Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 171: What is the most common cause of hydronephrosis in children?

A. Pelviureteric junction (PUJ) obstruction (Correct Answer)
B. Ureterocele
C. Posterior urethral valve
D. Ectopic ureter

Explanation: **Explanation:** **Pelviureteric Junction (PUJ) Obstruction** is the most common cause of congenital hydronephrosis in children. It occurs due to an anatomical or functional narrowing at the junction where the renal pelvis meets the ureter, leading to impaired urine flow and subsequent dilatation of the renal pelvis and calyces. **Analysis of Options:** * **A. PUJ Obstruction (Correct):** It is the leading cause of both neonatal and pediatric hydronephrosis. It is most commonly unilateral and often detected on antenatal ultrasound. * **B. Ureterocele:** This is a cystic dilation of the distal ureter. While it can cause hydroureteronephrosis, it is much less common than PUJ obstruction. * **C. Posterior Urethral Valve (PUV):** This is the most common cause of **bilateral** hydronephrosis in **male** infants. While clinically significant and a common cause of bladder outlet obstruction, its overall incidence is lower than PUJ obstruction. * **D. Ectopic Ureters:** These occur when the ureter terminates outside the bladder trigone. While they can cause obstruction or reflux, they are a relatively rare cause of hydronephrosis. **Clinical Pearls for NEET-PG:** * **Most common cause of unilateral hydronephrosis:** PUJ Obstruction. * **Most common cause of bilateral hydronephrosis in males:** Posterior Urethral Valve (PUV). * **Gold standard investigation for PUJ Obstruction:** DTPA or MAG-3 scan (Diuretic Renography) to assess the degree of obstruction and renal function. * **Classic Presentation:** Often asymptomatic (detected antenatally) or may present as a palpable flank mass or episodic "Dietl’s crisis" (intermittent flank pain associated with high fluid intake).

Question 172: What is the frequency of renal involvement in Henoch-Schonlein Purpura (HSP)?

A. 20-40%
B. >80%
C. 40-60% (Correct Answer)
D. 10%

Explanation: **Explanation:** Henoch-Schönlein Purpura (HSP), now commonly referred to as **IgA Vasculitis**, is the most common systemic vasculitis in children. It is characterized by the classic tetrad of palpable purpura, arthritis, abdominal pain, and renal involvement. **1. Why 40-60% is correct:** Renal involvement (HSP Nephritis) occurs in approximately **40-60%** of affected children. While the cutaneous and gastrointestinal symptoms often appear first, renal manifestations—ranging from microscopic hematuria and proteinuria to nephritic or nephrotic syndromes—typically develop within 4–6 weeks of the initial presentation. In most pediatric cases, the prognosis is excellent, but the severity of renal involvement is the primary determinant of long-term morbidity. **2. Analysis of Incorrect Options:** * **A (20-40%):** This range underestimates the prevalence. While some older studies cited lower figures, modern longitudinal tracking shows a higher incidence of urinary abnormalities. * **B (>80%):** This is too high for clinical HSP. While some studies suggest subclinical renal deposition of IgA might be higher, clinically detectable renal disease does not reach this frequency. * **D (10%):** This significantly underestimates the condition. Renal involvement is a hallmark feature, not a rare complication. **High-Yield Clinical Pearls for NEET-PG:** * **Pathogenesis:** Characterized by **IgA1-dominant immune complex deposition** in the mesangium (histologically identical to IgA Nephropathy/Berger’s disease). * **Monitoring:** Since 90% of renal involvement occurs within 2 months, children with HSP require **serial urinalysis and blood pressure monitoring** for at least 6 months. * **Prognosis:** The presence of **crescents** on renal biopsy is the most important predictor of poor outcome (progression to Chronic Kidney Disease). * **Treatment:** Steroids are effective for GI pain and arthritis but **do not prevent** the development of future renal disease.

Question 173: What is the daily maintenance fluid requirement for a child weighing 10 kg?

