Nephrology Practice Questions

Q: A 63-year-old man becomes oliguric 2 days following an open cholecystectomy. Which of the following findings would suggest that prerenal acute kidney injury is a major factor in the etiology?

Postural hypotension. ### Explanation **1. Why Postural Hypotension is Correct:** Prerenal Acute Kidney Injury (AKI) is caused by **decreased renal perfusion** without damage to the kidney parenchyma [1]. In a post-operative patient, this is often due to hypovolemia (blood loss, fluid shifts, or inadequate replacement). **Postural hypotension** (a drop in BP >20/10 mmHg upon standing) is a clinical hallmark of intravascular volume depletion. It indicates that the "pump" lacks sufficient "prime," leading to decreased glomerular filtration rate (GFR). **2. Why the Other Options are Incorrect:** * **Fractional Excretion of Sodium (FeNa) of 3%:** In prerenal AKI, the renal tubules are intact and aggressively reabsorb sodium to expand volume [2]. Therefore, **FeNa is typically 2–3% suggests Acute Tubular Necrosis (ATN), where damaged tubules cannot reabsorb sodium. * **Specific Gravity of 1.012:** In prerenal states, the kidneys secrete ADH to concentrate urine, resulting in a **high specific gravity (>1.020)**. A value of 1.012 is "isosthenuric" (similar to plasma), suggesting the kidneys have lost their concentrating ability (intrinsic AKI/ATN). * **Urine Sodium of 30 mEq/L:** To conserve volume, prerenal AKI presents with a **low urine sodium ( 20:1** (due to increased passive reabsorption of urea). * **Urine Osmolality:** High in prerenal (>500 mOsm/kg); low in ATN (<350 mOsm/kg). * **Sediment:** Prerenal AKI shows "bland" sediment or hyaline casts; ATN shows **"muddy brown" granular casts**. * **Management:** Prerenal AKI is reversible with prompt fluid resuscitation; delay can lead to ischemic ATN.

Q: Which of the following is NOT a cause of hypervolemic hyponatremia?

Hypothyroidism. To approach hyponatremia, it is essential to categorize it based on **volume status**: Hypovolemic, Euvolemic, or Hypervolemic [1]. ### **Why Hypothyroidism is the Correct Answer** **Hypothyroidism** is classically a cause of **euvolemic hyponatremia** [1]. In severe hypothyroidism (myxedema), there is a non-osmotic release of Antidiuretic Hormone (ADH) and a decrease in the glomerular filtration rate (GFR). This leads to impaired free water excretion. While there may be some interstitial accumulation of glycosaminoglycans (myxedema), there is no significant increase in effective arterial blood volume or clinical edema to classify it as hypervolemic. ### **Analysis of Incorrect Options (Hypervolemic Causes)** Hypervolemic hyponatremia occurs when there is an increase in both total body sodium and water, but the water increase exceeds the sodium increase, usually due to "effective" circulating volume depletion. * **Cirrhosis:** Peripheral vasodilation leads to decreased effective arterial blood volume, triggering ADH and the RAAS system, causing water and salt retention (edema/ascites) [1]. * **Nephrotic Syndrome:** Low oncotic pressure (due to hypoalbuminemia) causes fluid to shift into the interstitium, leading to compensatory water retention [1]. * **Chronic Renal Failure:** The kidneys lose the ability to excrete free water and sodium, leading to a state of total body fluid overload [1]. ### **NEET-PG High-Yield Pearls** * **Euvolemic Hyponatremia Mnemonic:** **SIADH** (most common), **G**lucocorticoid deficiency, **I**atrogenic, **P**sychogenic polydipsia, **H**ypothyroidism (**SI-GIPH**). * **Hypervolemic Hyponatremia:** Think of the

Q: In Bartter syndrome, which of the following is not typically seen?

