Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 231: Renal vein thrombosis (RVT) may be seen in:

A. Trauma
B. Renal Cell Carcinoma
C. Pregnancy
D. All of the above (Correct Answer)

Explanation: Renal Vein Thrombosis (RVT) occurs when there is a formation of a clot in the major renal veins or their tributaries. The underlying pathophysiology follows **Virchow’s Triad**: endothelial injury, stasis of blood flow, and hypercoagulability. * **Trauma (Option A):** Direct blunt or penetrating trauma to the abdomen or back can cause endothelial damage to the renal vessels, triggering the coagulation cascade and leading to acute thrombosis. * **Renal Cell Carcinoma (Option B):** RCC is notorious for its "angiotropic" nature. The tumor frequently invades the renal vein and can extend into the inferior vena cava (IVC) as a tumor thrombus [1]. This causes both mechanical obstruction (stasis) and a paraneoplastic prothrombotic state. * **Pregnancy (Option C):** Pregnancy is a physiological hypercoagulable state due to increased clotting factors and venous stasis caused by the gravid uterus compressing the pelvic veins and IVC. While rare, RVT can occur postpartum or as a complication of septic pelvic thrombophlebitis. **Clinical Pearls for NEET-PG:** * **Most Common Cause:** In adults, the most common cause of RVT is **Nephrotic Syndrome**, specifically **Membranous Nephropathy** (due to loss of Antithrombin III in urine). * **Clinical Presentation:** Acute RVT presents with flank pain, hematuria, and an enlarged kidney. * **Diagnosis:** The gold standard is **Selective Renal Venography**, but **Color Doppler Ultrasound** or CT/MR Angiography are the preferred initial investigations. * **Left vs. Right:** The left renal vein is more commonly involved due to its longer course and complex anatomy (e.g., Nutcracker syndrome).

Question 232: Bence Jones proteinuria is not seen in which of the following conditions?

A. Multiple myeloma
B. Chronic interstitial nephritis (Correct Answer)
C. Macroglobulinemia
D. Non-Hodgkins lymphoma

Explanation: Bence Jones proteins (BJP) are free monoclonal immunoglobulin light chains (kappa or lambda) produced by neoplastic plasma cells [1]. Their presence in urine is a hallmark of plasma cell dyscrasias and certain lymphoproliferative disorders. **Why Chronic Interstitial Nephritis is the correct answer:** Chronic interstitial nephritis is characterized by **tubular proteinuria**. In this condition, the damaged proximal tubules fail to reabsorb low-molecular-weight proteins that are normally filtered (such as $\beta_2$-microglobulin, retinol-binding protein, or lysozyme). While it involves protein in the urine, it does not involve the production of monoclonal light chains. Therefore, Bence Jones proteinuria is not a feature of this condition. **Analysis of Incorrect Options:** * **Multiple Myeloma:** This is the most common cause of Bence Jones proteinuria. Malignant plasma cells produce excessive light chains that exceed the renal reabsorptive capacity, leading to their excretion in urine [1]. * **Macroglobulinemia (Waldenström’s):** This is a lymphoplasmacytic lymphoma that produces monoclonal IgM. Like other plasma cell dyscrasias, it can be associated with the production of free light chains (BJP) [1]. * **Non-Hodgkin’s Lymphoma (NHL):** Certain B-cell lymphomas can have a circulating monoclonal component or differentiate into plasma cells, leading to the secretion of Bence Jones proteins [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Detection:** Bence Jones proteins precipitate at **40–60°C** and redissolve on boiling (**100°C**). * **Dipstick Limitation:** Standard urine dipsticks primarily detect **albumin**. A patient with Multiple Myeloma may have a "negative" dipstick but show heavy proteinuria on a 24-hour sulfosalicylic acid (SSA) test [1]. * **Diagnosis:** The gold standard for identifying BJP is **Urine Protein Electrophoresis (UPEP)** with immunofixation, showing a "M-spike." * **Renal Impact:** BJP are nephrotoxic and lead to "Myeloma Kidney" (Cast Nephropathy).

Question 233: Chronic Renal Failure is defined as residual renal functional mass less than what percentage?

