Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 191: A 65-year-old man has urine output of 10 mL/h following abdominal aortic aneurysmectomy. Acute tubular necrosis is suggested by the presence of which of the following?

A. Urine osmolality of more than 500 mOsm/kg
B. Urine sodium of more than 40 mEq/L (Correct Answer)
C. Fractional excretion of sodium of <1%
D. Blood urea nitrogen (BUN)-to-serum creatinine ratio (SCR) of more than 20

Explanation: **Explanation:** The clinical scenario describes oliguria following major surgery [1], suggesting a transition from **Prerenal Azotemia** (due to hypovolemia or cross-clamping of the aorta) to **Intrinsic Acute Kidney Injury (Acute Tubular Necrosis - ATN)**. **Why Option B is Correct:** In ATN, the tubular epithelial cells are damaged and lose their ability to reabsorb sodium and concentrate urine. Consequently, a large amount of sodium is "wasted" in the urine. A **Urine Sodium >40 mEq/L** is a hallmark of ATN, indicating tubular dysfunction. **Why the Other Options are Incorrect:** * **Option A (Urine Osmolality >500 mOsm/kg):** This indicates intact tubular concentrating ability, characteristic of **Prerenal Azotemia**. In ATN, the urine is iso-osmolar with plasma (typically <350 mOsm/kg) because the tubules cannot create a concentration gradient. * **Option C (FE_Na <1%):** The Fractional Excretion of Sodium (FE_Na) is the most sensitive test to differentiate these conditions. **FE_Na <1%** suggests prerenal states (kidneys are conserving sodium) [1]. In **ATN, FE_Na is >2%**. * **Option D (BUN:SCr Ratio >20):** A high ratio (>20:1) is seen in **Prerenal Azotemia** due to increased urea reabsorption in the proximal tubule alongside water. In ATN, the ratio is typically normal (**10-15:1**) because both BUN and Creatinine are handled similarly by the damaged tubules. **High-Yield Clinical Pearls for NEET-PG:** * **Microscopy:** Look for **"Muddy Brown" granular casts** or renal tubular epithelial cell casts in ATN. * **Exception to FE_Na:** FE_Na can be <1% in certain types of ATN, such as those induced by **contrast media, rhabdomyolysis, or sepsis**. * **Urine Specific Gravity:** In ATN, it is fixed at **1.010** (isosthenuria), reflecting the loss of concentrating capacity.

Question 192: What is the complication of the diuretic phase of acute renal failure?

A. Convulsion
B. Hyperkalemia
C. Increased sodium excretion in urine (Correct Answer)
D. Metabolic Alkalosis

Explanation: ### Explanation In the recovery phase of Acute Kidney Injury (AKI), specifically the **diuretic phase**, the kidneys regain their ability to filter blood before they regain the ability to concentrate urine or reabsorb electrolytes effectively. **Why Option C is Correct:** During this phase, the glomerular filtration rate (GFR) begins to normalize, but the newly regenerated tubular epithelial cells are still immature and lack full resorptive capacity [1]. This leads to an "osmotic diuresis" driven by the high levels of accumulated urea and a failure of the tubules to reabsorb sodium [4]. Consequently, there is a massive loss of water and **increased sodium excretion in the urine**, which can lead to profound dehydration and hyponatremia [2]. **Analysis of Incorrect Options:** * **A. Convulsion:** While severe electrolyte imbalances can cause seizures, they are more commonly associated with the uremic state of the *oliguric phase* or rapid shifts during dialysis (Dialysis Disequilibrium Syndrome) [3]. * **B. Hyperkalemia:** This is a hallmark of the *oliguric phase*. In the diuretic phase, the primary risk is actually **hypokalemia** due to excessive potassium loss in the urine. * **D. Metabolic Alkalosis:** AKI typically presents with High Anion Gap Metabolic Acidosis (HAGMA) [3]. While recovery occurs, metabolic alkalosis is not a standard complication of the diuretic phase unless there is external intervention (like excessive bicarbonate therapy). **High-Yield Clinical Pearls for NEET-PG:** * **Diuretic Phase Risk:** The most common cause of death in this phase is **hypokalemia** and secondary infections. * **Urine Output:** Can reach 4–5 Liters/day. * **Sequence of Recovery:** GFR recovers first $\rightarrow$ Tubular function (concentration/dilution) recovers last. * **Management:** Meticulous fluid and electrolyte replacement (especially $K^+$ and $Na^+$) is critical during this transition [1].

