Nephrology Practice Questions

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

Goodpasture syndrome. ### 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].

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

Chronic kidney disease. **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.

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

Nephrotic range proteinuria is an uncommon finding.. 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.

Q: 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?

Hypokalemia. 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.

Q: Indications for dialysis after failure of medical management include:

Hypotension. 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 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.

Q: Hallmark of IgA nephropathy is

Hematuria. **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.

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

Hypotension. **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.

Question 1

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

Accepted Answer

Goodpasture syndrome

Answer

Nephritic syndrome

Answer

Nephrotic syndrome

Answer

Guillain-Barré syndrome

Question 2

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

Accepted Answer

Chronic kidney disease

Answer

Nephrotic syndrome

Answer

Invasive renal cell carcinoma

Answer

Dehydration during pregnancy

Question 3

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

Accepted Answer

Nephrotic range proteinuria is an uncommon finding.

Answer

Polycystic kidney disease is an autosomal recessive disorder linked to a causative gene on the short arm of chromosome 16.

Answer

Erythropoietin levels are often low due to progressive renal failure.

Answer

Colonic diverticular disorder is a rare finding.

Question 4

What causes decreased fractional excretion of sodium?

Accepted Answer

Prerenal azotemia

Answer

Cortical ischemia

Answer

Glomerulonephritis

Answer

Renal tubular acidosis

Question 5

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?

Accepted Answer

Hypokalemia

Answer

Hypocalcemia

Answer

Hyponatremia

Answer

Hypoglycemia

Question 6

Indications for dialysis after failure of medical management include:

Accepted Answer

Hypotension

Answer

Hypervolemia

Answer

Hyperkalemia

Answer

Uremia

Question 7

What is the best treatment for atypical hemolytic uremic syndrome?

Accepted Answer

Plasmapheresis

Answer

Antibiotics

Answer

Intravenous immunoglobulin (IVIg)

Answer

Dialysis

Question 8

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?

Accepted Answer

Wegener's granulomatosis

Answer

Bacterial endocarditis

Answer

Goodpasture's syndrome

Answer

Lupus erythematosus

Question 9

Hallmark of IgA nephropathy is

Accepted Answer

Hematuria

Answer

Edema

Answer

Hypertension

Answer

Proteinuria

Question 10

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

Accepted Answer

Hypotension

Answer

Hyperkalemia

Answer

Metabolic acidosis

Answer

Low renin and low aldosterone

Nephrology — MCQs

Nephrology — MCQs

On this page

Practice by Chapter

Want unlimited practice?