Nephrology — MCQs
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A 32-year-old man complains of recurrent hematuria since his youth. The hematuria typically occurs following upper respiratory tract infections. Vital signs are normal. Urinalysis shows proteinuria, hematuria, and a few red blood cell casts. Laboratory studies disclose normal levels of BUN and creatinine. The ANA and ANCA tests are negative. Which of the following is the most likely diagnosis?
According to the RIFLE criteria, what defines acute kidney injury?
Which of the following findings is NOT associated with Adult Polycystic Kidney Disease?
What is the treatment of choice in acute hyperkalemia that is life-threatening to cardiac myocytes?
Uremia occurs when total GFR is reduced by approximately what percentage?
Nephrogenic diabetes insipidus is caused by all of the following except?
Urine analysis of a patient with haematuria and hypercalciuria is most likely to reveal which of the following?
Microalbuminuria is defined as:
Nephrocalcinosis is seen in all except:
Which of the following statements is NOT true about IgA nephropathy?
Nephrology Indian Medical PG Practice Questions and MCQs
Question 491: A 32-year-old man complains of recurrent hematuria since his youth. The hematuria typically occurs following upper respiratory tract infections. Vital signs are normal. Urinalysis shows proteinuria, hematuria, and a few red blood cell casts. Laboratory studies disclose normal levels of BUN and creatinine. The ANA and ANCA tests are negative. Which of the following is the most likely diagnosis?
- A. Amyloid nephropathy
- B. Berger disease (IgA nephropathy) (Correct Answer)
- C. Hereditary nephritis (Alport syndrome)
- D. Membranous glomerulopathy
Explanation: ### Explanation **1. Why Berger Disease (IgA Nephropathy) is Correct:** The clinical presentation is classic for **IgA Nephropathy**, the most common primary glomerulonephritis worldwide [1]. The hallmark is **synpharyngitic hematuria**—gross hematuria occurring concurrently or within 1–2 days of an upper respiratory tract infection (URTI) [1]. This happens because mucosal infections trigger overproduction of galactose-deficient IgA1, which forms immune complexes that deposit in the glomerular **mesangium** [1], [2]. The presence of RBC casts confirms a glomerular origin, while normal BUN/Creatinine and negative ANA/ANCA rule out systemic vasculitis or lupus. **2. Why the Other Options are Incorrect:** * **Amyloid Nephropathy:** Typically presents with massive proteinuria (nephrotic syndrome) and enlarged kidneys. It is not associated with episodic hematuria triggered by infections. * **Hereditary Nephritis (Alport Syndrome):** While it causes recurrent hematuria, it is usually associated with a positive family history, sensorineural hearing loss, and ocular defects (lenticonus). It does not typically show the "synpharyngitic" timing. * **Membranous Glomerulopathy:** This is a common cause of nephrotic syndrome in adults [2]. It presents with heavy proteinuria and edema, not episodic gross hematuria or RBC casts. **3. NEET-PG High-Yield Pearls:** * **Timing is Key:** IgA Nephropathy (Synpharyngitic: <3 days post-URTI) vs. Post-Streptococcal Glomerulonephritis (PSGN) (Post-infectious: 1–3 weeks post-URTI/skin infection) [1]. * **Diagnosis:** Gold standard is **Renal Biopsy**, showing **mesangial IgA deposits** on Immunofluorescence (IF) and mesangial hypercellularity on Light Microscopy [2]. * **Prognosis:** The most reliable predictor of poor prognosis is the degree of persistent proteinuria and hypertension [1]. * **Complement Levels:** Serum C3 and C4 levels are **normal** in IgA Nephropathy (unlike PSGN or Lupus).
Question 492: According to the RIFLE criteria, what defines acute kidney injury?
