis cannot be confirmed in just two occasions. Multiple readings are necessary to establish a trend. * **Options C & D:** The **90th percentile** (up to <95th percentile) is the threshold for **"Elevated Blood Pressure"** (formerly called Pre-hypertension), not clinical hypertension. **3. High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Measurement:** Auscultatory method using a mercury sphygmomanometer is preferred over oscillometric devices for confirming a diagnosis. * **Cuff Size:** The bladder width should be approximately **40%** of the arm circumference, and the length should cover **80–100%** of the circumference. * **Adolescents (≥13 years):** The definition aligns with adult guidelines: Hypertension is **≥130/80 mmHg**. * **Most Common Cause:** In young children, hypertension is usually **secondary** (Renal parenchymal disease is #1). In adolescents, **primary (essential)** hypertension is becoming more common due to obesity.

Question 64: What is true about Post-Streptococcal Glomerulonephritis?

A. 50% of cases occur after pharyngitis
B. Early treatment of pharyngitis eliminates the risk of PSGN
C. Glomerulonephritis secondary to skin infection is more common in summer (Correct Answer)
D. Recurrence is seen

Explanation: **Explanation:** Post-Streptococcal Glomerulonephritis (PSGN) is an immune-mediated glomerular injury following infection with nephritogenic strains of Group A Beta-Hemolytic Streptococcus (GABHS). **Why Option C is Correct:** PSGN can follow either pharyngeal or skin infections (impetigo). While pharyngitis-associated PSGN is more common in winter and spring, **skin-associated PSGN (Pyoderma)** is significantly more common in **summer and fall**, particularly in tropical or humid climates, due to increased insect bites and skin abrasions that facilitate streptococcal entry. **Analysis of Incorrect Options:** * **Option A:** In most clinical settings, skin infections (pyoderma/impetigo) are more frequently associated with PSGN than pharyngitis. The latent period for skin infection (3–6 weeks) is also longer than for pharyngitis (1–2 weeks). * **Option B:** Unlike Rheumatic Fever, where early antibiotic treatment of pharyngitis prevents the disease, **early treatment of streptococcal infections does NOT eliminate the risk of PSGN**, though it may limit the spread of the nephritogenic strain to others. * **Option D:** **Recurrence is extremely rare** in PSGN. This is because the initial infection confers long-lasting immunity against the specific nephritogenic strain of GABHS. **High-Yield Clinical Pearls for NEET-PG:** * **Complement Levels:** Low **C3** is a hallmark (returns to normal within 6–8 weeks). C4 is typically normal. * **Microscopy:** Light microscopy shows "Starry sky" or "Lumpy-bumpy" appearance; Electron microscopy shows **Subepithelial humps**. * **ASO Titer:** Elevated in pharyngitis-associated PSGN; **Anti-DNase B** is a more sensitive marker for skin-associated PSGN. * **Prognosis:** Excellent in children (>95% recover completely); more guarded in adults.

Question 65: Hypercoagulation in Nephrotic syndrome is caused by:

A. Loss of Antithrombin III (Correct Answer)
B. Decreased Fibrinogen
C. Decreased Metabolism of Vitamin K
D. Increase in Protein C

Explanation: **Explanation:** Nephrotic syndrome is characterized by a "hypercoagulable state," leading to an increased risk of venous and arterial thrombosis (most notably **Renal Vein Thrombosis**). **Why Option A is correct:** The primary mechanism for hypercoagulability is the **urinary loss of low-molecular-weight proteins** due to increased glomerular permeability. **Antithrombin III (AT-III)**, a natural anticoagulant that inhibits thrombin and factor Xa, has a relatively small molecular weight (approx. 58 kDa) and is easily lost in the urine. Low levels of AT-III shift the balance toward clot formation. **Why the other options are incorrect:** * **Option B:** In Nephrotic syndrome, there is actually an **increase in Fibrinogen** levels. The liver increases the synthesis of fibrinogen and other clotting factors (V, VII, VIII, X) as a reactive response to low oncotic pressure. * **Option C:** Vitamin K metabolism is not significantly altered in Nephrotic syndrome; the pathology is related to protein loss and hepatic overproduction, not vitamin deficiencies. * **Option D:** **Protein C and Protein S** levels are typically **decreased** (due to urinary loss), not increased. An increase in these proteins would provide an anticoagulant effect, which contradicts the clinical presentation. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site of thrombosis:** Renal Vein (especially in Membranous Nephropathy). * **Other factors:** Increased platelet aggregation and hemoconcentration (due to diuretics) further contribute to the prothrombotic state. * **Triad of Nephrotic Syndrome:** Massive proteinuria (>3.5g/day), Hypoalbuminemia (<3g/dL), and Generalized Edema. Hyperlipidemia is also a hallmark.

