Nephrology — MCQs

A 28-year-old woman presents with a recent episode of coughing up blood, frequent nosebleeds, and decreased urine output. Physical examination revealed an ulcerated nasal mucosa. Urinalysis is positive for protein and red blood cells, consistent with glomerulonephritis. Chest X-ray shows two cavitary lesions, and serology is positive for antineutrophil cytoplasmic antibodies (ANCA). Which of the following is the most likely diagnosis?

Q369Easy

Hallmark of IgA nephropathy is

Q370Medium

Gordon's syndrome is characterized by all of the following except?

Nephrology Indian Medical PG Practice Questions and MCQs

Question 361: A patient presents with hematuria and hemoptysis, and antinuclear membrane antibodies are present. What is the likely diagnosis?

A. Goodpasture syndrome (Correct Answer)
B. Nephritic syndrome
C. Nephrotic syndrome
D. Guillain-Barré syndrome

Explanation: ### Explanation **Correct Option: A. Goodpasture Syndrome** Goodpasture syndrome (also known as Anti-GBM disease) is a rare autoimmune disorder characterized by the presence of circulating **anti-glomerular basement membrane (anti-GBM) antibodies**. These antibodies target the alpha-3 chain of Type IV collagen, which is found in both the renal glomerular basement membrane and the pulmonary alveolar basement membrane [1]. This leads to the classic clinical dyad of **pulmonary hemorrhage (hemoptysis)** and **progressive glomerulonephritis (hematuria)**. **Why the other options are incorrect:** * **B. Nephritic Syndrome:** This is a clinical *syndrome* (characterized by hematuria, hypertension, and edema) rather than a specific diagnosis [2]. While Goodpasture syndrome presents as a nephritic syndrome, the specific combination of hemoptysis and anti-GBM antibodies points directly to Goodpasture [1]. * **C. Nephrotic Syndrome:** This is characterized by massive proteinuria (>3.5g/day), hypoalbuminemia, and hyperlipidemia [2]. It does not typically present with hemoptysis or anti-GBM antibodies. * **D. Guillain-Barré Syndrome:** This is an acute inflammatory demyelinating polyradiculoneuropathy presenting with ascending paralysis. It has no primary association with hematuria or hemoptysis. **High-Yield Clinical Pearls for NEET-PG:** * **Immunofluorescence (IF):** The hallmark finding on renal biopsy is **linear IgG deposition** along the glomerular capillaries. * **HLA Association:** Strongly associated with **HLA-DR2**. * **Treatment:** The standard of care is a combination of **plasmapheresis** (to remove circulating antibodies), corticosteroids, and cyclophosphamide [1]. * **Differential Diagnosis:** Always differentiate from Wegener’s Granulomatosis (GPA), which also causes pulmonary-renal syndrome but is associated with **c-ANCA** and lacks linear IF [1].

Question 362: Which of the following is not a cause of renal vein thrombosis?

A. Nephrotic syndrome
B. Invasive renal cell carcinoma
C. Chronic kidney disease (Correct Answer)
D. Dehydration during pregnancy

Explanation: **Explanation:** Renal Vein Thrombosis (RVT) occurs due to the classic Virchow’s triad: endothelial injury, stasis of blood flow, and hypercoagulability. **Why Chronic Kidney Disease (CKD) is the correct answer:** CKD itself is not a primary cause of RVT. While patients with advanced CKD may have altered coagulation profiles, the condition does not inherently create the acute hypercoagulable state or mechanical obstruction required to trigger RVT. In fact, RVT is more likely to be a *cause* of sudden renal function deterioration rather than a consequence of long-standing CKD. **Analysis of Incorrect Options:** * **Nephrotic Syndrome:** This is the **most common** cause of RVT in adults (especially Membranous Nephropathy). The loss of anticoagulant proteins (Antithrombin III, Protein S) in urine and increased hepatic synthesis of procoagulants create a profound hypercoagulable state. * **Invasive Renal Cell Carcinoma (RCC):** RCC is notorious for direct vascular invasion. The tumor thrombus can extend into the renal vein and even the inferior vena cava (IVC), causing mechanical obstruction and thrombosis. * **Dehydration during pregnancy:** Pregnancy is a physiological hypercoagulable state. When coupled with severe dehydration (which increases blood viscosity and slows flow), the risk of venous thrombosis, including RVT, increases significantly. **High-Yield Clinical Pearls for NEET-PG:** * **Most common association:** Membranous Nephropathy (up to 35% of patients develop RVT). * **Clinical Presentation:** Acute RVT presents with flank pain, hematuria, and an enlarged kidney; chronic RVT is often asymptomatic. * **Gold Standard Investigation:** Renal Venography (though CT Angiography/Doppler is used first-line). * **Pediatric Link:** In neonates, the most common cause is severe dehydration.