- A. Urine output < 0.5 ml/kg/h for > 8 hours
- B. Urine output < 0.5 ml/kg/h for > 12 hours (Correct Answer)
- C. Urine output < 0.3 ml/kg/h for > 24 hours
- D. Anuria for > 12 hours
Explanation: The **RIFLE criteria** (Risk, Injury, Failure, Loss, and End-stage renal disease) were developed by the ADQI group to standardize the definition of Acute Kidney Injury (AKI). The classification is based on two parameters: Serum Creatinine (SCr)/GFR and Urine Output (UO). [1] ### **Explanation of the Correct Option** **Option B** is correct because, under the RIFLE criteria, the **"Injury"** stage is defined by: * **Creatinine:** 2-fold increase in SCr or GFR decrease > 50%. * **Urine Output:** < 0.5 ml/kg/h for **> 12 hours**. ### **Analysis of Incorrect Options** * **Option A:** < 0.5 ml/kg/h for > 6 hours (not 8) defines the **"Risk"** stage. * **Option C:** < 0.3 ml/kg/h for > 24 hours defines the **"Failure"** stage. * **Option D:** Anuria for **> 12 hours** also defines the **"Failure"** stage. ### **High-Yield NEET-PG Clinical Pearls** 1. **RIFLE vs. AKIN:** The AKIN (Acute Kidney Injury Network) criteria later modified this, defining AKI as a SCr increase of ≥ 0.3 mg/dL within 48 hours or a 1.5-fold increase from baseline. [1] 2. **The "L" and "E" in RIFLE:** * **Loss:** Persistent ARF = complete loss of kidney function > 4 weeks. * **ESRD:** End-stage renal disease > 3 months. 3. **Sensitivity:** The UO criteria are generally more sensitive but less specific than creatinine changes for early detection of AKI. 4. **KDIGO:** Currently, the KDIGO criteria are the most widely used in clinical practice, combining elements of both RIFLE and AKIN.
Question 493: Which of the following findings is NOT associated with Adult Polycystic Kidney Disease?
- A. Autosomal dominant inheritance
- B. Mutations affecting cell-cell-matrix interaction
- C. Intracranial berry aneurysm
- D. Tricuspid valve prolapse (Correct Answer)
Explanation: ### Explanation **Autosomal Dominant Polycystic Kidney Disease (ADPKD)** is the most common inherited kidney disorder. The correct answer is **Option D** because ADPKD is associated with **Mitral Valve Prolapse (MVP)**, not Tricuspid Valve Prolapse. #### Why Option D is the Correct Answer: While ADPKD involves systemic connective tissue abnormalities, the cardiac valvular involvement typically manifests as **Mitral Valve Prolapse (up to 25% of patients)** and aortic root dilatation. Tricuspid valve involvement is not a recognized clinical feature of the disease. #### Analysis of Incorrect Options: * **Option A (Autosomal dominant inheritance):** ADPKD follows an autosomal dominant pattern [1]. It is primarily caused by mutations in the **PKD1** (85%, Chromosome 16) or **PKD2** (15%, Chromosome 4) genes [1]. * **Option B (Cell-cell-matrix interaction):** The protein products of PKD genes, **Polycystin-1 and Polycystin-2**, are located in the primary cilia of tubular epithelial cells. They regulate cell-cell and cell-matrix interactions. Mutations lead to abnormal proliferation and fluid secretion, resulting in cyst formation. * **Option C (Intracranial berry aneurysm):** This is a critical extra-renal manifestation. Approximately 5–10% of ADPKD patients have intracranial aneurysms (usually in the Circle of Willis), which can lead to subarachnoid hemorrhage. #### High-Yield Clinical Pearls for NEET-PG: * **Most common cause of death:** Cardiovascular disease (due to hypertension and LVH). * **Extra-renal cysts:** The **Liver** is the most common extra-renal site for cysts (Polycystic Liver Disease). * **Other associations:** Diverticulosis, abdominal/inguinal hernias, and seminal vesicle cysts. * **Diagnosis:** Ultrasonography is the screening modality of choice (standardized by Ravine’s or Unified Criteria). * **Treatment:** **Tolvaptan** (V2 receptor antagonist) is used to slow the progression of cyst growth and renal decline.
