Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 501: Nephrocalcinosis is seen in all except:

A. Sarcoidosis
B. Distal renal tubular acidosis
C. Milk alkali syndrome
D. Medullary cystic kidney disease (Correct Answer)

Explanation: **Explanation:** Nephrocalcinosis refers to the generalized deposition of calcium salts within the renal parenchyma (medulla or cortex). The correct answer is **Medullary Cystic Kidney Disease (MCKD)** because it is characterized by the formation of cysts at the corticomedullary junction and progressive interstitial fibrosis, but it does **not** typically involve calcium deposition [1]. **Why the other options are incorrect:** * **Sarcoidosis:** This granulomatous disease involves increased 1-alpha-hydroxylase activity in macrophages, leading to elevated Vitamin D levels, hypercalcemia, and hypercalciuria, which frequently results in medullary nephrocalcinosis. * **Distal Renal Tubular Acidosis (Type 1 RTA):** This is a classic cause of nephrocalcinosis. The inability to secrete hydrogen ions leads to alkaline urine, systemic acidosis (causing bone resorption), and hypocitraturia. This combination promotes the precipitation of calcium phosphate in the renal medulla. * **Milk Alkali Syndrome:** Excessive intake of calcium and absorbable alkali leads to hypercalcemia and metabolic alkalosis. The resulting hypercalciuria and alkaline urine environment facilitate calcium deposition in the kidneys. **NEET-PG High-Yield Pearls:** 1. **Medullary Nephrocalcinosis (95% of cases):** Most common causes are **Hyperparathyroidism**, **Distal RTA**, and **Medullary Sponge Kidney** [1]. 2. **Cortical Nephrocalcinosis (Rare):** Classically seen in **Acute Tubular Necrosis (ATN)**, **Chronic Glomerulonephritis**, and **Ethylene glycol poisoning**. 3. **Medullary Sponge Kidney vs. MCKD:** Do not confuse the two. Medullary Sponge Kidney is associated with nephrocalcinosis and "bouquet of flowers" appearance on IVP, whereas MCKD leads to small kidneys and renal failure without calcification [1].

Question 502: A patient presents with sudden onset headache and loss of consciousness. Examination reveals renal cysts and evidence of subarachnoid hemorrhage, consistent with a berry aneurysm. What is the most likely diagnosis considering these findings?

A. Autosomal Dominant Polycystic Kidney Disease (ADPKD) (Correct Answer)
B. Haemangioma of the liver
C. Meningioma
D. Head injury

Explanation: **Explanation:** The clinical presentation of **renal cysts** associated with a **subarachnoid hemorrhage (SAH)** due to a **berry aneurysm** is a classic triad for **Autosomal Dominant Polycystic Kidney Disease (ADPKD)** [1]. **1. Why ADPKD is Correct:** ADPKD is a multisystemic disorder caused by mutations in the *PKD1* (85%) or *PKD2* (15%) genes [1]. While the hallmark is the development of bilateral renal cysts leading to end-stage renal disease, it has significant extra-renal manifestations. The most life-threatening extra-renal complication is **intracranial "berry" aneurysms**, typically located in the Circle of Willis [1]. Rupture of these aneurysms leads to sudden onset "thunderclap" headache and loss of consciousness (SAH) [2]. **2. Why Incorrect Options are Wrong:** * **Haemangioma of the liver:** While liver cysts are the most common extra-renal manifestation of ADPKD, a haemangioma is a vascular tumor and is not specifically associated with renal cysts or berry aneurysms. * **Meningioma:** This is a benign tumor of the meninges. It does not correlate with renal cystic disease or the acute presentation of a ruptured aneurysm. * **Head injury:** While trauma can cause intracranial hemorrhage, it does not explain the presence of pre-existing renal cysts [3]. **3. NEET-PG High-Yield Pearls:** * **Most common extra-renal site:** Liver (Hepatic cysts). * **Most common cause of death:** Cardiovascular disease (Hypertension/LVH). * **Cardiac association:** Mitral Valve Prolapse (MVP). * **Other associations:** Diverticulosis, seminal vesicle cysts, and pancreatic cysts. * **Screening:** MRA is recommended for berry aneurysms only if there is a positive family history of SAH or in high-risk occupations (e.g., pilots).

Question 503: Deficiency of Factor I and Factor H causes which condition?

