Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 391: A 25-year-old man has IDDM for 5 years. Which is the best early indicator for diabetic nephropathy?

A. Albuminuria (Correct Answer)
B. Hypertension
C. Rising blood urea nitrogen
D. Rising creatinine

Explanation: **Explanation:** The earliest clinical hallmark of diabetic nephropathy (DN) is **Albuminuria**, specifically **Microalbuminuria** (defined as 30–300 mg/day) [1]. In patients with Type 1 Diabetes (IDDM), this typically manifests after 5 years of disease duration. **Why Albuminuria is the correct answer:** Hyperglycemia leads to non-enzymatic glycosylation of the glomerular basement membrane and efferent arteriolar vasoconstriction. This causes glomerular hyperfiltration and increased intraglomerular pressure, leading to the leakage of small amounts of albumin [1]. It precedes any decline in GFR or rise in nitrogenous waste, making it the most sensitive early screening tool [2]. **Why other options are incorrect:** * **Hypertension:** While hypertension is a key feature of DN, it usually develops concurrently with or after the onset of albuminuria. It is a consequence of renal damage rather than the earliest indicator. * **Rising Blood Urea Nitrogen (BUN) & Rising Creatinine:** These are markers of advanced renal dysfunction (decreased GFR). By the time these values rise, significant irreversible structural damage (Kimmelstiel-Wilson nodules) has already occurred [2]. They are late indicators, not early ones. **High-Yield Clinical Pearls for NEET-PG:** 1. **Natural History:** The stages of DN are: Hyperfiltration → Silent Phase (Thickened GBM) → **Microalbuminuria (Earliest clinical sign)** → Macroalbuminuria (Overt Nephropathy) → ESRD [2]. 2. **Screening:** In IDDM, screen for albuminuria 5 years after diagnosis. In NIDDM (Type 2), screen at the time of diagnosis. 3. **Pathology:** The most specific histological finding is **Kimmelstiel-Wilson (KW) nodules** (nodular glomerulosclerosis) [2]. 4. **Management:** ACE inhibitors or ARBs are the drugs of choice as they reduce intraglomerular pressure by dilating the efferent arteriole.

Question 392: What is the most common cause of nephrotic syndrome in elderly patients?

A. Minimal change glomerulonephritis
B. Membranous glomerulonephritis (Correct Answer)
C. IgA nephropathy
D. None of the above

Explanation: **Explanation:** **Membranous Nephropathy (MN)**, also known as Membranous Glomerulonephritis, is the most common cause of primary nephrotic syndrome in the elderly population (typically defined as >60 years). Pathologically, it is characterized by the thickening of the glomerular basement membrane due to the deposition of immune complexes (IgG and C3) in the subepithelial space, leading to a "spike and dome" appearance on electron microscopy [1]. In elderly patients, a significant proportion (up to 25%) of MN cases are **secondary**, most commonly associated with underlying **malignancies** (solid tumors of the lung, colon, or breast). **Analysis of Incorrect Options:** * **Minimal Change Disease (MCD):** This is the most common cause of nephrotic syndrome in **children**. While it can occur in adults, it is less frequent than MN in the elderly [1]. * **IgA Nephropathy:** This is the most common cause of **primary glomerulonephritis** worldwide, but it typically presents as **nephritic syndrome** (recurrent hematuria) in young adults, rather than pure nephrotic syndrome in the elderly [1]. * **Focal Segmental Glomerulosclerosis (FSGS):** Though not listed as a primary option, it is the most common cause of nephrotic syndrome in **young adults** and African Americans. **High-Yield Clinical Pearls for NEET-PG:** * **Primary MN:** 70-80% of cases are associated with antibodies against the **Phospholipase A2 Receptor (PLA2R)**. * **Secondary MN:** Always rule out malignancy, SLE, Hepatitis B, and drugs (NSAIDs, Gold, Penicillamine) in elderly patients. * **Complication:** MN has the highest risk of **renal vein thrombosis** among all nephrotic syndromes. * **Rule of Thumb:** Children = MCD; Young Adults = FSGS; Elderly = MN.

Question 393: A patient undergoing hemodialysis complains of muscle cramps. Which intervention is effective in relieving muscle cramps?

