Nephrology — MCQs

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?

Q69Medium

Heroin abuse is associated with which type of glomerulonephritis?

Q70Easy

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

Nephrology Indian Medical PG Practice Questions and MCQs

Question 61: A patient with acute kidney injury (creatinine > 4) has been undergoing dialysis in the ICU for 15 days and has developed deep vein thrombosis (DVT) due to immobilization. What is the most appropriate anticoagulant to administer?

A. Desirudin
B. Argatroban (Correct Answer)
C. Lepirudin
D. Aspirin

Explanation: ### Explanation The management of anticoagulation in patients with severe renal impairment (AKI or ESRD) requires careful selection based on the route of drug elimination. **Why Argatroban is the Correct Choice:** Argatroban is a parenteral Direct Thrombin Inhibitor (DTI) [1]. Its primary clinical advantage in this scenario is its **hepatic metabolism and biliary excretion**. Unlike many other anticoagulants, its clearance is independent of renal function. In a patient with a creatinine > 4 mg/dL undergoing dialysis, Argatroban can be administered without the risk of accumulation or toxicity, making it the safest choice among the options provided. **Analysis of Incorrect Options:** * **Desirudin & Lepirudin:** Both are recombinant hirudins (DTIs) that are **predominantly cleared by the kidneys**. In patients with renal failure, these drugs have a significantly prolonged half-life, leading to a high risk of life-threatening hemorrhage. (Note: Lepirudin has largely been withdrawn from many markets due to this risk and immunogenicity). * **Aspirin:** Aspirin is an antiplatelet agent, not an anticoagulant [1]. It is ineffective for the treatment of established Deep Vein Thrombosis (DVT). **NEET-PG High-Yield Pearls:** * **Drug of Choice for HIT:** Argatroban is also the preferred anticoagulant for patients with Heparin-Induced Thrombocytopenia (HIT) who have renal failure [1]. * **Monitoring:** Argatroban is monitored using **aPTT** (target 1.5–3 times the baseline). * **Renal vs. Hepatic:** Remember the mnemonic: **A**rgatroban = **A**liver (Liver/Hepatic clearance); **L**epirudin = **L**eaving via kidney (Renal clearance). * **LMWH/Fondaparinux:** These are generally contraindicated or require extreme caution/dose reduction when CrCl < 30 ml/min [1].

Question 62: High serum uric acid, high serum phosphates, and high serum creatinine in a patient will be observed in which of the following conditions?

A. Chronic lymphocytic leukemia (Correct Answer)
B. Obstructive jaundice
C. Status epilepticus
D. Typhoid

Explanation: The combination of hyperuricemia, hyperphosphatemia, and elevated creatinine is the classic biochemical signature of **Tumor Lysis Syndrome (TLS)**. ### **Explanation of the Correct Answer** **Chronic Lymphocytic Leukemia (CLL)** is a lymphoproliferative disorder characterized by a high burden of malignant white blood cells. When these cells undergo rapid turnover (either spontaneously or due to chemotherapy), they release their intracellular contents into the bloodstream: * **Hyperuricemia:** From the breakdown of nucleic acids (purines). Production of uric acid is increased in leukemia because of the increased breakdown of uric acid-rich white blood cells [1]. * **Hyperphosphatemia:** From the release of intracellular phosphorus. * **High Creatinine:** Resulting from **Acute Kidney Injury (AKI)** caused by the precipitation of uric acid crystals and calcium phosphate in the renal tubules [1]. ### **Why Other Options are Incorrect** * **Obstructive Jaundice:** Typically presents with elevated conjugated bilirubin and alkaline phosphatase. It does not cause rapid cell lysis or significant hyperphosphatemia. * **Status Epilepticus:** While it can cause rhabdomyolysis (leading to high creatinine and phosphate), it is not a primary cause of the massive nucleic acid turnover seen in hematological malignancies. Although status epilepticus is mentioned in the context of toxin exposures and organ dysfunction, it doesn't explain the full TLS triad . * **Typhoid:** An infectious disease presenting with "step-ladder" fever and bradycardia; it does not typically cause this specific triad of metabolic derangements. ### **NEET-PG High-Yield Pearls** * **TLS Electrolyte Triad:** Hyperkalemia, Hyperphosphatemia, and Hyperuricemia (with associated **Hypocalcemia**). * **Prophylaxis:** Aggressive hydration and **Allopurinol** (xanthine oxidase inhibitor). * **Treatment of Choice for Hyperuricemia:** **Rasburicase** (recombinant urate oxidase) is used if uric acid levels are already significantly elevated. * **Cairo-Bishop Definition:** The standard clinical criteria used to diagnose TLS.

