Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 121: A patient presents with hematuria, proteinuria, and hypertension. Which of the following conditions is most likely associated with normal serum complement levels in this clinical scenario?

A. Mixed essential cryoglobulinemia
B. Hepatitis C-associated membranoproliferative glomerulonephritis
C. Diffuse proliferative lupus nephritis
D. Henoch-Schonlein purpura (Correct Answer)

Explanation: ### Explanation The clinical triad of **hematuria, proteinuria, and hypertension** defines **Nephritic Syndrome** [1]. In NEET-PG, a common high-yield classification of glomerulonephritis (GN) is based on **serum complement levels (C3 and C4)**. **1. Why Henoch-Schönlein Purpura (HSP) is correct:** HSP (IgA Vasculitis) and IgA Nephropathy are characterized by the deposition of **IgA-dominant immune complexes** in the glomerular mesangium. Unlike the classical or lectin pathways, the activation of the alternative complement pathway in these conditions is usually mild and does not result in a detectable drop in systemic serum complement levels [1]. Therefore, **C3 and C4 levels remain normal.** [1] **2. Why the other options are incorrect:** * **Mixed Essential Cryoglobulinemia (Option A):** This condition is classically associated with **profoundly low C4** levels due to classical pathway activation by cryoglobulins. * **Hepatitis C-associated MPGN (Option B):** MPGN (Type I) is a "low complement" GN. When associated with Hep C, it often involves cryoglobulins, leading to **low C3 and C4.** * **Diffuse Proliferative Lupus Nephritis (Option C):** SLE (WHO Class IV) involves massive systemic immune complex deposition, leading to the consumption of both **C3 and C4.** --- ### High-Yield Clinical Pearls for NEET-PG To quickly differentiate GN based on complement levels, remember these categories: | **Low Complement (Hypocomplementemia)** | **Normal Complement** | | :--- | :--- | | 1. Post-Streptococcal GN (PSGN) | 1. **IgA Nephropathy / HSP** | | 2. Systemic Lupus Erythematosus (SLE) | 2. ANCA-associated Vasculitis (GPA, MPA) | | 3. Membranoproliferative GN (MPGN) | 3. Anti-GBM Disease (Goodpasture’s) | | 4. Cryoglobulinemia | 4. Polyarteritis Nodosa (PAN) | * **Rule of Thumb:** If the pathology is IgA-mediated or "Pauci-immune" (ANCA+), complements are **Normal**. * **PSGN Note:** In PSGN, C3 is low but usually returns to normal within **6–8 weeks**. If it remains low longer, suspect MPGN [1].

Question 122: Which of the following is false regarding Bartter syndrome?

A. Hypokalemia
B. Renal stones
C. Increased aldosterone
D. Metabolic acidosis (Correct Answer)

Explanation: **Explanation:** **Bartter syndrome** is a group of autosomal recessive disorders characterized by a defect in the thick ascending limb (TAL) of the loop of Henle. It mimics the effect of **Loop diuretics** (like Furosemide) by inhibiting the Na-K-2Cl cotransporter (NKCC2). **Why Metabolic Acidosis is the Correct Answer (False Statement):** Bartter syndrome causes **Metabolic Alkalosis**, not acidosis. The failure of sodium reabsorption in the TAL leads to increased distal delivery of sodium to the collecting duct. To reabsorb this sodium, the body exchanges it for Potassium ($K^+$) and Hydrogen ions ($H^+$) via the action of aldosterone [1]. The excessive loss of $H^+$ ions in the urine results in **hypokalemic metabolic alkalosis** [2]. **Analysis of Other Options:** * **A. Hypokalemia:** Increased distal delivery of sodium leads to excessive potassium secretion in the collecting ducts, causing significant hypokalemia [1]. * **B. Renal stones:** In the TAL, calcium reabsorption is dependent on the lumen-positive potential created by potassium recycling. In Bartter syndrome, this is disrupted, leading to **hypercalciuria**. This increased urinary calcium often leads to nephrocalcinosis or renal stones. * **C. Increased aldosterone:** The loss of salt and water leads to volume depletion, which activates the Renin-Angiotensin-Aldosterone System (RAAS), resulting in **secondary hyperaldosteronism** [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Bartter vs. Gitelman:** Bartter syndrome presents early in life with polyuria, polydipsia, and **hypercalciuria**. Gitelman syndrome (mimicking Thiazides) presents later in life and is characterized by **hypocalciuria** and hypomagnesemia. * **Blood Pressure:** Despite high renin and aldosterone levels, patients with Bartter syndrome are typically **normotensive** or hypotensive due to salt wasting. * **Key Association:** It is associated with juxtaglomerular apparatus hyperplasia.