Question 66: Frequent relapse in Nephrotic syndrome implies which of the following definitions?

A. Three or more relapses in a 1-year period
B. Relapse every month
C. Two or more relapses in a 6-month period following initial response (Correct Answer)
D. Relapse every 3 months

Explanation: **Explanation:** In pediatric nephrology, the definitions of treatment response and relapse patterns are strictly standardized to guide management strategies. **Why Option C is Correct:** According to the International Study of Kidney Disease in Children (ISKDC) and Indian Society of Pediatric Nephrology (ISPN) guidelines, **Frequent Relapse (FRNS)** is defined by either of the following criteria: 1. **Two or more relapses** within 6 months of the initial response. 2. **Four or more relapses** within any 12-month period. The underlying medical concept is to identify children who are steroid-sensitive but require frequent courses of steroids, putting them at high risk for steroid toxicity. This classification triggers the consideration of steroid-sparing agents (e.g., Levamisole, Cyclophosphamide, or Mycophenolate Mofetil). **Analysis of Incorrect Options:** * **Option A:** This is incorrect because the standard definition requires **four** or more relapses in a 1-year period, not three. * **Option B & D:** These are arbitrary timeframes. While a relapse every month would technically meet the "frequent" criteria, it is not the formal diagnostic definition used in clinical practice or exams. **High-Yield Clinical Pearls for NEET-PG:** * **Relapse:** Urinary protein ≥3+ (or >40 mg/m²/hr) for 3 consecutive days after having been in remission. * **Steroid Dependent (SDNS):** Two consecutive relapses occurring during corticosteroid therapy or within 14 days of its cessation. * **Steroid Resistant (SRNS):** Failure to achieve remission after 4 weeks of daily therapy with Prednisolone at 2 mg/kg/day. * **First-line treatment for FRNS:** Long-term, alternate-day Prednisolone (0.5–0.7 mg/kg) is often the initial strategy before moving to second-line immunosuppressants.

Question 67: An 8-year-old child presents with a blood pressure of 180/100 mmHg, urea of 90 mg/dL, creatinine of 5.3 mg/dL, and urinalysis showing 15-20 pus cells, 12 RBCs, and protein 1+. The child has no significant past history of similar complaints. What is the most likely diagnosis?

A. Post-infective glomerulonephritis
B. Accelerated hypertension with acute renal failure
C. Idiopathic rapidly progressive glomerulonephritis
D. Chronic interstitial nephritis with vesicoureteral reflux (Correct Answer)

