Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 411: A 22-year-old patient presents with hemoptysis and hematuria, and has basement membrane antibodies. What is the most likely diagnosis?

A. Wagner's Granulomatosis
B. Goodpasture's syndrome (Correct Answer)
C. Polyarteritis Nodosa
D. Churg-Strauss syndrome

Explanation: ### Explanation **Correct Option: B. Goodpasture's syndrome** Goodpasture’s syndrome is characterized by the clinical triad of **diffuse alveolar hemorrhage (hemoptysis)** and **glomerulonephritis (hematuria)**, mediated by **anti-glomerular basement membrane (anti-GBM) antibodies** [1], [2]. These antibodies are directed against the non-collagenous domain of the **alpha-3 chain of Type IV collagen**, which is found in both the glomerular and alveolar basement membranes. This leads to a Type II hypersensitivity reaction. On immunofluorescence, it classically shows a **linear deposition** of IgG along the basement membrane. **Why other options are incorrect:** * **A. Wegener’s Granulomatosis (GPA):** While it also presents with the pulmonary-renal syndrome (hemoptysis + hematuria), it is a small-vessel vasculitis associated with **c-ANCA (anti-PR3)**. It typically involves the upper respiratory tract (sinusitis, saddle nose deformity), which is absent here [2]. * **C. Polyarteritis Nodosa (PAN):** This is a medium-vessel vasculitis associated with Hepatitis B. It typically spares the lungs (no hemoptysis) and does not involve anti-GBM antibodies [2]. * **D. Churg-Strauss Syndrome (EGPA):** This is a small-vessel vasculitis characterized by **p-ANCA**, peripheral eosinophilia, and a strong history of asthma or allergic rhinitis [2]. **NEET-PG High-Yield Pearls:** * **Classic Triad:** Hemoptysis + Hematuria + Anti-GBM antibodies [1], [2]. * **Immunofluorescence:** Linear IgG pattern (Pathognomonic). * **Epidemiology:** Bimodal distribution (young men in their 20s and older women in their 60s). * **Treatment:** Plasmapheresis (to remove circulating antibodies) + Corticosteroids + Cyclophosphamide [1]. * **Key Distinction:** If only the kidney is involved (no lung hemorrhage), it is called **Anti-GBM Disease**; if both are involved, it is **Goodpasture’s Syndrome** [1], [2].

Question 412: What electrolyte disturbance is seen in rhabdomyolysis?

A. Hyperphosphatemia (Correct Answer)
B. Hyponatremia
C. Hypokalemia
D. Metabolic alkalosis

Explanation: Rhabdomyolysis involves the rapid breakdown of skeletal muscle, leading to the release of intracellular contents into the systemic circulation. **Why Hyperphosphatemia is correct:** Phosphate is a major intracellular anion [1]. When muscle cell membranes (sarcolemma) are damaged, massive amounts of inorganic phosphorus are leaked into the extracellular fluid [1]. This is further exacerbated if the patient develops secondary Acute Kidney Injury (AKI) due to myoglobinuria, as the kidneys become unable to excrete the excess phosphate load. **Analysis of Incorrect Options:** * **Hyponatremia:** While fluid shifts can occur, hyponatremia is not a classic hallmark of rhabdomyolysis. Electrolyte disturbances are primarily driven by the release of *intracellular* ions. * **Hypokalemia:** This is incorrect; **Hyperkalemia** is the most life-threatening electrolyte disturbance in rhabdomyolysis. Potassium is the primary intracellular cation, and its release from necrotic muscle can lead to dangerous cardiac arrhythmias. * **Metabolic alkalosis:** Rhabdomyolysis typically causes a **High Anion Gap Metabolic Acidosis (HAGMA)** due to the release of organic acids (like lactic acid) and the accumulation of sulfates/phosphates during renal failure. **High-Yield Clinical Pearls for NEET-PG:** 1. **Hypocalcemia (Early Phase):** Occurs because calcium deposits into damaged muscle (dystrophic calcification) and binds with excess phosphate. 2. **Hypercalcemia (Late/Recovery Phase):** As muscle heals, the deposited calcium is remobilized back into the blood. 3. **Diagnosis:** The most sensitive marker is an elevated **Serum Creatine Kinase (CK/CPK)**, typically >5 times the upper limit of normal. 4. **Urine Findings:** Urine appears "tea-colored" or "cola-colored." Dipstick is positive for blood (due to myoglobin), but microscopy shows **no RBCs**.

