Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 561: Which of the following is NOT a cause of acute renal failure?

A. Hypovolemia
B. Rhabdomyolysis
C. Snake bite
D. Pyelonephritis (Correct Answer)

Explanation: **Explanation:** Acute Renal Failure (now more commonly termed **Acute Kidney Injury - AKI**) is characterized by a sudden decline in GFR and a rise in serum creatinine [1]. To answer this question, one must distinguish between causes of AKI and causes of chronic or localized renal inflammation. **Why Pyelonephritis is the correct answer:** Pyelonephritis is an infection of the renal pelvis and parenchyma. While it causes significant morbidity, fever, and flank pain, **uncomplicated acute pyelonephritis** typically involves only one kidney or localized areas of the kidney. Because the unaffected nephrons compensate, it does **not** usually lead to systemic renal failure unless it is complicated by bilateral obstruction, emphysematous changes, or progresses to septic shock. **Analysis of Incorrect Options:** * **Hypovolemia:** This is the most common cause of **Pre-renal AKI**. Decreased renal perfusion leads to a drop in glomerular filtration pressure, causing a rapid rise in nitrogenous waste [1]. * **Rhabdomyolysis:** This causes **Intra-renal AKI**. Myoglobin released from damaged muscle is filtered by the glomerulus and becomes nephrotoxic (pigment nephropathy), especially in the presence of acidic urine, leading to Acute Tubular Necrosis (ATN) [1]. * **Snake Bite:** A common cause of AKI in tropical regions. It causes renal failure through multiple mechanisms: direct nephrotoxicity of the venom, hemolysis, rhabdomyolysis, and Disseminated Intravascular Coagulation (DIC) leading to Cortical Necrosis. **NEET-PG High-Yield Pearls:** * **Most common cause of AKI:** Pre-renal (Hypovolemia/Hypoperfusion) [1]. * **Most common cause of Intra-renal AKI:** Acute Tubular Necrosis (ATN). * **Fractional Excretion of Sodium (FeNa):** <1% in Pre-renal AKI; >2% in ATN. * **Urinary Casts:** "Muddy brown" granular casts are pathognomonic for ATN.

Question 562: Reversible diabetic nephropathy is characterized by which of the following?

A. Microalbuminuria (Correct Answer)
B. Macroalbuminuria
C. Kimmelstiel Wilson lesion
D. Diffuse glomerulosclerosis

Explanation: **Explanation:** Diabetic Nephropathy (DN) progresses through distinct stages. The hallmark of the **reversible stage** is **Microalbuminuria** (Stage III: Incipient Nephropathy) [1]. **1. Why Microalbuminuria is the Correct Answer:** Microalbuminuria is defined as the excretion of **30–300 mg/day** of albumin in the urine. At this stage, the damage is not yet structural or permanent. Strict glycemic control and the initiation of **ACE inhibitors or ARBs** can reduce intraglomerular pressure, stabilize the basement membrane, and potentially reverse the albuminuria back to normoalbuminuria [1], [2]. **2. Why the Other Options are Incorrect:** * **Macroalbuminuria (Option B):** Defined as >300 mg/day. This signifies Stage IV (Overt Nephropathy). At this point, there is a progressive decline in GFR, and the damage is generally considered irreversible, leading toward End-Stage Renal Disease (ESRD) [1]. * **Kimmelstiel-Wilson (KW) Lesion (Option C):** These are pathognomonic nodular glomerulosclerosis lesions seen on biopsy [1]. They represent advanced, irreversible structural damage [3]. * **Diffuse Glomerulosclerosis (Option D):** This is the most common histological change in DN. Like KW lesions, it represents permanent scarring and fibrosis of the glomeruli. **Clinical Pearls for NEET-PG:** * **Earliest functional change:** Hyperfiltration (Increased GFR). * **Earliest structural change:** Thickening of the Glomerular Basement Membrane (GBM) [1]. * **Most specific histological finding:** Kimmelstiel-Wilson nodules (Nodular sclerosis) [1]. * **Screening:** Patients with Type 2 DM should be screened for microalbuminuria at the time of diagnosis [2]; Type 1 DM patients should be screened 5 years after diagnosis.

Question 563: All are true of Nephrotic syndrome, except?

