Nephrology — MCQs
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What is the most common cause of nephrotic range proteinuria in an adult?
Which of the following is not associated with hyponatremia and normal osmolality?
What is the recommended treatment for early diabetic nephropathy manifested by microalbuminuria?
A 35-year-old man with AML and WBC of 100,000 cells/µl is treated with chemotherapy and develops oliguric renal failure. His urine is acidic and numerous crystals are noted in the urine. What is the most likely diagnosis?
Diuresis is seen in which phase of acute kidney injury?
Which chromosomes are involved in adult polycystic kidney disease (APKD)?
IgA nephropathy is characterized by all of the following except?
The Rifle Classification is used for staging which of the following conditions?
Which of the following has no role in the management of acute onset hyperkalemia?
Which of the following is NOT a component of dialysate in hemodialysis?
Nephrology Indian Medical PG Practice Questions and MCQs
Question 251: What is the most common cause of nephrotic range proteinuria in an adult?
- A. Diabetes Mellitus (Correct Answer)
- B. Amyloidosis
- C. Hypertensive nephropathy
- D. Wegener's Granulomatosis
Explanation: **Explanation:** **Diabetes Mellitus (DM)** is the most common cause of nephrotic-range proteinuria (>3.5 g/24h) in adults worldwide [1]. Diabetic Nephropathy (DN) begins with glomerular hyperfiltration, progressing to microalbuminuria and eventually overt proteinuria [1]. The underlying mechanism involves non-enzymatic glycosylation of the glomerular basement membrane (GBM) and efferent arteriolar vasoconstriction, leading to increased glomerular pressure and podocyte injury. **Analysis of Options:** * **Amyloidosis (Option B):** While amyloidosis is a classic cause of massive proteinuria and nephrotic syndrome, it is significantly less common in the general population compared to the high prevalence of Diabetes [2]. * **Hypertensive Nephropathy (Option C):** Hypertension typically causes "benign nephrosclerosis," which usually presents with sub-nephrotic range proteinuria (<1.5 g/day) and chronic renal failure. It rarely causes nephrotic-range proteinuria unless associated with malignant hypertension. * **Wegener’s Granulomatosis (Option D):** Now known as Granulomatosis with Polyangiitis (GPA), this typically presents as a **Nephritic Syndrome** (hematuria, RBC casts, and rapidly progressive renal failure) rather than isolated nephrotic-range proteinuria [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of Nephrotic Syndrome in adults:** Focal Segmental Glomerulosclerosis (FSGS) is the most common *primary* (idiopathic) cause [3], but **Diabetes** is the most common *secondary* (overall) cause. * **Pathognomonic finding in DN:** Kimmelstiel-Wilson (KW) nodules (nodular glomerulosclerosis). * **First clinical sign of DN:** Microalbuminuria (30–300 mg/day) [1]. * **Management:** ACE inhibitors or ARBs are the drugs of choice as they reduce intraglomerular pressure by dilating the efferent arteriole.
Question 252: Which of the following is not associated with hyponatremia and normal osmolality?
- A. Hyperlipidemia
- B. Hyperproteinemia
- C. Irrigation of bladder after TURP
- D. Congestive heart failure (CHF) (Correct Answer)
Explanation: ### Explanation The question asks to identify the condition **not** associated with hyponatremia and **normal osmolality** (Isotonic Hyponatremia). **1. Why Congestive Heart Failure (CHF) is the correct answer:** CHF is associated with **Hypotonic Hyponatremia** (low serum osmolality). In CHF, decreased effective arterial blood volume triggers the non-osmotic release of Antidiuretic Hormone (ADH). This leads to water retention and a dilutional drop in sodium. Because there is an excess of total body water relative to sodium, the serum osmolality is always **low** (<280 mOsm/kg). **2. Analysis of Incorrect Options (Isotonic Hyponatremia):** * **Hyperlipidemia & Hyperproteinemia (Pseudohyponatremia):** These conditions cause a "lab artifact." Sodium is restricted to the aqueous phase of plasma. When lipids or proteins occupy an abnormally large volume of the total plasma sample, the measured sodium concentration per unit of total volume appears low, even though the sodium concentration in the water phase and the overall **osmolality remain normal**. * **Irrigation after TURP:** During Transurethral Resection of the Prostate (TURP), non-conductive irrigation fluids (like glycine or mannitol) can be absorbed into the systemic circulation. These solutes are osmotically active and maintain a **normal serum osmolality** while diluting the serum sodium concentration [1]. **3. NEET-PG High-Yield Pearls:** * **Pseudohyponatremia** is becoming less common due to the use of direct ion-selective electrodes (ISE), which measure sodium only in the water phase. * **Hypertonic Hyponatremia** (High Osmolality) is most commonly caused by **Hyperglycemia**. For every 100 mg/dL rise in glucose above normal, the serum sodium drops by approximately 1.6 mEq/L. * Always check **Serum Osmolality** first when evaluating hyponatremia to differentiate between true (hypotonic) and factitious (isotonic/hypertonic) states. Note: Mannitol, mentioned in some contexts as an osmotic diuretic, is relevant to clinical states involving irrigation and fluid management during surgical procedures [1].