Question 494: What is the treatment of choice in acute hyperkalemia that is life-threatening to cardiac myocytes?
- A. Infusion of calcium gluconate (Correct Answer)
- B. Oral resins
- C. Intravenous infusion of insulin
- D. Beta-blockers
Explanation: ### Explanation In the management of life-threatening hyperkalemia, the immediate priority is **cardiac membrane stabilization**. **1. Why Calcium Gluconate is the Correct Answer:** Hyperkalemia increases the resting membrane potential of cardiac myocytes, bringing it closer to the threshold potential [2]. This leads to myocardial excitability and life-threatening arrhythmias (e.g., ventricular fibrillation). **Intravenous Calcium Gluconate** (or Calcium Chloride) acts within 1–3 minutes to antagonize the effect of potassium on the heart by shifting the threshold potential, thereby stabilizing the membrane [1]. It does **not** lower serum potassium levels; it merely protects the heart while other measures are initiated. **2. Why the Other Options are Incorrect:** * **B. Oral Resins (e.g., Polystyrene sulfonate):** These are cation-exchange resins that remove potassium from the body via the GI tract. They have a slow onset of action (hours to days) and are unsuitable for acute, life-threatening emergencies. * **C. IV Insulin (with Dextrose):** This is a first-line treatment to **lower** serum potassium by shifting it into the intracellular space. However, it takes 20–30 minutes to work. In a cardiac emergency, membrane stabilization (Calcium) must precede the shift (Insulin). * **D. Beta-blockers:** These are contraindicated. Beta-2 **agonists** (like Salbutamol) are used to shift potassium intracellularly. Beta-blockers can actually worsen hyperkalemia by preventing this shift. **3. High-Yield Clinical Pearls for NEET-PG:** * **ECG Changes:** The earliest sign is **Tall Tented T-waves**, followed by PR prolongation, loss of P-waves, and finally the **Sine Wave pattern** (pre-terminal) [2]. * **Calcium Choice:** 10 ml of 10% Calcium Gluconate is preferred over Calcium Chloride because it is less caustic to peripheral veins [1]. * **Digoxin Toxicity:** Use calcium with extreme caution in hyperkalemia caused by digoxin toxicity, as it may precipitate "stone heart." * **Definitive Treatment:** In patients with renal failure, **Hemodialysis** is the most effective way to remove potassium from the body.
Question 495: Uremia occurs when total GFR is reduced by approximately what percentage?
- A. 25%
- B. 50% (Correct Answer)
- C. 60%
- D. 80%
Explanation: **Explanation:** **1. Why 50% is Correct:** Uremia is a clinical syndrome resulting from the accumulation of nitrogenous waste products (like urea and creatinine) that are normally excreted by the kidneys. The kidneys possess a significant "functional reserve." Clinical symptoms of uremia and significant elevations in serum BUN/Creatinine typically do not manifest until the total Glomerular Filtration Rate (GFR) falls below **50% of its normal value**. [1] At this threshold, the remaining nephrons can no longer compensate for the loss of function, leading to the systemic manifestations of renal failure. [1] **2. Analysis of Incorrect Options:** * **A (25%):** A reduction of only 25% (leaving 75% function) is well within the kidney's compensatory capacity. Patients remain asymptomatic, and serum markers often stay within normal limits. * **C (60%) & D (80%):** While uremia is certainly present at these levels of reduction, the question asks for the approximate point at which uremia *begins* to occur. By the time GFR is reduced by 80% (leaving only 20% function), the patient is in Stage 4 Chronic Kidney Disease (CKD) and is often symptomatic with overt complications. [1] **3. NEET-PG High-Yield Pearls:** * **Azotemia vs. Uremia:** Azotemia is the biochemical abnormality (elevated BUN/Cr), while Uremia is the clinical syndrome (symptoms like pericarditis, encephalopathy, and asterixis). [1] * **The "Creatinine Blind" Zone:** Serum creatinine may remain within the "normal" range (e.g., 1.0 mg/dL) even if GFR has dropped by 50%. This is why GFR is a more sensitive indicator of renal function than creatinine alone. * **Stages of CKD:** Remember the KDOQI classification; Stage 3 (GFR 30-59 mL/min) is often where systemic complications become clinically evident. [1]
Question 496: Nephrogenic diabetes insipidus is caused by all of the following except?
