Nephrology Practice Questions

Q: A 72-year-old man develops acute renal failure following aortic angiography. He has gained weight, has rales at both lung bases, and is dyspneic. His fractional excretion of sodium is greater than 1. Peripheral smear shows eosinophilia, and his labs reveal an elevated erythrocyte sedimentation rate, proteinuria, and microscopic hematuria. What is the most likely cause of his renal failure?

Atheroembolic renal disease. ### Explanation **Atheroembolic Renal Disease (AERD)**, also known as cholesterol crystal embolism, is the most likely diagnosis. This condition occurs when cholesterol crystals are dislodged from atherosclerotic plaques in the aorta during invasive vascular procedures (like aortic angiography) [1]. **Why Option B is Correct:** The clinical triad of **recent vascular intervention**, **acute/subacute renal failure**, and **systemic inflammatory markers** is classic for AERD [1]. * **Inflammatory markers:** The presence of **eosinophilia**, elevated ESR, and low complement levels (hypocomplementemia) are hallmark features [1]. * **Urinalysis:** Unlike pure Acute Tubular Necrosis (ATN), AERD often presents with mild proteinuria and microscopic hematuria [1]. * **FENa > 1%:** This indicates intrinsic renal damage rather than a pre-renal state. **Why the Other Options are Incorrect:** * **A. Hypovolemia:** While it causes renal failure, it presents with a **FENa < 1%**, clear lungs, and no eosinophilia. * **C. Acute Tubular Necrosis (ATN):** Contrast-induced nephropathy (a form of ATN) is a common differential post-angiography. However, ATN does **not** typically cause eosinophilia or an elevated ESR [1]. * **D. Cardiogenic Shock:** While the patient has rales and dyspnea, there is no mention of hypotension or poor peripheral perfusion. **High-Yield Clinical Pearls for NEET-PG:** * **Pathognomonic finding:** Skin involvement like **Livedo Reticularis** or "Blue Toe Syndrome" (purple toes with palpable pulses) [1]. * **Histopathology:** Kidney biopsy shows pathognomonic **"Hollenhorst plaques"** or needle-shaped cholesterol clefts within the lumen of small arteries. * **Management:** Primarily supportive; avoid further anticoagulation as it may prevent the stabilization of the plaque [1].

Q: What is the new indication of tolvaptan as approved by FDA recently?

Polycystic kidney disease. **Explanation:** **Tolvaptan** is a selective, competitive **Vasopressin V2-receptor antagonist**. While it was initially approved for the treatment of hyponatremia (SIADH, heart failure, and cirrhosis), its most significant recent FDA approval is for **Autosomal Dominant Polycystic Kidney Disease (ADPKD)** [1]. **Why Polycystic Kidney Disease (PKD) is correct:** In ADPKD, arginine vasopressin (AVP) levels are often elevated. AVP binds to V2 receptors in the renal collecting ducts, increasing intracellular cyclic AMP (cAMP). This cAMP stimulates both the proliferation of cyst-lining epithelial cells and the secretion of fluid into the cysts. By blocking V2 receptors, Tolvaptan lowers cAMP levels, thereby **slowing the rate of cyst growth** and the decline in glomerular filtration rate (GFR). It is specifically indicated for adults at risk of rapidly progressing ADPKD [1]. **Why the other options are incorrect:** * **Phenylketonuria (A):** This is a metabolic disorder of amino acid metabolism (phenylalanine hydroxylase deficiency) treated primarily via dietary restriction, not vasopressin modulation. * **Pancreatic tumours (B):** Tolvaptan has no established role in the management of pancreatic oncology. * **Polycystic ovarian disease (C):** PCOS is an endocrine disorder involving insulin resistance and androgen excess; it does not involve the V2-receptor pathway. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** V2-receptor antagonist (Aquaretic). * **Major Side Effect:** Significant risk of **hepatotoxicity** (requires regular LFT monitoring). * **Common Side Effects:** Polyuria, thirst, and xerostomia (due to increased free water excretion). * **Contraindication:** Patients with underlying significant liver disease or those unable to sense/respond to thirst.

Q: What is the best prophylactic drug for a 60-year-old asthmatic female with microalbuminuria of 280mg?