A. 50%
B. 80%
C. 20% (Correct Answer)
D. 5%

Explanation: ### Explanation **Correct Option: C (20%)** Chronic Renal Failure (CRF) is clinically defined as a state where the residual renal functional mass (functioning nephrons) falls below **20% of normal**. At this threshold, the kidneys can no longer maintain the internal environment (homeostasis), leading to the clinical syndrome of uremia [1]. The progression of renal decline is generally categorized into four stages based on functional mass: 1. **Decreased Renal Reserve:** GFR is 50–80% of normal. Patients are asymptomatic. 2. **Renal Insufficiency:** GFR is 20–50% of normal. Azotemia appears, and anemia may begin. 3. **Renal Failure:** GFR is **<20% of normal**. Metabolic acidosis, edema, and overt uremia develop [1]. 4. **End-Stage Renal Disease (ESRD):** GFR is <5% of normal. Dialysis or transplant is mandatory for survival [1]. **Analysis of Incorrect Options:** * **A (50%):** This represents "Decreased Renal Reserve." The body compensates effectively, and serum creatinine levels usually remain within the normal range. * **B (80%):** This is considered normal or near-normal renal function. * **D (5%):** This defines **End-Stage Renal Disease (ESRD)**, the terminal stage of CRF where life cannot be sustained without renal replacement therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Definition of CKD:** According to KDIGO guidelines, CKD is defined as kidney damage or GFR **<60 ml/min/1.73m²** for **≥3 months** [1]. * **Most Common Cause:** Diabetes Mellitus is the #1 cause of CRF worldwide, followed by Hypertension. * **First Sign:** The earliest clinical sign of CRF is often **isosthenuria** (inability to concentrate or dilute urine, fixed specific gravity at 1.010). * **Small Kidneys:** Bilaterally shrunken kidneys on ultrasound (<9 cm) are a hallmark of CRF, *except* in Diabetes, Amyloidosis, and Polycystic Kidney Disease (PKD), where kidneys may be normal or enlarged.

Question 234: What is the initial treatment for hyperkalemia with bradycardia?

A. Calcium gluconate (Correct Answer)
B. Salbutamol
C. Steroids
D. Potassium resin binder

Explanation: The management of hyperkalemia is a high-yield topic for NEET-PG. The primary goal in severe hyperkalemia (especially when associated with ECG changes like bradycardia, peaked T-waves, or QRS widening) is **cardiac membrane stabilization.** [2] **1. Why Calcium Gluconate is Correct:** Hyperkalemia lowers the threshold potential of cardiac myocytes, leading to increased excitability and eventual conduction blocks (bradycardia). **Calcium gluconate** (10 ml of 10% solution) antagonizes the membrane effects of potassium by increasing the threshold potential, thereby restoring the normal gradient and stabilizing the myocardium. [1] It is the **initial** treatment because it acts within 1–3 minutes, preventing fatal arrhythmias. Note: It does *not* lower serum potassium levels. [1] **2. Why other options are incorrect:** * **Salbutamol:** This is a $\beta_2$-agonist that shifts potassium into the cells. While effective, its onset is slower (approx. 30 mins) and it does not provide immediate cardiac protection. * **Steroids:** These have no role in the acute management of hyperkalemia. * **Potassium resin binders (e.g., Kayexalate):** These remove potassium from the body via the GI tract. They have a very slow onset (hours to days) and are used for definitive removal, not emergency stabilization. **High-Yield Clinical Pearls for NEET-PG:** * **The "C-BIG-K" Mnemonic for Hyperkalemia:** **C**alcium gluconate (Stabilize), **B**eta-agonists/Bicarbonate (Shift), **I**nsulin + **G**lucose (Shift), **K**ayexalate/Kidney dialysis (Remove). * **Calcium Gluconate vs. Calcium Chloride:** Calcium gluconate is preferred in peripheral lines as it is less caustic to veins. * **Digoxin Toxicity:** Use calcium with extreme caution (traditionally avoided due to "stone heart" theory, though recent evidence is debated).

Question 235: Birefringent crystals in urine are seen with which condition?

