Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 161: Normal sized to enlarged kidneys in a patient with chronic failure is indicative of which of the following conditions?

A. Benign nephrosclerosis
B. Chronic glomerulonephritis
C. Chronic interstitial nephritis
D. Primary amyloidosis (Correct Answer)

Explanation: **Explanation:** In most cases of Chronic Kidney Disease (CKD), kidneys are typically shrunken and scarred (small, echogenic kidneys on ultrasound) [1]. However, certain conditions are classic exceptions where kidneys remain **normal-sized or enlarged** despite advanced renal failure. **1. Why Primary Amyloidosis is correct:** In Primary Amyloidosis (AL), there is an extracellular deposition of insoluble amyloid fibrils within the renal parenchyma (glomeruli, tubules, and interstitium). This progressive accumulation increases the overall mass and volume of the kidney, preventing the typical shrinkage seen in chronic failure. Even as the GFR declines, the kidneys remain large and "waxy." **2. Why the other options are incorrect:** * **Benign Nephrosclerosis:** This is the result of long-standing hypertension, leading to hyaline arteriolosclerosis and ischemic atrophy. It characteristically results in **symmetrically shrunken kidneys** with a finely granular surface. * **Chronic Glomerulonephritis:** This represents the end-stage of various glomerular diseases. It is the most common cause of **small, contracted kidneys** due to extensive fibrosis and loss of nephrons. * **Chronic Interstitial Nephritis:** Chronic inflammation of the tubules and interstitium leads to progressive tubular atrophy and interstitial fibrosis, resulting in **small, irregular kidneys [2].** **3. High-Yield Clinical Pearls for NEET-PG:** To remember the causes of **Large Kidneys in CKD**, use the mnemonic **"SHAPE"**: * **S:** **S**cleroderma (Systemic Sclerosis) * **H:** **H**IV-associated nephropathy (HIVAN) * **A:** **A**myloidosis * **P:** **P**olycystic Kidney Disease (ADPKD) * **E:** **E**ndocrinopathy (**Diabetes Mellitus** – the most common cause) *Note: In Diabetes, kidneys are enlarged in the early stages (hyperfiltration) and typically remain normal-sized even when renal failure develops.*

Question 162: Which of the following is NOT used in the management of hyperkalemia?

A. 50 ml of 50% dextrose (Correct Answer)
B. Sodium bicarbonate
C. Salbutamol
D. Calcium gluconate

Explanation: In the management of hyperkalemia, the goal is to stabilize the cardiac membrane, shift potassium into cells, and eventually remove it from the body. **Explanation of the Correct Answer:** **Option A (50 ml of 50% dextrose)** is the correct answer because it is **not** used alone. While insulin is a mainstay of treatment (shifting potassium into cells via Na+/K+ ATPase stimulation), dextrose is only administered alongside insulin to prevent hypoglycemia. Giving 50% dextrose alone can actually worsen hyperkalemia; the resulting hyperosmolality draws water out of cells, which pulls potassium into the extracellular space via "solvent drag," potentially exacerbating the arrhythmia risk. **Explanation of Incorrect Options:** * **B. Sodium Bicarbonate:** It induces alkalosis, which causes a hydrogen-potassium exchange, shifting K+ into the intracellular compartment [1]. It is particularly useful if metabolic acidosis is present. * **C. Salbutamol:** As a Beta-2 agonist, it stimulates the Na+/K+ ATPase pump, promoting the intracellular shift of potassium [2]. * **D. Calcium Gluconate:** This is the first-line treatment for hyperkalemia with ECG changes. It does not lower serum potassium levels but stabilizes the cardiac myocyte membrane to prevent lethal arrhythmias [1]. **NEET-PG High-Yield Pearls:** * **C-BIG-K Mnemonic:** **C**alcium gluconate (Stabilize), **B**icarbonate/Beta-agonists (Shift), **I**nsulin + **G**lucose (Shift), **K**ayexalate/Diuretics/Dialysis (Remove). * **Fastest Acting:** Calcium gluconate (1-3 minutes) but has the shortest duration [1]. * **Definitive Treatment:** Hemodialysis is the most effective method for potassium removal in patients with renal failure.

Question 163: In which one of the following conditions is a renal biopsy contraindicated?