Telmisartan. **Explanation:** The clinical presentation describes a patient with **Moderately Increased Albuminuria** (formerly microalbuminuria, defined as 30–300 mg/day) [1],[3]. In patients with albuminuria, the primary goal is to provide renoprotection by blocking the Renin-Angiotensin-Aldosterone System (RAAS) [1]. **Why Telmisartan is the Correct Answer:** Both ACE inhibitors (ACEIs) and Angiotensin II Receptor Blockers (ARBs) are first-line agents for renoprotection as they dilate the efferent arteriole, reducing intragulomerular pressure and protein excretion [1]. However, this patient is **asthmatic**. ACE inhibitors like **Enalapril** are associated with a dry cough (due to increased bradykinin and substance P) which can exacerbate respiratory symptoms or be confused with asthma symptoms [2]. **Telmisartan (an ARB)** provides the same renoprotective benefits without affecting bradykinin levels, making it the safer and preferred choice in an asthmatic patient [2]. **Analysis of Incorrect Options:** * **A & B (Amiloride & Spironolactone):** These are potassium-sparing diuretics. While Spironolactone has some role in resistant proteinuria, they are not first-line prophylactic agents for microalbuminuria and carry a high risk of hyperkalemia. * **C (Enalapril):** While effective for proteinuria, the risk of inducing a "bradykinin-mediated cough" [2] makes it less ideal than an ARB for a patient with a pre-existing reactive airway disease (asthma). **Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC)** for diabetic/hypertensive nephropathy: ACEIs or ARBs [1]. * **Mechanism:** Efferent arteriolar vasodilation → ↓ Glomerular capillary pressure [1],[2]. * **Contraindication:** Never combine ACEIs and ARBs (risk of hyperkalemia and acute kidney injury). * **Monitoring:** Always monitor serum creatinine and potassium levels within 1–2 weeks of starting RAAS blockers [2]. A rise in creatinine up to 30% is considered acceptable [1].

Q: A 43-year-old woman develops acute renal failure following an emergency resection of a leaking abdominal aortic aneurysm. One week after surgery, the following laboratory values are obtained: Serum electrolytes (mEq/L): Na+ 127, K+ 5.9, Cl- 92, HCO3- 15. Blood urea nitrogen: 82 mg/dL. Serum creatinine: 6.7 mg/dL. The patient has gained 4 kg since surgery and is mildly dyspneic at rest. Eight hours after these values are reported, the following electrocardiogram is obtained. Which of the following is the most appropriate initial treatment in the management of this patient?

10 mL of 10% calcium gluconate. ***10 mL of 10% calcium gluconate*** - **Hyperkalemia** (K+ 5.9 mEq/L) with ECG changes requires immediate **membrane stabilization** with calcium gluconate to prevent fatal arrhythmias. - Calcium gluconate is the **first-line treatment** for hyperkalemia with cardiac manifestations, stabilizing the cardiac membrane within minutes. *0.25 mg digoxin every 3 hours for 3 doses* - **Digoxin** is contraindicated in hyperkalemia as it can worsen **cardiac toxicity** and increase risk of arrhythmias. - High potassium levels increase sensitivity to digoxin, making this treatment potentially **life-threatening**. *100 mg lidocaine* - **Lidocaine** is used for ventricular arrhythmias but does not address the underlying **hyperkalemia** causing the ECG changes. - It provides no **membrane stabilization** against potassium-induced cardiac toxicity and delays appropriate treatment. *Emergent hemodialysis* - While **hemodialysis** is necessary for definitive potassium removal, it takes time to initiate and does not provide **immediate cardiac protection**. - **Membrane stabilization** with calcium must come first, followed by measures to shift potassium intracellularly, then removal via dialysis.

Q: What is the earliest sign of hyperkalemia on an ECG?

Tall T wave. **Explanation:** **1. Why "Tall T wave" is correct:** The earliest electrocardiographic manifestation of hyperkalemia is the appearance of **tall, peaked, "tented" T waves**, typically seen when serum potassium levels exceed 5.5 mEq/L. This occurs because high extracellular potassium increases the permeability of the cell membrane to potassium, leading to an **accelerated Phase 3 of the cardiac action potential** (rapid repolarization). This shortened repolarization time manifests on the ECG as a narrow-based, symmetrical, and tall T wave, most prominent in the precordial leads (V2–V4). **2. Why the other options are incorrect:** * **Flat and inverted T wave:** This is a classic sign of **hypokalemia** (low potassium) or myocardial ischemia, not hyperkalemia. * **Large P-wave:** In hyperkalemia, P-waves actually become **flattened or disappear** (atrial standstill) as the resting membrane potential becomes less negative, leading to decreased excitability. Large P-waves (P-pulmonale) are seen in right atrial enlargement. * **Prolonged Q-T interval:** Hyperkalemia typically **shortens** the QT interval due to rapid repolarization. A prolonged QT interval is characteristic of **hypocalcemia** or hypokalemia. **3. High-Yield Clinical Pearls for NEET-PG:** * **Progression of Hyperkalemia on ECG:** Tall T waves → Prolonged PR interval → Loss of P wave → Widening of QRS complex → **Sine wave pattern** (pre-terminal) → Ventricular fibrillation/Asystole. * **Management Priority:** If ECG changes are present, the immediate first step is **Intravenous Calcium Gluconate** to stabilize the cardiac membrane (it does not lower potassium levels). * **Pseudohyperkalemia:** Always rule out hemolysis during blood collection if ECG is normal despite high lab values.

Q: Which of the following is true about nephrogenic diabetes insipidus?