Question 253: What is the recommended treatment for early diabetic nephropathy manifested by microalbuminuria?
- A. Strict glycemic control
- B. Low protein diet
- C. Strict glycemic control and low protein diet (Correct Answer)
- D. Strict glycemic control, low protein diet, and ACE inhibitors
Explanation: **Explanation:** The management of early diabetic nephropathy (Stage III), characterized by microalbuminuria (30–300 mg/day), focuses on halting the progression to overt proteinuria and end-stage renal disease (ESRD). **Why Option C is Correct:** According to standard management guidelines for early diabetic nephropathy, the primary interventions are **strict glycemic control** and **dietary protein restriction** [4]. 1. **Strict Glycemic Control:** Maintaining an HbA1c < 7% reduces the hyperfiltration injury and slows the progression of albuminuria [3]. 2. **Low Protein Diet:** A protein intake of approximately **0.8 g/kg/day** is recommended. High protein intake increases intraglomerular pressure via afferent arteriole vasodilation; restricting it reduces this pressure, thereby decreasing microalbuminuria. **Analysis of Incorrect Options:** * **Option A & B:** These are incomplete. Both glycemic control and dietary modification are required synergistically to manage early nephropathy effectively. * **Option D:** While ACE inhibitors (or ARBs) are the drugs of choice for diabetic nephropathy, they are primarily indicated when the patient is **hypertensive** or has **persistent macroalbuminuria** [1]. In the specific context of "early" management where the focus is on metabolic and dietary stabilization, Option C represents the foundational conservative management. (Note: In many clinical scenarios, ACE inhibitors are started early, but for exam purposes, the combination of glycemic and dietary control is the established first-line physiological approach). **High-Yield NEET-PG Pearls:** * **Earliest sign of Diabetic Nephropathy:** Hyperfiltration (Increased GFR). * **First clinical sign:** Microalbuminuria (best detected by Urinary Albumin-Creatinine Ratio) [2]. * **Pathognomonic finding:** Kimmelstiel-Wilson (KW) nodules (nodular glomerulosclerosis) [2]. * **Target BP in Diabetic Nephropathy:** < 130/80 mmHg [3]. * **Drug of choice for HTN in Diabetics:** ACE inhibitors (e.g., Enalapril) as they dilate the efferent arteriole, reducing intraglomerular pressure [1].
Question 254: A 35-year-old man with AML and WBC of 100,000 cells/µl is treated with chemotherapy and develops oliguric renal failure. His urine is acidic and numerous crystals are noted in the urine. What is the most likely diagnosis?