A. RBC casts in urine (Correct Answer)
B. Hypoproteinemia
C. Edema
D. Hyperlipidemia

Explanation: To understand this question, one must distinguish between the two primary glomerular syndromes: **Nephrotic Syndrome** and **Nephritic Syndrome**. [1] ### **Why Option A is the Correct Answer** **RBC casts** are the hallmark of **Nephritic Syndrome** (e.g., Post-streptococcal glomerulonephritis). [2] They indicate active glomerular inflammation (glomerulitis) that allows red blood cells to leak into the nephron and get trapped in Tamm-Horsfall protein. [1] In contrast, Nephrotic syndrome is characterized by non-inflammatory podocyte injury, leading to massive protein leak without significant hematuria or cast formation. [1] ### **Explanation of Other Options (Features of Nephrotic Syndrome)** * **Hypoproteinemia (B):** Massive proteinuria (>3.5 g/day) leads to a drop in serum albumin levels (hypoalbuminemia). [1] * **Edema (C):** Decreased plasma oncotic pressure (due to low albumin) and compensatory sodium/water retention lead to generalized edema (Anasarca). [1] * **Hyperlipidemia (D):** To compensate for low oncotic pressure, the liver increases the synthesis of lipoproteins. Additionally, there is decreased clearance of lipids due to reduced lipoprotein lipase activity. ### **High-Yield Clinical Pearls for NEET-PG** 1. **The Nephrotic Tetrad:** Massive proteinuria (>3.5g/24hr), Hypoalbuminemia (<3g/dL), Generalized Edema, and Hyperlipidemia/Hyperlipiduria (Fatty casts/Oval fat bodies). 2. **Hypercoagulability:** Patients are at high risk for venous thromboembolism (especially **Renal Vein Thosis**) due to the urinary loss of Antithrombin III, Protein C, and S. 3. **Infection Risk:** Increased susceptibility to encapsulated organisms (e.g., *S. pneumoniae*) due to loss of IgG and complement factors in urine. [1] 4. **Maltese Cross Appearance:** Seen under polarized microscopy in the urine of nephrotic patients due to lipiduria.

Question 564: What is the best treatment for anemia associated with Chronic Renal Failure (CRF)?

A. Iron
B. Erythropoietin (Correct Answer)
C. Blood transfusion
D. Folic acid

Explanation: **Explanation:** **1. Why Erythropoietin (EPO) is the Correct Answer:** The primary cause of anemia in Chronic Renal Failure (CRF) is the **deficiency of Erythropoietin** [1]. EPO is a glycoprotein hormone synthesized by the **peritubular interstitial cells** of the kidney [1]. As renal function declines, the production of EPO decreases, leading to normocytic, normochromic anemia. Therefore, Recombinant Human Erythropoietin (rhEPO) or Darbepoetin alfa is the treatment of choice as it addresses the underlying hormonal deficiency [1]. **2. Analysis of Incorrect Options:** * **Iron (Option A):** While iron deficiency often coexists in CRF (due to poor absorption or dialysis blood loss), iron is considered a **supportive treatment**. It is essential to ensure adequate iron stores (Transferrin saturation >30%, Ferritin >500 ng/mL) for EPO to work effectively, but it is not the primary treatment for the anemia of renal origin itself. * **Blood Transfusion (Option C):** This is avoided unless the patient is symptomatic or has acute hemorrhage. Frequent transfusions lead to **iron overload** and **HLA sensitization**, which can complicate future kidney transplantations. * **Folic Acid (Option D):** While water-soluble vitamins are lost during dialysis, folate deficiency is a minor contributor compared to EPO deficiency. **3. High-Yield Clinical Pearls for NEET-PG:** * **Target Hemoglobin:** In CRF, the goal is **10–11.5 g/dL**. Aiming for >13 g/dL is associated with increased risks of stroke and cardiovascular events (CHOIR and CREATE trials). * **Most Common Side Effect of EPO:** Hypertension (due to rapid increase in red cell mass and peripheral resistance). * **EPO Resistance:** The most common cause of non-response to EPO therapy is **Iron Deficiency**. * **HIF-PH Inhibitors (e.g., Roxadustat):** A newer class of oral drugs for CRF anemia that stabilizes Hypoxia-Inducible Factor.

Question 565: Which of the following is not a feature of rapidly progressive glomerulonephritis (RPGN)?