Renal tubule is unresponsive to ADH. **Explanation:** **Nephrogenic Diabetes Insipidus (NDI)** is a clinical syndrome characterized by the inability of the kidneys to concentrate urine despite the presence of adequate levels of Antidiuretic Hormone (ADH/Vasopressin) [1]. 1. **Why Option A is Correct:** The fundamental defect in NDI is the **resistance of the renal collecting ducts to ADH**. This is usually due to mutations in the V2 receptor (X-linked recessive) or the Aquaporin-2 water channels, or acquired causes like Lithium toxicity and hypercalcemia [1], [2]. Since the tubules cannot respond to ADH, water reabsorption fails, leading to polyuria. 2. **Why Other Options are Incorrect:** * **Option B:** A central decrease in ADH secretion defines **Central Diabetes Insipidus**, not nephrogenic. In NDI, ADH levels are actually normal or elevated. * **Option C:** Patients lose free water in the urine, leading to hemoconcentration. Therefore, **Hypernatremia** (high serum sodium) is the classic finding, especially if the patient's thirst mechanism is impaired or access to water is restricted. * **Option D:** In the **Water Deprivation Test**, NDI is distinguished by a **failure to increase urine osmolality** after exogenous ADH (Desmopressin) administration [2], because the "end-organ" (kidney) is unresponsive. **High-Yield Clinical Pearls for NEET-PG:** * **Most common inherited cause:** X-linked recessive mutation in the **V2 receptor**. * **Most common drug-induced cause:** **Lithium** (it enters via ENaC channels and inhibits signaling). * **Electrolyte triggers:** **Hypercalcemia** and **Hypokalemia** can both induce NDI [2]. * **Treatment:** Thiazide diuretics (paradoxical effect), NSAIDs (Indomethacin), and a low-salt diet. Amiloride is specifically used for Lithium-induced NDI.

Question 1

Which disease recurs after kidney transplantation?

Accepted Answer

Systemic Lupus Erythematosus

Answer

Diabetes Mellitus

Answer

Membranoproliferative Glomerulonephritis

Answer

Mesangial proliferative glomerulonephritis

Question 2

A 72-year-old man develops acute renal failure following aortic angiography. He has gained weight, has rales at both lung bases, and is dyspneic. His fractional excretion of sodium is greater than 1. Peripheral smear shows eosinophilia, and his labs reveal an elevated erythrocyte sedimentation rate, proteinuria, and microscopic hematuria. What is the most likely cause of his renal failure?

Accepted Answer

Atheroembolic renal disease

Answer

Hypovolemia

Answer

Acute tubular necrosis

Answer

Cardiogenic shock

Question 3

What is the new indication of tolvaptan as approved by FDA recently?

Accepted Answer

Polycystic kidney disease

Answer

Phenylketonuria

Answer

Pancreatic tumours

Answer

Polycystic ovarian disease

Question 4

What is the best prophylactic drug for a 60-year-old asthmatic female with microalbuminuria of 280mg?

Accepted Answer

Telmisartan

Answer

Amiloride

Answer

Spironolactone

Answer

Enalapril

Question 5

A 43-year-old woman develops acute renal failure following an emergency resection of a leaking abdominal aortic aneurysm. One week after surgery, the following laboratory values are obtained: Serum electrolytes (mEq/L): Na+ 127, K+ 5.9, Cl- 92, HCO3- 15. Blood urea nitrogen: 82 mg/dL. Serum creatinine: 6.7 mg/dL. The patient has gained 4 kg since surgery and is mildly dyspneic at rest. Eight hours after these values are reported, the following electrocardiogram is obtained. Which of the following is the most appropriate initial treatment in the management of this patient?

Accepted Answer

10 mL of 10% calcium gluconate

Answer

0.25 mg digoxin every 3 hours for 3 doses

Answer

100 mg lidocaine

Answer

Emergent hemodialysis

Question 6

What is the earliest sign of hyperkalemia on an ECG?

Accepted Answer

Tall T wave

Answer

Flat and inverted T wave

Answer

Large P-wave

Answer

Prolonged Q-T interval

Question 7

Hypokalemia is seen in all the following conditions except?

Accepted Answer

21 hydroxylase deficiency

Answer

Bartter syndrome

Answer

Hypokalemic periodic paralysis

Answer

Reninoma (juxtaglomerular cell tumor)

Question 8

Renal Tubular Acidosis (RTA) shows all except?

Accepted Answer

Vitamin D deficiency

Answer

Urine pH always >5.5

Answer

Anion gap normal

Answer

Bicarbonaturia

Question 9

Which of the following is true about nephrogenic diabetes insipidus?

Accepted Answer

Renal tubule is unresponsive to ADH

Answer

There is central decrease in secretion of ADH

Answer

Serum sodium is low

Answer

Urine osmolality is increased after administration of ADH

Question 10

Which investigation is most crucial for the diagnosis of idiopathic membranous glomerulopathy?

Accepted Answer

Antibody to PLA2R on podocytes

Answer

Kidney biopsy with immunofluorescent staining

Answer

C3, C4, and CH50 levels

Answer

c-ANCA titers

Nephrology — MCQs

Nephrology — MCQs

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