Question 413: Which of the following statements is FALSE about calciphylaxis?

A. It is a calcific arteriopathy seen in chronic kidney disease.
B. Livedo reticularis can be a clinical manifestation.
C. Vascular calcification is a characteristic feature.
D. It is typically associated with hypoparathyroidism. (Correct Answer)

Explanation: ### Explanation **Calciphylaxis**, also known as **Calcific Uremic Arteriolopathy (CUA)**, is a rare but life-threatening syndrome characterized by systemic calcification of the tunica media of small-to-medium-sized dermo-hypodermal arteries. **Why Option D is the Correct Answer (False Statement):** Calciphylaxis is typically associated with **Secondary or Tertiary Hyperparathyroidism**, not hypoparathyroidism [1]. Elevated levels of Parathyroid Hormone (PTH), along with an elevated Calcium-Phosphate product (>55 mg²/dL²), promote the deposition of calcium in the vascular walls. Hyperparathyroidism drives the mineral bone disorder that leads to this extra-skeletal calcification [2]. **Analysis of Other Options:** * **Option A:** It is indeed a **calcific arteriopathy** most commonly seen in patients with End-Stage Renal Disease (ESRD) or Stage 4-5 **Chronic Kidney Disease (CKD)** [1]. * **Option B:** The clinical presentation often begins with **livedo reticularis** or violaceous plaques, which progress to extremely painful, necrotic, non-healing skin ulcers with an eschar. * **Option C:** **Vascular calcification** and intimal fibrosis leading to luminal narrowing and tissue ischemia are the hallmark histopathological features. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Female gender, obesity, diabetes mellitus, and use of **Warfarin** (which inhibits Matrix Gla Protein, a calcification inhibitor). * **Diagnosis:** Primarily clinical; however, a **skin biopsy** (deep punch) showing medial calcification and endovascular fibrosis is the gold standard. * **Management:** Multi-modal approach including wound care, lowering PTH, and the use of **Sodium Thiosulfate** (which helps dissolve calcium deposits). * **Prognosis:** Very poor, with high mortality rates usually due to secondary sepsis.

Question 414: Which mode of vascular access for dialysis has the least chance of infection?

A. Arteriovenous fistula (Correct Answer)
B. Tunneled catheter
C. Venous catheter
D. Arteriovenous graft

Explanation: The choice of vascular access is critical in hemodialysis management, as infection and thrombosis are the leading causes of morbidity. ### **Explanation** **Arteriovenous (AV) Fistula** is the "gold standard" for hemodialysis access [1]. It is created by a direct surgical anastomosis between a native artery and a native vein (e.g., Radiocephalic or Brachiocephalic). * **Why it has the lowest infection risk:** Since it uses the patient's own native vessels and is located entirely under the skin once healed, there is no foreign material (like plastic or synthetic fabric) involved. Once the skin over the fistula is cleaned for needle insertion, the risk of pathogen entry is minimal compared to synthetic or percutaneous options. ### **Analysis of Incorrect Options** * **B & C (Tunneled and Venous Catheters):** These carry the **highest risk** of infection (catheter-related bloodstream infections or CRBSI). They provide a direct conduit from the skin surface to the central venous system [1]. Even "tunneled" catheters, which have a dacron cuff to inhibit bacterial migration, have significantly higher infection rates than fistulas. * **D (AV Graft):** These involve the use of synthetic material (usually PTFE) to connect an artery and vein. Because the graft is a **foreign body**, it is more prone to colonization by bacteria (especially *Staphylococcus aureus*) and is harder to sterilize once infected compared to native tissue. ### **NEET-PG High-Yield Pearls** * **Order of preference for access:** AV Fistula > AV Graft > Tunneled Catheter > Non-tunneled Catheter. * **Rule of 6s for Fistula Maturation:** Should be evaluated 6 weeks after creation; diameter >6 mm; depth <6 mm; blood flow >600 mL/min. * **Most common site:** Radiocephalic fistula (Brescia-Cimino). * **Most common cause of fistula failure:** Intimal hyperplasia leading to stenosis (usually at the venous end). * **Most common organism in access infections:** *Staphylococcus aureus*.