A. Phosphaturia
B. Uricosuria (Correct Answer)
C. Cystinuria
D. Struvite stones

Explanation: **Explanation:** The correct answer is **Uricosuria** (Uric acid crystals). **1. Why Uricosuria is correct:** Uric acid crystals are a classic example of **birefringent** crystals [1]. Under polarized light microscopy, they exhibit "polychromatic" or strong birefringence, appearing in various colors. Morphologically, they are typically yellow-brown, diamond-shaped, or rhomboid plates. They precipitate in acidic urine (pH < 5.5). **2. Why the other options are incorrect:** * **Phosphaturia (Amorphous Phosphates):** These appear as granular, non-crystalline precipitates in alkaline urine. They do not exhibit the characteristic birefringence seen in uric acid. * **Cystinuria:** Cystine crystals are pathognomonic "hexagonal plates." While they are highly specific for cystinuria, they are typically **non-birefringent** or only weakly birefringent. * **Struvite stones (Triple Phosphate):** Composed of magnesium ammonium phosphate, these are "coffin-lid" shaped crystals seen in alkaline urine associated with urease-producing bacteria (e.g., *Proteus*). They are not typically characterized by birefringence in clinical microscopy. **3. NEET-PG High-Yield Pearls:** * **Ethylene Glycol Poisoning:** Associated with **Calcium Oxalate Monohydrate** crystals, which are needle-shaped and **strongly birefringent**. * **Calcium Oxalate Dihydrate:** The most common crystal; "envelope" or "octahedral" shaped; weakly birefringent. * **Maltese Cross Appearance:** Seen in **Lipiduria** (Nephrotic syndrome) under polarized light due to cholesterol esters [2]. * **Drug-induced crystals:** Sulfonamides (sheaves of wheat) and Indinavir (starburst) can also show birefringence.

Question 236: What is the cause of salt-losing nephropathy?

A. Interstitial nephropathy (Correct Answer)
B. Maintenance phase of acute tubular necrosis
C. Post-streptococcal glomerulonephritis
D. IgA nephropathy

Explanation: **Explanation:** **1. Why Interstitial Nephropathy is Correct:** Salt-losing nephropathy refers to a state where the kidneys are unable to conserve sodium despite low systemic levels. This occurs primarily due to damage to the **renal tubules and the interstitium**. In chronic interstitial nephritis (interstitial nephropathy), the structural integrity of the distal tubules and collecting ducts is compromised [1]. Since these segments are responsible for the fine-tuning of sodium reabsorption, their dysfunction leads to "obligatory" sodium loss in the urine, potentially causing hyponatremia and volume depletion. **2. Why the Other Options are Incorrect:** * **Maintenance phase of ATN:** Salt losing typically occurs during the **Recovery (Diuretic) phase** of Acute Tubular Necrosis, not the maintenance phase. In the maintenance phase, GFR is at its lowest, and the patient is usually oliguric with fluid retention. * **Post-streptococcal glomerulonephritis (PSGN):** This is a nephritic syndrome characterized by glomerular inflammation [2]. The hallmark is salt and water **retention** (leading to hypertension and edema), rather than salt wasting [2]. * **IgA Nephropathy:** Similar to PSGN, this is a glomerular disease. While it can progress to chronic kidney disease, it does not typically present as a primary salt-wasting state unless it reaches advanced stages of interstitial fibrosis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Common Causes of Salt-Wasting:** Medullary cystic disease, Polycystic kidney disease (PKD), Obstructive uropathy, and Chronic Pyelonephritis. * **Distinction:** Do not confuse "Salt-losing nephropathy" with "Cerebral Salt Wasting Syndrome" (which is CNS-mediated). * **Clinical Sign:** Patients often present with "orthostatic hypotension" and a craving for salt. * **Key Concept:** Tubulointerstitial diseases affect the **concentrating ability** and **electrolyte reabsorption** long before the GFR significantly drops.