Explanation: ### Explanation The key to this question lies in recognizing the clinical picture of **Reflux Nephropathy** (Chronic Interstitial Nephritis secondary to Vesicoureteral Reflux). **1. Why Option D is Correct:** The presence of **sterile pyuria** (15-20 pus cells) combined with mild hematuria and proteinuria in a child with severe hypertension and advanced renal failure (Creatinine 5.3 mg/dL) is classic for chronic tubulointerstitial damage. In children, the most common cause of such presentation is **Vesicoureteral Reflux (VUR)**. VUR leads to recurrent subclinical infections and pressure-induced scarring, eventually causing chronic kidney disease (CKD). The severe hypertension (180/100 mmHg) is a hallmark of renal scarring. **2. Why Other Options are Incorrect:** * **Option A (PSGN):** While PSGN presents with hypertension and hematuria, the creatinine is rarely this high (5.3 mg/dL) unless it's a crescentic transformation. Furthermore, PSGN typically presents with "coca-cola" colored urine and significant RBC casts, not predominant pus cells. * **Option B (Accelerated HTN with ARF):** This is a descriptive diagnosis rather than an etiological one. In a pediatric context, one must identify the underlying cause of the renal failure. * **Option C (RPGN):** RPGN presents with a rapid decline in GFR and nephritic sediment. However, the presence of significant pus cells and the specific demographic more strongly point toward a structural/interstitial pathology like VUR. **3. Clinical Pearls for NEET-PG:** * **Reflux Nephropathy** is the most common cause of childhood hypertension and a leading cause of CKD in children. * **Gold Standard Investigation:** Voiding Cystourethrogram (VCUG) is used to diagnose VUR, while DMSA scan is the gold standard for detecting renal scarring. * **Pus cells without significant bacteria** (Sterile pyuria) in a hypertensive child should always raise suspicion of chronic interstitial nephritis or renal tuberculosis.

Question 68: All of the following are causes of hematuria in a child except?

A. Polycystic kidney disease (PCKD)
B. Porphyria (Correct Answer)
C. Renal vein thrombosis
D. Idiopathic hypercalciuria

Explanation: **Explanation:** The core concept in this question is distinguishing between **true hematuria** (presence of intact RBCs in urine) and **discoloration of urine** (pseudohematuria). **Why Porphyria is the correct answer:** In **Porphyria**, the urine turns a characteristic "port-wine" or dark red color upon standing. This is due to the oxidation of porphobilinogen (PBG) into porphobilin or the presence of uroporphyrins. Crucially, there are **no red blood cells** present in the urine. Therefore, it causes red-colored urine but not hematuria. **Analysis of incorrect options:** * **Polycystic Kidney Disease (PCKD):** Both Autosomal Dominant (ADPKD) and Autosomal Recessive (ARPKD) forms can cause hematuria. In ADPKD, it often results from cyst rupture or associated nephrolithiasis. * **Renal Vein Thrombosis (RVT):** This is a classic cause of hematuria in neonates (often presenting with a flank mass and thrombocytopenia). The venous congestion leads to capillary rupture and bleeding into the collecting system. * **Idiopathic Hypercalciuria:** This is one of the most common causes of isolated asymptomatic microscopic hematuria in children. High urinary calcium levels cause micro-calculi that irritate the urothelium, leading to bleeding even in the absence of a visible stone. **High-Yield Clinical Pearls for NEET-PG:** * **Dipstick vs. Microscopy:** If a urine dipstick is positive for blood but microscopy shows **no RBCs**, consider **Hemoglobinuria** (intravascular hemolysis), **Myoglobinuria** (rhabdomyolysis), or **Porphyria** (though Porphyria may not always trigger the heme-reagent strip). * **Dysmorphic RBCs:** Presence of acanthocytes or dysmorphic RBCs suggests a **glomerular** source of hematuria (e.g., Post-streptococcal glomerulonephritis). * **Commonest cause:** The most common cause of gross hematuria in children is **UTI**, while the most common glomerular cause is **IgA Nephropathy** (Berger’s disease).

Question 69: Low C3 levels are seen in which of the following conditions?

A. IgA nephropathy
B. Minimal change disease
C. Mesangial capillary glomerulonephritis (Correct Answer)
D. Focal segmental glomerulosclerosis