- A. Toxicity of lithium
- B. Amyloidosis
- C. Hypocalcemia (Correct Answer)
- D. Hypokalemia
Explanation: Nephrogenic Diabetes Insipidus (NDI) occurs when the renal tubules are resistant to the action of Antidiuretic Hormone (ADH/Vasopressin), leading to an inability to concentrate urine [1]. **Why Hypocalcemia is the correct answer:** The correct answer is **Hypocalcemia** because it is actually **Hypercalcemia** that causes NDI. High serum calcium levels lead to the activation of calcium-sensing receptors in the thick ascending limb, which inhibits the accumulation of intracellular cAMP and interferes with the insertion of Aquaporin-2 channels in the collecting duct. This induces a state of ADH resistance. **Analysis of other options:** * **Lithium Toxicity:** This is the most common drug-induced cause of NDI. Lithium enters the principal cells through ENaC channels and interferes with the ADH-mediated signaling pathway. * **Amyloidosis:** This is an infiltrative disease. Deposition of amyloid proteins in the renal medulla disrupts the medullary osmotic gradient and damages the tubular response to ADH. * **Hypokalemia:** Low potassium levels cause downregulation of Aquaporin-2 channels and can lead to structural changes (vacuolization) in the proximal and distal tubules, resulting in ADH resistance. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Electrolyte Mnemonic:** "High Ca, Low K" (Hypercalcemia and Hypokalemia) cause NDI. * **Drug of Choice:** For Lithium-induced NDI, **Amiloride** is preferred as it blocks the ENaC channels, preventing lithium entry into cells. * **General Treatment:** Thiazide diuretics (paradoxical effect) and NSAIDs (which inhibit prostaglandins that normally antagonize ADH). * **Congenital NDI:** Most commonly X-linked recessive (mutation in V2 receptor) or Autosomal recessive (mutation in Aquaporin-2) [1].
Question 497: Urine analysis of a patient with haematuria and hypercalciuria is most likely to reveal which of the following?
- A. Isomorphic RBCs (Correct Answer)
- B. RBC casts
- C. Nephrotic range proteinuria
- D. Eosinophilluria
Explanation: ### Explanation The presence of **haematuria and hypercalciuria** in a patient typically points toward a **non-glomerular** cause of bleeding [1]. Hypercalciuria can cause irritation or micro-calculi formation in the renal pelvis or collecting system, leading to "urological" or extra-glomerular bleeding [2]. **1. Why Isomorphic RBCs is correct:** In extra-glomerular bleeding (e.g., stones, malignancy, or hypercalciuria-induced irritation), the red blood cells do not pass through the glomerular basement membrane [1]. Consequently, they maintain their normal size and biconcave shape. These are termed **isomorphic RBCs**. In contrast, glomerular bleeding causes RBCs to become "dysmorphic" (e.g., acanthocytes) due to mechanical trauma and osmotic shifts during their passage through the nephron. **2. Why other options are incorrect:** * **RBC Casts:** These are pathognomonic for **glomerular disease** (e.g., Glomerulonephritis). Casts form in the distal convoluted tubule when RBCs are trapped in a Tamm-Horsfall protein matrix. * **Nephrotic range proteinuria:** This indicates severe glomerular basement membrane damage (e.g., Minimal Change Disease, FSGS). Hypercalciuria-related haematuria is typically associated with minimal or no proteinuria [1]. * **Eosinophiluria:** This is a classic marker for **Acute Interstitial Nephritis (AIN)**, often drug-induced (e.g., NSAIDs, Penicillins), not hypercalciuria. **Clinical Pearls for NEET-PG:** * **Acanthocytes (G1 cells):** If >5% of total urinary RBCs are acanthocytes, it is highly specific for glomerular haematuria. * **Hypercalciuria:** Defined as >4 mg/kg/day of calcium excretion. It is the most common metabolic abnormality in children with unexplained isolated haematuria. * **Rule of Thumb:** Glomerular bleeding = Dysmorphic RBCs + RBC Casts + Significant Proteinuria. Extra-glomerular bleeding = Isomorphic RBCs + No Casts + Minimal Proteinuria [1].