A. Oliguria
B. Edema
C. Hypertension
D. Rapid recovery (Correct Answer)

Explanation: **Rapidly Progressive Glomerulonephritis (RPGN)**, also known as **Crescentic Glomerulonephritis**, is a clinical syndrome characterized by a rapid and profound impairment of glomerular function [1]. ### **Explanation of the Correct Answer** * **D. Rapid recovery:** This is the correct answer because it is **not** a feature of RPGN. Without aggressive intervention (such as high-dose steroids, cyclophosphamide, or plasmapheresis), RPGN typically progresses to **End-Stage Renal Disease (ESRD)** [1]. Recovery is rarely spontaneous or "rapid"; it requires intensive immunosuppression to halt the crescent formation [1]. ### **Explanation of Incorrect Options** RPGN is a form of **Nephritic Syndrome**, and thus presents with its classic features: * **A. Oliguria:** A common finding due to the severe inflammatory collapse of glomerular capillaries and the physical obstruction of Bowman’s space by "crescents," leading to a drastic reduction in urine output. * **B. Edema:** Reduced GFR leads to salt and water retention, manifesting as periorbital or peripheral edema. * **C. Hypertension:** Resulting from fluid overload and the activation of the Renin-Angiotensin-Aldosterone System (RAAS) due to impaired renal perfusion. ### **High-Yield Clinical Pearls for NEET-PG** * **Hallmark Pathology:** The presence of **Crescents** in >50% of glomeruli on light microscopy [1]. Crescents are composed of proliferating parietal epithelial cells and infiltrating monocytes/macrophages [1]. * **Classification by Immunofluorescence (IF):** 1. **Type I (Anti-GBM):** Linear deposits (e.g., Goodpasture Syndrome) [1]. 2. **Type II (Immune Complex):** Lumpy-bumpy/Granular deposits (e.g., PSGN, SLE) [1]. 3. **Type III (Pauci-immune):** No deposits; associated with ANCA (e.g., Wegener’s/GPA, Microscopic Polyangiitis) [1]. * **Key Marker:** Rupture of the **Glomerular Basement Membrane (GBM)** is the inciting event for crescent formation.

Question 566: A 63-year-old man becomes oliguric 2 days following an open cholecystectomy. Which of the following findings would suggest that prerenal acute kidney injury is a major factor in the etiology?

A. Postural hypotension (Correct Answer)
B. Fractional excretion of sodium is 3%
C. Specific gravity is 1.012
D. Urine sodium is 30 mEq/L

Explanation: ### Explanation **1. Why Postural Hypotension is Correct:** Prerenal Acute Kidney Injury (AKI) is caused by **decreased renal perfusion** without damage to the kidney parenchyma [1]. In a post-operative patient, this is often due to hypovolemia (blood loss, fluid shifts, or inadequate replacement). **Postural hypotension** (a drop in BP >20/10 mmHg upon standing) is a clinical hallmark of intravascular volume depletion. It indicates that the "pump" lacks sufficient "prime," leading to decreased glomerular filtration rate (GFR). **2. Why the Other Options are Incorrect:** * **Fractional Excretion of Sodium (FeNa) of 3%:** In prerenal AKI, the renal tubules are intact and aggressively reabsorb sodium to expand volume [2]. Therefore, **FeNa is typically <1%**. A FeNa >2–3% suggests Acute Tubular Necrosis (ATN), where damaged tubules cannot reabsorb sodium. * **Specific Gravity of 1.012:** In prerenal states, the kidneys secrete ADH to concentrate urine, resulting in a **high specific gravity (>1.020)**. A value of 1.012 is "isosthenuric" (similar to plasma), suggesting the kidneys have lost their concentrating ability (intrinsic AKI/ATN). * **Urine Sodium of 30 mEq/L:** To conserve volume, prerenal AKI presents with a **low urine sodium (<20 mEq/L)** [2]. A value of 30 mEq/L points toward intrinsic renal damage. **3. Clinical Pearls for NEET-PG:** * **BUN:Creatinine Ratio:** In prerenal AKI, the ratio is typically **>20:1** (due to increased passive reabsorption of urea). * **Urine Osmolality:** High in prerenal (>500 mOsm/kg); low in ATN (<350 mOsm/kg). * **Sediment:** Prerenal AKI shows "bland" sediment or hyaline casts; ATN shows **"muddy brown" granular casts**. * **Management:** Prerenal AKI is reversible with prompt fluid resuscitation; delay can lead to ischemic ATN.