Question 123: A 30-year-old man presents with generalized edema and hypertension. Urine examination shows sub-nephrotic proteinuria (< 2 gm) and microscopic hematuria. Serum complement levels are decreased and he is positive for anti-hepatitis C antibodies. What is the most likely diagnosis?

A. Post-streptococcal Glomerulonephritis (PSGN)
B. Mixed cryoglobulinemia
C. Membranoproliferative glomerulonephritis (MPGN) (Correct Answer)
D. Focal segmental Glomerulosclerosis (FSGS)

Explanation: ### Explanation The clinical presentation of edema, hypertension, hematuria, and sub-nephrotic proteinuria points toward a **Nephritic-Nephrotic syndrome** pattern [1]. The definitive clues in this case are the **low serum complement levels** and the positive **Hepatitis C (HCV)** status. **Why MPGN is the correct answer:** Membranoproliferative Glomerulonephritis (specifically Type 1) is classically associated with chronic infections, most notably **Hepatitis C**. HCV triggers the formation of immune complexes (often involving mixed cryoglobulins) that deposit in the glomerular basement membrane, activating the classical complement pathway. This leads to **hypocomplementemia** (low C3 and C4). While it can present as pure nephrotic syndrome, it frequently presents with a mixed nephritic-nephrotic picture, as seen here [1]. **Why the other options are incorrect:** * **PSGN:** While it presents with low complement and hematuria, it typically follows a streptococcal throat or skin infection (not HCV) and usually occurs in a younger age group with a more acute onset [1]. * **Mixed Cryoglobulinemia:** This is a systemic vasculitis strongly associated with HCV and often *causes* MPGN. However, when the question asks for the specific renal diagnosis based on glomerular findings, MPGN is the pathological entity. * **FSGS:** This typically presents with massive proteinuria (nephrotic range) and is associated with HIV or heroin use, not HCV [1]. Crucially, complement levels are **normal** in FSGS. **High-Yield Clinical Pearls for NEET-PG:** * **Low Complement Glomerulonephritis (The "P-M-S" Mnemonic):** **P**SGN, **M**PGN, and **S**LE (Lupus Nephritis). * **HCV Associations:** Always look for MPGN or Mixed Cryoglobulinemia in a patient with Hepatitis C. * **Morphology:** On light microscopy, MPGN shows a characteristic **"tram-track" appearance** (double contouring) of the glomerular basement membrane due to mesangial interposition.

Question 124: Which of the following is NOT a feature of the maintenance phase of acute kidney injury?

A. Hyperuricemia
B. Hypermagnesemia
C. Hypernatremia
D. Hypercalcemia (Correct Answer)

Explanation: In the **maintenance phase** of Acute Kidney Injury (AKI), the Glomerular Filtration Rate (GFR) reaches its nadir, leading to the accumulation of metabolic waste and electrolyte imbalances. ### **Why Hypercalcemia is the Correct Answer** **Hypocalcemia**, not hypercalcemia, is the classic feature of the maintenance phase of AKI. This occurs due to two primary mechanisms: 1. **Reduced Vitamin D activation:** The damaged renal parenchyma cannot convert 25-hydroxyvitamin D into its active form (1,21-dihydroxyvitamin D). 2. **Hyperphosphatemia:** Elevated phosphate levels (due to decreased excretion) lead to the precipitation of calcium-phosphate salts in soft tissues, further lowering serum calcium [1]. *Note: Hypercalcemia is only seen during the **recovery (diuretic) phase** if there is mobilization of calcium from tissues or underlying rhabdomyolysis.* ### **Explanation of Incorrect Options** * **Hyperuricemia (A):** Reduced GFR leads to decreased renal clearance of uric acid, causing its accumulation. * **Hypermagnesemia (B):** Magnesium is primarily excreted by the kidneys. In AKI, impaired excretion leads to elevated levels, which can cause neuromuscular depression. * **Hypernatremia (C):** While hyponatremia is more common (due to water retention), hypernatremia can occur if there is a disproportionate loss of free water or excessive administration of sodium-containing fluids [1]. ### **High-Yield Clinical Pearls for NEET-PG** * **Most common electrolyte abnormality in AKI:** Hyperkalemia (due to decreased distal delivery of sodium and reduced K+ secretion). * **Metabolic state:** High anion gap metabolic acidosis (due to retention of organic acids like phosphates and sulfates). * **Recovery Phase:** Watch for **hypokalemia** and **hypomagnesemia** due to osmotic diuresis as the tubular function lags behind GFR recovery.

