Nephrology Practice Questions

Q: Which of the following can cause renal vein thrombosis?

All of the above. Renal Vein Thrombosis (RVT) occurs when a thrombus forms in one or both renal veins, leading to venous congestion and potential renal dysfunction. The correct answer is **All of the above** because RVT results from the classic Virchow’s Triad: hypercoagulability, endothelial injury, and venous stasis. 1. **Nephrotic Syndrome (Option A):** This is the most common medical cause of RVT in adults. The loss of low-molecular-weight anticoagulants (like **Antithrombin III**) and Proteins C and S in the urine, combined with increased hepatic synthesis of pro-coagulants (Fibrinogen), creates a profound **hypercoagulable state**. It is most frequently associated with **Membranous Nephropathy**. 2. **Invasive Renal Cell Carcinoma (Option B):** RCC is notorious for its "angiotropic" nature [1]. The tumor can directly invade the renal vein and propagate into the Inferior Vena Cava (IVC), causing mechanical obstruction and local stasis [1]. 3. **Dehydration (Option C):** Severe volume depletion leads to hemoconcentration and decreased renal blood flow (stasis). This is a particularly common cause of RVT in **neonates** and infants. **Clinical Pearls for NEET-PG:** * **Gold Standard Investigation:** Renal Venography (though CT Angiography/Doppler is usually the first-line clinical choice). * **Classic Presentation:** Flank pain, hematuria, and a sudden decline in GFR (in acute cases). * **High-Yield Association:** Among nephrotic syndromes, **Membranous Nephropathy** has the highest incidence of RVT (up to 30-50% of cases). * **Left-sided RVT:** Can present with a **left-sided varicocele** because the left gonadal vein drains directly into the left renal vein.

Q: Which statement is true regarding post-streptococcal glomerulonephritis?

Renal biopsy is indicated in severe renal dysfunction.. Post-streptococcal glomerulonephritis (PSGN) is a classic nephritic syndrome following a skin (impetigo) or throat (pharyngitis) infection with Group A Beta-hemolytic Streptococcus [1]. **Why Option A is correct:** PSGN is typically a clinical diagnosis in children with a recent history of infection, hematuria, edema, and hypertension. A renal biopsy is **not** routinely required. However, it becomes mandatory if there is **severe renal dysfunction** (e.g., rapidly rising creatinine suggesting RPGN), atypical features (absence of latent period), or if the clinical course is prolonged (persistent low C3 beyond 8 weeks), to rule out other glomerular diseases like IgA nephropathy or Lupus nephritis [1]. **Why the other options are incorrect:** * **Option B:** While gross hematuria ("cola-colored urine") usually resolves within 1–2 weeks, **microscopic hematuria** can persist for up to **1 to 2 years** post-recovery. * **Option C:** PSGN is characterized by the activation of the alternative complement pathway [1]. Therefore, **Serum C3 levels are characteristically low** (hypocomplementemia) in >90% of patients during the acute phase, typically returning to normal within 6–8 weeks. * **Option D:** Elevated triglycerides are a hallmark of **Nephrotic Syndrome** (due to increased hepatic lipoprotein synthesis). PSGN is a **Nephritic Syndrome**, where lipid profiles are typically normal. **High-Yield Clinical Pearls for NEET-PG:** * **Latent Period:** 1–3 weeks after pharyngitis; 3–6 weeks after pyoderma. * **Light Microscopy:** "Starry sky" appearance or "Lumpy-bumpy" deposits [1]. * **Electron Microscopy:** Pathognomonic **subepithelial humps**. * **Immunofluorescence:** Granular deposits of IgG and C3. * **Prognosis:** Excellent in children (>95% complete recovery); more guarded in adults [1].

Q: What is the most common infectious agent associated with chronic pyelonephritis?