Question 415: Alport syndrome is associated with all except?

A. Sensorineural deafness
B. Posterior lenticonus
C. Peripheral retinal fleck (Correct Answer)
D. Hematuria

Explanation: Explanation: Alport Syndrome is a hereditary disorder of basement membranes caused by mutations in the genes encoding the **alpha-3, alpha-4, or alpha-5 chains of type IV collagen**. This collagen is a crucial structural component of the glomerular basement membrane (GBM), the cochlea, and the eye [1]. **Why "Peripheral retinal fleck" is the correct answer:** The characteristic ocular finding in Alport syndrome is **Macular flecks** (perimacular retinopathy), which are yellowish-white spots around the fovea. These are typically asymptomatic and do not affect vision. **Peripheral** retinal flecks are more commonly associated with other conditions (like Benign Familial Fleck Retina) rather than the classic presentation of Alport Syndrome. **Analysis of other options:** * **Sensorineural deafness (A):** This is the most common extra-renal manifestation. It is bilateral and usually develops in late childhood or adolescence due to defects in the cochlear basement membrane. * **Posterior lenticonus (B):** This is a **pathognomonic** finding for Alport syndrome. It involves a conical protrusion of the posterior aspect of the lens into the vitreous chamber due to a weak lens capsule. * **Hematuria (D):** This is the earliest and most common clinical sign [1]. It typically presents as persistent microscopic hematuria, often with episodes of gross hematuria following upper respiratory infections. **NEET-PG High-Yield Pearls:** * **Inheritance:** Most common is **X-linked Dominant** (COL4A5 mutation). * **Electron Microscopy:** Shows a characteristic **"Basket-weave" appearance** (irregular thinning and thickening of the GBM) [1]. * **Clinical Triad:** Hereditary nephritis (hematuria/ESRD), sensorineural hearing loss, and ocular abnormalities (Posterior lenticonus). * **Leiomyomatosis:** Diffuse leiomyomatosis of the esophagus and tracheobronchial tree can be associated with certain X-linked deletions in Alport syndrome.

Question 416: In Type II Renal Tubular Acidosis (RTA), what is the typical serum potassium level?

A. Low (Correct Answer)
B. Normal
C. 5.7 mEq/L
D. >7 mEq/L

Explanation: **Explanation:** **Type II Renal Tubular Acidosis (Proximal RTA)** is characterized by a defect in the proximal tubule's ability to reabsorb filtered bicarbonate ($HCO_3^-$) [1]. This leads to significant bicarbonate wasting in the urine. **Why the correct answer is Low (Hypokalemia):** The primary mechanism for hypokalemia in Type II RTA is twofold: 1. **Increased Distal Delivery of Sodium Bicarbonate:** The failure of the proximal tubule to reabsorb $HCO_3^-$ leads to an increased load of non-reabsorbable anions (bicarbonate) reaching the distal tubule. To maintain electrical neutrality, sodium follows. 2. **Hyperaldosteronism:** The resulting volume depletion (due to osmotic diuresis from bicarbonate) activates the Renin-Angiotensin-Aldosterone System (RAAS) [1]. Aldosterone acts on the collecting duct to reabsorb sodium in exchange for potassium, leading to significant urinary potassium wasting. **Analysis of Incorrect Options:** * **B (Normal):** Potassium is rarely normal in untreated Type II RTA; the physiological response to bicarbonate wasting almost always drives levels down. * **C & D (Elevated levels):** Hyperkalemia is a hallmark of **Type IV RTA** (Hypoaldosteronism/Resistance), not Type II. Levels above 7 mEq/L are medical emergencies and are not characteristic of any RTA unless associated with acute renal failure. **NEET-PG High-Yield Pearls:** * **Type II RTA** is often associated with **Fanconi Syndrome** (phosphaturia, glycosuria, aminoaciduria). * **Urine pH:** Initially >5.5, but can become **<5.5** once the plasma bicarbonate level drops below the "renal threshold," allowing the distal tubule to acidify the urine normally [1]. * **Comparison:** Both Type I (Distal) and Type II (Proximal) RTA present with **hypokalemia**, whereas Type IV presents with **hyperkalemia**. * **Treatment Caution:** Giving bicarbonate to Type II RTA patients can actually worsen hypokalemia by increasing distal bicarbonate delivery.

