Nephrology — MCQs

During a routine physical examination, a 42-year-old female is found to have an elevated blood pressure of 150/100 mmHg. Workup reveals a small left kidney and a normal-sized right kidney. Laboratory examination reveals elevated serum renin levels, and renal vein renin levels are increased on the left but decreased on the right. This patient's hypertension is most likely the result of?

Q219Medium

Which feature differentiates prerenal azotemia from acute tubular necrosis (ATN)?

Q220Medium

Which of the following treatments is appropriate for tall peaked T waves on ECG?

Nephrology Indian Medical PG Practice Questions and MCQs

Question 211: Hyperkalemia is seen in which type of Renal Tubular Acidosis?

A. Type 1 RTA
B. Type 2 RTA
C. Type 3 RTA
D. Type 4 RTA (Correct Answer)

Explanation: **Explanation:** The hallmark of **Type 4 Renal Tubular Acidosis (RTA)**, also known as Hyperkalemic RTA, is the presence of **hyperkalemia**. This condition is primarily caused by either **aldosterone deficiency** or **aldosterone resistance** (pseudohypoaldosteronism). Aldosterone normally acts on the principal cells of the collecting duct to reabsorb sodium and secrete potassium and hydrogen ions [1]. When aldosterone action is impaired, potassium is retained in the blood, and the distal tubule fails to excrete $H^+$ ions, leading to a metabolic acidosis with high serum potassium levels. **Analysis of Incorrect Options:** * **Type 1 RTA (Distal RTA):** Characterized by a failure of distal intercalated cells to secrete $H^+$. This leads to an inability to acidify urine (pH > 5.5) and is typically associated with **hypokalemia**, as potassium is lost in exchange for sodium [2]. * **Type 2 RTA (Proximal RTA):** Caused by a defect in proximal bicarbonate reabsorption. The resulting bicarbonaturia leads to potassium wasting, typically causing **hypokalemia**. * **Type 3 RTA:** This is a rare, historical term referring to a hybrid of Type 1 and Type 2 features (seen in carbonic anhydrase II deficiency). Like Types 1 and 2, it is generally associated with **hypokalemia**. **High-Yield Clinical Pearls for NEET-PG:** * **Type 4 RTA** is the most common form of RTA in clinical practice, frequently seen in patients with **Diabetes Mellitus** (Hyporeninemic hypoaldosteronism). * **Urine pH:** In Type 4 RTA, the urine pH is typically **< 5.5** (the distal acidification mechanism is intact, but the buffer capacity is low due to low ammonia production). * **Drugs causing Type 4 RTA:** ACE inhibitors, ARBs, NSAIDs, Heparin, and Spironolactone [1]. * **Mnemonic:** "Type **4** is the only one with **High** K+" (4 looks like an 'H' for High).

Question 212: Proximal renal tubular acidosis has all the following features except?

A. Hypokalemia
B. Bicarbonate wasting
C. Nephrocalcinosis (Correct Answer)
D. Hyperchloremia

Explanation: The correct answer is **Nephrocalcinosis**. **Why Nephrocalcinosis is the correct answer:** Nephrocalcinosis (calcium deposition in the renal parenchyma) and nephrolithiasis are characteristic features of **Distal RTA (Type 1)**, not Proximal RTA (Type 2). In Type 1 RTA, the inability to secrete hydrogen ions leads to alkaline urine, which promotes calcium phosphate precipitation. Additionally, distal RTA is associated with **hypocitraturia** (citrate normally inhibits stone formation). In contrast, Proximal RTA involves a defect in bicarbonate reabsorption; as the filtrate moves to the distal tubule, the urine can still be acidified (pH < 5.5), and citrate excretion remains relatively normal, making stone formation rare. **Analysis of Incorrect Options:** * **Hypokalemia (A):** In Proximal RTA, the failure to reabsorb HCO₃⁻ leads to increased delivery of sodium bicarbonate to the distal tubule. This stimulates aldosterone-mediated sodium reabsorption in exchange for potassium, leading to significant potassium wasting. * **Bicarbonate wasting (B):** This is the primary pathophysiology of Type 2 RTA [2]. The proximal tubule fails to reabsorb the filtered load of bicarbonate (usually 85%), leading to massive bicarbonaturia until a lower steady-state plasma level is reached [2]. * **Hyperchloremia (D):** All primary RTAs are characterized by a **Normal Anion Gap Metabolic Acidosis (NAGMA)** [1]. To maintain electroneutrality as bicarbonate is lost, the kidneys retain chloride, resulting in hyperchloremia [1]. **NEET-PG High-Yield Pearls:** * **Type 2 RTA (Proximal):** Associated with **Fanconi Syndrome** (phosphaturia, glycosuria, aminoaciduria) [3]. * **Urine pH:** In Type 2, urine pH is initially >7.5 but can drop below **5.5** once the plasma bicarbonate level falls below the renal threshold [1]. In Type 1, urine pH is **persistently >5.5** [1]. * **Treatment:** Type 2 requires very high doses of bicarbonate; Type 1 requires much lower doses.