Question 63: All of the following are seen in Hemolytic Uremic Syndrome (HUS) except?

A. Thrombocytopenia
B. Altered sensorium (Correct Answer)
C. Hemolytic anemia
D. Renal failure

Explanation: Hemolytic Uremic Syndrome (HUS) is characterized by a classic **triad** of clinical features [2]. The correct answer is **Altered sensorium** because neurological involvement is typically absent or minimal in HUS, serving as a key clinical differentiator from its sister condition, Thrombotic Thrombocytopenic Purpura (TTP) [1]. **Why "Altered Sensorium" is the correct answer:** While HUS and TTP share many features, TTP is defined by a **pentad** that includes the HUS triad plus **fever** and **neurological symptoms** (like altered sensorium, seizures, or focal deficits). In HUS, the pathology is primarily localized to the renal microvasculature, whereas TTP involves systemic microthrombi affecting the brain. **Analysis of incorrect options (The HUS Triad):** * **Thrombocytopenia (Option A):** Occurs due to the consumption of platelets in the formation of microthrombi within small blood vessels [2]. * **Hemolytic Anemia (Option C):** Specifically, **Microangiopathic Hemolytic Anemia (MAHA)**. Red blood cells are mechanically shredded as they pass through fibrin-occluded capillaries, leading to the presence of **schistocytes** (helmet cells) on a peripheral smear [1]. * **Renal Failure (Option D):** Acute Kidney Injury (AKI) is a hallmark of HUS, often manifesting as oliguria, hematuria, and elevated creatinine due to glomerular endothelial damage [2]. **NEET-PG High-Yield Pearls:** * **Typical HUS:** Most common in children; associated with **Shiga toxin-producing E. coli (STEC)**, specifically serotype **O157:H7** [1]. It usually follows an episode of bloody diarrhea. * **Atypical HUS:** Associated with uncontrolled complement activation (e.g., mutations in **Factor H**). * **Key Lab Finding:** Negative Coomb's test (since hemolysis is mechanical, not immune-mediated). * **Management:** Primarily supportive (fluids, dialysis). Antibiotics and anti-motility agents are generally avoided in STEC-HUS as they may increase toxin release.

Question 64: Which of the following symptoms do you expect to see in a patient diagnosed with acute pyelonephritis?

A. Jaundice and flank pain
B. Costovertebral angle tenderness and chills (Correct Answer)
C. Burning sensation on urination
D. Polyuria and nocturia

Explanation: **Explanation:** **Acute Pyelonephritis** is a common clinical entity in NEET-PG, characterized by an infection of the renal parenchyma and pelvis [1], [2], typically ascending from the lower urinary tract [1]. **1. Why Option B is Correct:** The classic clinical triad of acute pyelonephritis includes **fever/chills, flank pain (manifesting as costovertebral angle tenderness - CVAT), and nausea/vomiting.** [1], [2] Chills and rigors signify systemic involvement (bacteremia), while CVAT is the hallmark physical finding indicating inflammation of the renal capsule [2]. **2. Analysis of Incorrect Options:** * **Option A (Jaundice):** Jaundice is not a feature of pyelonephritis. While severe sepsis can cause cholestasis, jaundice typically points toward hepatobiliary pathology (e.g., cholecystitis or hepatitis). * **Option C (Burning sensation):** This describes **dysuria**, which is a symptom of lower urinary tract infections (Cystitis). While pyelonephritis can coexist with cystitis, the presence of systemic symptoms and CVAT specifically differentiates "upper" from "lower" UTI [1]. * **Option D (Polyuria and nocturia):** These are symptoms of chronic renal conditions (like Chronic Pyelonephritis or Diabetes) where the concentrating ability of the kidney is lost. Acute pyelonephritis presents with acute inflammatory symptoms rather than chronic volume changes. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most Common Organism:** *E. coli* (uropathogenic strains). * **Diagnosis:** Primarily clinical; however, **WBC casts** in urine microscopy are pathognomonic for pyelonephritis (distinguishing it from cystitis). * **Imaging:** Not routinely required unless the patient is diabetic, immunocompromised, or fails to respond to antibiotics within 72 hours (to rule out perinephric abscess or emphysematous pyelonephritis). * **Treatment:** Empiric Fluoroquinolones (e.g., Ciprofloxacin) or Ceftriaxone are first-line agents.

Question 65: Which of the following statements about prerenal azotaemia is false?

