Nephrology Practice Questions

Q: In which of the following conditions is the serum C3 level not persistently low?

Poststreptococcal glomerulonephritis. In nephrology, glomerulonephritides (GN) are often categorized by their effect on the complement system. This question tests the ability to distinguish between **transient** and **persistent** hypocomplementemia. ### **Explanation of the Correct Answer** **A. Poststreptococcal Glomerulonephritis (PSGN):** In PSGN, serum C3 levels are characteristically low due to the activation of the alternative complement pathway [1]. However, this decrease is **transient**. C3 levels typically return to normal within **6 to 8 weeks** after the onset of symptoms [1]. If hypocomplementemia persists beyond 8 weeks, an alternative diagnosis (like MPGN) must be considered. ### **Analysis of Incorrect Options** * **B. Membranoproliferative Glomerulonephritis (MPGN):** This is a classic "low complement" GN. In Type I, C3 is low due to classical pathway activation; in Type II (Dense Deposit Disease), C3 is **persistently low** due to C3 nephritic factor, which stabilizes C3 convertase [1]. * **C. Lupus Nephritis:** Systemic Lupus Erythematosus (SLE) involves chronic immune complex deposition. C3 and C4 levels remain low during active disease and flares, reflecting ongoing consumption. * **D. Endocarditis-related GN:** Chronic infections like subacute bacterial endocarditis or "shunt nephritis" cause continuous antigenemia, leading to **persistent** consumption of complement until the underlying infection is eradicated. ### **NEET-PG High-Yield Pearls** * **The "Big Three" Low Complement GNs:** Remember the mnemonic **"P-M-L"** (PSGN, MPGN, Lupus). * **C3 vs. C4:** In PSGN and MPGN Type II, **only C3** is usually low (Alternative pathway) [1]. In Lupus and Endocarditis, both C3 and C4 are low (Classical pathway). * **The 8-Week Rule:** Any patient suspected of PSGN whose C3 remains low after 2 months requires a renal biopsy to rule out MPGN.

Q: Gross hematuria is seen in which of the following conditions?

IgA nephropathy. **Explanation:** **IgA Nephropathy (Berger’s Disease)** is the most common cause of primary glomerulonephritis worldwide. It characteristically presents as **synpharyngitic hematuria**—episodes of **gross (macroscopic) hematuria** occurring concurrently or within 1–2 days of an upper respiratory tract infection [1]. The underlying pathology involves the deposition of IgA immune complexes in the glomerular mesangium, leading to inflammation and rupture of glomerular capillaries [3]. **Analysis of Incorrect Options:** * **Minimal Change Disease (MCD):** This is the classic cause of **Nephrotic Syndrome** in children [2]. It typically presents with massive proteinuria, edema, and hypoalbuminemia, but **not** gross hematuria. * **Chronic Renal Failure (CRF):** CRF is a state of progressive loss of kidney function. While microscopic hematuria can occur depending on the primary cause, gross hematuria is not a hallmark feature of chronic kidney disease itself. * **Nephritic Syndrome:** While nephritic syndrome (e.g., Post-streptococcal GN) presents with hematuria, it is usually described as **"cola-colored" or "smoky" urine** [4]. While it can be gross, IgA nephropathy is the most classic and frequent association with recurrent, visible gross hematuria in exam scenarios. (Note: If both are options, IgA is the more specific "textbook" answer for recurrent gross hematuria). **High-Yield Clinical Pearls for NEET-PG:** * **Timing is Key:** IgA Nephropathy = **Synpharyngitic** (1-2 days after infection); PSGN = **Post-pharyngitic** (1-3 weeks after infection) [1]. * **Diagnosis:** Definitive diagnosis requires renal biopsy showing **mesangial IgA deposits** on immunofluorescence [3]. * **Prognosis:** The most reliable predictor of poor prognosis in IgA nephropathy is the severity of **proteinuria** and hypertension at presentation.

Q: How can acute and chronic renal failure be differentiated?