Question 193: Sensorineural deafness may be a feature of all of the following conditions, EXCEPT?

A. Alport syndrome
B. Batten disease
C. Nail-patella syndrome (Correct Answer)
D. Distal renal tubular acidosis

Explanation: **Explanation:** The correct answer is **Nail-patella syndrome (Option C)**. This is an autosomal dominant condition caused by mutations in the **LMX1B gene**. While it is characterized by the clinical tetrad of nail hypoplasia/dysplasia, absent or hypoplastic patellae, iliac horns (pathognomonic), and elbow abnormalities, it is **not** associated with sensorineural hearing loss (SNHL). Renal involvement occurs in about 40% of cases, typically presenting as proteinuria or focal segmental glomerulosclerosis (FSGS). **Analysis of other options:** * **Alport Syndrome (Option A):** A classic cause of hereditary nephritis due to mutations in Type IV collagen (COL4A3/4/5). The most common extra-renal manifestation is **bilateral sensorineural deafness** (high-frequency), alongside ocular defects like anterior lenticonus. * **Batten Disease (Option B):** Also known as Neuronal Ceroid Lipofuscinosis (NCL), this group of neurodegenerative disorders involves the accumulation of lipopigments. While primarily causing vision loss and seizures, certain subtypes are associated with progressive hearing impairment. * **Distal Renal Tubular Acidosis (Type 1 RTA) (Option D):** Specifically, the autosomal recessive form of distal RTA (associated with mutations in *ATP6V1B1* or *ATP6V0A4*) is frequently associated with **early-onset sensorineural hearing loss** [1]. **NEET-PG High-Yield Pearls:** * **Iliac Horns:** Pathognomonic radiological sign for Nail-patella syndrome. * **Alport Syndrome:** Look for the

Question 194: Which is not a feature of classic distal renal tubular acidosis?

A. Hyperkalemia (Correct Answer)
B. Urine pH >5.5
C. Positive urine anion gap
D. Nephrocalcinosis

Explanation: ### Explanation **Distal Renal Tubular Acidosis (Type 1 RTA)** is characterized by a defect in the alpha-intercalated cells of the distal tubule, leading to an inability to secrete hydrogen ions ($H^+$) [1]. **1. Why Hyperkalemia is the correct answer:** In classic Type 1 RTA, the primary defect is the failure of the $H^+$-ATPase pump. To maintain electrical neutrality, the kidney excretes potassium ($K^+$) instead of hydrogen ions. This results in **hypokalemia**, not hyperkalemia. Hyperkalemia is a hallmark of **Type 4 RTA** (Hypoaldosteronism), making it the "odd one out" for distal RTA. **2. Analysis of Incorrect Options:** * **Urine pH > 5.5:** This is the most characteristic feature [1]. Because the distal tubule cannot secrete $H^+$, the urine cannot be acidified below a pH of 5.5, even in the presence of systemic acidemia [1]. * **Positive Urine Anion Gap (UAG):** UAG ($Na + K - Cl$) is a surrogate marker for urinary ammonium ($NH_4^+$) excretion. In Type 1 RTA, $NH_4^+$ production is impaired due to the distal defect, leading to a low chloride concentration and a **positive** UAG. * **Nephrocalcinosis:** Chronic acidemia leads to bone resorption (releasing calcium) and inhibits citrate reabsorption. The combination of hypercalciuria and hypocitraturia in alkaline urine causes calcium phosphate stones and medullary nephrocalcinosis. **Clinical Pearls for NEET-PG:** * **Type 1 (Distal):** Hypokalemia, Urine pH > 5.5, Stones (Nephrocalcinosis). * **Type 2 (Proximal):** Hypokalemia, Urine pH < 5.5 (eventually), associated with **Fanconi Syndrome**. * **Type 4 (Hyperkalemic):** Only RTA with **Hyperkalemia**; associated with Diabetes Mellitus and Addison’s disease. * **Mnemonic:** "Distal is **D**istant from 7 (pH is high/alkaline)" and "Type **4** adds **K** (Hyperkalemia)."

Question 195: Which of the following is characteristic of CRF?