A. Increase the rate of dialysis
B. Infuse normal saline solution (Correct Answer)
C. Administer a 5% dextrose solution
D. Encourage active range of motion exercises

Explanation: ### Explanation **Correct Option: B (Infuse normal saline solution)** Muscle cramps are one of the most common complications of hemodialysis [1], typically occurring due to **hypovolemia** and **hypotension** caused by rapid fluid removal (ultrafiltration). When the intravascular volume is depleted, it leads to muscle hypoperfusion and electrolyte shifts across the cell membrane, triggering involuntary contractions. Infusing a bolus of **Normal Saline (0.9% NaCl)** or hypertonic saline increases the plasma osmolality and intravascular volume [2], which improves muscle perfusion and rapidly alleviates the cramp. **Analysis of Incorrect Options:** * **A. Increase the rate of dialysis:** This would accelerate fluid removal and solute clearance, likely worsening hypotension and exacerbating muscle cramps. * **C. Administer a 5% dextrose solution:** Dextrose 5% (D5W) is an isotonic solution that becomes hypotonic once the glucose is metabolized [2]. It does not stay in the intravascular space effectively and can lead to hyposmolality, which may actually trigger or worsen cramps. * **D. Active range of motion exercises:** While passive stretching of the affected muscle can provide temporary relief, active exercise during a dialysis-induced hypotensive episode is impractical and does not address the underlying volume deficit. **Clinical Pearls for NEET-PG:** * **Most common cause of cramps in HD:** Excessive or rapid ultrafiltration (hypovolemia). * **Prevention:** Accurate assessment of "dry weight," reducing sodium modeling, and avoiding heavy meals during dialysis. * **First-line management:** Reducing the ultrafiltration rate to zero and administering a 100–200 mL bolus of Normal Saline. * **Alternative treatment:** Hypertonic solutions (e.g., 23.4% saline or 50% dextrose) can be used as they create an osmotic shift of fluid into the intravascular space.

Question 394: An 18-year-old student presents with dark urine, fever, and flank pain, and is diagnosed with acute glomerulonephritis. What is the most likely preceding event in this student's health history?

A. Renal calculi
B. Renal trauma
C. Recent sore throat (Correct Answer)
D. Family history of acute glomerulonephritis

Explanation: ### Explanation The clinical presentation of dark urine (hematuria), fever, and flank pain in a young patient is classic for **Post-Streptococcal Glomerulonephritis (PSGN)**. This is a Type III hypersensitivity reaction occurring after an infection with nephritogenic strains of Group A Beta-hemolytic *Streptococcus* (GABHS). **Why "Recent sore throat" is correct:** PSGN typically follows a **pharyngeal infection** (sore throat) or a **skin infection** (impetigo). There is a characteristic latent period between the infection and the onset of renal symptoms: 1–3 weeks after pharyngitis and 3–6 weeks after pyoderma. The deposition of immune complexes in the glomerular basement membrane leads to the "lumpy-bumpy" appearance on immunofluorescence and the classic "coke-colored" or smoky urine [1]. **Why the other options are incorrect:** * **Renal calculi:** While stones cause flank pain and hematuria, they do not typically cause the systemic inflammatory features of glomerulonephritis (like RBC casts or significant proteinuria) unless complicated by obstructive pyelonephritis. * **Renal trauma:** This would cause gross hematuria and pain immediately following an injury, not a systemic nephritic syndrome. * **Family history:** While some nephropathies (like Alport syndrome) are hereditary, the acute onset following a febrile illness strongly points toward an infectious trigger rather than a genetic predisposition [1]. **NEET-PG High-Yield Pearls:** * **Most common cause** of acute nephritic syndrome in children/young adults worldwide. * **Lab findings:** Low C3 levels (complement consumption) and elevated ASO titers (after pharyngitis) or Anti-DNAse B (after skin infection). * **Light Microscopy:** "Starry sky" appearance or "Lumpy-bumpy" deposits of IgG and C3. * **Electron Microscopy:** Subepithelial "humps." * **Prognosis:** Excellent in children (95% recover), but more guarded in adults.