Explanation: **Explanation:** The measurement of serum complement (C3) levels is a crucial diagnostic step in pediatric nephrology to differentiate between various glomerular diseases. **1. Why Mesangial Capillary Glomerulonephritis (MCGN) is correct:** MCGN, also known as **Membranoproliferative Glomerulonephritis (MPGN)**, is characterized by the persistent activation of the complement pathway. * **Type I MPGN:** Activation of the classical pathway (low C3 and C4). * **Type II MPGN (Dense Deposit Disease):** Activation of the alternative pathway due to **C3 nephritic factor** (an autoantibody that stabilizes C3 convertase), leading to profound and persistent **low C3** with normal C4 levels. **2. Why the other options are incorrect:** * **IgA Nephropathy:** This is a "normocomplementemic" nephropathy. While the alternative pathway is involved locally in the kidney, systemic serum C3 levels remain **normal**. * **Minimal Change Disease (MCD):** This is a non-inflammatory podocytopathy. There is no complement activation; hence, C3 levels are **normal**. * **Focal Segmental Glomerulosclerosis (FSGS):** Similar to MCD, FSGS is generally a non-immune complex-mediated disease (except in rare secondary forms), and serum C3 levels are typically **normal**. **High-Yield Clinical Pearls for NEET-PG:** * **Low C3 + Low C4:** Systemic Lupus Erythematosus (SLE), Cryoglobulinemia, MPGN Type I. * **Low C3 + Normal C4:** Post-Streptococcal Glomerulonephritis (PSGN), MPGN Type II. * **Transient Low C3:** In PSGN, C3 levels typically return to normal within **6–8 weeks**. If C3 remains low beyond 8 weeks, suspect MPGN. * **Normal C3 Glomerular Diseases:** IgA Nephropathy, HSP (Henoch-Schönlein Purpura), MCD, FSGS, and Alport Syndrome.

Question 70: A 5-year-old male child presents with complaints of fever and abdominal distension. On examination, there are 6-8 pus cells/hpf in urine. WBC count shows 78% neutrophils. What is the best line of management?

A. Send urine for culture and sensitivity and wait for results.
B. Send urine for culture and sensitivity and start antibiotics immediately. (Correct Answer)
C. Send urine for culture and perform an USG.
D. Radionuclide scan.

Explanation: **Explanation:** The clinical presentation of fever, abdominal distension, and pyuria (6-8 pus cells/hpf) in a 5-year-old child is highly suggestive of a **Urinary Tract Infection (UTI)**. In pediatric patients, especially those presenting with systemic symptoms like fever and neutrophilia (78%), there is a high risk of **Pyelonephritis** and potential renal scarring if treatment is delayed. **1. Why Option B is Correct:** The standard of care for a suspected UTI in a symptomatic child is to obtain a **urine culture** (the gold standard for diagnosis) and then **initiate empirical antibiotic therapy immediately**. Waiting for culture results (which take 48-72 hours) increases the risk of urosepsis and permanent renal parenchymal damage. **2. Why Other Options are Incorrect:** * **Option A:** Waiting for results is dangerous in a symptomatic child with fever and leukocytosis; empirical therapy must bridge the gap until sensitivity results are available. * **Option C:** While an Ultrasonogram (USG) is part of the workup to rule out structural anomalies (like VUR or PUV), it is not the immediate management priority over starting antibiotics. * **Option D:** Radionuclide scans (like DMSA for scarring or MCU for reflux) are performed later in the diagnostic algorithm, usually after the acute infection has subsided. **Clinical Pearls for NEET-PG:** * **Pyuria Definition:** Significant pyuria in children is typically >5 WBCs/hpf in centrifuged urine. * **Gold Standard:** Urine culture is the definitive test for UTI. * **Imaging Timing:** In a first febrile UTI, USG is recommended. A DMSA scan is the most sensitive for acute pyelonephritis/scarring, while Voiding Cystourethrogram (VCUG/MCU) is the investigation of choice for Vesicoureteral Reflux (VUR). * **Common Organism:** *E. coli* remains the most common cause of pediatric UTI.

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Urinary Tract Infections

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Vesicoureteral Reflux

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Glomerulonephritis

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Nephrotic Syndrome

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Acute Kidney Injury

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Chronic Kidney Disease

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Renal Tubular Disorders

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Congenital Anomalies of the Kidney

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Hydronephrosis

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Hypertension in Children

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Hemolytic Uremic Syndrome

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Renal Replacement Therapy in Children

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Nephrology — MCQs

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