Question 498: Microalbuminuria is defined as:
- A. 0.3-0.5 g of 24-hour urine protein
- B. 0.03-0.3 g of 24-hour urine protein
- C. 0.03-0.3 g of 24-hour urine albumin (Correct Answer)
- D. > 2.5 g of 24-hour urine protein
Explanation: **Explanation:** **Microalbuminuria** (now clinically referred to as **Moderately Increased Albuminuria**) is a critical marker for early-stage diabetic nephropathy and cardiovascular risk [1]. It represents a level of albumin excretion that is higher than normal but below the detection limit of a standard urine dipstick [1]. 1. **Why Option C is Correct:** The standard definition of microalbuminuria is an albumin excretion rate of **30–300 mg/day** (24-hour collection). Converting milligrams to grams, this equals **0.03–0.3 g of albumin**. It is essential to distinguish between *total protein* and *albumin*; microalbuminuria specifically measures the latter [3]. 2. **Analysis of Incorrect Options:** * **Option A (0.3–0.5 g protein):** This range exceeds the threshold for microalbuminuria and refers to "Macroalbuminuria" or overt proteinuria [3]. * **Option B (0.03–0.3 g protein):** This is incorrect because it specifies "protein." Total protein includes globulins and Tamm-Horsfall proteins; microalbuminuria is specific to albumin [2]. * **Option D (> 2.5 g protein):** This range approaches the **Nephrotic range proteinuria** (> 3.5 g/day), indicating severe glomerular damage. **High-Yield Clinical Pearls for NEET-PG:** * **Albumin-to-Creatinine Ratio (ACR):** In a spot urine sample, microalbuminuria is defined as an ACR of **30–300 mg/g**. * **Gold Standard:** The 24-hour urine collection remains the gold standard, but ACR is preferred for screening due to convenience. * **Clinical Significance:** It is the earliest clinical sign of diabetic nephropathy [3]. At this stage, the damage is potentially **reversible** with strict glycemic control and ACE inhibitors/ARBs. * **Diagnosis:** To confirm microalbuminuria, 2 out of 3 specimens collected over a 3-to-6-month period should be elevated (as transient elevation can occur due to exercise, fever, or CHF).