A. Typical Hemolytic Uremic Syndrome (HUS)
B. Atypical Hemolytic Uremic Syndrome (HUS) (Correct Answer)
C. Thrombotic Thrombocytopenic Purpura (TTP)
D. Acute Thrombotic Thrombocytopenic Purpura (TTP)

Explanation: ### Explanation **1. Why the Correct Answer is Right:** Atypical Hemolytic Uremic Syndrome (aHUS) is primarily a disease of **complement dysregulation**. Under normal physiological conditions, **Factor H** and **Factor I** act as essential regulatory proteins that inhibit the alternative complement pathway, preventing it from attacking the body's own cells. * **Factor H** is a cofactor for Factor I and competes with Factor B. * **Factor I** is a serine protease that cleaves C3b. A genetic deficiency or mutation in these factors leads to uncontrolled activation of the alternative pathway, resulting in the formation of the Membrane Attack Complex (MAC) on vascular endothelial cells. This triggers systemic microvascular thrombosis, leading to the classic triad of microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and acute kidney injury. **2. Why the Incorrect Options are Wrong:** * **Typical HUS (Option A):** This is caused by **Shiga toxin-producing E. coli (STEC)**, usually serotype O157:H7 [1, 2]. It is typically preceded by bloody diarrhea and is not caused by primary genetic complement deficiencies. * **TTP / Acute TTP (Options C & D):** Thrombotic Thrombocytopenic Purpura is caused by a severe deficiency of the metalloproteinase **ADAMTS13** (either congenital or acquired via autoantibodies). This leads to large von Willebrand factor (vWF) multimers that cause platelet aggregation. While it presents with similar features (MAHA and thrombocytopenia), the underlying molecular defect is not in the complement system. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common mutation in aHUS:** Factor H (approx. 30% of cases). * **Treatment of choice for aHUS:** **Eculizumab** (a monoclonal antibody against C5). * **Differentiating TTP from HUS:** TTP often presents with prominent neurological symptoms and a "pentad" (fever, anemia, thrombocytopenia, renal failure, neuro symptoms), whereas HUS is dominated by renal failure [1, 2]. * **ADAMTS13 Activity:** In TTP, activity is typically **<10%**. In aHUS, it is usually normal.

Question 504: A 20-year-old male with end-stage renal failure since age 13 has had progressive renal insufficiency, initially with episodes of painless hematuria. He also has progressive deafness. His brother suffers from a similar illness. What is the most likely diagnosis?

A. Alport syndrome (Correct Answer)
B. Henoch-Schönlein vasculitis
C. Familial lupus
D. Wegener's granulomatosis

Explanation: ### Explanation **Correct Answer: A. Alport Syndrome** **Reasoning:** Alport syndrome is a hereditary type IV collagen synthesis disorder (most commonly X-linked, involving the *COL4A5* gene) [1]. It typically presents with a clinical triad of: 1. **Renal Involvement:** Persistent microscopic or gross painless hematuria progressing to End-Stage Renal Disease (ESRD), often by the second or third decade of life. 2. **Sensorineural Hearing Loss:** Progressive, bilateral high-frequency deafness (due to collagen defects in the cochlea). 3. **Ocular Abnormalities:** Such as anterior lenticonus (pathognomonic) or maculopathy. The patient’s age, history of painless hematuria, progression to ESRD, deafness, and positive family history (brother affected) are classic indicators of Alport syndrome. **Why other options are incorrect:** * **B. Henoch-Schönlein Purpura (HSP):** This is a small-vessel vasculitis characterized by a tetrad of palpable purpura, arthritis, abdominal pain, and hematuria. It does not cause deafness or follow a strong hereditary pattern leading to ESRD in multiple siblings. * **C. Familial Lupus:** While SLE can cause nephritis, it is rarely "familial" in a Mendelian sense and is not associated with progressive sensorineural deafness. * **D. Wegener’s Granulomatosis (GPA):** This is an ANCA-associated vasculitis. While it involves the kidneys and ears (otitis media), it typically presents with upper/lower respiratory tract symptoms (sinusitis, lung nodules) and is not a hereditary condition. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** 80% are **X-linked Dominant**; therefore, males are more severely affected. * **Pathology:** Electron microscopy shows characteristic **"Basket-weave appearance"** (irregular thinning and thickening of the Glomerular Basement Membrane) [1]. * **Ocular Hallmark:** **Anterior Lenticonus** is highly specific for Alport syndrome. * **Post-Transplant Complication:** Patients with Alport syndrome who receive a kidney transplant may develop **Anti-GBM disease** (Goodpasture-like syndrome) because their immune system recognizes the type IV collagen in the new kidney as foreign.