Question 125: Which of the following statements is WRONG regarding adult polycystic kidney disease?

A. Kidneys are enlarged in size
B. The presentation is bilateral (Correct Answer)
C. Patients tend to have extra-renal congenital anomalies
D. Mitral valve prolapse may be present

Explanation: **Explanation:** Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common hereditary kidney disease [1]. The question asks for the **WRONG** statement regarding this condition. **Why Option B is the Correct Answer (The Wrong Statement):** While ADPKD is a systemic, genetic disorder that affects both kidneys, the clinical presentation is often **asymmetrical**. One kidney may enlarge significantly faster or develop more symptomatic cysts (hemorrhage, infection) than the other [1]. However, the question's logic in a competitive exam context often hinges on the fact that while the *pathology* is bilateral, the *initial clinical or radiological presentation* can occasionally appear unilateral in early stages, or more importantly, it is a **systemic genetic condition** where "bilateral" is a defining feature, not a complication. *Note: In many standard texts, ADPKD is strictly bilateral; if this option is marked "wrong," it implies that the disease is inherently bilateral and thus the statement "The presentation is bilateral" is actually a CORRECT fact, making the question's premise or the provided key slightly controversial. However, in the context of NEET-PG, if B is the intended "wrong" statement, it suggests the examiner is focusing on the potential for asymmetrical clinical findings.* **Analysis of Other Options:** * **Option A (Correct Fact):** Kidneys are progressively enlarged due to the relentless growth of fluid-filled cysts, often reaching massive sizes palpable on abdominal exam [1]. * **Option C (Correct Fact):** ADPKD is a systemic ciliopathy. Extra-renal manifestations include **Polycystic Liver Disease** (most common), pancreatic cysts, and seminal vesicle cysts. * **Option D (Correct Fact):** Cardiovascular involvement is common. **Mitral Valve Prolapse (MVP)** occurs in up to 25% of patients. Other associations include Berry aneurysms (Circle of Willis) and diverticulosis. **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Mutation in **PKD1** (Chromosome 16 - 85% cases, more severe) or **PKD2** (Chromosome 4) [1]. * **Most common extra-renal site:** Liver (Cysts). * **Most common cause of death:** Cardiovascular disease (not renal failure). * **Screening:** Ultrasound is the gold standard for family screening. * **Associated Risk:** Subarachnoid hemorrhage due to rupture of **Berry Aneurysms**.

Question 126: Hemodialysis can be performed for long periods from the same site due to which of the following?

A. Arteriovenous fistula reduces bacterial contamination of site
B. Arteriovenous fistula results in aerialization of vein (Correct Answer)
C. Arteriovenous fistula reduces chances of graft failure
D. Arteriovenous fistula facilitates small bore needles for high flow rates

Explanation: **Explanation:** The correct answer is **B. Arteriovenous fistula results in arterialization of vein.** **Understanding the Concept:** Hemodialysis requires high blood flow rates (typically 300–400 mL/min) that normal peripheral veins cannot provide. An **Arteriovenous (AV) Fistula** is created by surgically connecting an artery directly to a vein (e.g., Cimino-Brescia fistula) [1]. The high-pressure arterial blood flowing into the vein causes **"arterialization"** (also known as maturation). This process involves: 1. **Vascular Remodeling:** The vein wall thickens (hypertrophy) and the lumen dilates. 2. **Durability:** This thickened wall can withstand repeated punctures with large-bore needles over several years without collapsing or scarring excessively. 3. **High Flow:** It provides the necessary volume for efficient solute clearance [1]. **Analysis of Incorrect Options:** * **Option A:** AV fistulas do not inherently reduce bacteria; in fact, any skin puncture carries a risk. However, they have lower infection rates compared to catheters. * **Option B:** In haemodialysis, there is diffusion of solutes from blood to dialysate across a semi-permeable membrane down a concentration gradient [2]. * **Option C:** This is a circular argument. A fistula is a type of access; "graft failure" refers specifically to synthetic AV grafts, which actually have *higher* failure rates than native fistulas. * **Option D:** High flow rates require **large-bore needles** (typically 15-17 gauge), not small-bore needles, to prevent hemolysis and provide adequate clearance. **High-Yield Clinical Pearls for NEET-PG:** * **Standard Site:** The Radiocephalic fistula (Cimino-Brescia) at the wrist is the gold standard. * **Maturation Time:** A native AV fistula typically requires **6–8 weeks** to mature before it can be used. * **Physical Exam:** A functioning fistula must have a palpable **thrill** and an audible **bruit**. Loss of these signs indicates thrombosis. * **Complication:** "Steal Syndrome" can occur if too much blood is diverted from the distal extremity, leading to ischemia.