A. Parenchymal damage to kidney (Correct Answer)
B. Physiological response to renal hypoperfusion
C. Certain drugs can provoke acute prerenal failure
D. Persistent renal hypoperfusion leads to ischaemic acute tubular necrosis

Explanation: ### Explanation **Prerenal Azotaemia** is characterized by a decrease in the Glomerular Filtration Rate (GFR) due to reduced renal blood flow (hypoperfusion) without any initial structural damage to the kidney tissue [1]. **1. Why Option A is the Correct Answer (False Statement):** In prerenal azotaemia, the kidney parenchyma (glomeruli and tubules) remains **structurally intact**. The condition is purely functional and reversible if the underlying cause of hypoperfusion is corrected [1]. If there were "parenchymal damage," the condition would be classified as **Intrinsic Renal Failure** (e.g., Acute Tubular Necrosis). **2. Analysis of Other Options:** * **Option B:** This is true. Prerenal azotaemia is a **physiological compensatory response** to systemic hypotension or volume depletion. The kidneys attempt to maintain GFR through autoregulation (afferent vasodilation and efferent vasoconstriction) [2]. * **Option C:** This is true. Drugs like **NSAIDs** (block prostaglandins, causing afferent vasoconstriction) and **ACE inhibitors/ARBs** (block Angiotensin II, causing efferent vasodilation) can impair renal autoregulation and provoke prerenal failure. * **Option D:** This is true. If renal hypoperfusion is severe or prolonged, the compensatory mechanisms fail, leading to cellular hypoxia and eventually **Ischaemic Acute Tubular Necrosis (ATN)**, marking the transition from prerenal to intrinsic renal failure [1]. **High-Yield Clinical Pearls for NEET-PG:** * **BUN:Creatinine Ratio:** Typically **>20:1** in prerenal azotaemia (due to increased proximal tubular reabsorption of urea). * **Fractional Excretion of Sodium (FeNa):** Characteristically **<1%** as the tubules are intact and aggressively reabsorbing sodium to restore volume. * **Urine Osmolality:** Usually high (**>500 mOsm/kg**) because the concentrating mechanism is preserved. * **Urinary Sediment:** Usually normal or contains "hyaline casts"; "muddy brown casts" are seen in ATN [1].

Question 66: What is the leading cause of hyperkalemia?

A. Redistribution of potassium
B. Reduced renal excretion (Correct Answer)
C. Adrenal neurohormonal surge
D. Drugs

Explanation: **Explanation:** The correct answer is **B. Reduced renal excretion**. The kidneys are the primary regulators of potassium balance, responsible for excreting approximately 90% of the daily potassium intake. Under normal physiological conditions, the distal convoluted tubule and collecting duct can adapt to high potassium loads by increasing secretion. Hyperkalemia occurs most frequently when this excretory capacity is compromised, typically due to **Acute Kidney Injury (AKI)** or **Chronic Kidney Disease (CKD)**. Even in cases of increased intake or redistribution, healthy kidneys can usually clear the excess; therefore, impaired renal handling is the most common underlying mechanism for sustained hyperkalemia. **Analysis of Incorrect Options:** * **A. Redistribution of potassium:** This refers to the shift of $K^+$ from the intracellular to the extracellular compartment (e.g., metabolic acidosis, insulin deficiency, or cell lysis). While a significant cause, it is less common than renal impairment. * **C. Adrenal neurohormonal surge:** This is not a standard cause of hyperkalemia. In fact, a surge in catecholamines (like epinephrine) typically causes *hypokalemia* by shifting potassium into cells via $\beta_2$-receptors. * **D. Drugs:** While medications (ACE inhibitors, ARBs, Spironolactone, NSAIDs) are a very frequent *trigger* for hyperkalemia, they primarily act by **reducing renal excretion** (interfering with the Renin-Angiotensin-Aldosterone System). Thus, "Reduced renal excretion" is the broader, more definitive physiological cause. **High-Yield Clinical Pearls for NEET-PG:** * **ECG Changes:** The earliest sign is **Tall Tented T-waves**, followed by PR prolongation, loss of P-wave, and eventually the "Sine wave" pattern. * **Treatment Priority:** The first step in management with ECG changes is **Calcium Gluconate** (stabilizes the cardiac membrane), followed by insulin/dextrose to shift $K^+$ intracellularly. * **Pseudohyperkalemia:** Always rule this out if the patient is asymptomatic; it is often caused by hemolysis during venipuncture or severe thrombocytosis/leukocytosis.

Question 67: Which disease recurs after kidney transplantation?