Question 505: What is the most common complication of dialysis?

A. Hypotension (Correct Answer)
B. Anaphylaxis
C. Dialysis dysequilibrium syndrome
D. Amyloidosis

Explanation: **Explanation:** **Intradialytic Hypotension (IDH)** is the most common complication of hemodialysis [1], occurring in approximately 20–30% of dialysis sessions. The primary mechanism is the **rapid removal of fluid (ultrafiltration)** from the intravascular compartment at a rate that exceeds the compensatory "plasma refill" from the interstitial space. This leads to decreased venous return, reduced cardiac output, and a subsequent drop in blood pressure. Other contributing factors include autonomic dysfunction (common in diabetics) and the use of antihypertensive medications before dialysis. **Analysis of Incorrect Options:** * **B. Anaphylaxis:** This is a rare, acute complication typically associated with "First-use syndrome" (hypersensitivity to ethylene oxide used for sterilizing new dialyzers or polyacrylonitrile membranes). * **C. Dialysis Dysequilibrium Syndrome (DDS):** This occurs due to the rapid removal of urea from the blood, creating an osmotic gradient that shifts water into brain cells (cerebral edema). While high-yield, it is much less common than hypotension and usually occurs during a patient's first few sessions. * **D. Amyloidosis:** Specifically **$̢_2$-microglobulin amyloidosis**, this is a *chronic* complication of long-term dialysis (usually >5–10 years), not an acute complication of the procedure itself. **High-Yield Clinical Pearls for NEET-PG:** * **Management of IDH:** Place the patient in the Trendelenburg position, reduce the ultrafiltration rate, and administer a bolus of normal saline. * **Most common cause of death in dialysis patients:** Cardiovascular disease (Arrhythmias/MI). * **Most common infection in hemodialysis:** Staphylococcus aureus (via vascular access). * **Prevention of DDS:** Use a lower blood flow rate and shorter duration for the initial dialysis sessions.

Question 506: Salt-losing nephritis is a feature of which of the following conditions?

A. Interstitial nephritis (Correct Answer)
B. Polycystic kidney disease
C. Lupus nephritis
D. Renal amyloidosis

Explanation: **Explanation:** **Salt-losing nephritis** refers to a clinical syndrome where the kidneys are unable to conserve sodium despite low dietary intake, leading to hyponatremia and volume depletion. **1. Why Interstitial Nephritis is Correct:** The primary site of sodium reabsorption is the renal tubules (specifically the proximal tubule and the thick ascending limb). In **Chronic Interstitial Nephritis (CIN)**, the inflammatory process and subsequent fibrosis primarily damage the **tubulointerstitial compartment** rather than the glomeruli [1]. This structural damage impairs the tubular response to aldosterone and disrupts the medullary osmotic gradient, leading to a profound "salt-wasting" effect. Common causes include analgesic nephropathy and chronic pyelonephritis [1]. **2. Why the Other Options are Incorrect:** * **Polycystic Kidney Disease (PKD):** While PKD can involve tubular dysfunction in late stages, it is primarily characterized by cyst formation and progressive renal failure. It is not the classic or most common prototype for salt-losing nephritis. * **Lupus Nephritis:** This is primarily a **glomerular disease** (immune-complex mediated glomerulonephritis). Glomerular diseases typically present with salt *retention*, edema, and hypertension rather than salt wasting [2]. * **Renal Amyloidosis:** This typically presents as **Nephrotic Syndrome** due to amyloid deposition in the glomeruli [2]. Similar to lupus, it leads to massive proteinuria and sodium retention (edema). **Clinical Pearls for NEET-PG:** * **Differential Diagnosis for Salt-Wasting:** Chronic interstitial nephritis, Medullary cystic kidney disease, Bartter syndrome, and the recovery phase of Acute Tubular Necrosis (ATN). * **Key Finding:** Patients with salt-losing nephritis often require high dietary salt intake to prevent hypotension and azotemia. * **Distinction:** Do not confuse this with SIADH; in salt-losing nephritis, the patient is **hypovolemic**, whereas in SIADH, the patient is **euvolemic**.

Question 507: Which one of the following is not a feature of adult polycystic kidney disease?