Escherichia coli. ### Explanation **Correct Answer: D. Escherichia coli** **Medical Concept:** Chronic pyelonephritis is a clinicopathologic entity characterized by chronic tubulointerstitial inflammation and renal scarring, typically resulting from recurrent or persistent urinary tract infections (UTIs) associated with vesicoureteral reflux (V reflux) or chronic obstruction [2]. **Escherichia coli** is the most common causative agent because it is the predominant uropathogen in the fecal flora. It possesses specific virulence factors, such as **P-pili (adhesins)**, which allow it to adhere to the uroepithelium and ascend the urinary tract, even in the presence of anatomical abnormalities. **Analysis of Incorrect Options:** * **A. Proteus vulgaris:** While *Proteus* species are significant in nephrology, they are more specifically associated with **struvite (staghorn) calculi** due to their urease-producing ability, which alkalinizes the urine. * **B. Klebsiella pneumonia:** This is a common cause of hospital-acquired UTIs and can cause pyelonephritis, but its overall prevalence is lower than *E. coli*. * **C. Staphylococcus aureus:** This organism usually reaches the kidney via **hematogenous spread** (seeding from the blood) rather than the ascending route. It is more commonly associated with renal abscesses in the setting of bacteremia. **High-Yield Clinical Pearls for NEET-PG:** * **Pathognomonic Finding:** The presence of **"Thyroidization" of the kidney** (proteinaceous casts in dilated tubules resembling thyroid follicles) is the classic histological hallmark of chronic pyelonephritis. * **Radiology:** Look for **coarse cortical scarring** overlying a blunted/dilated calyx (U-shaped scars), typically at the poles. * **Xanthogranulomatous Pyelonephritis:** A rare variant of chronic pyelonephritis often associated with *Proteus* infections and characterized by "foamy macrophages." [1]

Q: Which of the following is FALSE regarding acute tubular necrosis?

BUN/Creatinine ratio > 20. ### Explanation Acute Tubular Necrosis (ATN) is an intrinsic renal cause of acute kidney injury (AKI) characterized by damage to the tubular epithelial cells [1]. The key to answering this question lies in distinguishing **Intrinsic AKI (ATN)** from **Prerenal Azotemia** [2]. **1. Why Option A is False (The Correct Answer):** In ATN, the tubular cells are damaged and cannot reabsorb urea effectively. Consequently, urea is excreted, and the **BUN/Creatinine ratio remains low ( 20:1** is a classic hallmark of **Prerenal Azotemia**, where intact tubules increase urea reabsorption in response to hypovolemia (passive reabsorption follows sodium and water). **2. Analysis of Other Options (True for ATN):** * **Option B (Urinary Sodium > 40 mEq/L):** Damaged tubules lose the ability to reabsorb sodium, leading to high urinary sodium concentration. * **Option C (FeNa > 2%):** The Fractional Excretion of Sodium (FeNa) is the most reliable indicator. In ATN, the "leaky" tubules cannot conserve sodium, resulting in a FeNa > 2% (often > 1%). * **Option D (U/P Creatinine Ratio < 40):** Since the tubules cannot reabsorb water effectively, the urine is not concentrated. This leads to a low Urine-to-Plasma Creatinine ratio (typically 500 mOsm/kg). * **FeNa Exception:** FeNa can be < 1% in certain ATN cases like contrast-induced nephropathy or rhabdomyolysis.

Q: Anti-GBM antibody-mediated Rapidly Progressive Glomerulonephritis is seen in which condition?

Goodpasture syndrome. **Goodpasture Syndrome** is the correct answer because it is defined by the presence of circulating **anti-glomerular basement membrane (anti-GBM) antibodies**. [1] These antibodies specifically target the non-collagenous domain of the **alpha-3 chain of Type IV collagen**, which is found in the basement membranes of the renal glomeruli and pulmonary alveoli. This leads to a Type II hypersensitivity reaction, manifesting as Rapidly Progressive Glomerulonephritis (RPGN) and alveolar hemorrhage. On immunofluorescence, it characteristically shows **linear IgG deposits**. [1] **Analysis of Incorrect Options:** * **Postinfectious Glomerulonephritis (PIGN):** This is a Type III hypersensitivity reaction caused by immune complex deposition (subepithelial "humps"). It shows a "starry sky" or granular pattern on immunofluorescence, not anti-GBM antibodies. * **IgA Nephropathy (Berger’s Disease):** This involves the deposition of IgA immune complexes in the mesangium. It is the most common glomerulonephritis worldwide but is not mediated by anti-GBM antibodies. [1] * **Lupus Nephritis:** This is caused by the deposition of DNA-anti-DNA immune complexes (Type III hypersensitivity). It typically shows a "full house" pattern on immunofluorescence (IgG, IgM, IgA, C3, and C4). **High-Yield Clinical Pearls for NEET-PG:** * **Classification:** Anti-GBM disease is classified as **RPGN Type I**. * **Immunofluorescence:** The hallmark is **smooth, continuous linear IgG deposition** along the GBM. [1] * **Clinical Presentation:** Hematuria, proteinuria, and hemoptysis (if lungs are involved). * **Treatment:** The mainstay of treatment is **plasmapheresis** (to remove circulating antibodies) combined with corticosteroids and cyclophosphamide. [1] * **HLA Association:** Strongly associated with **HLA-DR2**.

Q: Which one of the following is not a feature of type I renal tubular acidosis?