A. Acute renal failure
B. Uncontrolled hypertension (Correct Answer)
C. Nephrotic syndrome
D. Isolated hematuria

Explanation: **Explanation:** Renal biopsy is a percutaneous procedure typically performed under ultrasound guidance. Because the kidney is a highly vascular organ, the most significant risk associated with the procedure is **hemorrhage**. **1. Why Uncontrolled Hypertension is the Correct Answer:** Uncontrolled hypertension is considered an **absolute contraindication** for a renal biopsy. High systemic blood pressure significantly increases the risk of post-procedural bleeding, hematoma formation, and the potential loss of the kidney. The procedure should only be performed once the blood pressure is stabilized (typically <140/90 mmHg) to ensure hemostasis. **2. Why the Other Options are Incorrect:** * **A. Acute Renal Failure (ARF):** Biopsy is often indicated in ARF (specifically Rapidly Progressive Glomerulonephritis) to determine the underlying etiology and guide urgent immunosuppressive therapy. * **C. Nephrotic Syndrome:** This is one of the most common indications for a renal biopsy in adults to differentiate between causes like Minimal Change Disease, FSGS, or Membranous Nephropathy. * **D. Isolated Hematuria:** While not always mandatory, a biopsy is indicated if isolated hematuria is associated with declining renal function, proteinuria, or if a glomerular origin (like IgA Nephropathy) is suspected. **NEET-PG High-Yield Pearls:** * **Absolute Contraindications:** Uncontrolled hypertension, uncorrectable bleeding diathesis, active renal infection (e.g., pyelonephritis), and an uncooperative patient. * **Relative Contraindications:** Solitary kidney (except in transplants), polycystic kidney disease, and small echogenic kidneys (indicative of end-stage renal disease where biopsy won't change management). * **Most Common Complication:** Microscopic hematuria (occurs in almost all patients); the most common *significant* complication is a perinephric hematoma. Note: The provided references discussing renal artery stenosis, cholesterol emboli, ultrasound imaging techniques, and hematuria diagnostic steps do not explicitly list the contraindications for renal biopsy.

Question 164: What is the earliest finding in diabetic nephropathy?

A. Shrunken kidney
B. Fibrin caps
C. Elevated creatinine clearance
D. Urine albumin > 30 mg/dl (Correct Answer)

Explanation: ### Explanation **1. Why the correct answer is right:** The natural history of diabetic nephropathy (DN) begins with a phase of **hyperfiltration**, followed by the development of **Microalbuminuria**. Microalbuminuria, defined as a urine albumin excretion of **30–300 mg/day** (or >30 mg/dl in a spot sample), is clinically recognized as the **earliest detectable sign** of impending nephropathy [1]. It reflects early glomerular damage and serves as a critical predictor of progression to overt proteinuria and end-stage renal disease (ESRD). **2. Why the incorrect options are wrong:** * **A. Shrunken kidney:** This is a late-stage finding in most chronic kidney diseases. Notably, in diabetic nephropathy, kidneys often remain **normal or enlarged** in size even when renal function is significantly impaired, making shrunken kidneys an incorrect choice for an "earliest" finding. * **B. Fibrin caps:** These are hyaline deposits in the Bowman’s capsule or glomerular capillaries. While characteristic of DN, they are **histopathological** findings seen in the stage of established Kimmelstiel-Wilson (KW) lesions, not the earliest clinical finding [2]. * **C. Elevated creatinine clearance:** While an increase in Glomerular Filtration Rate (GFR) and creatinine clearance (Hyperfiltration) is technically the *first physiological change* (Stage 1 of Mogensen’s classification), it is often transient and rarely used as a diagnostic marker in clinical practice. In the context of standard NEET-PG questions, **Microalbuminuria** is the preferred answer for the earliest clinical sign. **3. Clinical Pearls for NEET-PG:** * **Mogensen’s Stages:** Stage 1 (Hyperfiltration), Stage 2 (Silent/Structural changes), Stage 3 (Incipient DN/Microalbuminuria), Stage 4 (Overt DN/Macroalbuminuria), Stage 5 (ESRD). * **Pathognomonic Finding:** Kimmelstiel-Wilson (KW) nodules (nodular glomerulosclerosis) are the most specific histological finding [2]. * **Screening:** Type 1 DM patients should be screened 5 years after diagnosis; Type 2 DM patients should be screened at the time of diagnosis [1]. * **Management:** ACE inhibitors or ARBs are the drugs of choice as they reduce intraglomerular pressure and slow the progression of albuminuria.

Question 165: Which of the following is a common feature of Gitelman syndrome?