A. Hypertension
B. Intermittent renal colic
C. Massive proteinuria (Correct Answer)
D. Macroscopic haematuria

Explanation: **Explanation:** Autosomal Dominant Polycystic Kidney Disease (ADPKD) is primarily a **tubulointerstitial disorder**, not a primary glomerular disease. Therefore, while mild to moderate proteinuria (usually <1 g/day) is common due to tubular dysfunction and secondary focal segmental glomerulosclerosis, **massive proteinuria (>3.5 g/day or nephrotic range) is not a feature** of ADPKD. If present, it suggests a superimposed glomerular pathology. **Analysis of Options:** * **Hypertension (Option A):** This is the most common early manifestation (seen in 70-80% of patients). It results from intrarenal ischemia caused by cyst expansion, which triggers the **Renin-Angiotensin-Aldosterone System (RAAS)**. * **Intermittent Renal Colic (Option B):** This occurs frequently due to the passage of blood clots (following cyst rupture) or the high incidence of **nephrolithiasis** (calcium oxalate stones) seen in these patients [1]. * **Macroscopic Haematuria (Option C):** A classic feature often precipitated by minor trauma or strenuous exercise [1]. It occurs when a cyst ruptures into the renal collecting system. **High-Yield Clinical Pearls for NEET-PG:** 1. **Extra-renal Manifestations:** The most common is **Liver cysts** (Polycystic Liver Disease). The most serious is **Berry Aneurysms** (Circle of Willis), which can lead to Subarachnoid Hemorrhage (SAH). 2. **Genetics:** Most cases (85%) are due to **PKD1** mutation (Chromosome 16), which progresses to ESRD faster than **PKD2** (Chromosome 4) [1]. 3. **Diagnosis:** Ultrasonography is the screening modality of choice (Ravine’s criteria). 4. **Treatment:** Tolvaptan (V2-receptor antagonist) is used to slow cyst growth and disease progression.

Question 508: Nephrocalcinosis is seen in all the following conditions except:

A. Sarcoidosis
B. Distal RTA
C. Milk alkali syndrome
D. Medullary cystic kidney disease (Correct Answer)

Explanation: **Explanation:** Nephrocalcinosis refers to the generalized deposition of calcium salts within the renal parenchyma (medullary or cortical) [1]. To solve this question, one must distinguish between conditions that cause hypercalcemia/hypercalciuria and those that involve structural cysts. **Why Medullary Cystic Kidney Disease (MCKD) is the correct answer:** MCKD (now often classified under Autosomal Dominant Tubulointerstitial Kidney Disease) is characterized by the formation of cysts at the corticomedullary junction, tubular atrophy, and interstitial fibrosis [3]. It typically presents with "salt-wasting" and progressive renal failure. Crucially, it is **not** associated with hypercalcemia or hypercalciuria; therefore, it does not cause nephrocalcinosis. **Analysis of Incorrect Options:** * **Sarcoidosis:** Causes increased production of 1,25-dihydroxyvitamin D by macrophages in granulomas, leading to hypercalcemia and hypercalciuria [2], which results in medullary nephrocalcinosis. * **Distal RTA (Type 1):** This is a classic cause of medullary nephrocalcinosis [1]. The systemic acidosis leads to bone resorption and decreased citrate excretion (hypocitraturia). Calcium precipitates easily in the alkaline urine characteristic of this condition. * **Milk Alkali Syndrome:** Caused by excessive ingestion of calcium and absorbable alkali. The resulting triad of hypercalcemia [2], metabolic alkalosis, and renal insufficiency leads to calcium deposition in the kidneys. **NEET-PG High-Yield Pearls:** * **Medullary Nephrocalcinosis (Most Common):** Causes include Distal RTA (Type 1), Hyperparathyroidism, Medullary Sponge Kidney, and Vitamin D toxicity [1]. * **Cortical Nephrocalcinosis (Rare):** Classically caused by Acute Tubular Necrosis (ATN) [1], Chronic Glomerulonephritis, and Ethylene glycol poisoning. * **Mnemonic for Medullary Nephrocalcinosis:** "M-I-L-K" (Milk alkali, Idiopathic, Limey bile/Low citrate, Kidney-RTA).

Question 509: Routine use of recombinant erythropoietin in patients with chronic kidney disease obviates the need for which of the following?