Question 237: Hyponatremia is seen in all of the following conditions except:

A. Congestive heart failure
B. Kidney problems
C. Diabetes insipidus (Correct Answer)
D. Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Explanation: **Explanation:** The core concept in this question is the balance between water and sodium. **Diabetes Insipidus (DI)** is characterized by either a deficiency of Antidiuretic Hormone (ADH) or a lack of response to it. This leads to the inability of the kidneys to concentrate urine, resulting in massive excretion of dilute urine (polyuria). Because the body is losing pure water in excess of sodium, the serum sodium concentration rises, leading to **hypernatremia**, not hyponatremia. **Analysis of other options:** * **Congestive Heart Failure (CHF):** This is a classic cause of **hypervolemic hyponatremia** [2]. Decreased effective arterial blood volume triggers the release of ADH (non-osmotic release), causing water retention that outweighs sodium retention, thus diluting serum sodium [1]. * **Kidney Problems:** Chronic Kidney Disease (CKD) or acute renal failure often leads to hyponatremia because the kidneys lose the ability to excrete free water effectively, leading to a dilutional state [2]. * **SIADH:** This is the prototype for **euvolemic hyponatremia** [2]. Excessive, unregulated ADH secretion causes continuous water reabsorption in the collecting ducts, diluting the extracellular fluid [1]. **High-Yield Clinical Pearls for NEET-PG:** 1. **DI vs. SIADH:** Think of them as opposites. DI = Low ADH/Effect → High Serum Sodium. SIADH = High ADH → Low Serum Sodium [2]. 2. **Urine Osmolality:** In DI, urine is inappropriately dilute (<200 mOsm/kg); in SIADH, urine is inappropriately concentrated (>100 mOsm/kg) [1]. 3. **Correction Speed:** Rapid correction of hyponatremia can lead to **Osmotic Demyelination Syndrome (Central Pontine Myelinolysis)**. Rule of thumb: Do not exceed 8–10 mEq/L in 24 hours.

Question 238: In adult polycystic kidney disease, all the following are true except?

A. Hypertension is rare (Correct Answer)
B. Hematuria is a common symptom
C. Cysts are seen in the liver, spleen, and pancreas
D. Autosomal dominant transmission is seen

Explanation: **Explanation:** Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common inherited kidney disorder [1]. The correct answer is **Option A** because hypertension is actually a **hallmark feature** of ADPKD, occurring in approximately 70-80% of patients before the onset of renal failure. **Why Option A is the correct answer (The Exception):** Hypertension is **not rare**; it is often the presenting symptom. It results from the activation of the **Renin-Angiotensin-Aldosterone System (RAAS)**. As cysts enlarge, they compress intrarenal vasculature, causing localized ischemia, which triggers renin release even when GFR is still normal [1]. **Analysis of other options:** * **Option B (Hematuria):** This is a very common symptom. It occurs due to the rupture of a cyst into the renal pelvis or associated nephrolithiasis [1]. * **Option C (Extra-renal cysts):** ADPKD is a systemic disorder. While the kidneys are primarily affected, cysts are frequently found in the **liver** (most common extra-renal site), pancreas, spleen, and seminal vesicles. * **Option D (Transmission):** As the name implies, it follows an **Autosomal Dominant** pattern, primarily involving mutations in the **PKD1** (Chromosome 16 - 85% cases) and **PKD2** (Chromosome 4 - 15% cases) genes [1]. **NEET-PG High-Yield Pearls:** * **Most common extra-renal manifestation:** Polycystic Liver Disease. * **Most serious complication:** Berry Aneurysm (Circle of Willis), which can lead to Subarachnoid Hemorrhage (SAH). * **Diagnosis:** Ultrasonography is the screening modality of choice (Ravine’s criteria). * **Treatment:** Tolvaptan (V2-receptor antagonist) is used to slow cyst growth and disease progression.

Question 239: In active lupus nephritis, which one of the following prostaglandins is increased in the urine?