Increased anion gap. Renal Tubular Acidosis (RTA) is characterized by a **Normal Anion Gap Metabolic Acidosis (NAGMA)**. In NAGMA, the loss of bicarbonate is compensated by a reciprocal increase in serum chloride levels (hyperchloremic acidosis), keeping the anion gap within the normal range (8–12 mEq/L) [1]. Therefore, an **Increased Anion Gap** is not a feature of Type I RTA; it is instead seen in conditions like ketoacidosis, lactic acidosis, or renal failure [1]. **Analysis of Options:** * **Option A (Lower tubule re-absorption of calcium):** In Type I RTA, chronic metabolic acidosis leeches calcium from bones and inhibits distal tubule calcium reabsorption. This leads to hypercalciuria, often resulting in nephrolithiasis and nephrocalcinosis. * **Option B (Defective bicarbonate absorption in distal tubule):** While Type I is primarily a defect in **hydrogen ion (H+) secretion** by the alpha-intercalated cells, this failure to acidify urine prevents the "regeneration" and reclamation of bicarbonate, leading to a systemic deficit. * **Option C (Low serum potassium level):** Hypokalemia is a hallmark of Type I RTA. To compensate for the inability to secrete H+, the distal tubule increases potassium secretion to maintain electrical neutrality. **High-Yield Clinical Pearls for NEET-PG:** * **Type I (Distal) RTA:** Urinary pH is characteristically **> 5.5** (inability to acidify urine despite systemic acidosis) [1]. * **Associations:** Often associated with autoimmune diseases like Sjögren’s syndrome or Amphotericin B toxicity. * **Mnemonic:** Remember **"Distal = Stone"** (Type I is associated with kidney stones, whereas Type II/Proximal is not). * **Anion Gap Rule:** All RTAs (Type I, II, and IV) present with **NAGMA**. If a question mentions an elevated anion gap, look for causes other than RTA.

Question 1

Which of the following can cause renal vein thrombosis?

Accepted Answer

All of the above

Answer

Nephrotic syndrome

Answer

Invasive renal cell carcinoma

Answer

Dehydration

Question 2

Which statement is true regarding post-streptococcal glomerulonephritis?

Accepted Answer

Renal biopsy is indicated in severe renal dysfunction.

Answer

Microscopic hematuria resolves within 2 weeks.

Answer

Serum C3 levels are normal.

Answer

Serum triglyceride levels are elevated.

Question 3

Which of the following is associated with non-oliguric renal failure?

Accepted Answer

Aminoglycoside toxicity

Answer

Hypovolemia

Answer

NSAIDS

Answer

Post-streptococcal glomerulonephritis

Question 4

Dementia in a patient with chronic renal failure undergoing chronic hemodialysis is most commonly due to which of the following?

Accepted Answer

Aluminium toxicity

Answer

Uremia

Answer

Cerebral amyloid angiopathy

Answer

Beta-amyloid deposition

Question 5

What is the most common infectious agent associated with chronic pyelonephritis?

Accepted Answer

Escherichia coli

Answer

Proteus vulgaris

Answer

Klebsiella pneumonia

Answer

Staphylococcus aureus

Question 6

Which of the following is FALSE regarding acute tubular necrosis?

Accepted Answer

BUN/Creatinine ratio > 20

Answer

Urinary sodium > 40 mEq/L

Answer

FeNa > 2%

Answer

Urinary creatinine/Plasma creatinine ratio < 40

Question 7

Anti-GBM antibody-mediated Rapidly Progressive Glomerulonephritis is seen in which condition?

Accepted Answer

Goodpasture syndrome

Answer

Postinfectious glomerulonephritis

Answer

IgA nephropathy

Answer

Lupus nephritis

Question 8

What are the characteristic electrolyte imbalances associated with Congestive Heart Failure (CHF)?

Accepted Answer

Hypervolemic hyponatremia with urinary sodium < 20 mEq/L

Answer

Hypovolemic hyponatremia with urinary sodium < 20 mEq/L

Answer

Euvolemic hyponatremia with urinary sodium < 20 mEq/L

Answer

None of the above

Question 9

What has the maximum chance of infection in dialysis?

Accepted Answer

Venous catheter

Answer

AV fistula

Answer

Tunnel catheter

Answer

AV graft fistula

Question 10

Which one of the following is not a feature of type I renal tubular acidosis?

Accepted Answer

Increased anion gap

Answer

Lower tubule re-absorption of calcium

Answer

Defective bicarbonate absorption in distal tubule

Answer

Low serum potassium level

Nephrology — MCQs

Nephrology — MCQs

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