Nephrology Practice Questions

Q: Which of the following findings is suggestive of acute renal failure?

FENa < 1. Explanation: Acute Renal Failure (ARF), now more commonly termed Acute Kidney Injury (AKI), is broadly classified into Pre-renal, Intrinsic, and Post-renal causes [1]. The question focuses on the biochemical markers used to differentiate Pre-renal Azotemia (where the kidney is structurally intact but under-perfused) from Acute Tubular Necrosis (ATN). 1. Why FENa < 1% is correct: The Fractional Excretion of Sodium (FENa) is the most reliable index to differentiate these states. In pre-renal failure, the kidneys respond to hypoperfusion by maximizing sodium and water reabsorption to restore blood volume. Consequently, very little sodium is excreted in the urine, leading to a FENa 2%. 2. Analysis of Incorrect Options: * Renal Failure Index (RFI) 20:1 because urea reabsorption is increased alongside sodium/water, while creatinine is not. A ratio 1.010: This refers to Specific Gravity. In pre-renal states, urine is highly concentrated (> 500 mOsm/kg or SG > 1.020). A value of 1.010 (Isosthenuria) indicates the kidney has lost its concentrating ability, which is characteristic of ATN, not early pre-renal ARF. Clinical Pearls for NEET-PG: * Pre-renal: FENa 500 mOsm/kg [1]. * Intrinsic (ATN): FENa > 2%, Urine Na > 40 mEq/L, Urine Osmolality < 350 mOsm/kg. * Exception: FENa can be < 1% in certain intrinsic conditions like Contrast-induced nephropathy and Acute Glomerulonephritis.

Q: Gross hematuria can be seen in which of the following conditions?

Both IgA nephropathy and sickle cell disease. Gross hematuria (visible blood in urine) is a significant clinical finding that can arise from both glomerular and non-glomerular pathologies [1]. **Why Option C is Correct:** * **IgA Nephropathy (Berger’s Disease):** This is the most common cause of primary glomerulonephritis worldwide. It characteristically presents as **synpharyngitic hematuria**—episodes of gross hematuria occurring concurrently or within 1–2 days of an upper respiratory tract infection [2]. * **Sickle Cell Disease (SCD):** Gross hematuria in SCD (and Sickle Cell Trait) is typically non-glomerular. It occurs due to **renal papillary necrosis** or vasa recta occlusion caused by sickling in the hypoxic, hypertonic environment of the renal medulla. **Analysis of Other Options:** * **Option A & B:** While both cause gross hematuria, selecting either individually is incomplete as both conditions are well-recognized triggers for this presentation. * **Option D (MPGN):** While MPGN can cause microscopic hematuria and occasionally gross hematuria during acute nephritic presentations, it is less classically associated with recurrent "gross" episodes compared to the hallmark presentation of IgA nephropathy or the structural vascular damage in Sickle Cell Disease. **High-Yield Clinical Pearls for NEET-PG:** * **IgA Nephropathy:** Look for the "short latent period" (24–48 hours) after an infection [2]. In contrast, Post-Streptococcal Glomerulonephritis (PSGN) has a longer latent period (1–3 weeks). * **Sickle Cell Nephropathy:** The most common renal manifestation is **hyposthenuria** (inability to concentrate urine). Gross hematuria is often painless and more common from the left kidney (due to the longer left renal vein). * **Differential for Gross Hematuria:** Always consider malignancy (RCC, Bladder Cancer) in older patients, and IgA nephropathy or Alport syndrome in younger patients [2][3].

Q: Which of the following is associated with adult polycystic kidney disease?

Berry aneurysms in Circle of Willis. **Explanation:** **Autosomal Dominant Polycystic Kidney Disease (ADPKD)** is a systemic multisystem disorder caused by mutations in the *PKD1* (85%) or *PKD2* (15%) genes [1]. These genes encode polycystin proteins, which are essential for the structural integrity of both renal tubules and vascular smooth muscle/endothelium. **Why Option A is Correct:** The most significant extrarenal vascular manifestation of ADPKD is the formation of **intracranial "berry" aneurysms** in the Circle of Willis. These occur in approximately 5–10% of patients (rising to 20% in those with a positive family history). Rupture of these aneurysms leads to subarachnoid hemorrhage, a major cause of morbidity in these patients. **Why Other Options are Incorrect:** * **Options B & C:** While ADPKD is associated with vascular abnormalities like mitral valve prolapse and aortic root dilatation, it is not classically associated with isolated **saccular or fusiform aortic aneurysms**. These are more typically linked to atherosclerosis, hypertension, or connective tissue disorders like Marfan syndrome. * **Option D:** **Leutic aneurysms** are a manifestation of tertiary syphilis (specifically syphilitic aortitis), involving the vasa vasorum of the ascending aorta. They have no association with ADPKD. **High-Yield Clinical Pearls for NEET-PG:** * **Most common extrarenal site:** Hepatic cysts (usually asymptomatic). * **Cardiac associations:** Mitral Valve Prolapse (MVP) is the most common valvular abnormality. * **Other associations:** Pancreatic cysts, colonic diverticula, and seminal vesicle cysts. * **Screening:** Routine screening for berry aneurysms is not recommended for all patients; it is reserved for those with a family history of intracranial hemorrhage or those in high-risk occupations (e.g., pilots) [1].