Peripheral neuropathy in chronic renal failure. To differentiate between Acute Kidney Injury (AKI) and Chronic Kidney Disease (CKD), clinicians must look for signs of chronicity. While many biochemical markers overlap, certain clinical and radiological findings are specific to long-standing renal impairment [1]. ### **Explanation of the Correct Option** **C. Peripheral Neuropathy:** This is a definitive sign of chronicity. Uremic peripheral neuropathy (typically a symmetric distal sensory-motor neuropathy) takes months to years of persistent azotemia to develop. It is virtually never seen in AKI, making it a reliable clinical differentiator. ### **Explanation of Incorrect Options** * **A. Anemia:** While classic teaching suggests anemia favors CKD (due to decreased Erythropoietin), it is **not** a reliable differentiator [1]. Patients with AKI can develop rapid anemia due to hemodilution, hemolysis, or gastrointestinal bleeding (stress ulcers). Conversely, some CKD patients (e.g., Polycystic Kidney Disease) may maintain normal hemoglobin levels. * **B. Hyperphosphatemia:** This occurs in both AKI and CKD [2]. In AKI, it results from a sudden drop in GFR and decreased excretion; in CKD, it is part of the Mineral Bone Disorder (MBD) spectrum. Therefore, it cannot be used to distinguish between the two. ### **High-Yield Clinical Pearls for NEET-PG** 1. **Kidney Size:** The most reliable radiological differentiator is kidney size on Ultrasound. **Small, shrunken kidneys (<9 cm)** indicate CKD. * *Exceptions (Large kidneys in CKD):* Diabetes Mellitus, Amyloidosis, Polycystic Kidney Disease (PCKD), and HIV-associated nephropathy. 2. **Renal Osteodystrophy:** Radiological evidence of subperiosteal resorption (best seen in hand phalanges) is pathognomonic for CKD. 3. **Broad Casts:** The presence of "Broad Casts" (wider than ordinary granular casts) in urine sediment suggests compensatory hypertrophy of remaining nephrons, indicating CKD.

Q: Calculate the water deficit in a 50 kg male patient with a serum sodium level of 160 mEq/L.

2.9 L of half normal saline. ### Explanation To solve this question, we must first calculate the **Free Water Deficit (FWD)** using the standard formula: **FWD = Total Body Water (TBW) × [(Serum Na / 140) – 1]** 1. **Calculate TBW:** In an adult male, TBW is approximately 60% of body weight [2]. * TBW = 50 kg × 0.6 = **30 L** 2. **Calculate the Deficit:** * FWD = 30 × [(160 / 140) – 1] * FWD = 30 × [1.142 – 1] = 30 × 0.142 = **4.26 L** While the pure water deficit is ~4.3 L, the clinical management of hypernatremia often involves using hypotonic solutions. Among the options provided, **2.9 L of half-normal saline (0.45% NaCl)** is the most appropriate choice because it provides the necessary free water while addressing potential volume depletion [1]. #### Why the other options are incorrect: * **Option A (Hypertonic Saline):** This contains 3% NaCl. Giving more sodium to a patient with a serum sodium of 160 mEq/L would worsen the hypernatremia and is contraindicated. * **Options C & D (1.5 L Dextrose):** While 5% Dextrose (D5W) is technically "free water" [2], the calculated volume (1.5 L) is significantly lower than the required deficit (~4.3 L), making these options inadequate. #### High-Yield Clinical Pearls for NEET-PG: * **Rate of Correction:** Never correct sodium faster than **0.5 mEq/L per hour** (or max 8–10 mEq/L in 24 hours). Rapid correction leads to **Cerebral Edema** due to the sudden shift of water into brain cells. * **TBW Constants:** Use 0.6 for men, 0.5 for women/elderly men, and 0.45 for elderly women. * **Preferred Fluid:** If the patient is hypovolemic and hypernatremic, start with Normal Saline (0.9%) until hemodynamically stable, then switch to hypotonic fluids (0.45% Saline or D5W) [1].