Decreased urinary calcium. **Explanation:** **Bartter syndrome** is a group of autosomal recessive disorders caused by mutations in the ion transporters of the **thick ascending limb (TAL)** of the Loop of Henle. It functionally mimics the effect of **Loop diuretics** (e.g., Furosemide). **Why "Decreased urinary calcium" is the correct answer:** In the TAL, the reabsorption of sodium, potassium, and chloride via the **NKCC2 transporter** creates a positive luminal potential that drives the paracellular reabsorption of Calcium and Magnesium. In Bartter syndrome, this transporter is defective. Consequently, calcium is not reabsorbed and is instead excreted in the urine, leading to **Hypercalciuria**. This is a key diagnostic feature that distinguishes it from Gitelman syndrome (which presents with hypocalciuria). **Analysis of incorrect options:** * **Metabolic alkalosis:** The loss of fluid and NaCl leads to volume depletion, activating the Renin-Angiotensin-Aldosterone System (RAAS). Increased aldosterone promotes H+ secretion in the distal tubule, causing metabolic alkalosis [2]. * **Hypokalemia:** High aldosterone levels increase sodium reabsorption in exchange for potassium secretion in the collecting duct, leading to significant potassium wasting [1]. * **Hypomagnesemia:** Since the TAL is also responsible for magnesium reabsorption via the same electrochemical gradient as calcium, magnesium wasting occurs, though it is usually milder than in Gitelman syndrome. **NEET-PG High-Yield Pearls:** * **Bartter vs. Gitelman:** Bartter = Loop Diuretic-like (Hypercalciuria); Gitelman = Thiazide-like (Hypocalciuria). * **Clinical Presentation:** Polyhydramnios in utero, salt wasting, and growth retardation. * **Blood Pressure:** Characterized by **normotension** or hypotension despite high renin/aldosterone levels (due to volume depletion). * **Juxtaglomerular Apparatus (JGA):** Hyperplasia of the JGA is a classic pathological finding.

Q: Which of the following statements about contrast-induced acute kidney injury is true?

Dialysis requirement is usually uncommon.. **Explanation:** Contrast-Induced Acute Kidney Injury (CI-AKI) is a form of acute tubular necrosis (ATN) caused by the administration of iodinated contrast media. **Why Option C is correct:** CI-AKI is typically a self-limiting condition. While it causes a transient decline in renal function, the injury is usually mild. **Dialysis is required in less than 1% of cases** in the general population, though the risk increases slightly in patients with pre-existing advanced chronic kidney disease or cardiogenic shock. **Analysis of Incorrect Options:** * **Option A:** Serum creatinine typically begins to rise within **24 to 48 hours** after contrast exposure, not 12 hours. * **Option B:** The peak serum creatinine level is usually reached within **3 to 5 days**, with levels typically returning to baseline within 7 to 10 days. A 2-week timeframe is too long for the peak of CI-AKI. * **Option D:** Unlike most forms of ATN, CI-AKI often presents with a **low fractional excretion of sodium (FeNa < 1%)**. This is due to the intense renal medullary vasoconstriction that precedes tubular injury, mimicking a pre-renal pattern. **Clinical Pearls for NEET-PG:** * **Definition:** An absolute increase in serum creatinine of $\geq$ 0.3 mg/dL or a $\geq$ 50% increase from baseline within 48–72 hours [1]. * **Risk Factors:** Pre-existing CKD (most important), Diabetes Mellitus, heart failure, and volume depletion. * **Prevention:** The most effective preventive strategy is **intravenous hydration** with isotonic saline (0.9% NaCl) before and after the procedure. * **Contrast Type:** Low-osmolar or iso-osmolar contrast agents are preferred to reduce nephrotoxicity.

Q: A patient presents with hematuria of several days and dysmorphic red blood cell casts in the urine. What is the most likely site of origin for the bleeding?