A. Regular blood transfusions (Correct Answer)
B. Iron supplementation
C. Dialysis
D. Hyperkalemia

Explanation: ### Explanation **Correct Answer: A. Regular blood transfusions** **Mechanism and Rationale:** The primary cause of anemia in Chronic Kidney Disease (CKD) is the deficiency of **Erythropoietin (EPO)**, a glycoprotein hormone produced by the peritubular interstitial cells of the kidney [1]. As renal function declines, EPO production decreases, leading to normocytic normochromic anemia. Before the advent of **Recombinant Human Erythropoietin (rhEPO)**, patients with end-stage renal disease (ESRD) were dependent on frequent blood transfusions to maintain hemoglobin levels. The routine use of rhEPO stimulates the bone marrow to produce red blood cells naturally, thereby **obviating (eliminating) the need for regular blood transfusions** and reducing associated risks like iron overload (hemosiderosis) and HLA sensitization [1]. **Why the other options are incorrect:** * **B. Iron supplementation:** rhEPO therapy actually **increases** the demand for iron because of accelerated erythropoiesis. Most patients require concurrent iron supplementation (often IV) to ensure adequate stores (Target Ferritin >200 ng/mL) for the EPO to be effective. * **C. Dialysis:** rhEPO treats the hematologic complication of CKD but does not improve the Glomerular Filtration Rate (GFR) or the kidney's ability to filter toxins. Dialysis remains necessary for renal replacement. * **D. Hyperkalemia:** Hyperkalemia is a metabolic complication of renal failure. rhEPO has no direct effect on potassium excretion; in fact, a rapid rise in hematocrit can occasionally worsen hypertension or indirectly affect dialysis efficiency. **High-Yield Clinical Pearls for NEET-PG:** * **Target Hemoglobin:** In CKD patients on rhEPO, the target Hb is **10–11.5 g/dL**. Aiming for "normal" levels (>13 g/dL) is avoided due to increased risks of stroke, hypertension, and cardiovascular events (as per the CHOIR and CREATE trials). * **Most common side effect:** New-onset or worsening **Hypertension**. * **Resistance to EPO:** The most common cause of "EPO resistance" is **Iron Deficiency**. Other causes include chronic inflammation, malnutrition, and aluminum toxicity.

Question 510: Nephrotic syndrome may be caused by the following except?

A. Renal cell carcinoma
B. Minimal change nephropathy
C. Diabetes mellitus
D. Rheumatoid arthritis (Correct Answer)

Explanation: The core concept tested here is the distinction between causes of **Nephrotic Syndrome** (characterized by massive proteinuria >3.5g/day, hypoalbuminemia, and edema) and systemic diseases that primarily affect the kidney in other ways [3]. **Why Rheumatoid Arthritis (RA) is the correct answer:** While RA is a systemic inflammatory disease, it typically does **not** directly cause nephrotic syndrome as a primary manifestation. Renal involvement in RA is usually secondary to treatment (e.g., NSAID-induced interstitial nephritis or gold/penicillamine-induced membranous nephropathy) or the development of **Secondary (AA) Amyloidosis**. While AA amyloidosis *can* cause nephrotic syndrome [2], RA itself is classically associated with **analgesic nephropathy** or **mesangial glomerulonephritis**, making it the "least likely" primary cause among the options. **Analysis of Incorrect Options:** * **Minimal Change Nephropathy (MCN):** This is the classic cause of nephrotic syndrome, especially in children [1]. It involves T-cell mediated podocyte effacement. * **Diabetes Mellitus:** Diabetic Nephropathy is the **most common cause** of nephrotic syndrome in adults worldwide [3]. It progresses from microalbuminuria to overt nephrotic-range proteinuria due to Kimmelstiel-Wilson nodules. * **Renal Cell Carcinoma (RCC):** Paraneoplastic syndromes associated with solid tumors (like RCC or lung cancer) frequently manifest as **Membranous Nephropathy**, a leading cause of nephrotic syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of Nephrotic Syndrome in children:** Minimal Change Disease [2]. * **Most common cause in adults:** Diabetes Mellitus (Systemic); Membranous Nephropathy (Primary/Idiopathic). * **Most common cause in HIV/Heroin users:** Focal Segmental Glomerulosclerosis (FSGS) [1]. * **Association:** Hodgkin’s Lymphoma is specifically linked to Minimal Change Disease, whereas solid tumors (RCC, GI) are linked to Membranous Nephropathy.

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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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