A. Prostaglandin E
B. Prostaglandin L (Correct Answer)
C. Prostaglandin A
D. None of the above

Explanation: **Explanation:** In the context of **Systemic Lupus Erythematosus (SLE)** and active lupus nephritis, the urinary excretion of specific prostaglandins serves as a marker of renal inflammation and hemodynamic compensation. **Why Prostaglandin L (PGI2/Prostacyclin) is correct:** Active lupus nephritis involves significant glomerular injury and inflammation. To maintain renal blood flow and glomerular filtration rate (GFR) in the face of this injury, the kidneys increase the production of vasodilatory prostaglandins. **Prostacyclin (PGI2)**, often referred to in older literature or specific biochemical contexts as **Prostaglandin L**, is a potent vasodilator synthesized by the vascular endothelium and glomerular cells. Studies have shown that urinary levels of 6-keto-PGF1α (the stable metabolite of PGI2) are significantly elevated during the active phase of lupus nephritis, reflecting the intrarenal response to inflammatory damage. **Why other options are incorrect:** * **Prostaglandin E (PGE2):** While PGE2 is also a renal vasodilator, clinical studies specifically highlight the marked elevation of PGI2 metabolites as the primary indicator of active lupus-related glomerular damage compared to PGE2. * **Prostaglandin A (PGA):** PGA is generally considered a dehydration product of PGE and does not play a significant clinical or diagnostic role in the pathogenesis or monitoring of lupus nephritis. **NEET-PG High-Yield Pearls:** * **Thromboxane A2 (TXA2):** In contrast to the vasodilatory PGI2, levels of Thromboxane B2 (metabolite of TXA2, a vasoconstrictor) are also increased in lupus nephritis and are associated with declining renal function and platelet activation. * **Monitoring:** Urinary prostaglandin levels can sometimes correlate with the histological activity index of the disease. * **Clinical Correlation:** The use of NSAIDs in lupus patients is risky because they inhibit these protective prostaglandins (PGI2/PGE2), potentially leading to acute renal failure.

Question 240: Which of the following is NOT a feature of type 4 A (Alport syndrome)?

A. Mild renal failure
B. Hyperkalemia
C. Hypochloremic acidosis (Correct Answer)
D. Occurs in diabetic nephropathy

Explanation: The question refers to **Type 4 Renal Tubular Acidosis (RTA)**, also known as hyperkalemic RTA. The confusion in the question stem regarding "Type 4 A (Alport syndrome)" is a common nomenclature error; in the context of RTA, Type 4 refers to **Hypoaldosteronism** or resistance to aldosterone, not Alport syndrome (which is a collagen IV disorder). **1. Why "Hypochloremic acidosis" is the correct answer:** Type 4 RTA is characterized by **Hyperchloremic Metabolic Acidosis** (Normal Anion Gap Acidosis) [1]. In this condition, the lack of aldosterone effect leads to decreased potassium and hydrogen ion secretion in the distal tubule [1]. This results in the retention of chloride to maintain electrical neutrality, leading to high serum chloride levels, not low. Therefore, **Hypochloremic acidosis is incorrect** for Type 4 RTA. **2. Analysis of incorrect options:** * **Mild renal failure (A):** Type 4 RTA is frequently associated with mild to moderate chronic kidney disease (CKD), where the reduction in functioning nephrons contributes to impaired potassium excretion. * **Hyperkalemia (B):** This is the **hallmark** of Type 4 RTA [1]. Unlike Types 1 and 2 RTA (which cause hypokalemia), Type 4 is the only RTA characterized by high serum potassium due to aldosterone deficiency or resistance [1]. * **Occurs in diabetic nephropathy (D):** Diabetic nephropathy is the **most common cause** of Type 4 RTA. It often leads to a state of "Hyporeninemic Hypoaldosteronism" due to damage to the juxtaglomerular apparatus. **Clinical Pearls for NEET-PG:** * **Urine pH:** In Type 4 RTA, the urine pH is typically **< 5.5** (the distal acidification mechanism is intact, but the total acid excretion is low due to decreased ammonia production). * **Mnemonic:** Remember **"Type 4 is the only one with High K+"**. * **Common Causes:** Diabetes mellitus, NSAIDs, ACE inhibitors, and Heparin [1].

Practice by Chapter

Acute Kidney Injury

Practice Questions

Chronic Kidney Disease

Practice Questions

Glomerular Diseases

Practice Questions

Tubulointerstitial Diseases

Practice Questions

Nephrotic and Nephritic Syndromes

Practice Questions

Urinary Tract Infections

Practice Questions

Renal Replacement Therapy

Practice Questions

Fluid and Electrolyte Disorders

Practice Questions

Acid-Base Disorders

Practice Questions

Kidney in Systemic Diseases

Practice Questions

Kidney Stones and Obstructive Uropathy

Practice Questions

Hypertension in Kidney Disease

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Nephrology — MCQs

Nephrology — MCQs

On this page

Practice by Chapter

Want unlimited practice?