Q: The ECG in hyperkalemia classically shows:

Increased QRS duration. ### Explanation Hyperkalemia is a critical electrolyte abnormality that affects the resting membrane potential of cardiac myocytes, leading to delayed depolarization and repolarization [1]. **1. Why "Increased QRS duration" is correct:** As potassium levels rise, the resting membrane potential becomes less negative (partially depolarized). This leads to a decrease in the velocity of the upstroke of the action potential (Phase 0), which slows down intraventricular conduction. On an ECG, this manifests as a **widening of the QRS complex** [1]. If left untreated, the QRS can eventually merge with the T wave, forming a "sine wave" pattern, a precursor to ventricular fibrillation or asystole. **2. Why the other options are incorrect:** * **Shortened PR interval:** In hyperkalemia, the PR interval actually **prolongs** due to delayed conduction through the AV node. Eventually, P waves may disappear entirely (atrial standstill) [1]. * **Prominent U waves:** These are characteristic of **hypokalemia**, not hyperkalemia. Hyperkalemia is associated with tall, "tented" or peaked T waves [1]. * **Increased R wave amplitude:** Hyperkalemia typically causes a **decrease** in R wave amplitude and S wave deepening as conduction slows. **3. High-Yield Clinical Pearls for NEET-PG:** * **Sequential ECG Changes:** Tall peaked T waves (earliest sign) → PR prolongation/P wave flattening → QRS widening → Sine wave pattern → VF/Asystole [1]. * **Treatment Priority:** The first step in management when ECG changes are present is **Intravenous Calcium Gluconate** (to stabilize the cardiac membrane), followed by insulin/dextrose to shift potassium intracellularly. * **Pseudohyperkalemia:** Always rule out hemolysis during blood collection if the ECG is normal despite very high lab values.

Question 1

Which of the following is NOT a complication of hemodialysis?

Accepted Answer

Hypotension

Answer

Peritonitis

Answer

Hypertension

Answer

Bleeding tendency

Question 2

What is true regarding IgA nephropathy?

Accepted Answer

Recurrent gross hematuria following respiratory infections.

Answer

Usually seen in children <10 years of age.

Answer

Microscopic hematuria is a common presentation.

Answer

Decreased serum IgA.

Question 3

Which of the following findings cannot be used to differentiate between acute pyelonephritis and uncomplicated urinary tract infection?

Accepted Answer

Organisms in excess of 100,000 colony-forming units per milliliter

Answer

WBC cast

Answer

Concentrating defect

Answer

Antibody to Tamm-Horsfall protein

Question 4

In which of the following conditions is the serum C3 level not persistently low?

Accepted Answer

Poststreptococcal glomerulonephritis

Answer

Membranoproliferative glomerulonephritis

Answer

Lupus nephritis

Answer

Glomerulonephritis related to bacterial endocarditis

Question 5

Gross hematuria is seen in which of the following conditions?

Accepted Answer

IgA nephropathy

Answer

Minimal change disease

Answer

Chronic renal failure

Answer

Nephritic syndrome

Question 6

How can acute and chronic renal failure be differentiated?

Accepted Answer

Peripheral neuropathy in chronic renal failure

Answer

Anemia in chronic renal failure

Answer

Hyperphosphatemia in chronic renal failure

Answer

None of the above

Question 7

All of the following statements about Bartter syndrome and Gitelman syndrome are true, EXCEPT:

Accepted Answer

Genetic defect in Bartter syndrome involves the Na+-Cl- cotransporter in the distal tubule

Answer

Autosomal recessive inheritance

Answer

Bartter syndrome presents earlier in life than Gitelman syndrome

Answer

Hypercalciuria is more common in Bartter syndrome

Question 8

Calculate the water deficit in a 50 kg male patient with a serum sodium level of 160 mEq/L.

Accepted Answer

2.9 L of half normal saline

Answer

2.9 L of hypertonic saline

Answer

1.5 L of 5% dextrose in water

Answer

1.5 L of 10% dextrose in water

Question 9

Which of the following is NOT a uremic manifestation that improves with dialysis?

Accepted Answer

Osteodystrophy

Answer

Metabolic acidosis

Answer

Asterixis

Answer

Nausea, vomiting, and anorexia

Question 10

The ECG in hyperkalemia classically shows:

Accepted Answer

Increased QRS duration

Answer

Shortened PR interval

Answer

Prominent U waves

Answer

Increased R wave amplitude

Nephrology — MCQs

Nephrology — MCQs

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