A. Hyperkalemia
B. Metabolic alkalosis (Correct Answer)
C. Hypermagnesemia
D. High calcium excretion

Explanation: **Explanation:** **Gitelman syndrome** is an autosomal recessive salt-wasting tubulopathy caused by a loss-of-function mutation in the **SLC12A3 gene**, which encodes the **thiazide-sensitive sodium-chloride (Na-Cl) cotransporter** in the distal convoluted tubule (DCT). 1. **Why Metabolic Alkalosis is Correct:** The defect in the Na-Cl cotransporter leads to increased delivery of sodium and water to the collecting duct. This stimulates the Renin-Angiotensin-Aldosterone System (RAAS). Aldosterone promotes sodium reabsorption in exchange for potassium and **hydrogen ions (H+)** in the intercalated cells. The excessive loss of H+ ions results in **hypokalemic metabolic alkalosis**, mimicking the chronic use of thiazide diuretics. 2. **Analysis of Incorrect Options:** * **A. Hyperkalemia:** Incorrect. Increased distal delivery of sodium and high aldosterone levels lead to significant potassium wasting, resulting in **hypokalemia**. * **C. Hypermagnesemia:** Incorrect. Gitelman syndrome is uniquely characterized by profound **hypomagnesemia** due to magnesium wasting in the DCT. * **D. High calcium excretion:** Incorrect. Unlike Bartter syndrome (which presents with hypercalciuria), Gitelman syndrome is characterized by **hypocalciuria** (low urinary calcium). This occurs because the reduced intracellular sodium in the DCT cells enhances the activity of the basolateral Na/Ca exchanger, promoting calcium reabsorption. **NEET-PG High-Yield Pearls:** * **Gitelman vs. Bartter:** Gitelman presents later (adolescence/adulthood) and features **hypocalciuria** and **hypomagnesemia**. Bartter presents earlier (infancy) with **hypercalciuria** (mimicking loop diuretics). * **Mnemonic:** **G**itelman = **G**radual (late onset) + **G**ood (low) urinary calcium. * **Clinical Presentation:** Patients often present with muscle cramps, fatigue, and salt craving.

Question 166: All of the following statements are true about adult polycystic kidney disease, except:

A. Autosomal dominant inheritance
B. Hypertension is rare (Correct Answer)
C. Can be associated with cysts in liver, lungs and pancreas
D. Pyelonephritis is common

Explanation: Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common hereditary kidney disease [1]. Understanding its systemic nature is crucial for NEET-PG. **Why Option B is the correct answer (The False Statement):** Contrary to the option, **hypertension is very common** in ADPKD, occurring in approximately 70-80% of patients even before a significant decline in GFR. The underlying mechanism is the activation of the **Renin-Angiotensin-Aldosterone System (RAAS)**. As cysts enlarge, they compress intrarenal vasculature, causing localized ischemia, which triggers renin release. Controlling hypertension is the primary intervention to slow disease progression. **Analysis of other options:** * **Option A:** ADPKD follows an **Autosomal Dominant** inheritance pattern, primarily involving mutations in the *PKD1* (85%, Chromosome 16) or *PKD2* (15%, Chromosome 4) genes [1]. * **Option C:** ADPKD is a systemic ciliopathy. **Polycystic Liver Disease (PLD)** is the most common extrarenal manifestation. Cysts can also occur in the pancreas, spleen, and seminal vesicles. * **Option D:** Urinary tract infections, including **pyelonephritis** and infected cysts, are frequent complications due to stasis and structural abnormalities within the distorted renal parenchyma. **NEET-PG High-Yield Pearls:** 1. **Most common extrarenal manifestation:** Liver cysts (70% of patients). 2. **Most serious extrarenal complication:** Berry Aneurysms (Circle of Willis), which can lead to Subarachnoid Hemorrhage (SAH). 3. **Diagnosis:** Ultrasonography is the first-line screening tool (Ravine’s criteria). 4. **Treatment:** ACE inhibitors/ARBs are the drugs of choice for hypertension; **Tolvaptan** (V2 receptor antagonist) is used to slow cyst growth.