Question 567: Which of the following conditions is associated with hypokalemia, except?

A. Type I Renal Tubular Acidosis (Correct Answer)
B. Type II Renal Tubular Acidosis
C. Type IV Renal Tubular Acidosis
D. Penicillin therapy

Explanation: The correct answer is **C. Type IV Renal Tubular Acidosis**. ### **Explanation** The fundamental concept to remember for NEET-PG is that **Type I and Type II RTA are associated with hypokalemia**, whereas **Type IV RTA is the only RTA associated with hyperkalemia.** 1. **Type IV RTA (Correct Answer):** Also known as Hyperkalemic RTA, it is caused by either **aldosterone deficiency** or **aldosterone resistance** (pseudohypoaldosteronism). Since aldosterone is responsible for secreting $K^+$ and $H^+$ in the distal tubule, its absence leads to potassium retention, resulting in **hyperkalemia** [1]. 2. **Type I RTA (Distal):** Caused by a failure of $H^+$ secretion in the distal tubule. To maintain electrical neutrality, the kidney excretes $K^+$ instead of $H^+$, leading to **hypokalemia** [2]. 3. **Type II RTA (Proximal):** Caused by a failure to reabsorb $HCO_3^-$ in the proximal tubule. The resulting bicarbonaturia increases distal sodium delivery, which stimulates aldosterone-mediated $K^+$ secretion, leading to **hypokalemia** [2]. 4. **Penicillin Therapy:** High doses of sodium penicillin act as **non-reabsorbable anions** in the distal tubule. This increases the lumen-negative potential, which "pulls" $K^+$ out of the cells into the urine, causing **hypokalemia**. ### **High-Yield Clinical Pearls for NEET-PG** * **Type I RTA:** Associated with **nephrolithiasis** (high urinary pH > 5.5 and hypocitraturia) [2]. * **Type II RTA:** Associated with **Fanconi Syndrome** (phosphaturia, glycosuria, aminoaciduria). * **Type IV RTA:** Most common cause is **Diabetes Mellitus** (Hyporeninemic Hypoaldosteronism). * **Mnemonic:** "Type **4** is the only one where $K^+$ goes **up** (Hyperkalemia)."

Question 568: Which of the following is NOT a cause of hypervolemic hyponatremia?

A. Hypothyroidism (Correct Answer)
B. Cirrhosis
C. Chronic renal failure
D. Nephrotic syndrome

Explanation: To approach hyponatremia, it is essential to categorize it based on **volume status**: Hypovolemic, Euvolemic, or Hypervolemic [1]. ### **Why Hypothyroidism is the Correct Answer** **Hypothyroidism** is classically a cause of **euvolemic hyponatremia** [1]. In severe hypothyroidism (myxedema), there is a non-osmotic release of Antidiuretic Hormone (ADH) and a decrease in the glomerular filtration rate (GFR). This leads to impaired free water excretion. While there may be some interstitial accumulation of glycosaminoglycans (myxedema), there is no significant increase in effective arterial blood volume or clinical edema to classify it as hypervolemic. ### **Analysis of Incorrect Options (Hypervolemic Causes)** Hypervolemic hyponatremia occurs when there is an increase in both total body sodium and water, but the water increase exceeds the sodium increase, usually due to "effective" circulating volume depletion. * **Cirrhosis:** Peripheral vasodilation leads to decreased effective arterial blood volume, triggering ADH and the RAAS system, causing water and salt retention (edema/ascites) [1]. * **Nephrotic Syndrome:** Low oncotic pressure (due to hypoalbuminemia) causes fluid to shift into the interstitium, leading to compensatory water retention [1]. * **Chronic Renal Failure:** The kidneys lose the ability to excrete free water and sodium, leading to a state of total body fluid overload [1]. ### **NEET-PG High-Yield Pearls** * **Euvolemic Hyponatremia Mnemonic:** **SIADH** (most common), **G**lucocorticoid deficiency, **I**atrogenic, **P**sychogenic polydipsia, **H**ypothyroidism (**SI-GIPH**). * **Hypervolemic Hyponatremia:** Think of the

Question 569: A patient with Hepatitis C exhibits hypocomplementemia with 2 gm/day proteinuria and hematuria. What is the most probable diagnosis?