- A. Urate nephropathy (Correct Answer)
- B. Nephrocalcinosis
- C. Leukemic infiltration of the kidneys
- D. Acute tubular necrosis secondary to a nephrotoxic effect of his chemotherapy
Explanation: The clinical scenario describes **Acute Urate Nephropathy**, a classic manifestation of **Tumor Lysis Syndrome (TLS)**. In patients with high-grade hematologic malignancies (like AML) and a high tumor burden (WBC >100,000/µl), rapid cell lysis following chemotherapy releases massive amounts of intracellular purines. These are metabolized into **uric acid**. [2] 1. **Why Urate Nephropathy is correct:** Uric acid is poorly soluble in the acidic environment of the distal tubules and collecting ducts. This leads to the precipitation of uric acid crystals, causing intrarenal obstruction and oliguric acute kidney injury (AKI). [1] The presence of **acidic urine** and **numerous crystals** is pathognomonic. [2] 2. **Why other options are incorrect:** * **Nephrocalcinosis:** This involves calcium phosphate deposition in the renal parenchyma, usually seen in chronic hypercalcemic states or distal RTA, not typically presenting as acute oliguric failure post-chemotherapy. * **Leukemic infiltration:** While it can cause renal enlargement, it rarely causes sudden, acute oliguric renal failure immediately following the initiation of chemotherapy. * **Acute Tubular Necrosis (ATN):** While some chemo agents are nephrotoxic, the specific mention of high WBC count, acidic urine, and crystals points specifically to urate crystal-induced obstruction rather than direct tubular cell death. **High-Yield Clinical Pearls for NEET-PG:** * **Uric Acid/Creatinine Ratio:** In acute urate nephropathy, the ratio is typically **>1.0**, whereas in other causes of AKI, it is <1.0. * **Prevention:** Aggressive hydration and **Allopurinol** (xanthine oxidase inhibitor). * **Treatment of Choice:** **Rasburicase** (recombinant urate oxidase) which converts uric acid to highly soluble allantoin. * **Urine pH:** Alkalinization of urine (pH >7.0) increases uric acid solubility but is now controversial as it may promote calcium phosphate precipitation.
Question 255: Diuresis is seen in which phase of acute kidney injury?
- A. Initiation
- B. Maintenance phase
- C. Recovery phase (Correct Answer)
- D. Oliguric phase
Explanation: Acute Kidney Injury (AKI) typically progresses through four distinct clinical phases. Understanding the physiological changes in each phase is crucial for NEET-PG. [1] ### **Explanation of the Correct Answer** **C. Recovery Phase:** This phase begins when the underlying cause of AKI is corrected and the tubular epithelium starts to regenerate. It is characterized by a **progressive increase in urine volume**, often leading to **polyuria (diuresis)**. Diuresis occurs because: 1. The glomerular filtration rate (GFR) begins to normalize. 2. The newly regenerated tubular cells are still immature and lack the full capacity to reabsorb water and electrolytes (impaired concentrating ability). 3. There is an osmotic effect from the accumulated urea and waste products being filtered. ### **Analysis of Incorrect Options** * **A. Initiation Phase:** This is the period from the onset of the renal insult (e.g., toxins, ischemia) to the development of actual kidney injury. [1] Urine output starts to decline, but diuresis is not present. * **B. Maintenance Phase:** Also known as the established phase, GFR stabilizes at its nadir (usually <10 mL/min). Complications like uremia, hyperkalemia, and metabolic acidosis are most severe here. [2] * **D. Oliguric Phase:** This is a subset of the maintenance phase where urine output is **<400 mL/day**. [3] It is the opposite of diuresis. ### **Clinical Pearls for NEET-PG** * **The "Diuretic Phase" Danger:** During recovery, patients can lose massive amounts of fluid and electrolytes. The most common electrolyte imbalances to watch for are **hypokalemia** and **hyponatremia**. [2] * **Prognostic Marker:** The first sign of recovery is often an increase in urine output, followed by a gradual fall in serum creatinine. * **Non-oliguric AKI:** Some patients never enter an oliguric phase (common in aminoglycoside toxicity); they maintain normal urine volume despite a rising creatinine. [3] * **Most common cause of death in AKI:** Infections/Sepsis, followed by cardiovascular complications (hyperkalemia/fluid overload).
Question 256: Which chromosomes are involved in adult polycystic kidney disease (APKD)?
- A. 4 and 11
- B. 4 and 16 (Correct Answer)
- C. 4 and 12
- D. 4 and 17
Explanation: **Explanation:** Autosomal Dominant Polycystic Kidney Disease (ADPKD), often referred to as adult polycystic kidney disease, is a multisystemic genetic disorder characterized by the progressive formation of fluid-filled cysts in the renal parenchyma [1]. **Why Option B is correct:** ADPKD is primarily caused by mutations in two specific genes: 1. **PKD1 Gene:** Located on **Chromosome 16p13.3**. It encodes the protein **Polycystin-1**. This mutation accounts for approximately **85%** of cases and is associated with a more severe phenotype and earlier progression to End-Stage Renal Disease (ESRD) (mean age ~54 years) [1]. 2. **PKD2 Gene:** Located on **Chromosome 4q21**. It encodes **Polycystin-2**. This mutation accounts for roughly **15%** of cases and generally presents with a milder clinical course and later onset of ESRD (mean age ~74 years) [1]. **Why other options are incorrect:** * **Options A, C, and D:** While Chromosome 4 is correctly associated with the PKD2 gene, chromosomes 11, 12, and 17 do not harbor the primary genes responsible for ADPKD. (Note: Chromosome 6 is associated with Autosomal Recessive PKD/ARPKD via the PKHD1 gene). **High-Yield Clinical Pearls for NEET-PG:** * **Extra-renal manifestations:** The most common is **Liver cysts**. The most life-threatening is **Berry Aneurysms** (Circle of Willis), which can lead to Subarachnoid Hemorrhage (SAH). Other features include Mitral Valve Prolapse (MVP) and diverticulosis. * **Diagnosis:** Ultrasonography is the first-line screening tool (Ravine’s criteria). * **Management:** Tolvaptan (Vasopressin V2 receptor antagonist) is used to slow cyst growth and disease progression.