Question 417: Which of the following statements about adult polycystic kidney disease is true?

A. Autosomal recessive disorder
B. Low erythropoietin level
C. Hematuria can occur (Correct Answer)
D. Berry aneurysms are not associated with polycystic kidney disease

Explanation: **Explanation:** **Autosomal Dominant Polycystic Kidney Disease (ADPKD)** is the most common inherited cystic kidney disease [1]. It is characterized by the progressive development of numerous cysts in the renal parenchyma, leading to kidney enlargement and eventual renal failure [1]. **Why Option C is Correct:** **Hematuria** is a common clinical presentation in ADPKD. It occurs due to the **rupture of a cyst** into the renal collecting system or as a result of associated nephrolithiasis (kidney stones). It can manifest as either microscopic or gross hematuria and is often accompanied by flank pain [1]. **Analysis of Incorrect Options:** * **Option A:** ADPKD is an **Autosomal Dominant** disorder (linked to *PKD1* on chromosome 16 or *PKD2* on chromosome 4) [1]. Autosomal Recessive PKD (ARPKD) is a distinct entity typically seen in infancy/childhood. * **Option B:** Erythropoietin (EPO) levels are usually **normal or elevated** in ADPKD. Unlike other causes of chronic kidney disease where EPO is deficient, the cysts in ADPKD can produce EPO locally, often maintaining hemoglobin levels despite declining renal function. * **Option D:** **Berry aneurysms** (Circle of Willis) are a classic extra-renal association of ADPKD, occurring in approximately 5-10% of patients. Subarachnoid hemorrhage is a major cause of morbidity. **NEET-PG High-Yield Pearls:** * **Most common extra-renal manifestation:** Hepatic cysts (usually asymptomatic). * **Cardiac association:** Mitral Valve Prolapse (MVP). * **Other associations:** Diverticulosis, pancreatic cysts, and seminal vesicle cysts. * **Diagnosis:** Ultrasonography is the primary screening tool (Ravine’s criteria). * **Treatment:** Tolvaptan (V2 receptor antagonist) is used to slow cyst progression.

Question 418: A patient with chronic kidney disease on haemodialysis complains of chest pain and back pain shortly after dialysis initiation. The symptoms resolve spontaneously with reassurance. What is the most likely cause of these symptoms?

A. Anxiety related to the dialysis procedure
B. Type B anaphylactoid reaction to the dialyser (Correct Answer)
C. Anaphylaxis to ethylene oxide used for sterilization
D. Febrile non-haemolytic transfusion reaction

Explanation: ### Explanation The patient is experiencing a **Type B Dialyser Reaction**, also known as the **"First-use syndrome" (non-specific type)**. **1. Why Option B is Correct:** Type B reactions are relatively common and occur within 15–30 minutes of starting dialysis. The underlying mechanism is likely **complement activation** triggered by the blood's contact with the dialyser membrane (historically more common with cuprophane membranes). The classic presentation includes **vague chest pain and back pain**. Unlike Type A reactions, these symptoms are typically mild and **resolve spontaneously** as dialysis continues, requiring only reassurance and symptomatic care [1]. **2. Why Other Options are Incorrect:** * **Option C (Type A Anaphylactoid Reaction):** This is a severe, immediate hypersensitivity reaction (IgE-mediated) often due to **ethylene oxide** gas used for sterilization. It presents within minutes with urticaria, bronchospasm, and hypotension. It is a medical emergency and does *not* resolve spontaneously. * **Option A:** While dialysis can be stressful, the specific combination of chest and back pain shortly after initiation is a recognized physiological reaction to the extracorporeal circuit [1]. * **Option D:** This occurs during blood transfusions, presenting with fever and chills, not isolated chest/back pain resolving with reassurance. **3. High-Yield Clinical Pearls for NEET-PG:** * **Type A Reaction:** "Immediate/Severe" – Think Ethylene oxide or AN69 membranes (especially in patients on ACE inhibitors). Stop dialysis immediately; do **not** return the blood. * **Type B Reaction:** "Delayed/Mild" – Think Complement activation. Continue dialysis; symptoms usually subside. * **Prevention:** Using biocompatible membranes (synthetic) and "reusing" dialysers (which reduces the concentration of residual sterilants and modifies the membrane surface) decreases the incidence of these reactions [1].

Question 419: Clinical manifestations of acute glomerulonephritis include which of the following?