Question 363: Which of the following statements about polycystic kidney disease is true?

A. Polycystic kidney disease is an autosomal recessive disorder linked to a causative gene on the short arm of chromosome 16.
B. Erythropoietin levels are often low due to progressive renal failure.
C. Colonic diverticular disorder is a rare finding.
D. Nephrotic range proteinuria is an uncommon finding. (Correct Answer)

Explanation: Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common hereditary kidney disease [1]. Understanding its systemic and renal manifestations is crucial for NEET-PG. **Why Option D is Correct:** In ADPKD, the primary pathology involves the formation of cysts from the renal tubules, leading to architectural disruption rather than primary glomerular injury [1]. While mild to moderate proteinuria is common due to tubular dysfunction or secondary focal segmental glomerulosclerosis (FSGS), **nephrotic-range proteinuria (>3.5g/day) is very uncommon**. If present, it usually suggests a superimposed glomerular disease. **Analysis of Incorrect Options:** * **Option A:** ADPKD is primarily **Autosomal Dominant**. While the PKD1 gene is indeed on the short arm of **chromosome 16** (85% of cases), the statement incorrectly labels the inheritance as recessive [1]. Autosomal Recessive PKD (ARPKD) is linked to the PKHD1 gene on chromosome 6. * **Option B:** Unlike other causes of chronic kidney disease (CKD), patients with ADPKD often maintain **higher hemoglobin levels**. This is because the cyst epithelial cells produce **erythropoietin**, which can lead to erythrocytosis or at least delay the onset of anemia. * **Option C:** **Colonic diverticula** are actually the most common extra-renal intestinal manifestation of ADPKD, especially in patients with end-stage renal disease. It is not a rare finding. **High-Yield Clinical Pearls for NEET-PG:** * **Extra-renal manifestations:** Berry aneurysms (Circle of Willis), Hepatic cysts (most common extra-renal site), Mitral Valve Prolapse (MVP), and Pancreatic cysts. * **Diagnosis:** Ultrasonography is the first-line screening tool (Ravine’s criteria). * **Treatment:** Tolvaptan (V2 receptor antagonist) is used to slow the progression of cyst growth and renal decline.

Question 364: What causes decreased fractional excretion of sodium?

A. Prerenal azotemia (Correct Answer)
B. Cortical ischemia
C. Glomerulonephritis
D. Renal tubular acidosis

Explanation: ### Explanation **Fractional Excretion of Sodium (FeNa)** is a critical diagnostic index used to differentiate between causes of acute kidney injury (AKI) [1]. It measures the percentage of sodium filtered by the kidney that is actually excreted in the urine. **1. Why Prerenal Azotemia is Correct:** In **Prerenal Azotemia**, the primary pathology is decreased renal perfusion (e.g., dehydration, heart failure). The kidneys are structurally intact and respond physiologically to the perceived volume depletion by activating the **Renin-Angiotensin-Aldosterone System (RAAS)** [2]. This leads to maximal tubular reabsorption of sodium and water to restore blood volume. Consequently, very little sodium is excreted in the urine, resulting in a **FeNa < 1%**. **2. Why the Other Options are Incorrect:** * **Cortical Ischemia:** This is a form of Acute Tubular Necrosis (ATN). When the tubules are damaged, they lose their ability to reabsorb sodium. Sodium "leaks" into the urine, leading to a **FeNa > 2%**. * **Glomerulonephritis:** While some cases of acute GN can present with low FeNa due to decreased GFR and intact tubular function, it is not the classic or most common cause compared to Prerenal Azotemia in the context of this question. * **Renal Tubular Acidosis (RTA):** RTA involves defects in tubular secretion or reabsorption. Specifically, in Type 2 (Proximal) RTA, there is a failure to reabsorb bicarbonate, often dragging sodium with it, typically resulting in a higher FeNa. **3. High-Yield Clinical Pearls for NEET-PG:** * **FeNa Formula:** $(U_{Na} imes P_{Cr}) / (P_{Na} imes U_{Cr}) imes 100$. * **FeNa < 1%:** Prerenal Azotemia, Hepatorenal Syndrome, and early Acute Glomerulonephritis. * **FeNa > 2%:** Acute Tubular Necrosis (ATN). * **Exception:** FeNa is unreliable in patients taking **diuretics** (use **Fractional Excretion of Urea/FeUrea** instead; <35% suggests prerenal). * **Urine Osmolality:** In Prerenal Azotemia, urine is concentrated (>500 mOsm/kg); in ATN, it is isosthenuric (~300 mOsm/kg) [2].