Question 257: IgA nephropathy is characterized by all of the following except?
- A. Hypertension
- B. Hematuria
- C. Nephritic syndrome
- D. Renal biopsy showing a thin basement membrane (Correct Answer)
Explanation: **Explanation:** **IgA Nephropathy (Berger’s Disease)** is the most common primary glomerulonephritis worldwide [1]. It is characterized by the deposition of IgA-dominant immune complexes in the glomerular mesangium [1]. **Why Option D is the correct answer:** A **Thin Basement Membrane (TBM)** is the hallmark of **Thin Basement Membrane Nephropathy (Benign Familial Hematuria)**, not IgA nephropathy. In IgA nephropathy, the classic finding on Light Microscopy is **mesangial hypercellularity and matrix expansion**. Immunofluorescence (the gold standard for diagnosis) shows **granular IgA and C3 deposits** in the mesangium [1]. Electron microscopy shows electron-dense deposits in the mesangial area, rather than thinning of the basement membrane. **Why other options are incorrect:** * **A & C (Hypertension & Nephritic Syndrome):** IgA nephropathy typically presents as a nephritic syndrome, which includes the triad of hypertension, hematuria, and mild-to-moderate proteinuria [1]. While many patients have an indolent course, hypertension is a significant prognostic factor for progression to chronic kidney disease [1]. * **B (Hematuria):** This is the most common clinical presentation. It often manifests as **synpharyngitic hematuria**—gross hematuria occurring concurrently with or within 1–2 days of an upper respiratory tract infection [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Association:** Often associated with Henoch-Schönlein Purpura (HSP), which is considered the systemic form of IgA deposition. * **Diagnosis:** Definitive diagnosis requires renal biopsy showing mesangial IgA deposits [1]. * **Prognosis:** The most reliable predictor of poor prognosis is the degree of proteinuria and the presence of hypertension at presentation [1]. * **Oxford Classification (MEST-C score):** Used to grade the severity of IgA nephropathy on biopsy.
Question 258: The Rifle Classification is used for staging which of the following conditions?
- A. Acute kidney injury (Correct Answer)
- B. Chronic kidney disease
- C. Diabetic nephropathy
- D. Amyloidosis
Explanation: The **RIFLE criteria** (Risk, Injury, Failure, Loss, and End-stage renal disease) were developed by the Acute Dialysis Quality Initiative (ADQI) group to provide a standardized definition and classification for **Acute Kidney Injury (AKI)**. [1] The classification is based on two primary parameters: **Serum Creatinine (SCr) / Glomerular Filtration Rate (GFR)** and **Urine Output (UO)**. The first three stages (Risk, Injury, Failure) represent increasing severity of acute dysfunction, while the last two (Loss, End-stage) represent clinical outcomes. **Why other options are incorrect:** * **Chronic Kidney Disease (CKD):** Staged based on the **KDIGO classification**, which utilizes GFR categories (G1–G5) and Albuminuria categories (A1–A3). * **Diabetic Nephropathy:** Traditionally staged using the **Mogensen Classification** (Stages I–V), ranging from hyperfiltration to end-stage renal failure. * **Amyloidosis:** Staged using the **Mayo Staging System**, which relies on cardiac biomarkers (NT-proBNP and Troponin) rather than renal parameters, as prognosis is often driven by cardiac involvement. **High-Yield Clinical Pearls for NEET-PG:** * **AKIN Criteria:** A modified version of RIFLE that uses smaller increments in creatinine (≥0.3 mg/dL) to define Stage 1 AKI. * **KDIGO Criteria:** The current global standard, which merges RIFLE and AKIN. * **Loss (L):** Defined as complete loss of kidney function for >4 weeks. * **End-stage (E):** Defined as loss of kidney function for >3 months. * **Earliest Marker:** Urine output is often the earliest indicator of AKI, whereas Serum Creatinine is a lagging marker.