A. Chills and flank pain
B. Oliguria and generalized edema
C. Hematuria and proteinuria (Correct Answer)
D. Dysuria and hypotension

Explanation: ### Explanation Acute Glomerulonephritis (AGN) is characterized by an inflammatory process within the renal glomeruli, leading to the classic **Nephritic Syndrome** [1]. **1. Why Hematuria and Proteinuria are correct:** The hallmark of AGN is glomerular capillary wall damage. This leads to increased permeability, allowing red blood cells and proteins to leak into the urine. * **Hematuria:** Often presents as "cola-colored" or smoky urine due to the presence of dysmorphic RBCs and RBC casts (pathognomonic for glomerular bleeding) [1], [3]. * **Proteinuria:** Usually in the sub-nephrotic range (<3.5 g/day), though it is a consistent finding due to the loss of the glomerular basement membrane's integrity [1]. **2. Analysis of Incorrect Options:** * **A. Chills and flank pain:** These are classic symptoms of **Acute Pyelonephritis** (upper urinary tract infection), not primary glomerular inflammation. * **B. Oliguria and generalized edema:** While these *can* occur in AGN (due to decreased GFR and salt/water retention), they are not as universally defining as the presence of blood and protein in the urine [1]. Generalized edema (anasarca) is more characteristic of Nephrotic Syndrome. * **C. Dysuria and hypotension:** Dysuria suggests a lower UTI (cystitis). AGN is typically associated with **hypertension** (due to fluid overload and renin activation), not hypotension [2]. * **Classic Triad of Nephritic Syndrome:** Hematuria, Hypertension, and Oliguria/Edema [1], [2]. * **Most common cause worldwide:** IgA Nephropathy (Berger’s disease) [2]. * **Post-Streptococcal GN (PSGN):** Occurs 1–3 weeks after a sore throat or skin infection; characterized by low C3 levels and "lumpy-bumpy" subepithelial humps on electron microscopy [1]. * **Red Cell Casts:** Their presence is the most specific indicator of a glomerular source of bleeding [3].

Question 420: Which of the following is NOT a feature of Alport syndrome according to the FLINTER diagnostic criteria?

A. Positive family history
B. Typical changes in renal biopsy specimen
C. High tone sensorineural deafness
D. Cardiovascular changes (Correct Answer)

Explanation: Alport Syndrome is a hereditary disorder of basement membranes caused by mutations in genes encoding the **Type IV collagen** alpha chains ($\alpha$3, $\alpha$4, or $\alpha$5) [1]. This leads to structural defects in the Glomerular Basement Membrane (GBM), cochlea, and eye. **Why Cardiovascular changes is the correct answer:** The **Flinter Criteria** (1989) were established to standardize the diagnosis of Alport Syndrome. The four classic criteria focus on the renal, auditory, and ocular manifestations. **Cardiovascular changes are not part of the Flinter criteria**, nor are they a primary feature of Alport syndrome. While some patients may develop hypertension secondary to chronic kidney disease (CKD), it is a complication rather than a diagnostic hallmark. **Analysis of Incorrect Options (Flinter Criteria components):** * **Positive family history (A):** A history of hematuria or progression to end-stage renal disease (ESRD) in male relatives is a core criterion. * **Typical changes in renal biopsy (B):** Electron microscopy (the gold standard) shows characteristic **"basket-weave" appearance** (thickening, thinning, and splitting of the GBM) [1]. * **High-tone sensorineural deafness (C):** Bilateral sensorineural hearing loss, typically affecting high frequencies, is a classic extra-renal manifestation. * *(Note: The fourth Flinter criterion is **Ocular lesions**, specifically anterior lenticonus or maculopathy).* [1] **High-Yield Facts for NEET-PG:** * **Inheritance:** Most common is **X-linked Dominant** (85%, COL4A5 mutation). * **Ocular Hallmark:** **Anterior Lenticonus** (pathognomonic) and "Dot-and-fleck" retinopathy. * **Diagnosis:** Diagnosis is now increasingly made via genetic testing or skin biopsy (looking for absence of $\alpha$5 chain). * **Clinical Presentation:** Persistent microscopic hematuria in childhood, progressing to proteinuria and ESRD by the 2nd–3rd decade in males.

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Glomerular 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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Nephrology — MCQs

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