Question 213: Broad casts in urinary sediments are specific for:

A. Acute renal failure
B. Rapidly progressive renal failure
C. Chronic renal failure (Correct Answer)
D. Asymptomatic urinary abnormality

Explanation: **Explanation:** **Broad casts** (also known as "Renal Failure Casts") are a hallmark finding in **Chronic Renal Failure (CRF)** [1]. 1. **Why Chronic Renal Failure is correct:** Broad casts are significantly wider than ordinary casts. They form in the **large collecting ducts** that have undergone compensatory **dilation and hypertrophy** due to the loss of surrounding functioning nephrons [1]. This structural remodeling is a characteristic feature of end-stage renal disease or advanced chronic kidney disease (CKD) [1]. Their presence indicates severe reduction in nephron number and stasis in these dilated tubules. 2. **Why other options are incorrect:** * **Acute Renal Failure (ARF):** Typically characterized by **Muddy Brown (Granular) casts**, which represent acute tubular necrosis (ATN). The tubules have not had time to undergo the chronic dilation required to form broad casts. * **Rapidly Progressive Renal Failure (RPGN):** This is clinically associated with **Red Blood Cell (RBC) casts**, signifying glomerular inflammation (crescentic glomerulonephritis). * **Asymptomatic Urinary Abnormality:** This usually presents with isolated proteinuria or hematuria (e.g., IgA nephropathy) without the extensive tubular remodeling seen in advanced renal failure. **High-Yield Clinical Pearls for NEET-PG:** * **Broad Casts:** Specific for Chronic Renal Failure/End-stage renal disease. * **RBC Casts:** Pathognomonic for Glomerulonephritis. * **WBC Casts:** Suggestive of Pyelonephritis or Interstitial Nephritis. * **Fatty Casts ("Maltese Cross"):** Seen in Nephrotic Syndrome. * **Hyaline Casts:** Can be normal (after exercise/dehydration) or seen in concentrated urine. * **Waxy Casts:** Found in chronic renal states; they represent the final stage of granular cast degeneration.

Question 214: Renal osteodystrophy is characterized by all EXCEPT?

A. Calcium level
B. Phosphorus level
C. Alkaline phosphatase (Correct Answer)
D. Parathormone levels

Explanation: **Explanation:** Renal Osteodystrophy (ROD) is a component of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). The question asks which parameter does **not** characterize the condition. While Alkaline Phosphatase (ALP) is often elevated in high-turnover bone disease (like osteitis fibrosa cystica), it is a **non-specific marker**. It can be elevated in liver disease or other bone pathologies, making it the least characteristic diagnostic feature compared to the direct hormonal and mineral derangements of CKD. **Analysis of Options:** * **Phosphorus (B):** Hyperphosphatemia is the primary trigger. As GFR declines, phosphate excretion decreases, leading to its accumulation in the blood [2]. * **Calcium (A):** Hypocalcemia occurs due to hyperphosphatemia (calcium-phosphate precipitation) and a deficiency of 1,25-dihydroxyvitamin D (Calcitriol) because the failing kidney cannot perform 1-alpha hydroxylation [1]. * **Parathormone (D):** Secondary Hyperparathyroidism is a hallmark. Low calcium and high phosphorus stimulate the parathyroid glands to secrete PTH to mobilize calcium from bones, leading to bone resorption [2]. * **Alkaline Phosphatase (C):** While bone-specific ALP rises during active bone remodeling, it is not a defining biochemical criterion for the *pathophysiology* of ROD in the same way that the Ca-P-PTH axis is. **High-Yield Pearls for NEET-PG:** * **Sequence of events:** ↓ GFR → ↑ Phosphate → ↓ 1,25(OH)₂D₃ → ↓ Calcium → ↑ PTH [2]. * **Most common bone lesion:** Osteitis fibrosa cystica (due to high PTH) [2]. * **Adynamic Bone Disease:** Characterized by **low** PTH and **low** ALP, often due to over-suppression of the parathyroid gland [2]. * **Radiology:** "Rugger-jersey spine" is a classic sign of renal osteodystrophy.