A. Membranoproliferative glomerulonephritis (MPGN) (Correct Answer)
B. Cryoglobulinemia
C. Membranous glomerulopathy
D. Post-infectious glomerulonephritis

Explanation: ### Explanation **1. Why Membranoproliferative Glomerulonephritis (MPGN) is Correct:** The clinical triad of **Hepatitis C (HCV)** infection, **hypocomplementemia**, and a nephritic-nephrotic presentation (proteinuria and hematuria) is a classic association for **Type I MPGN**. HCV triggers the formation of immune complexes (often involving mixed cryoglobulins) that deposit in the subendothelial space of the glomerulus [1]. This activates the classical complement pathway, leading to low C3 and C4 levels. Histologically, this results in the characteristic "tram-track" appearance of the glomerular basement membrane. **2. Why the Other Options are Incorrect:** * **Cryoglobulinemia:** While HCV is the leading cause of Essential Mixed Cryoglobulinemia, "Cryoglobulinemia" itself is a systemic vasculitis syndrome. The specific *renal manifestation* of cryoglobulinemia is Type I MPGN. In the context of a renal diagnosis, MPGN is the more precise pathological term for the glomerular injury described. * **Membranous Glomerulopathy:** While associated with Hepatitis B, it is less commonly associated with Hepatitis C [1]. Furthermore, Membranous Nephropathy typically presents with pure nephrotic syndrome and **normal complement levels**, unlike the hypocomplementemia seen here. * **Post-infectious Glomerulonephritis (PSGN):** While it presents with hematuria and low complement, it typically follows a streptococcal skin or throat infection (not chronic HCV) and usually resolves spontaneously [1]. **3. Clinical Pearls for NEET-PG:** * **HCV Association:** Always link Hepatitis C with **MPGN** and **Cryoglobulinemia**. * **HBV Association:** Always link Hepatitis B with **Membranous Nephropathy** and **Polyarteritis Nodosa (PAN)**. * **Complement Profile:** MPGN is one of the few chronic glomerulonephritides characterized by persistently **low complement levels** (C3 and C4). * **Morphology:** Look for "tram-track" appearance or "double contouring" of the GBM on Silver/PAS stain in MPGN cases [1].

Question 570: In Bartter syndrome, which of the following is not typically seen?

A. Metabolic alkalosis
B. Hypokalemia
C. Hypomagnesemia
D. Decreased urinary calcium (Correct Answer)

Explanation: **Explanation:** **Bartter syndrome** is a group of autosomal recessive disorders caused by mutations in the ion transporters of the **thick ascending limb (TAL)** of the Loop of Henle. It functionally mimics the effect of **Loop diuretics** (e.g., Furosemide). **Why "Decreased urinary calcium" is the correct answer:** In the TAL, the reabsorption of sodium, potassium, and chloride via the **NKCC2 transporter** creates a positive luminal potential that drives the paracellular reabsorption of Calcium and Magnesium. In Bartter syndrome, this transporter is defective. Consequently, calcium is not reabsorbed and is instead excreted in the urine, leading to **Hypercalciuria**. This is a key diagnostic feature that distinguishes it from Gitelman syndrome (which presents with hypocalciuria). **Analysis of incorrect options:** * **Metabolic alkalosis:** The loss of fluid and NaCl leads to volume depletion, activating the Renin-Angiotensin-Aldosterone System (RAAS). Increased aldosterone promotes H+ secretion in the distal tubule, causing metabolic alkalosis [2]. * **Hypokalemia:** High aldosterone levels increase sodium reabsorption in exchange for potassium secretion in the collecting duct, leading to significant potassium wasting [1]. * **Hypomagnesemia:** Since the TAL is also responsible for magnesium reabsorption via the same electrochemical gradient as calcium, magnesium wasting occurs, though it is usually milder than in Gitelman syndrome. **NEET-PG High-Yield Pearls:** * **Bartter vs. Gitelman:** Bartter = Loop Diuretic-like (Hypercalciuria); Gitelman = Thiazide-like (Hypocalciuria). * **Clinical Presentation:** Polyhydramnios in utero, salt wasting, and growth retardation. * **Blood Pressure:** Characterized by **normotension** or hypotension despite high renin/aldosterone levels (due to volume depletion). * **Juxtaglomerular Apparatus (JGA):** Hyperplasia of the JGA is a classic pathological finding.

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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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