A. Chronic Renal Failure (CRF) (Correct Answer)
B. Acute Glomerulonephritis (Ac GN)
C. Acute Renal Failure (ARF)
D. Renal Tuberculosis (Renal TB)

Explanation: **Explanation:** The hallmark of **Chronic Renal Failure (CRF)**, now more commonly referred to as Chronic Kidney Disease (CKD), is the irreversible and progressive loss of nephron function over a period of at least three months. The characteristic features that distinguish CRF from acute conditions include **bilateral small, shrunken kidneys** (on ultrasound), **secondary hyperparathyroidism**, and **renal osteodystrophy**. The presence of broad waxy casts in urinary sediment is also a specific indicator of the dilated, hypertrophied nephrons seen in end-stage renal disease. **Analysis of Options:** * **Acute Glomerulonephritis (Ac GN):** This is characterized by the sudden onset of hematuria (coca-cola colored urine), hypertension, and edema. It is an inflammatory process, not a failure state, and is typically reversible. * **Acute Renal Failure (ARF/AKI):** ARF involves a rapid decline in GFR (hours to days). Key differentiators from CRF include **normal-sized kidneys** and the potential for full recovery of renal function once the underlying insult is removed. * **Renal Tuberculosis:** This typically presents with "sterile pyuria" (pus cells in urine without bacterial growth on routine culture) and characteristic imaging findings like infundibular stenosis or "putty kidney," rather than generalized renal failure. **NEET-PG High-Yield Pearls:** * **Kidney Size Exception:** While small kidneys are characteristic of CRF, certain conditions cause **CRF with large/normal kidneys**: Diabetes Mellitus (most common), Amyloidosis, Polycystic Kidney Disease (PCKD), and HIV-associated nephropathy. * **Anemia:** Normocytic normochromic anemia due to Erythropoietin deficiency is a classic sign of CRF. * **Electrolytes:** CRF typically presents with hypocalcemia, hyperphosphatemia, and hyperkalemia.

Question 196: In urinary system disease, gastrointestinal symptoms appear due to which phenomenon?

A. Chemical reactions
B. Renogastric reflex (Correct Answer)
C. Peritoneal reactions
D. Reflux phenomenon

Explanation: ### Explanation The correct answer is **B. Renogastric reflex**. **1. Why Renogastric Reflex is Correct:** The renogastric reflex is a visceral autonomic reflex mediated primarily by the **vagus nerve** and the **celiac ganglion** [1]. The kidneys and the gastrointestinal tract share a common nerve supply (T10–L1 segments). When there is acute distension of the renal capsule or ureter (as seen in renal colic or pyelonephritis), the sensory afferent impulses trigger a reflex arc that inhibits gastric motility and stimulates the vomiting center in the medulla [1]. This explains why patients with acute renal pathology frequently present with nausea, vomiting, and abdominal distension (paralytic ileus). **2. Why Other Options are Incorrect:** * **A. Chemical reactions:** While metabolic waste accumulation (uremia) in chronic kidney disease can cause "uremic gastritis," the immediate GI symptoms in acute urinary diseases are neurogenic, not primarily due to local chemical reactions [2]. * **C. Peritoneal reactions:** Although the kidneys are retroperitoneal, severe inflammation can irritate the overlying peritoneum (peritonism). However, this is a secondary complication rather than the primary physiological mechanism for GI symptoms in standard urinary diseases. * **D. Reflux phenomenon:** This term usually refers to Vesicoureteral Reflux (VUR) [3] or Gastroesophageal Reflux (GERD), which are structural/functional flow issues and do not describe the neurogenic link between the kidney and the stomach. **3. Clinical Pearls for NEET-PG:** * **Shared Innervation:** The kidney and stomach both receive autonomic input from the celiac plexus. * **Differential Diagnosis:** Because of the renogastric reflex, acute renal colic can mimic an "acute abdomen" (like appendicitis or cholecystitis) due to referred pain and associated GI distress. * **Uremic Fetor:** In chronic renal failure, the ammonia-like breath is due to the bacterial breakdown of urea in saliva, a "chemical" GI manifestation distinct from the acute reflex mechanism [2].

Question 197: A 20-year-old female presents with a blood pressure of 160/110 mm Hg. Clinical examination reveals a bruit in both flanks. Which of the following statements about this patient is not true?