Question 215: Which of the following is the common extrarenal involvement in autosomal dominant polycystic kidney disease?

A. Mitral valve prolapse
B. Hepatic cysts (Correct Answer)
C. Splenic cysts
D. Colonic diverticulosis

Explanation: **Explanation:** Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a multisystemic disorder characterized by the growth of numerous cysts in the kidneys and various extrarenal manifestations [1]. **Why Hepatic Cysts are the Correct Answer:** **Hepatic cysts** are the **most common extrarenal manifestation** of ADPKD, occurring in approximately 70–90% of patients during their lifetime (detected via MRI). These cysts arise from the biliary epithelium. While they are numerous, they rarely lead to hepatic failure because the intervening liver parenchyma remains functional. They are more common and more extensive in females, particularly those who have been pregnant, due to the influence of estrogen. **Analysis of Incorrect Options:** * **A. Mitral Valve Prolapse (MVP):** This is the most common **valvular** abnormality in ADPKD (occurring in ~25% of patients), but it is less frequent than hepatic cysts. * **C. Splenic Cysts:** These occur in ADPKD but are much rarer (approx. 5%) compared to hepatic involvement. * **D. Colonic Diverticulosis:** There is an increased association between ADPKD and diverticulosis (and diverticulitis), especially in patients with end-stage renal disease, but it is not the most common extrarenal finding. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of death:** Cardiovascular disease (due to hypertension and LVH). * **Most common extrarenal manifestation:** Hepatic cysts. * **Most serious/dreaded complication:** Rupture of **Berry Aneurysms** (Circle of Willis), leading to Subarachnoid Hemorrhage (SAH). * **Genetics:** Mutation in **PKD1** (Chromosome 16 - 85% cases, more severe) or **PKD2** (Chromosome 4 - 15% cases [1], slower progression). * **Other associations:** Pancreatic cysts, seminal vesicle cysts, and abdominal/inguinal hernias.

Question 216: What is the primary diagnostic laboratory finding in nephrotic syndrome?

A. Elevated blood urea
B. Severe anaemia
C. Massive albuminuria (Correct Answer)
D. Hyperglycemia

Explanation: **Explanation:** Nephrotic syndrome is a clinical triad characterized by the disruption of the glomerular filtration barrier (specifically the podocytes and basement membrane), leading to increased permeability to plasma proteins [1]. **1. Why "Massive albuminuria" is correct:** The hallmark of nephrotic syndrome is **heavy proteinuria**, specifically defined as **>3.5 g/24 hours** (or a protein-to-creatinine ratio >3000 mg/g) [1]. Because albumin is the smallest and most abundant plasma protein, it is the primary constituent lost. This massive loss leads to hypoalbuminemia (<3 g/dL), which subsequently causes a decrease in plasma oncotic pressure, resulting in generalized edema and compensatory hyperlipidemia [1]. **2. Why the other options are incorrect:** * **Elevated blood urea:** This is a feature of **Azotemia/Uremia**, more commonly associated with Nephritic syndrome or Acute/Chronic Kidney Injury [1]. While it can occur in late-stage nephrotic diseases, it is not a diagnostic criterion. * **Severe anaemia:** While chronic kidney disease (CKD) leads to anemia due to decreased erythropoietin, it is not a primary diagnostic finding for nephrotic syndrome. * **Hyperglycemia:** This is a finding in Diabetes Mellitus. While Diabetic Nephropathy is a leading cause of nephrotic syndrome [1], hyperglycemia itself is not a diagnostic feature of the renal syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **The Nephrotic Triad:** Proteinuria (>3.5g/day), Hypoalbuminemia (<3g/dL), and Generalized Edema. * **Hyperlipidemia:** The liver increases lipoprotein synthesis (including LDL and VLDL) to compensate for low oncotic pressure. Look for **"Oval Fat Bodies"** or **"Maltese Cross"** appearance in urine sediment under polarized light. * **Hypercoagulability:** Loss of **Antithrombin III** in urine increases the risk of venous thromboembolism, especially Renal Vein Thrombosis (most common in Membranous Nephropathy). * **Most common cause:** Minimal Change Disease (Children); Focal Segmental Glomerulosclerosis (Adults) [1].