Kidney. **Explanation:** The presence of **dysmorphic red blood cells (RBCs)** and **RBC casts** is a pathognomonic finding for **glomerular bleeding**, indicating that the source of hematuria is the **Kidney** (specifically the renal parenchyma/glomerulus) [1]. 1. **Why Kidney is correct:** When RBCs pass through the damaged glomerular basement membrane (GBM) and travel through the renal tubules, they undergo mechanical trauma and osmotic stress, leading to a "dysmorphic" appearance (e.g., acanthocytes) [1]. Furthermore, RBCs get trapped in a matrix of **Tamm-Horsfall mucoprotein** within the distal convoluted tubule or collecting duct, forming **RBC casts** [1]. The presence of these casts confirms that the bleeding originated within the nephron. 2. **Why other options are incorrect:** * **Ureter, Bladder, and Urethra:** These represent the post-renal or "lower" urinary tract. Bleeding from these sites is typically characterized by **isomorphic (uniform) RBCs** and the **absence of casts**, as the blood enters the urine stream after the site of protein matrix formation in the tubules [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Acanthocytes:** RBCs with "mickey mouse ears" or blebs; if they constitute >5% of the urine RBCs, it is highly specific for glomerular disease [1]. * **Glomerular vs. Non-Glomerular Hematuria:** * **Glomerular:** Smoky/Cola-colored urine, RBC casts, dysmorphic RBCs, and significant proteinuria [1]. * **Non-Glomerular:** Bright red urine, blood clots (never seen in glomerular bleeding), and isomorphic RBCs. * **Common Causes:** Glomerular bleeding is often due to IgA Nephropathy (most common worldwide), Post-Streptococcal Glomerulonephritis (PSGN), or Alport Syndrome.

Q: Which of the following is a common feature of NSAID-induced allergic interstitial nephritis?

Heavy proteinuria. ### Explanation **Correct Option: D (Heavy proteinuria)** NSAID-induced **Acute Interstitial Nephritis (AIN)** is a unique clinical entity that differs significantly from classic drug-induced AIN (e.g., caused by Penicillins or Sulfonamides). The hallmark of NSAID-induced AIN is the frequent association with **Minimal Change Disease (MCD)** or Membranous Nephropathy, leading to **nephrotic-range proteinuria (>3.5g/day)** [1]. This occurs because NSAIDs inhibit cyclooxygenase, diverting arachidonic acid metabolism toward the lipoxygenase pathway. This results in an overproduction of leukotrienes, which can alter glomerular permeability and cause podocyte foot process effacement. **Why other options are incorrect:** * **A, B, and C (Fever, Rash, Eosinophilia):** These constitute the "classic triad" of drug-induced AIN. While common in hypersensitivity reactions to antibiotics (like Methicillin), this triad is **notoriously absent** in NSAID-induced cases. Patients typically present months after starting the drug, often lacking systemic allergic features [1]. **High-Yield Clinical Pearls for NEET-PG:** * **The "Classic Triad":** Fever, rash, and eosinophilia are seen in only **10–15%** of all AIN cases; their absence does not rule out the diagnosis [1]. * **Latency Period:** Unlike most drugs which cause AIN within days, NSAID-induced AIN can occur after **months** of chronic use. * **Urinalysis:** Look for "sterile pyuria" (WBCs without bacteria) and WBC casts. Eosinophiluria (Hansel’s stain) is suggestive but not pathognomonic [1]. * **Management:** The first step is the immediate cessation of the offending NSAID. Corticosteroids may be used if renal function does not improve.

Q: What is seen in Bartter syndrome?