A. Enalapril may deteriorate renal function.
B. The most definitive diagnostic procedure is contrast-enhanced angiography.
C. The condition is nearly always bilateral. (Correct Answer)
D. Surgical intervention may be used.

Explanation: ### **Explanation** The clinical presentation of a young female with severe hypertension and bilateral abdominal bruits is classic for **Fibromuscular Dysplasia (FMD)** causing Renovascular Hypertension. **1. Why Option C is the Correct Answer (The "Not True" Statement):** While FMD is frequently bilateral (occurring in approximately 35–50% of cases), it is **not "nearly always" bilateral**. In many patients, it presents as unilateral involvement. In contrast, the question implies a near-universal bilateral occurrence, which is clinically inaccurate. **2. Analysis of Other Options:** * **Option A (Enalapril/ACE inhibitors):** In the presence of bilateral renal artery stenosis (suggested by bilateral bruits), ACE inhibitors like Enalapril can lead to a sharp decline in GFR and acute renal failure. This occurs because they block Angiotensin II-mediated vasoconstriction of the efferent arteriole, which is necessary to maintain glomerular capillary pressure. * **Option B (Contrast-enhanced angiography):** Digital Subtraction Angiography (DSA) remains the **gold standard** and most definitive diagnostic tool. It characteristically shows a "string of beads" appearance in FMD. * **Option D (Surgical intervention):** While Percutaneous Transluminal Renal Angioplasty (PTRA) is the treatment of choice for FMD, surgical revascularization is a valid alternative if angioplasty fails or if the stenosis involves complex branch arteries. ### **High-Yield Clinical Pearls for NEET-PG** * **FMD vs. Atherosclerosis:** FMD typically affects young females and involves the **distal two-thirds** of the renal artery. Atherosclerotic stenosis affects older males and involves the **ostium/proximal third**. * **Pathology:** The most common histological type of FMD is **medial fibroplasia**. * **Screening:** Renal Doppler ultrasound or CT Angiography are initial screening tools, but catheter-based angiography is definitive [1]. * **Treatment:** Unlike atherosclerotic stenosis, FMD responds exceptionally well to angioplasty **without** stenting.

Question 198: Renal vein thrombosis is caused by all of the following except?

A. Lupus nephritis (Correct Answer)
B. Invasive renal cell carcinoma
C. Pregnancy
D. Dehydration

Explanation: **Explanation:** Renal Vein Thrombosis (RVT) occurs due to the classic Virchow’s triad: endothelial injury, stasis of blood flow, and hypercoagulability. **Why Lupus Nephritis is the correct answer (the "Except"):** While Lupus Nephritis (LN) is a glomerular disease, it is **not** a primary cause of RVT unless it progresses to **Nephrotic Syndrome** [1]. Among the nephrotic syndromes, RVT is most strongly associated with **Membranous Nephropathy (MN)** [2], followed by Minimal Change Disease and FSGS. LN itself, without the profound protein loss and loss of Antithrombin III seen in nephrotic states, does not typically cause RVT. **Analysis of Incorrect Options:** * **Invasive Renal Cell Carcinoma (RCC):** This is a classic cause of RVT due to direct **vascular invasion**. The tumor thrombus often extends into the renal vein and can reach the Inferior Vena Cava (IVC). * **Pregnancy:** Pregnancy is a systemic **hypercoagulable state** due to increased clotting factors and venous stasis from the gravid uterus compressing the IVC, increasing the risk of thromboembolic events, including RVT. * **Dehydration:** This is the most common cause of RVT in **neonates and infants**. Hemoconcentration leads to increased blood viscosity and stasis, triggering thrombus formation. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Investigation:** Selective Renal Venography. * **Investigation of Choice (Non-invasive):** CT Angiography or Doppler Ultrasound. * **Clinical Presentation:** Flank pain, hematuria, and a sudden increase in proteinuria or decline in GFR. * **Most Common Association:** Membranous Nephropathy (up to 30-50% of patients may develop subclinical RVT) [2].

Question 199: A 30-year-old male presents with hemoptysis, facial puffiness, microscopic hematuria, and increased serum creatinine. Which of the following investigations should be included?