Question 167: All of the following are examples of microvascular causes of acute kidney injury, EXCEPT:

A. Antiphospholipid antibody syndrome
B. Radiation nephritis
C. Thrombotic thrombocytopenic purpura
D. Renal vein thrombosis (Correct Answer)

Explanation: Explanation: Acute Kidney Injury (AKI) can be categorized by the size and location of the vessels involved. The distinction between **microvascular** and **macrovascular** causes is a high-yield concept for NEET-PG. **1. Why Renal Vein Thrombosis is the Correct Answer:** Renal vein thrombosis (RVT) is a **macrovascular** cause of AKI. It involves the obstruction of the main renal vein or its major branches. Because it affects a large vessel rather than the microscopic capillary beds or arterioles, it does not fall under the "microvascular" category. Clinically, RVT is most commonly associated with Nephrotic Syndrome (especially Membranous Nephropathy). **2. Analysis of Incorrect Options (Microvascular Causes):** * **Thrombotic Thrombocytopenic Purpura (TTP):** This is a classic **Thrombotic Microangiopathy (TMA)** [1]. It involves the formation of microthrombi in the small arterioles and capillaries due to ADAMTS13 deficiency, leading to microvascular AKI [1]. * **Antiphospholipid Antibody Syndrome (APS):** While APS can cause macrovascular events (like DVT), **APS Nephropathy** specifically involves small-vessel vaso-occlusion, including glomerular capillary thrombosis and fibrous intimal hyperplasia of interlobular arteries. * **Radiation Nephritis:** Chronic or acute exposure to radiation leads to endothelial damage of the **small vessels** (capillaries and arterioles), resulting in a TMA-like picture and subsequent nephrosclerosis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Macrovascular AKI:** Includes Renal Artery Stenosis/Embolism, Renal Vein Thrombosis, and Large-vessel Vasculitis (e.g., Takayasu Arteritis) [2]. * **Microvascular AKI:** Includes HUS/TTP, DIC, Pre-eclampsia, Scleroderma Renal Crisis, and Malignant Hypertension [1]. * **Key Association:** The most common cause of Renal Vein Thrombosis in adults is **Membranous Nephropathy**. * **Triad of RVT:** Flank pain, hematuria, and an increase in kidney size (on ultrasound).

Question 168: Pre-renal azotemia is associated with which of the following characteristic features?

A. Urinary sodium < 10 mmol/L (Correct Answer)
B. Renal failure index > 1
C. Urine osmolality < 500 mOsm/kg
D. Urinary creatinine/plasma creatinine ratio < 20

Explanation: **Explanation:** Pre-renal azotemia occurs due to decreased renal perfusion (e.g., dehydration, hemorrhage, or heart failure) without structural damage to the kidney parenchyma. In this state, the kidneys function normally but respond to hypovolemia by activating the **Renin-Angiotensin-Aldosterone System (RAAS)** and increasing ADH secretion. [1] 1. **Why Option A is Correct:** Aldosterone acts on the distal tubules to maximize sodium reabsorption to expand intravascular volume. Consequently, the **Urinary Sodium is typically low (< 20 mmol/L, often < 10 mmol/L)**. This is a hallmark of intact tubular function attempting to conserve salt and water. 2. **Why the other options are incorrect:** * **Option B (Renal Failure Index > 1):** The RFI (Urinary Na / [Urine Cr / Plasma Cr]) is **< 1** in pre-renal states. An RFI > 1 (or > 2) indicates Acute Tubular Necrosis (ATN), where tubules lose the ability to reabsorb sodium. * **Option C (Urine Osmolality < 500 mOsm/kg):** In pre-renal azotemia, high ADH levels cause the kidneys to produce highly concentrated urine to conserve water. [1] Thus, **Urine Osmolality is typically > 500 mOsm/kg**. Low osmolality (< 350 mOsm/kg) suggests ATN. * **Option D (U/P Creatinine Ratio < 20):** Because the tubules are intact, they reabsorb water, which concentrates creatinine in the urine. Therefore, the **Urine/Plasma Creatinine ratio is > 40** in pre-renal states. A ratio < 20 indicates tubular dysfunction (ATN). **High-Yield Clinical Pearls for NEET-PG:** * **Fractional Excretion of Sodium (FeNa):** The most reliable indicator. **FeNa < 1%** suggests Pre-renal azotemia; **FeNa > 2%** suggests ATN. * **BUN/Creatinine Ratio:** Typically **> 20:1** in pre-renal states (due to increased passive urea reabsorption) compared to 10-15:1 in intrinsic renal failure. * **Urinary Sediment:** Usually "bland" or contains hyaline casts in pre-renal states, whereas "muddy brown" granular casts are pathognomonic for ATN.