Question 259: Which of the following has no role in the management of acute onset hyperkalemia?
- A. Intravenous bicarbonate (Correct Answer)
- B. Nebulization with salbutamol
- C. Calcium chloride
- D. Intravenous regular insulin
Explanation: Explanation: The management of acute hyperkalemia focuses on three goals: stabilizing the cardiac membrane, shifting potassium into cells, and eliminating potassium from the body [1]. **1. Why Intravenous Bicarbonate is the Correct Answer:** Current clinical guidelines (including KDIGO and AHA) state that **intravenous sodium bicarbonate** has no role in the *acute* management of hyperkalemia, especially when not associated with metabolic acidosis. While it was historically used to shift potassium into cells, evidence shows it is ineffective as a bolus and works too slowly to be useful in an emergency. It may only be considered in cases of severe pre-existing metabolic acidosis (pH < 7.1). **2. Analysis of Other Options:** * **Calcium chloride (Option C):** This is the **first-line** treatment for hyperkalemia with ECG changes [1]. It antagonizes the membrane-excitability effects of potassium, stabilizing the cardiac myocyte membrane to prevent arrhythmias [1]. It does *not* lower serum potassium levels. * **Intravenous regular insulin (Option D):** Usually given with 25-50g of Dextrose, insulin stimulates the Na+/K+-ATPase pump, shifting potassium into the intracellular compartment. It is the most reliable agent for rapid potassium reduction. * **Nebulization with salbutamol (Option B):** Beta-2 agonists also stimulate the Na+/K+-ATPase pump to shift potassium intracellularly. It acts synergistically with insulin. **High-Yield Clinical Pearls for NEET-PG:** * **Fastest onset of action:** Calcium gluconate/chloride (1-3 mins) – but it is **cardioprotective only.** [1] * **Most effective for shifting K+:** Insulin + Dextrose. * **Calcium Gluconate vs. Chloride:** Calcium chloride contains 3x more elemental calcium than gluconate but is more irritating to peripheral veins. * **Definitive treatment:** Hemodialysis is the most effective method for potassium removal if medical therapy fails or in renal failure.
Question 260: Which of the following is NOT a component of dialysate in hemodialysis?
- A. Sodium
- B. Potassium
- C. Aluminium (Correct Answer)
- D. Glucose
Explanation: **Explanation:** The goal of hemodialysis is to mimic the filtration function of the kidney by removing metabolic waste products and excess electrolytes while maintaining physiological balance [1]. **Why Aluminium is the correct answer:** Aluminium is **not** a component of dialysate; in fact, its presence is strictly avoided. Historically, aluminium toxicity was a major complication in dialysis patients (leading to **Dialysis Encephalopathy**, osteomalacia, and microcytic anemia) due to its presence in untreated tap water used for dialysate or the use of aluminium-containing phosphate binders [2]. Modern dialysis requires highly purified water (via Reverse Osmosis) to ensure aluminium levels are negligible. **Why the other options are incorrect:** * **Sodium (A):** Dialysate sodium is typically kept at 135–145 mEq/L. It is essential to maintain serum osmolality and prevent "Dialysis Disequilibrium Syndrome." * **Potassium (B):** Potassium is a vital component, usually kept at 0–4 mEq/L. The concentration is adjusted based on the patient's pre-dialysis serum potassium levels to facilitate the removal of excess potassium via a concentration gradient [1]. * **Glucose (D):** Glucose is added to the dialysate (typically 100–200 mg/dL) to prevent hypoglycemia during the procedure and to provide a small osmotic gradient to assist in fluid removal. **High-Yield Clinical Pearls for NEET-PG:** * **Dialysis Encephalopathy:** Characterized by speech disturbances, seizures, and progressive dementia due to aluminium toxicity. * **Water Purification:** Reverse Osmosis (RO) is the gold standard for preparing water for dialysate to remove contaminants like aluminium, copper, and chloramines. * **Bicarbonate:** Modern dialysate uses bicarbonate as a buffering agent instead of acetate to correct metabolic acidosis.
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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