A. Chest X-ray
B. Antinuclear antibody (ANA) (Correct Answer)
C. Antineutrophil cytoplasmic antibody (ANCA)
D. CT scan of the chest

Explanation: This clinical presentation describes **Pulmonary-Renal Syndrome (PRS)**, characterized by the triad of diffuse alveolar hemorrhage (hemoptysis) and rapidly progressive glomerulonephritis (hematuria, puffiness, and elevated creatinine) [1]. ### **Explanation of the Correct Answer** The differential diagnosis for PRS includes Systemic Lupus Erythematosus (SLE), ANCA-associated vasculitis (e.g., Granulomatosis with polyangiitis), and Goodpasture’s syndrome [4]. In the context of this specific question (likely based on a previous year's pattern), **Antinuclear antibody (ANA)** is prioritized as a primary screening tool [2]. SLE is a multisystem disease that frequently presents in young patients with both pulmonary hemorrhage [3] and lupus nephritis. ANA has a very high sensitivity (>95%) for SLE, making it an essential initial investigation to rule out a systemic autoimmune etiology [2]. ### **Analysis of Incorrect Options** * **ANCA (Option C):** While ANCA is crucial for diagnosing vasculitides like GPA or MPA, ANA is often considered a broader initial screen in young patients to rule out SLE, which can mimic many vasculitic presentations [2]. * **Chest X-ray (Option A) & CT Chest (Option D):** These are imaging modalities used to confirm the presence of alveolar hemorrhage (showing bilateral opacities) [3]. While clinically necessary, they are **supportive** investigations. They do not provide the **etiological diagnosis** required to guide specific immunosuppressive therapy, unlike serological markers. ### **NEET-PG High-Yield Pearls** * **Pulmonary-Renal Syndrome Triad:** Hemoptysis + Hematuria + Acute Kidney Injury. * **Most common cause of PRS:** ANCA-associated vasculitis (specifically GPA) [4]. * **Goodpasture’s Syndrome:** Caused by anti-GBM antibodies; involves the lungs and kidneys only (no systemic involvement). * **Diagnostic Gold Standard:** Renal biopsy (shows crescentic glomerulonephritis) and Serology (ANA, ANCA, Anti-GBM) [1].

Question 200: What is the most common cause of hypovolemic hyponatremia in a hospitalized patient?

A. Intravenous fluids
B. Diuretic-induced (Correct Answer)
C. Severe pain
D. Congestive heart failure

Explanation: ### Explanation **Correct Option: B. Diuretic-induced** Hypovolemic hyponatremia occurs when there is a loss of both water and sodium, but the sodium loss is disproportionately greater [1]. In hospitalized patients, **diuretics (especially Thiazides)** are the most common cause [1]. * **Mechanism:** Diuretics inhibit sodium reabsorption (Thiazides at the distal convoluted tubule; Loop diuretics at the Thick Ascending Limb). This leads to volume depletion, which triggers the non-osmotic release of **Antidiuretic Hormone (ADH)**. ADH causes water retention in the collecting ducts via V2 receptors and aquaporin channels, further diluting the serum sodium and resulting in hyponatremia [2]. **Analysis of Incorrect Options:** * **A. Intravenous fluids:** While common in hospitals, IV fluids (like 5% Dextrose) typically cause **euvolemic** hyponatremia due to the administration of free water, rather than hypovolemic hyponatremia [1]. * **C. Severe pain:** Pain, stress, and nausea are potent stimulators of ADH secretion (SIADH physiology). This leads to **euvolemic** hyponatremia, as there is no primary fluid volume deficit [1]. * **D. Congestive heart failure (CHF):** CHF is a classic cause of **hypervolemic** hyponatremia [1]. Despite low effective arterial blood volume, the total body water and sodium are increased (edematous state). **NEET-PG High-Yield Pearls:** * **Thiazides vs. Loop Diuretics:** Thiazides cause hyponatremia more frequently than Loop diuretics because they do not interfere with the medullary osmotic gradient, allowing ADH to work more effectively. * **Urinary Sodium Check:** In hypovolemic hyponatremia, if $U_{Na} < 20$ mEq/L, the loss is extra-renal (e.g., vomiting/diarrhea). If $U_{Na} > 40$ mEq/L, the loss is renal (e.g., diuretics or Addison’s disease) [1]. * **Management:** The mainstay of treatment for hypovolemic hyponatremia is **Isotonic (0.9%) Saline** to restore volume and shut off the ADH stimulus [3].

Practice by Chapter

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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