Question 365: A 46-year-old male presented to the emergency with muscle weakness and cramping. He has been taking hydrochlorothiazide for recently diagnosed hypertension. Which of the following is the most likely cause of his symptoms?

A. Hypocalcemia
B. Hyponatremia
C. Hypokalemia (Correct Answer)
D. Hypoglycemia

Explanation: The patient is presenting with classic symptoms of electrolyte imbalance—muscle weakness and cramping—following the initiation of a Thiazide diuretic. **1. Why Hypokalemia is correct:** Thiazide diuretics (like hydrochlorothiazide) act on the distal convoluted tubule (DCT) by inhibiting the Na+/Cl- symporter. This increases the delivery of sodium and water to the collecting duct. In the collecting duct, the increased sodium load promotes sodium reabsorption via ENaC channels, which is coupled with the secretion of potassium (K+) and hydrogen ions (H+) into the urine [1]. This process leads to **Hypokalemia** and metabolic alkalosis. Low serum potassium levels hyperpolarize the muscle cell membrane, leading to muscle weakness, cramps, and in severe cases, paralysis or arrhythmias [1]. **2. Why the other options are incorrect:** * **Hypocalcemia:** Thiazides actually **increase** calcium reabsorption in the DCT (Hypocalciuric effect). Therefore, they are more likely to cause *hypercalcemia*, not hypocalcemia. * **Hyponatremia:** While Thiazides can cause hyponatremia, it typically presents with neurological symptoms (confusion, lethargy, seizures) rather than isolated muscle cramping and weakness. * **Hypoglycemia:** Thiazides are associated with "metabolic side effects" including **hyperglycemia** (due to impaired insulin secretion) and hyperuricemia, not hypoglycemia. **Clinical Pearls for NEET-PG:** * **Thiazide Side Effects (Mnemonic: GLUC):** Hyper**G**lycemia, Hyper**L**ipidemia, Hyper**U**ricemia, Hyper**C**alcemia. * **Electrolyte "Lowers":** Thiazides lower Na+, K+, and Mg2+. * **Drug of Choice:** Thiazides are the preferred diuretics for hypertensive patients with osteoporosis because they decrease urinary calcium excretion, helping to preserve bone density.

Question 366: Indications for dialysis after failure of medical management include:

A. Hypervolemia
B. Hyperkalemia
C. Hypotension (Correct Answer)
D. Uremia

Explanation: The question asks for the condition that is **NOT** an indication for dialysis. In clinical nephrology, the standard indications for urgent dialysis are remembered by the mnemonic **AEIOU**. 1. **A – Acidosis:** Severe metabolic acidosis (pH <7.1) refractory to medical therapy. 2. **E – Electrolytes:** Refractory hyperkalemia (Potassium >6.5 mEq/L or ECG changes) [2]. 3. **I – Intoxication:** Poisoning with dialyzable substances (e.g., Lithium, Salicylates, Ethylene glycol). 4. **O – Overload:** Refractory hypervolemia/pulmonary edema. 5. **U – Uremia:** Symptomatic uremia causing complications like pericarditis, encephalopathy, or neuropathy [3]. **Why Hypotension is the Correct Answer:** Hypotension is a **contraindication** (specifically for hemodialysis) rather than an indication [1]. Hemodialysis requires stable hemodynamics because the process involves extracorporeal circulation and fluid removal, which can further drop blood pressure. In patients with AKI and hypotension, **CRRT** (Continuous Renal Replacement Therapy) is preferred over standard hemodialysis. **Analysis of Incorrect Options:** * **Hypervolemia (A):** Fluid overload unresponsive to diuretics is a classic indication to prevent pulmonary edema. * **Hyperkalemia (B):** Life-threatening potassium levels are the most common acute indication for dialysis [2]. * **Uremia (D):** Uremic complications (especially pericarditis) are absolute indications for initiating dialysis [3]. **NEET-PG High-Yield Pearls:** * **Absolute Indication:** Uremic pericarditis (due to risk of cardiac tamponade). * **Dialyzable Drugs (SLIME):** **S**alicylates, **L**ithium, **I**sopropanol, **M**ethanol, **E**thylene glycol [1]. * **Preferred Access:** Internal Jugular Vein is preferred over Subclavian to avoid stenosis.