Question 395: Glomerulonephritis associated with sensory neural deafness are features of?

A. Alport's syndrome (Correct Answer)
B. Nail patella syndrome
C. Down's syndrome
D. Fabry's syndrome

Explanation: Explanation: **Alport’s Syndrome** is the correct answer. It is a hereditary type IV collagen disorder caused by mutations in the genes encoding the $\alpha$-3, $\alpha$-4, or $\alpha$-5 chains of **Type IV collagen** [1]. Since Type IV collagen is a structural component of the basement membranes in the kidney (GBM), cochlea, and eye, the clinical triad includes: 1. **Hereditary Nephritis:** Progressing from microscopic hematuria to End-Stage Renal Disease (ESRD). In Alport's syndrome, the normal collagen network is disrupted and replaced by $\alpha$1 and $\alpha$2 chains, leading to characteristic splitting and degeneration of the GBM [1]. 2. **Sensorineural Hearing Loss:** Typically bilateral and high-frequency. 3. **Ocular Abnormalities:** Most characteristically **Anterior Lenticonus** (pathognomonic) and maculopathy. **Analysis of Incorrect Options:** * **Nail-Patella Syndrome:** Characterized by hypoplastic nails, absent/small patellae, and iliac horns. While it involves nephropathy, it is not associated with deafness. * **Down’s Syndrome:** Associated with congenital heart defects (AVSD) and early-onset Alzheimer’s, but not typically with glomerulonephritis or primary sensorineural deafness. * **Fabry’s Disease:** An X-linked lysosomal storage disorder (alpha-galactosidase A deficiency). It causes renal failure and acroparesthesia, but the classic extra-renal features are **angiokeratomas** and corneal verticillata, not sensorineural deafness. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most common is **X-linked Dominant** (85%). * **Electron Microscopy (EM):** Shows a characteristic **"Basket-weave appearance"** due to irregular thinning and thickening of the GBM [1]. * **Diagnosis:** Skin biopsy can sometimes be used for diagnosis (staining for $\alpha$-5 chain) as an alternative to renal biopsy. * **Post-Transplant Complication:** Patients with Alport’s may develop **Anti-GBM disease (Goodpasture-like syndrome)** after a kidney transplant because their immune system recognizes the normal collagen in the graft as foreign.

Question 396: All of the following may occur due to hyperkalemia, except?

A. Prolonged PR interval
B. Prolonged QRS interval
C. Prolonged QT interval (Correct Answer)
D. Ventricular asystole

Explanation: Hyperkalemia is a critical electrolyte abnormality that alters the resting membrane potential of cardiac myocytes, leading to characteristic sequential ECG changes [1]. **Why "Prolonged QT interval" is the correct answer:** Hyperkalemia typically causes a **shortened QT interval**. This occurs because high extracellular potassium levels increase the speed of repolarization (Phase 3 of the action potential), leading to narrow, symmetrical, and "tented" T-waves [1]. In contrast, **prolonged QT interval** is a hallmark of **hypocalcemia** or **hypokalemia**. **Explanation of incorrect options:** * **Prolonged PR interval:** As potassium levels rise (typically >6.5 mEq/L), atrial conduction slows, leading to PR interval prolongation and eventual flattening/disappearance of the P-wave [1]. * **Prolonged QRS interval:** When potassium levels exceed 7.0 mEq/L, ventricular conduction slows significantly, causing the QRS complex to widen [1]. If untreated, this progresses to a "sine wave" pattern. * **Ventricular asystole:** This is the terminal event of severe hyperkalemia. The myocardium becomes refractory to excitation, leading to ventricular fibrillation or asystole [1]. **High-Yield NEET-PG Pearls:** 1. **Sequential ECG changes in Hyperkalemia:** Tall T-waves → Prolonged PR interval → Loss of P-wave → Widened QRS (Sine wave) → V-fib/Asystole [1]. 2. **Treatment Priority:** The first step in management with ECG changes is **Intravenous Calcium Gluconate** (stabilizes the cardiac membrane), though it does not lower potassium levels [2]. 3. **Pseudohyperkalemia:** Always consider this if the patient is asymptomatic and has high platelet or WBC counts (lysis during clotting).