A. Diabetes Mellitus
B. Membranoproliferative Glomerulonephritis
C. Systemic Lupus Erythematosus (Correct Answer)
D. Mesangial proliferative glomerulonephritis

Explanation: The recurrence of primary disease in a renal allograft is a significant cause of long-term graft failure. [1] **Correct Option: C (Systemic Lupus Erythematosus)** While SLE is a systemic autoimmune disease, it is a classic example of a condition that can recur in the transplanted kidney (Lupus Nephritis). [2] However, the clinical recurrence rate is relatively low (approx. 2–10%) because the potent immunosuppressive regimen used to prevent graft rejection (such as Mycophenolate Mofetil and Steroids) also effectively treats the underlying SLE. [2] **Analysis of Incorrect Options:** * **A. Diabetes Mellitus:** While hyperglycemia will eventually cause diabetic nephropathy in the new graft, this is considered a "de novo" development of the disease over years rather than an immediate "recurrence" of the primary glomerular pathology in the same sense as GN. * **B. Membranoproliferative Glomerulonephritis (MPGN):** This is a "trick" option. While MPGN (especially Type II/Dense Deposit Disease) has a very high recurrence rate, the question asks for the specific answer based on standard NEET-PG patterns where SLE is frequently highlighted. *Note: In clinical practice, MPGN Type II actually has a higher recurrence rate than SLE.* * **D. Mesangial Proliferative GN:** This is a non-specific histological pattern. While IgA nephropathy (a form of mesangial proliferative GN) recurs frequently, "Mesangial Proliferative GN" as a general category is less commonly cited as the primary answer compared to SLE in this specific question context. **NEET-PG High-Yield Pearls:** * **Highest rate of recurrence:** Dense Deposit Disease (MPGN Type II) – nearly 100% histological recurrence. * **Fastest recurrence leading to graft loss:** Focal Segmental Glomerulosclerosis (FSGS) – can recur within hours to days. * **Least likely to recur:** Polycystic Kidney Disease (PKD) and Alport Syndrome (as these are genetic structural defects). * **De novo disease:** Membranous Nephropathy is the most common de novo glomerulonephritis in a transplant.

Question 68: 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?

A. Hypovolemia
B. Atheroembolic renal disease (Correct Answer)
C. Acute tubular necrosis
D. Cardiogenic shock

Explanation: ### 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].

Question 69: Heroin abuse is associated with which type of glomerulonephritis?

A. Focal segmental glomerulosclerosis (Correct Answer)
B. Crescentic glomerulonephritis
C. Membranous glomerulonephritis
D. Diffuse proliferative glomerulonephritis

Explanation: **Explanation:** **Heroin-Associated Nephropathy (HAN)** is a classic clinical entity characterized by the development of **Focal Segmental Glomerulosclerosis (FSGS)** [1]. 1. **Why FSGS is correct:** Intravenous heroin use leads to a specific form of secondary FSGS [1]. The pathophysiology involves direct toxicity to podocytes [2], chronic inflammation, and potential contaminants in the drug. Patients typically present with massive proteinuria (nephrotic syndrome) [2] and a rapid progression to End-Stage Renal Disease (ESRD). On biopsy, it shows segmental scarring of some (but not all) glomeruli, similar to the collapsing variant seen in HIV-associated nephropathy (HIVAN) [1]. 2. **Why other options are incorrect:** * **Crescentic GN:** This is the hallmark of Rapidly Progressive Glomerulonephritis (RPGN) [3], associated with conditions like Goodpasture syndrome [4] or ANCA-associated vasculitis, not typically heroin. * **Membranous GN:** This is most commonly associated with Hepatitis B, Hepatitis C, gold therapy, or malignancies. While heroin users may have Hep B/C, the direct association of heroin itself is with FSGS [3]. * **Diffuse Proliferative GN:** This is the classic pattern for SLE (Class IV) or post-streptococcal GN [1]. **High-Yield Clinical Pearls for NEET-PG:** * **The "Collapsing" Variant:** Both Heroin and HIV are strongly associated with the collapsing variant of FSGS, which has the worst prognosis. * **Race Factor:** HAN is significantly more common in the African American population. * **Differential Diagnosis:** If a question mentions an IV drug user with **fever and hematuria**, think of **Staph. aureus Endocarditis** leading to Post-Infectious GN. If it mentions **painless nephrotic syndrome**, think of **FSGS**. * **Other FSGS associations:** Obesity, Sickle Cell Disease, and Pamidronate use.

Question 70: What is the new indication of tolvaptan as approved by FDA recently?

A. Phenylketonuria
B. Pancreatic tumours
C. Polycystic ovarian disease
D. Polycystic kidney disease (Correct Answer)

Explanation: **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.

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Acute Kidney Injury

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Chronic Kidney Disease

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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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Kidney Stones and Obstructive Uropathy

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Hypertension in Kidney Disease

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Nephrology — MCQs

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