Question 367: What is the best treatment for atypical hemolytic uremic syndrome?

A. Plasmapheresis (Correct Answer)
B. Antibiotics
C. Intravenous immunoglobulin (IVIg)
D. Dialysis

Explanation: **Explanation:** **Atypical Hemolytic Uremic Syndrome (aHUS)** is a condition characterized by the triad of microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and acute kidney injury [1]. Unlike typical HUS (caused by Shiga toxin-producing *E. coli*), aHUS is primarily a disease of **uncontrolled complement activation** due to genetic mutations in complement regulatory proteins (e.g., Factor H, Factor I) [1]. **Why Plasmapheresis is the correct answer:** Plasmapheresis (Plasma Exchange) is considered the traditional first-line treatment. It works by: 1. Removing defective complement regulatory proteins and autoantibodies (like anti-factor H antibodies). 2. Replacing deficient functional regulatory proteins via the donor plasma. *Note: While **Eculizumab** (a monoclonal antibody against C5) is now the gold-standard "best" treatment in modern clinical practice, Plasmapheresis remains the standard answer in many exam formats when Eculizumab is not listed.* **Why other options are incorrect:** * **Antibiotics:** These are generally contraindicated in HUS (especially typical HUS) as they can trigger the release of more toxins and worsen the condition. * **IVIg:** This has no proven role in the pathophysiology of aHUS, which is complement-mediated rather than a simple immunoglobulin deficiency or standard autoimmune process. * **Dialysis:** While dialysis manages the complications of renal failure (uremia, fluid overload), it does not treat the underlying disease process or stop the systemic microangiopathy [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of HUS:** Hemolytic anemia (Schistocytes on smear), Thrombocytopenia, and Renal failure [2]. * **Typical HUS:** Associated with *E. coli* O157:H7; usually follows bloody diarrhea [1]. * **aHUS:** No diarrhea prodrome; high risk of progression to End-Stage Renal Disease (ESRD) [1]. * **Drug of Choice (Modern):** Eculizumab (C5 inhibitor). If Eculizumab is an option alongside Plasmapheresis, Eculizumab is the superior choice.

Question 368: A 28-year-old woman presents with a recent episode of coughing up blood, frequent nosebleeds, and decreased urine output. Physical examination revealed an ulcerated nasal mucosa. Urinalysis is positive for protein and red blood cells, consistent with glomerulonephritis. Chest X-ray shows two cavitary lesions, and serology is positive for antineutrophil cytoplasmic antibodies (ANCA). Which of the following is the most likely diagnosis?

A. Wegener's granulomatosis (Correct Answer)
B. Bacterial endocarditis
C. Goodpasture's syndrome
D. Lupus erythematosus

Explanation: ### Explanation The clinical presentation of **Wegener’s Granulomatosis** (now known as **Granulomatosis with Polyangiitis - GPA**) is characterized by a classic triad of upper respiratory tract, lower respiratory tract, and renal involvement. **1. Why Option A is Correct:** The patient exhibits the hallmark features of GPA: * **Upper Respiratory:** Nasal mucosal ulceration and epistaxis (can lead to a saddle-nose deformity) [2]. * **Lower Respiratory:** Hemoptysis and **cavitary lesions** on chest X-ray (highly characteristic of GPA) [2]. * **Renal:** Glomerulonephritis (hematuria/proteinuria), typically presenting as Pauci-immune Crescentic GN [1]. * **Serology:** The presence of **c-ANCA (anti-PR3)** is highly specific for this condition [1]. **2. Why Other Options are Incorrect:** * **B. Bacterial Endocarditis:** While it can cause hematuria (via embolic GN) and lung issues (septic emboli), it would typically present with fever, new heart murmurs, and positive blood cultures rather than chronic nasal ulceration. * **C. Goodpasture’s Syndrome:** This involves a "Pulmonary-Renal Syndrome" (hemoptysis + GN) caused by anti-GBM antibodies [2]. However, it **spares the upper respiratory tract** (no nasal ulcers) and lung lesions are typically diffuse alveolar hemorrhage, not cavitary nodules. * **D. Lupus Erythematosus:** SLE can cause multi-organ failure and nephritis, but cavitary lung lesions and destructive nasal ulcerations are not standard features [3]. Serology would show ANA/anti-dsDNA rather than ANCA. **High-Yield Clinical Pearls for NEET-PG:** * **GPA Triad:** Upper Respiratory + Lower Respiratory + Kidneys. * **Marker:** c-ANCA (Proteinase-3/PR3 antibodies) is the most specific marker [1]. * **Biopsy Gold Standard:** Shows necrotizing granulomatous inflammation [2]. * **Treatment:** Induction with Corticosteroids + Cyclophosphamide (or Rituximab) [1]. * **Differential:** Remember that **Microscopic Polyangiitis (MPA)** also involves the lung and kidney but **lacks granulomas** and is associated with **p-ANCA** [2].