Hypokalemia. **Explanation:** **Bartter syndrome** is a group of autosomal recessive genetic disorders characterized by a defect in the thick ascending limb (TAL) of the loop of Henle [3]. It mimics the chronic use of **loop diuretics** (like Furosemide). 1. **Why Hypokalemia is correct:** The primary defect involves the NKCC2 transporter (or related channels like ROMK). This leads to a failure of sodium, chloride, and potassium reabsorption in the TAL. The resulting increased distal delivery of sodium to the collecting duct triggers aldosterone-mediated sodium reabsorption in exchange for potassium and hydrogen ions [1]. This leads to profound **hypokalemia** and metabolic alkalosis [2]. 2. **Why other options are incorrect:** * **Metabolic Acidosis (A):** Bartter syndrome causes **Metabolic Alkalosis** due to increased hydrogen ion secretion in the distal tubule (stimulated by aldosterone and volume depletion) [2]. * **Hyperkalemia (C):** This is the opposite of what occurs; potassium is lost excessively in the urine. * **Decrease in urinary calcium (D):** In the TAL, the reabsorption of Ca²⁺ and Mg²⁺ depends on the positive lumen potential created by potassium recycling. Since this mechanism is defective in Bartter syndrome, calcium is not reabsorbed, leading to **Hypercalciuria** (unlike Gitelman syndrome, which causes hypocalciuria). **High-Yield Clinical Pearls for NEET-PG:** * **Bartter vs. Gitelman:** Bartter mimics **Loop diuretics** (High urinary calcium); Gitelman mimics **Thiazides** (Low urinary calcium). * **Presentation:** Polyuria, polydipsia, and growth retardation in childhood. * **Key Lab Findings:** Hypokalemia, Metabolic Alkalosis, Hypercalciuria, and High Renin/Aldosterone levels with **Normal Blood Pressure**.

Question 1

A 63-year-old man becomes oliguric 2 days following an open cholecystectomy. Which of the following findings would suggest that prerenal acute kidney injury is a major factor in the etiology?

Accepted Answer

Postural hypotension

Answer

Fractional excretion of sodium is 3%

Answer

Specific gravity is 1.012

Answer

Urine sodium is 30 mEq/L

Question 2

Which of the following is NOT a cause of hypervolemic hyponatremia?

Accepted Answer

Hypothyroidism

Answer

Cirrhosis

Answer

Chronic renal failure

Answer

Nephrotic syndrome

Question 3

A patient with Hepatitis C exhibits hypocomplementemia with 2 gm/day proteinuria and hematuria. What is the most probable diagnosis?

Accepted Answer

Membranoproliferative glomerulonephritis (MPGN)

Answer

Cryoglobulinemia

Answer

Membranous glomerulopathy

Answer

Post-infectious glomerulonephritis

Question 4

In Bartter syndrome, which of the following is not typically seen?

Accepted Answer

Decreased urinary calcium

Answer

Metabolic alkalosis

Answer

Hypokalemia

Answer

Hypomagnesemia

Question 5

A patient is to undergo angiography for unstable angina and has an elevated serum creatinine. Which of the following measures is NOT used to prevent contrast nephropathy?

Accepted Answer

Fenoldopam

Answer

Haemofiltration

Answer

N-acetylcysteine

Answer

0.9% saline

Question 6

Which of the following statements about contrast-induced acute kidney injury is true?

Accepted Answer

Dialysis requirement is usually uncommon.

Answer

Serum creatinine rises after 12 hours.

Answer

Peak serum creatinine occurs within 2 weeks.

Answer

High fractional excretion of sodium is a common finding.

Question 7

A patient presents with hematuria of several days and dysmorphic red blood cell casts in the urine. What is the most likely site of origin for the bleeding?

Accepted Answer

Kidney

Answer

Ureter

Answer

Bladder

Answer

Urethra

Question 8

Which of the following is a common feature of NSAID-induced allergic interstitial nephritis?

Accepted Answer

Heavy proteinuria

Answer

Fever

Answer

Rash

Answer

Eosinophilia

Question 9

Which of the following are characteristic features of medullary sponge kidney?

Accepted Answer

Autosomal dominant, Nephrocalcinosis, and Minimal proteinuria

Answer

Autosomal dominant, Nephrocalcinosis, and More common in females

Answer

Autosomal dominant and Nephrocalcinosis

Question 10

What is seen in Bartter syndrome?

Accepted Answer

Hypokalemia

Answer

Metabolic acidosis

Answer

Hyperkalemia

Answer

Decrease in urinary calcium

Nephrology — MCQs

Nephrology — MCQs

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