Q: Which of the following are causes of chloride-responsive alkalosis?

Severe vomiting, Frusemide therapy. Metabolic alkalosis is classified based on the urinary chloride concentration and the response to saline (chloride) infusion. **1. Why Option A is Correct (Chloride-Responsive Alkalosis):** Chloride-responsive alkalosis is characterized by **Urinary Chloride < 20 mEq/L**. It occurs due to the loss of chloride-rich fluids, leading to ECF volume depletion [1]. * **Severe Vomiting:** Loss of HCl leads to both chloride depletion and metabolic alkalosis [1]. The kidney attempts to conserve sodium and water, resulting in low urinary chloride. [2] * **Frusemide Therapy:** While diuretics initially increase urinary chloride, once the drug effect wears off, the resulting volume contraction leads to avid chloride reabsorption (post-diuretic phase). Both conditions are corrected by administering Isotonic Saline (NaCl). **2. Why Other Options are Incorrect:** * **Bartter’s Syndrome (Options B, C, D):** This is a **Chloride-Resistant** alkalosis. It mimics chronic loop diuretic use but is caused by a genetic defect in the NKCC2 transporter. It presents with **Urinary Chloride > 40 mEq/L** and normotension; it does not resolve with saline infusion. * **Milk-Alkali Syndrome (Option C):** This is caused by excessive intake of calcium and absorbable alkali [1]. It is chloride-resistant and typically associated with hypercalcemia and renal failure. **NEET-PG High-Yield Pearls:** * **Chloride-Responsive (UCl 40):** * *Hypertensive:* Conn’s syndrome, Cushing’s syndrome, Liddle’s syndrome [1]. * *Normotensive:* Bartter’s syndrome, Gitelman’s syndrome. * **Saline Test:** If metabolic alkalosis is corrected by 0.9% NaCl, it confirms a chloride-responsive state.

Q: In which of the following conditions is the serum C3 level not persistently low?

Poststreptococcal glomerulonephritis. In nephrology, glomerulonephritides (GN) are often categorized by their effect on the complement system. This question tests the ability to distinguish between **transient** and **persistent** hypocomplementemia. ### **Explanation of the Correct Answer** **A. Poststreptococcal Glomerulonephritis (PSGN):** In PSGN, serum C3 levels are characteristically low due to the activation of the alternative complement pathway [1]. However, this decrease is **transient**. C3 levels typically return to normal within **6 to 8 weeks** after the onset of symptoms [1]. If hypocomplementemia persists beyond 8 weeks, an alternative diagnosis (like MPGN) must be considered. ### **Analysis of Incorrect Options** * **B. Membranoproliferative Glomerulonephritis (MPGN):** This is a classic "low complement" GN. In Type I, C3 is low due to classical pathway activation; in Type II (Dense Deposit Disease), C3 is **persistently low** due to C3 nephritic factor, which stabilizes C3 convertase [1]. * **C. Lupus Nephritis:** Systemic Lupus Erythematosus (SLE) involves chronic immune complex deposition. C3 and C4 levels remain low during active disease and flares, reflecting ongoing consumption. * **D. Endocarditis-related GN:** Chronic infections like subacute bacterial endocarditis or "shunt nephritis" cause continuous antigenemia, leading to **persistent** consumption of complement until the underlying infection is eradicated. ### **NEET-PG High-Yield Pearls** * **The "Big Three" Low Complement GNs:** Remember the mnemonic **"P-M-L"** (PSGN, MPGN, Lupus). * **C3 vs. C4:** In PSGN and MPGN Type II, **only C3** is usually low (Alternative pathway) [1]. In Lupus and Endocarditis, both C3 and C4 are low (Classical pathway). * **The 8-Week Rule:** Any patient suspected of PSGN whose C3 remains low after 2 months requires a renal biopsy to rule out MPGN.

Q: Anti-neutrophil cytoplasmic antibodies (ACNA) are sensitive and specific for which of the following conditions?