Question 217: A patient with autosomal dominant polycystic kidney disease (ADPKD) is taking tolvaptan and is complaining of abdominal pain and loose stools. What is the likely cause of these symptoms?

A. Colonic diverticulosis
B. Diverticulitis
C. Appendicitis
D. Side effects of tolvaptan (Correct Answer)

Explanation: **Explanation:** **Correct Answer: D. Side effects of tolvaptan** Tolvaptan is a selective **vasopressin V2-receptor antagonist** used to slow the progression of cyst growth in ADPKD. While its most common side effects are related to its aquaretic effect (polyuria, polydipsia, and thirst), it is also frequently associated with **gastrointestinal disturbances**, including abdominal pain, dyspepsia, and diarrhea (loose stools). In the context of a patient recently starting or currently on tolvaptan, these symptoms are most likely pharmacological side effects rather than a new surgical pathology. **Analysis of Incorrect Options:** * **A & B (Colonic Diverticulosis/Diverticulitis):** While patients with ADPKD have a higher incidence of extra-renal manifestations like colonic diverticula compared to the general population, these typically present with localized left lower quadrant pain, fever, or hematochezia. The presence of "loose stools" specifically linked to the medication profile points more strongly toward a drug effect. Adult PKD common clinical features include vague discomfort in the loin or abdomen due to increasing mass [1]. * **C (Appendicitis):** There is no increased association between ADPKD and appendicitis. This would typically present with migratory pain to the right iliac fossa and signs of peritoneal irritation, which is less likely than a common drug side effect in this clinical scenario. **High-Yield Clinical Pearls for NEET-PG:** * **Tolvaptan Monitoring:** The most serious side effect of Tolvaptan is **hepatotoxicity**. Liver function tests (ALT, AST, and bilirubin) must be monitored monthly for the first 18 months. * **Extra-renal Manifestations of ADPKD:** 1. **Cysts:** Liver (most common), Pancreas, Spleen. 2. **Vascular:** Berry aneurysms (Circle of Willis) leading to SAH, Mitral Valve Prolapse (MVP). 3. **Abdominal Wall:** Hernias (Inguinal/Incisional). 4. **GI:** Colonic diverticula. * **Mechanism:** Tolvaptan works by decreasing intracellular cAMP, which inhibits cyst fluid secretion and cell proliferation [1].

Question 218: During a routine physical examination, a 42-year-old female is found to have an elevated blood pressure of 150/100 mmHg. Workup reveals a small left kidney and a normal-sized right kidney. Laboratory examination reveals elevated serum renin levels, and renal vein renin levels are increased on the left but decreased on the right. This patient's hypertension is most likely the result of?

A. Atherosclerotic narrowing of the left renal artery
B. Atherosclerotic narrowing of the right renal artery
C. Fibromuscular hyperplasia of the left renal artery (Correct Answer)
D. Fibromuscular hyperplasia of the right renal artery

Explanation: The clinical presentation describes **Renovascular Hypertension** caused by **Renal Artery Stenosis (RAS)**. The key to this diagnosis lies in the "Two-Kidney, One-Clip" model of hypertension. 1. **Why Option C is Correct:** * **Pathophysiology:** Stenosis of the left renal artery leads to decreased perfusion to the left kidney. This triggers the Juxtaglomerular apparatus to secrete **Renin**, activating the Renin-Angiotensin-Aldosterone System (RAAS). [1] * **Renin Lateralization:** The affected (left) kidney shows high renin levels. The contralateral (right) kidney senses the resulting systemic hypertension and suppresses its own renin production (negative feedback), explaining the decreased right renal vein renin. * **Demographics:** In a **young to middle-aged female (42 years)**, the most common cause of RAS is **Fibromuscular Dysplasia (FMD)**, often described histologically as fibromuscular hyperplasia. 2. **Why Other Options are Incorrect:** * **Options B & D:** The right kidney is normal-sized and has decreased renin levels, indicating it is the "healthy" kidney responding to systemic high pressure. * **Option A:** While atherosclerosis also causes RAS, it typically affects **older males** with cardiovascular risk factors (smoking, diabetes, hyperlipidemia) and usually involves the ostium of the renal artery. **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis:** Digital Subtraction Angiography (DSA) showing a **"String of Beads"** appearance is classic for FMD. * **Renin Ratio:** A renal vein renin ratio (affected: unaffected) of **>1.5** is diagnostic of significant stenosis. * **Physical Sign:** Listen for an abdominal bruit (systolic-diastolic) in the epigastrium or flank. * **Treatment:** Percutaneous Transluminal Angioplasty (PTA) is the treatment of choice for FMD. ACE inhibitors are contraindicated if stenosis is bilateral or in a solitary kidney. [1]