Question 369: Hallmark of IgA nephropathy is

A. Edema
B. Hematuria (Correct Answer)
C. Hypertension
D. Proteinuria

Explanation: **Explanation:** **IgA Nephropathy (Berger’s Disease)** is the most common primary glomerulonephritis worldwide. The hallmark clinical presentation is **recurrent episodes of gross or microscopic hematuria**, typically occurring shortly after (within 24–48 hours) an upper respiratory tract infection (synpharyngitic hematuria) [1]. 1. **Why Hematuria is the correct answer:** The underlying pathophysiology involves the deposition of abnormally glycosylated IgA1 molecules in the glomerular mesangium. This triggers an inflammatory response that damages the capillary wall, leading to the leakage of red blood cells into the urine [1]. Hematuria is the most sensitive and characteristic sign of this condition [1]. 2. **Why other options are incorrect:** * **Edema & Proteinuria:** While these can occur if the patient develops nephrotic-range proteinuria or progressive renal failure, they are not the "hallmark." IgA nephropathy typically presents with a nephritic pattern rather than a pure nephrotic pattern. * **Hypertension:** This is a common complication as the disease progresses to chronic kidney disease (CKD), but it is a secondary feature rather than the defining clinical hallmark [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Synpharyngitic Hematuria:** Hematuria occurs simultaneously or within 1–2 days of a sore throat (unlike Post-Streptococcal Glomerulonephritis, which has a latent period of 1–3 weeks) [1]. * **Diagnosis:** Gold standard is **Renal Biopsy**, showing mesangial IgA deposits on Immunofluorescence (IF) and mesangial hypercellularity on Light Microscopy. * **Prognosis:** The most reliable predictor of poor prognosis is the degree of persistent proteinuria and hypertension [1]. * **Association:** Often associated with **Henoch-Schönlein Purpura (HSP)**, which is considered the systemic version of the same disease process.

Question 370: Gordon's syndrome is characterized by all of the following except?

A. Hyperkalemia
B. Metabolic acidosis
C. Low renin and low aldosterone
D. Hypotension (Correct Answer)

Explanation: **Explanation:** **Gordon’s Syndrome**, also known as **Pseudohypoaldosteronism Type II (PHA II)**, is a rare genetic disorder caused by mutations in WNK kinases (WNK1 and WNK4). These mutations lead to overactivity of the **Sodium-Chloride Cotransporter (NCC)** in the distal convoluted tubule. 1. **Why Hypotension is the correct answer:** Increased NCC activity leads to excessive reabsorption of sodium and chloride. This results in volume expansion and **Hypertension**, not hypotension. Therefore, Option D is the false statement. 2. **Analysis of other options:** * **Hyperkalemia (Option A):** Increased sodium reabsorption in the distal tubule reduces the delivery of sodium to the collecting duct. This decreases the electrical gradient required for potassium secretion, leading to hyperkalemia [1]. * **Metabolic Acidosis (Option B):** The reduced distal delivery of sodium also impairs hydrogen ion secretion, resulting in a hyperchloremic metabolic acidosis [1]. * **Low Renin and Low Aldosterone (Option C):** The chronic volume expansion caused by salt retention suppresses the Renin-Angiotensin-Aldosterone System (RAAS), leading to low levels of both renin and aldosterone. **Clinical Pearls for NEET-PG:** * **"Mirror Image" of Gitelman Syndrome:** While Gitelman’s presents with hypotension and hypokalemia (due to NCC loss-of-function), Gordon’s presents with hypertension and hyperkalemia (due to NCC gain-of-function). * **Treatment:** It is uniquely sensitive to **Thiazide diuretics**, which directly inhibit the overactive NCC transporter. * **Inheritance:** Usually Autosomal Dominant.

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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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