Question 127: A 30-year-old man presents with hematuria. Examination reveals an elevated blood pressure of 164/94 mm Hg. An ultrasound of the kidneys shows multiple renal cysts in both kidneys. His father had a similar condition. Which of the following is NOT associated with this syndrome?

A. Liver cysts
B. Intracranial aneurysms
C. Autosomal dominant inheritance
D. Rheumatoid arthritis (RA) (Correct Answer)

Explanation: The clinical presentation of a young male with hypertension, hematuria, bilateral multiple renal cysts, and a positive family history (father) is diagnostic of **Autosomal Dominant Polycystic Kidney Disease (ADPKD)** [1]. **Why Option D is the Correct Answer:** **Rheumatoid Arthritis (RA)** is an autoimmune inflammatory joint disease and has **no known association** with ADPKD. ADPKD is a systemic genetic disorder involving connective tissue and epithelial cell abnormalities, but it does not predispose patients to RA. **Analysis of Incorrect Options:** * **Option A (Liver cysts):** Polycystic liver disease is the **most common extra-renal manifestation** of ADPKD. While usually asymptomatic, they increase in frequency with age [1]. * **Option B (Intracranial aneurysms):** Approximately 5-10% of ADPKD patients develop "Berry aneurysms" in the Circle of Willis. Rupture leads to subarachnoid hemorrhage, a major cause of mortality. * **Option C (Autosomal dominant inheritance):** ADPKD follows an autosomal dominant pattern, typically caused by mutations in the **PKD1** (Chromosome 16 - 85% cases) or **PKD2** (Chromosome 4 - 15% cases) genes [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of death:** Cardiovascular disease (due to hypertension and LVH). * **Other Extra-renal manifestations:** Pancreatic cysts, Mitral Valve Prolapse (MVP), diverticulosis, and seminal vesicle cysts. * **Diagnosis:** Ultrasound is the primary screening tool. Criteria are based on the number of cysts relative to age (e.g., ≥3 cysts bilaterally in ages 15–39). * **Treatment:** Tolvaptan (V2-receptor antagonist) is used to slow disease progression in rapidly progressing cases.

Question 128: Which of the following leads to hyponatremia and low osmolality?

A. Hyperlipidemia
B. Hyperproteinemia
C. IVIG therapy
D. CHF (Correct Answer)

Explanation: **Explanation:** The correct answer is **CHF (Congestive Heart Failure)**. **1. Why CHF is correct:** Hyponatremia is classified based on serum osmolality. CHF causes **hypoosmolar hypervolemic hyponatremia** [1]. In CHF, decreased effective arterial blood volume (EABV) triggers the baroreceptors, leading to a non-osmotic release of **Antidiuretic Hormone (ADH)**. ADH acts on the V2 receptors in the collecting ducts, causing water retention that exceeds sodium retention [1]. This results in a "dilutional" hyponatremia where both serum sodium and serum osmolality are low. **2. Why the other options are incorrect:** * **Hyperlipidemia (A) and Hyperproteinemia (B):** These cause **Pseudohyponatremia**. In these conditions, the lipid or protein fraction of the plasma is increased, leading to a falsely low sodium measurement when using older flame photometry. Crucially, the **serum osmolality remains normal** (Isotonic hyponatremia). * **IVIG therapy (C):** High-dose IVIG can lead to **Translocational Hyponatremia**. The infusion of sucrose (often used as a stabilizer in IVIG) increases plasma osmolality, drawing water from the intracellular to the extracellular space. This results in hyponatremia with **high serum osmolality** (Hypertonic hyponatremia). **3. High-Yield NEET-PG Pearls:** * **True Hyponatremia** is always associated with **low serum osmolality** (<280 mOsm/kg). * **Hypertonic Hyponatremia:** Think Hyperglycemia or Mannitol [2]. * **Isotonic Hyponatremia (Pseudohyponatremia):** Think Hypertriglyceridemia or Paraproteinemia (Multiple Myeloma). * **Urine Sodium in CHF:** Typically **<20 mEq/L** (due to RAAS activation), helping differentiate it from renal causes of volume overload [1].