Question 219: Which feature differentiates prerenal azotemia from acute tubular necrosis (ATN)?

A. Urine osmolality > 500 mosmol/kg (Correct Answer)
B. Urinary sodium excretion < 10 mEq/L
C. Plasma transferrin/Ig ratio
D. All the above

Explanation: The differentiation between prerenal azotemia and acute tubular necrosis (ATN) hinges on the functional integrity of the renal tubules. [1] **1. Why Option A is correct:** In **prerenal azotemia**, the kidneys are structurally intact but under-perfused. To compensate for low blood volume, the tubules maximize water reabsorption under the influence of ADH. This results in highly concentrated urine with a **Urine Osmolality > 500 mOsm/kg**. In contrast, in **ATN**, the tubular cells are damaged and lose their concentrating ability (isosthenuria), typically resulting in a urine osmolality < 350 mOsm/kg. **2. Why other options are incorrect:** * **Option B:** While a low urinary sodium is characteristic of prerenal states, the standard diagnostic threshold is **< 20 mEq/L**, not < 10 mEq/L. Furthermore, Urine Osmolality is considered a more reliable physiological indicator of tubular water-handling capacity in this specific comparison. * **Option C:** The Plasma transferrin/Ig ratio is not a standard clinical parameter used to differentiate these two conditions; it is more relevant in specific proteinuric or nutritional assessments. **Clinical Pearls for NEET-PG:** To master this topic, remember the

Question 220: Which of the following treatments is appropriate for tall peaked T waves on ECG?

A. Atropine IV
B. Nitroprusside IV
C. Inhaled Salbutamol (Correct Answer)
D. Inhaled betamethasone

Explanation: **Explanation:** **Tall peaked T waves** on an ECG are the earliest and most characteristic sign of **Hyperkalemia**. Management focuses on three goals: stabilizing the cardiac membrane, shifting potassium into cells, and removing potassium from the body. **Why Inhaled Salbutamol is correct:** Salbutamol is a $\beta_2$-adrenergic agonist. It stimulates the Na⁺/K⁺-ATPase pump in skeletal muscle, which promotes the **intracellular shift of potassium**, thereby rapidly lowering serum potassium levels. It is an effective "shifter" therapy, often used alongside insulin-dextrose. **Analysis of Incorrect Options:** * **A. Atropine IV:** Used for symptomatic bradycardia or AV blocks; it has no effect on serum potassium levels. * **B. Nitroprusside IV:** A potent vasodilator used in hypertensive emergencies; it does not treat electrolyte imbalances. * **D. Inhaled Betamethasone:** While some corticosteroids have mineralocorticoid activity that can lower potassium over long periods, inhaled steroids have no role in the acute management of hyperkalemia. **NEET-PG High-Yield Pearls:** 1. **Immediate First Step:** If the ECG shows changes (like peaked T waves or QRS widening), the first drug to administer is **IV Calcium Gluconate** (10 ml of 10%). It stabilizes the cardiac membrane but does *not* lower potassium. 2. **The "Shifters":** Insulin with Dextrose (most reliable), Inhaled Salbutamol, and IV Sodium Bicarbonate (if metabolic acidosis is present). 3. **Definitive Removal:** Loop diuretics (Furosemide), Potassium-binding resins (Patiromer, Lokelma), or **Hemodialysis** (the gold standard for refractory hyperkalemia). 4. **ECG Progression:** Peaked T waves $\rightarrow$ P wave flattening/PR prolongation $\rightarrow$ QRS widening $\rightarrow$ "Sine wave" pattern $\rightarrow$ Ventricular Fibrillation.

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Acute Kidney Injury

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Glomerular Diseases

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Tubulointerstitial 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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Kidney in Systemic Diseases

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Nephrology — MCQs

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