Idiopathic crescentic glomerulonephritis. Anti-neutrophil cytoplasmic antibodies (ANCA) are the hallmark of **Pauci-immune Small Vessel Vasculitis** [1]. Idiopathic crescentic glomerulonephritis (Type III RPGN) is characterized by a rapidly progressive decline in renal function and crescent formation on biopsy, but notably lacks significant immune complex or complement deposits (hence "pauci-immune") [1]. Over 80–90% of patients with this condition are ANCA-positive (C-ANCA/PR3 or P-ANCA/MPO) [1]. It is considered a renal-limited form of systemic vasculitis like Granulomatosis with Polyangiitis (GPA) or Microscopic Polyangiitis (MPA) [1]. **Why the incorrect options are wrong:** * **Post-streptococcal glomerulonephritis (PSGN):** This is an **immune-complex-mediated** (Type II RPGN) condition [2]. Diagnosis relies on low C3 levels and elevated ASO/anti-DNase B titers, not ANCA [2]. * **Diffuse glomerulosclerosis:** This is the characteristic pathological finding in **Diabetic Nephropathy** (Kimmelstiel-Wilson lesions). It is a metabolic/hemodynamic complication, not an autoimmune vasculitis. * **Henoch-Schönlein purpura (IgA Vasculitis):** While this is a small vessel vasculitis, it is mediated by **IgA1 immune complex deposition** [3]. ANCA is typically negative; diagnosis is confirmed by IgA deposits on skin or renal biopsy [3]. **High-Yield Clinical Pearls for NEET-PG:** * **C-ANCA (PR3):** Highly specific for Granulomatosis with Polyangiitis (Wegener’s). * **P-ANCA (MPO):** Associated with Microscopic Polyangiitis and Churg-Strauss Syndrome. * **RPGN Classification:** * Type I: Anti-GBM (Goodpasture’s) * Type II: Immune Complex (SLE, PSGN) * Type III: Pauci-immune (ANCA-associated)

Question 1

Which of the following findings is suggestive of acute renal failure?

Accepted Answer

FENa < 1

Answer

Renal Failure Index < 1

Answer

Blood urea nitrogen/creatinine ratio < 20

Answer

Urine osmolality > 1.010

Question 2

Gross hematuria can be seen in which of the following conditions?

Accepted Answer

Both IgA nephropathy and sickle cell disease

Answer

IgA nephropathy

Answer

Sickle cell disease

Answer

Membranoproliferative glomerulonephritis

Question 3

Which of the following is NOT a complication of hemodialysis?

Accepted Answer

Hypotension

Answer

Peritonitis

Answer

Hypertension

Answer

Bleeding tendency

Question 4

What is the cause of a large kidney in chronic renal failure (CRF)?

Accepted Answer

Benign nephrosclerosis

Answer

Diabetes Mellitus (DM)

Answer

Amyloidosis

Answer

Diffuse glomerulonephritis (GN)

Question 5

Which of the following is associated with adult polycystic kidney disease?

Accepted Answer

Berry aneurysms in Circle of Willis

Answer

Saccular aneurysms of the aorta

Answer

Fusiform aneurysms of the aorta

Answer

Leutic aneurysms

Question 6

Which of the following are causes of chloride-responsive alkalosis?

Accepted Answer

Severe vomiting, Frusemide therapy

Answer

Bartter's syndrome, Frusemide therapy

Answer

Severe vomiting, Bartter's syndrome, Milk alkali syndrome

Answer

Severe vomiting, Bartter's syndrome

Question 7

A 50-year-old man with a long-standing history of diabetes presents with a poor urinary stream, hesitancy, difficulty in micturition, and incomplete bladder emptying. What is the most likely diagnosis?

Accepted Answer

Autonomic neuropathy

Answer

Benign Prostatic Hyperplasia (BPH)

Answer

Urinary Tract Infection (UTI)

Answer

Atonic bladder

Question 8

Which of the following findings cannot be used to differentiate between acute pyelonephritis and uncomplicated urinary tract infection?

Accepted Answer

Organisms in excess of 100,000 colony-forming units per milliliter

Answer

WBC cast

Answer

Concentrating defect

Answer

Antibody to Tamm-Horsfall protein

Question 9

In which of the following conditions is the serum C3 level not persistently low?

Accepted Answer

Poststreptococcal glomerulonephritis

Answer

Membranoproliferative glomerulonephritis

Answer

Lupus nephritis

Answer

Glomerulonephritis related to bacterial endocarditis

Question 10

Anti-neutrophil cytoplasmic antibodies (ACNA) are sensitive and specific for which of the following conditions?

Accepted Answer

Idiopathic crescentic glomerulonephritis

Answer

Post-streptococcal glomerulonephritis

Answer

Diffuse glomerulosclerosis

Answer

Henoch-Schönlein purpura

Nephrology — MCQs

Nephrology — MCQs

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