Question 397: What is a common cause of chronic renal failure?

A. Hypotension
B. Hypertension (Correct Answer)
C. Diabetes insipidus
D. Malaria

Explanation: **Explanation:** Chronic Kidney Disease (CKD) or Chronic Renal Failure is characterized by progressive, irreversible loss of renal function [1]. **Why Hypertension is the correct answer:** Hypertension is the **second most common cause** of CKD worldwide (after Diabetes Mellitus) [2]. It creates a "vicious cycle": high systemic pressure causes **hyaline arteriolosclerosis** of the afferent arterioles and glomerular hypertension. This leads to hyperfiltration injury, glomerulosclerosis, and nephron loss. As the kidneys fail, they activate the Renin-Angiotensin-Aldosterone System (RAAS), further worsening the hypertension and accelerating renal decline. **Analysis of Incorrect Options:** * **A. Hypotension:** This typically causes **Acute Kidney Injury (AKI)** via decreased renal perfusion, leading to Prerenal Azotemia or Acute Tubular Necrosis (ATN). It is not a primary cause of chronic, progressive failure. * **C. Diabetes Insipidus:** This is a disorder of water balance (ADH deficiency or resistance) leading to polyuria and polydipsia. While it affects the collecting ducts, it does not typically cause parenchymal destruction or chronic renal failure. * **D. Malaria:** Severe *P. falciparum* malaria is a known cause of **AKI** (Blackwater fever due to hemolysis or ATN), but it is not a leading cause of chronic renal failure compared to systemic metabolic/vascular diseases. **High-Yield NEET-PG Pearls:** * **Most common cause of CKD:** Diabetes Mellitus (Type 2 > Type 1) [2]. * **Second most common cause:** Hypertension [2]. * **Most common cause of death in CKD patients:** Cardiovascular disease (not uremia). * **Pathological hallmark:** Glomerulosclerosis and tubulointerstitial fibrosis. * **Staging:** Based on GFR; Stage 5 (End-Stage Renal Disease) is defined as GFR <15 ml/min/1.73m² [1].

Question 398: Which of the following is included in the definition of Nephrotic syndrome?

A. Microalbuminuria
B. Massive Proteinuria (Correct Answer)
C. Microscopic haematuria
D. All of the above

Explanation: **Explanation:** Nephrotic syndrome is a clinical triad resulting from increased glomerular permeability to plasma proteins [1]. The hallmark of this condition is **Massive Proteinuria**, defined as protein excretion **>3.5 g/24 hours** (or a protein-to-creatinine ratio >3000 mg/g) in adults [1]. This massive loss leads to hypoalbuminemia (<3 g/dL), which decreases oncotic pressure, resulting in generalized edema and compensatory hyperlipidemia/lipiduria. **Analysis of Options:** * **Massive Proteinuria (Option B):** This is the primary diagnostic criterion. Without "nephrotic-range" proteinuria, the diagnosis cannot be made [2]. * **Microalbuminuria (Option A):** This refers to a small increase in albumin excretion (30–300 mg/day). It is an early marker of diabetic nephropathy but is significantly below the threshold required for nephrotic syndrome [1]. * **Microscopic Hematuria (Option C):** While it can occur in some nephrotic conditions (like Membranoproliferative Glomerulonephritis), it is the hallmark of **Nephritic Syndrome**, not Nephrotic [2]. Nephrotic syndrome is primarily characterized by "bland" urinary sediment (fats/casts rather than RBCs). **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause in children:** Minimal Change Disease (MCD) [1]. * **Most common cause in adults:** Focal Segmental Glomerulosclerosis (FSGS) is currently the most common primary cause globally, though Membranous Nephropathy is a close second [2]. * **Hypercoagulability:** Patients are at high risk for venous thromboembolism (especially Renal Vein Thrombosis) due to the loss of Antithrombin III in urine. * **Infection Risk:** Increased susceptibility to encapsulated organisms (e.g., *S. pneumoniae*) due to loss of IgG and complement factors.

Question 399: All of the following infections have a well-recognized association with nephropathies except?