Question 499: Nephrocalcinosis is seen in all except:
- A. Sarcoidosis
- B. Distal renal tubular acidosis
- C. Milk alkali syndrome
- D. Medullary cystic kidney disease (Correct Answer)
Explanation: **Explanation:** Nephrocalcinosis refers to the generalized deposition of calcium salts within the renal parenchyma (medulla or cortex) [1]. To solve this question, one must distinguish between conditions that cause hypercalcemia/hypercalciuria and those that cause structural cysts. **Why Medullary Cystic Kidney Disease (MCKD) is the correct answer:** MCKD (now often classified under Autosomal Dominant Tubulointerstitial Kidney Disease) is characterized by the formation of cysts at the corticomedullary junction, tubular atrophy, and interstitial fibrosis [1]. While it involves the medulla, it **does not** typically lead to calcium deposition. In contrast, **Medullary Sponge Kidney** is a classic cause of nephrocalcinosis; students often confuse these two distinct entities [1]. **Analysis of Incorrect Options:** * **Sarcoidosis:** Causes increased production of 1,25-dihydroxyvitamin D by macrophages in granulomas, leading to hypercalcemia and hypercalciuria, which results in calcium deposition. * **Distal Renal Tubular Acidosis (Type 1 RTA):** This is the most common cause of medullary nephrocalcinosis [1]. The alkaline urine, hypocitraturia (citrate normally inhibits stone formation), and systemic acidosis leading to bone resorption create the perfect environment for calcium phosphate deposition. * **Milk Alkali Syndrome:** Excessive intake of calcium and absorbable alkali leads to hypercalcemia and metabolic alkalosis, directly causing metastatic calcification in the kidneys. **NEET-PG High-Yield Pearls:** * **Most common cause of Medullary Nephrocalcinosis:** Distal RTA (Type 1) [1]. * **Cortical Nephrocalcinosis:** Classically seen in Acute Tubular Necrosis (ATN), Chronic Glomerulonephritis, and Alport Syndrome [1]. * **Medullary Sponge Kidney vs. MCKD:** Remember, "Sponge" collects calcium (nephrocalcinosis), while "Cystic" (MCKD) leads to small kidneys and renal failure without calcification [1].
Question 500: Which of the following statements is NOT true about IgA nephropathy?
- A. The pathological changes are proliferative and usually confined to mesangial cells; usually focal and segmental.
- B. Hematuria may be gross or microscopic.
- C. On immunofluorescence, deposits contain IgA and IgG.
- D. Absence of associated proteinuria is pathognomic. (Correct Answer)
Explanation: **Explanation:** IgA Nephropathy (Berger’s Disease) is the most common primary glomerulonephritis worldwide. The correct answer is **D** because the statement is factually incorrect; proteinuria is a common feature of the disease and its presence (especially >1g/day) is a significant poor prognostic marker. There is no "pathognomonic" absence of proteinuria in this condition. [1] **Analysis of Options:** * **Option A:** This is **true**. Light microscopy typically shows mesangial hypercellularity and matrix expansion. These changes are often focal (involving some glomeruli) and segmental (involving parts of the glomerulus). [1] * **Option B:** This is **true**. Patients classically present with "synpharyngitic hematuria" (gross hematuria occurring concurrently with an upper respiratory infection) [1]. However, many patients are diagnosed via incidental microscopic hematuria found during routine screening. * **Option C:** This is **true**. Immunofluorescence (IF) is the gold standard for diagnosis, showing granular deposits of **IgA** (predominantly IgA1) in the mesangium [1]. These deposits are frequently accompanied by **C3 and IgG/IgM**. **NEET-PG High-Yield Pearls:** * **Pathogenesis:** Associated with "galactose-deficient IgA1" and the formation of anti-glycan antibodies. * **Clinical Presentation:** Synpharyngitic hematuria (short latent period of <2-3 days), unlike Post-Streptococcal Glomerulonephritis (PSGN), which has a longer latent period (1-3 weeks) [1]. * **Prognosis:** The **Oxford Classification (MEST-C score)** is used to predict clinical outcomes based on histology. * **Serum Complement:** Unlike PSGN or Lupus Nephritis, serum complement levels (C3, C4) are typically **normal** in IgA Nephropathy.
Practice by Chapter
Acute Kidney Injury
Practice Questions
Chronic Kidney Disease
Practice Questions
Glomerular Diseases
Practice Questions
Tubulointerstitial Diseases
Practice Questions
Nephrotic and Nephritic Syndromes
Practice Questions
Urinary Tract Infections
Practice Questions
Renal Replacement Therapy
Practice Questions
Fluid and Electrolyte Disorders
Practice Questions
Acid-Base Disorders
Practice Questions
Kidney in Systemic Diseases
Practice Questions
Kidney Stones and Obstructive Uropathy
Practice Questions
Hypertension in Kidney Disease
Practice Questions
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