Question 129: All of the following are true about Rhabdomyolysis, except:

A. Hyperuricemia
B. Hyperphosphatemia
C. Hypercalcemia (Correct Answer)
D. Elevated Creatine kinase

Explanation: Explanation: Rhabdomyolysis involves the rapid breakdown of skeletal muscle, leading to the release of intracellular contents into the systemic circulation. **Why Hypercalcemia is the Correct Answer (The Exception):** In the **acute phase** of rhabdomyolysis, **hypocalcemia** (low calcium) is typically observed rather than hypercalcemia. This occurs because calcium deposits into the damaged muscle tissues (dystrophic calcification) and binds with the excess phosphate released from cells. While hypercalcemia can occur later during the recovery phase (due to the mobilization of these deposits), it is not a characteristic feature of the initial presentation. **Analysis of Other Options:** * **Hyperuricemia (A):** Muscle breakdown releases purines, which are metabolized by the liver into uric acid. This can lead to secondary gout or contribute to acute kidney injury (AKI). * **Hyperphosphatemia (B):** Phosphorus is a major intracellular anion. Massive cell lysis releases large amounts of phosphate into the blood. * **Elevated Creatine Kinase (D):** CK is the most sensitive marker for muscle damage. Levels typically exceed five times the upper limit of normal (often >10,000 U/L) and are diagnostic of the condition. **NEET-PG High-Yield Pearls:** * **Classic Triad:** Muscle pain, weakness, and dark (tea-colored) urine. * **Urinalysis Paradox:** The dipstick is positive for "blood" (due to myoglobinuria), but microscopy shows **no RBCs**. * **Most Common Electrolyte Abnormality:** Hyperkalemia (the most life-threatening complication). * **Treatment:** Aggressive fluid resuscitation (Normal Saline) to maintain urine output and prevent Myoglobin-induced AKI.

Question 130: A 12-year-old boy presented with severe vomiting and diarrhea. He was brought to the hospital due to severe oliguria. He was given IV fluids and furosemide without any diuresis. Blood biochemistry revealed: Urea 120 mg% and serum creatinine 4 mg%. What is the most likely diagnosis?

A. Prerenal azotemia
B. Hemolytic uremic syndrome (Correct Answer)
C. Acute glomerulonephritis
D. Acute tubular necrosis

Explanation: ### Explanation The correct diagnosis is **Hemolytic Uremic Syndrome (HUS)**. **Why it is correct:** The clinical triad of HUS consists of **Microangiopathic Hemolytic Anemia (MAHA), Thrombocytopenia, and Acute Kidney Injury (AKI)** [1], [2]. In children, the most common form is "D+ HUS" (Diarrhea-associated), typically caused by Shiga toxin-producing *E. coli* (O157:H7) [1]. The patient’s history of severe diarrhea followed by oliguria and significantly elevated nitrogenous waste (Urea 120, Creatinine 4) is a classic presentation [2]. The **failure to respond to IV fluids and furosemide** indicates established intrinsic renal damage (thrombotic microangiopathy), which is characteristic of HUS rather than simple dehydration [1]. **Why incorrect options are wrong:** * **Prerenal Azotemia:** While diarrhea causes dehydration, prerenal AKI should respond to aggressive fluid resuscitation with an increase in urine output. The lack of diuresis here points toward intrinsic damage. * **Acute Tubular Necrosis (ATN):** While ATN can follow severe dehydration, the specific prodrome of diarrhea in a pediatric patient strongly favors HUS. In exams, "diarrhea + renal failure" in a child is HUS until proven otherwise. * **Acute Glomerulonephritis (AGN):** AGN typically presents with hematuria (cola-colored urine), hypertension, and edema, usually following a respiratory or skin infection (e.g., PSGN), not a diarrheal illness. **Clinical Pearls for NEET-PG:** * **Most common cause of AKI in children:** HUS. * **Pathogenesis:** Shiga toxin causes endothelial injury, leading to platelet microthrombi in the glomerular capillaries [1]. * **Peripheral Smear:** Look for **Schistocytes** (fragmented RBCs) [1]. * **Management:** Primarily supportive (dialysis if needed). Antibiotics and anti-motility agents are generally avoided as they may worsen toxin release.

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

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Nephrology — MCQs

Nephrology — MCQs

On this page

Practice by Chapter

Want unlimited practice?