A. Staphylococcus Epidermidis
B. Salmonella Typhi
C. Hepatitis A (Correct Answer)
D. Legionnaire's disease

Explanation: **Explanation:** The association between systemic infections and glomerular diseases is a high-yield topic in Nephrology. The correct answer is **Hepatitis A**, as it is primarily an acute, self-limiting infection and is **not** typically associated with chronic immune-complex mediated nephropathies [2]. **1. Why Hepatitis A is the correct answer:** Unlike Hepatitis B and C, which are notorious for causing chronic infections and subsequent glomerular damage (like Membranous Nephropathy or Cryoglobulinemic Vasculitis), Hepatitis A does not lead to chronicity [2]. While rare cases of transient acute kidney injury (AKI) due to ATN or interstitial nephritis have been reported, it lacks a "well-recognized" association with specific nephropathies. **2. Analysis of incorrect options:** * **Staphylococcus epidermidis:** Well-recognized for causing **"Shunt Nephritis."** This occurs when infected ventriculoatrial shunts lead to chronic antigenemia and immune-complex deposition in the glomeruli (MPGN pattern) [1]. * **Salmonella typhi:** Associated with **Glomerulonephritis** during the course of typhoid fever. It can present with proteinuria and hematuria due to immune-complex deposition in the mesangium. * **Legionnaire's disease:** Frequently associated with renal involvement, most commonly **Acute Tubular Necrosis (ATN)** or tubulointerstitial nephritis, often presenting with microscopic hematuria and proteinuria. **Clinical Pearls for NEET-PG:** * **Hepatitis B:** Most commonly associated with **Membranous Nephropathy (MGN)** and Polyarteritis Nodosa (PAN). * **Hepatitis C:** Most strongly associated with **Type I MPGN** and **Mixed Cryoglobulinemia** [2]. * **HIV:** Classically associated with **Collapsing variant of FSGS** (HIVAN) [1]. * **Syphilis:** A classic infectious cause of Membranous Nephropathy.

Question 400: What is the most common type of nephropathy found in HIV patients?

A. Membranous glomerulonephritis
B. Fibrillary glomerulopathy
C. Collapsing glomerulonephritis (Correct Answer)
D. Rapidly progressive glomerulonephritis (RPGN)

Explanation: The correct answer is **Collapsing glomerulonephritis**, which is the hallmark histological pattern of **HIV-Associated Nephropathy (HIVAN)**. **1. Why Collapsing Glomerulonephritis is Correct:** HIVAN is a classic complication of HIV infection, particularly in patients of African descent with the **APOL1 risk alleles**. It is characterized by a "collapsing" variant of **Focal Segmental Glomerulosclerosis (FSGS)** [1]. The underlying mechanism involves direct infection of the renal tubular and glomerular visceral epithelial cells (podocytes) by the HIV virus. This leads to podocyte proliferation and subsequent collapse of the glomerular tuft, resulting in heavy proteinuria and a rapid decline in renal function. **2. Why the Other Options are Incorrect:** * **Membranous Glomerulonephritis (MGN):** While MGN can be associated with infections like Hepatitis B or C, it is not the most common or characteristic finding in HIV. [1] * **Fibrillary Glomerulopathy:** This is a rare condition characterized by organized microtubular deposits; it is not specifically linked to HIV. * **Rapidly Progressive Glomerulonephritis (RPGN):** RPGN is a clinical syndrome (characterized by crescents on biopsy) caused by vasculitis or anti-GBM disease [1]. While HIV patients can develop various nephropathies, RPGN is not the primary histological pattern associated with the virus. **3. High-Yield Clinical Pearls for NEET-PG:** * **Classic Presentation:** Nephrotic-range proteinuria + Normal-sized or enlarged kidneys on ultrasound (unlike the shrunken kidneys seen in most chronic kidney diseases). * **Demographics:** Strongest association is with the **APOL1 gene** in the Black population. * **Treatment:** Highly Active Antiretroviral Therapy (HAART) is the mainstay of treatment and can significantly slow progression. * **Biopsy Finding:** Look for "microcystic tubular dilation" and "tubuloreticular inclusions" (the latter are induced by high levels of Interferon-alpha).

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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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