Question 169: What is the most common organism isolated in emphysematous pyelonephritis?

A. Escherichia coli (Correct Answer)
B. Proteus
C. Pseudomonas
D. Klebsiella

Explanation: **Explanation:** **Emphysematous Pyelonephritis (EPN)** is a severe, necrotizing infection of the renal parenchyma characterized by the presence of gas within the kidney or perinephric space. It is a urological emergency, predominantly seen in patients with uncontrolled diabetes mellitus (approx. 90% of cases) or urinary tract obstruction. [1] **Why Escherichia coli is correct:** * **E. coli** is the most common organism isolated, accounting for approximately **60-70%** of cases. [1] * **Pathophysiology:** In diabetic patients, high tissue glucose levels provide a substrate for facultative anaerobes like *E. coli*. These bacteria undergo mixed-acid fermentation, producing carbon dioxide ($CO_2$) and hydrogen ($H_2$) gas, which accumulates in the renal tissues. **Why other options are incorrect:** * **Klebsiella pneumoniae:** This is the second most common cause (approx. 10-20%). While it also performs fermentation leading to gas production, its prevalence is significantly lower than *E. coli*. * **Proteus mirabilis:** Though associated with staghorn calculi and urease-producing infections, it is a rare cause of EPN compared to the coliforms. * **Pseudomonas aeruginosa:** This is an uncommon isolate in EPN, usually seen in healthcare-associated infections or post-instrumentation, but it is not the primary causative agent. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Diabetes Mellitus (most common) and Female gender. [1] * **Diagnosis:** **NCCT Abdomen** is the gold standard (shows gas in the renal parenchyma). * **Management:** Medical management with IV antibiotics and percutaneous drainage (PCD) is the first line. Emergency nephrectomy is reserved for patients who fail conservative therapy. * **Classification:** Often classified using the **Wan et al.** or **Huang and Tseng** criteria based on CT findings.

Question 170: A patient presents with the following blood biochemical values: Calcium 6 mg/dL; Uric acid 13 mg/dL; Phosphorus 12 mg/dL; Creatinine 6 mg/dL. Which of the following is a possible diagnosis?

A. Krait bite
B. Uric acid nephropathy (Correct Answer)
C. Hypercalcemic nephropathy
D. Rickets

Explanation: ### Explanation The biochemical profile provided—**Hyperuricemia** (13 mg/dL), **Hyperphosphatemia** (12 mg/dL), **Hypocalcemia** (6 mg/dL), and **Acute Kidney Injury** (Creatinine 6 mg/dL)—is the classic metabolic signature of **Tumor Lysis Syndrome (TLS)**, which leads to **Uric Acid Nephropathy** [1]. **1. Why Uric Acid Nephropathy is Correct:** In conditions with high cell turnover (like leukemia or lymphoma), massive release of intracellular contents occurs [2]. * **Uric Acid:** Purine catabolism leads to extreme hyperuricemia. These crystals precipitate in the renal tubules, causing obstructive uropathy. * **Phosphorus:** Intracellular phosphate release causes hyperphosphatemia. * **Calcium:** High phosphate levels lead to calcium-phosphate precipitation, resulting in secondary hypocalcemia. The combination of high uric acid and high phosphorus in the setting of renal failure is a hallmark of this diagnosis [1]. **2. Why Other Options are Incorrect:** * **Krait Bite:** Typically presents with neurological symptoms (neuromuscular blockade/paralysis). While Russell’s Viper bite causes AKI (via hemolysis/rhabdomyolysis), Krait bites usually lack significant nephrotoxicity. * **Hypercalcemic Nephropathy:** This would present with **high** calcium levels (e.g., >12 mg/dL), not the low levels (6 mg/dL) seen here [3]. * **Rickets:** Characterized by low/normal calcium and **low** phosphorus (due to PTH action), with normal creatinine. It does not cause acute renal failure. **3. NEET-PG High-Yield Pearls:** * **Uric Acid/Creatinine Ratio:** A ratio **>1.0** in a random urine sample suggests acute uric acid nephropathy (TLS), whereas a ratio <1.0 suggests other causes of AKI. * **Prevention:** Aggressive hydration and **Rasburicase** (recombinant urate oxidase) are preferred for high-risk TLS. **Allopurinol** is used for prophylaxis but does not reduce existing uric acid. * **Phosphate-Calcium Product:** If [Ca] x [Phos] > 55–60, the risk of metastatic calcification increases significantly.

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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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