A. 1000 ml/day (Correct Answer)
B. 800 ml/day
C. 500 ml/day
D. 1200 ml/day

Explanation: The calculation of maintenance fluid in pediatrics is based on the **Holliday-Segar Formula**, which estimates caloric expenditure and subsequent fluid needs based on body weight. This is a high-yield concept for NEET-PG. ### **Explanation of the Correct Answer** According to the Holliday-Segar rule, maintenance fluid requirements are calculated as follows: * **First 10 kg:** 100 ml/kg/day * **Next 10 kg (11–20 kg):** 1000 ml + 50 ml/kg for every kg over 10 kg * **Each kg above 20 kg:** 1500 ml + 20 ml/kg for every kg over 20 kg For a child weighing **10 kg**, the calculation is: $10\text{ kg} \times 100\text{ ml/kg/day} = \mathbf{1000\text{ ml/day}}$. ### **Analysis of Incorrect Options** * **B (800 ml/day):** This would be the requirement for an 8 kg infant. * **C (500 ml/day):** This is insufficient for a 10 kg child and represents the requirement for a 5 kg infant. * **D (1200 ml/day):** This would be the requirement for a 14 kg child ($1000\text{ ml} + [4\text{ kg} \times 50\text{ ml}]$). ### **Clinical Pearls for NEET-PG** 1. **Hourly Rate Rule (4-2-1 Rule):** To calculate the hourly infusion rate: * 0–10 kg: 4 ml/kg/hr * 11–20 kg: 40 ml + 2 ml/kg for every kg > 10 * >20 kg: 60 ml + 1 ml/kg for every kg > 20 2. **Neonatal Exception:** The Holliday-Segar formula is **not** used for neonates (<28 days), as their fluid requirements change daily during the first week of life. 3. **Composition:** Isotonic solutions (e.g., 0.9% Normal Saline in D5) are now preferred over hypotonic solutions to prevent hospital-acquired hyponatremia.

Question 174: What is the primary pathology underlying edema in nephrotic syndrome?

A. Reduced plasma protein concentration
B. Sodium and water retention (Correct Answer)
C. Increased venous pressure
D. Hyperlipidemia

Explanation: **Explanation:** The primary pathology underlying edema in nephrotic syndrome is **Sodium and water retention**, specifically through the **"Overfill Mechanism."** While traditional teaching emphasized the "Underfill" theory (low albumin leading to decreased oncotic pressure), modern evidence and NEET-PG standards prioritize the Overfill theory as the primary driver. 1. **Why the correct answer is right:** In nephrotic syndrome, there is a primary intrarenal defect in the distal nephron (specifically the ENaC channels in the cortical collecting duct). This leads to **primary sodium retention** regardless of the plasma volume status. This excess sodium causes water retention, leading to an expansion of the extracellular fluid (ECF) volume, which then leaks into the interstitium, causing edema. 2. **Why the incorrect options are wrong:** * **Reduced plasma protein concentration:** While hypoalbuminemia occurs, it is considered a *contributory* factor (Underfill theory) rather than the primary initiator of edema in most adult and many pediatric cases. * **Increased venous pressure:** This is the mechanism for edema in Congestive Heart Failure (CHF), not nephrotic syndrome. * **Hyperlipidemia:** This is a diagnostic criterion for nephrotic syndrome (due to increased hepatic lipoprotein synthesis), but it does not physiologically contribute to edema formation. **High-Yield Clinical Pearls for NEET-PG:** * **Overfill Theory:** Primary renal sodium retention (most common in adults/MCD). * **Underfill Theory:** Decreased oncotic pressure → Secondary activation of RAAS (more common in severe hypoalbuminemia <2.0 g/dL). * **Site of Sodium Retention:** The **ENaC (Epithelial Sodium Channel)** in the collecting duct is the chief site of resistance to ANP and increased sodium reabsorption. * **Initial Sign:** Edema in nephrotic syndrome typically presents first as **periorbital puffiness** (dependent edema).

Question 175: Nephrotic range of proteinuria is defined as:

A. greater than 30 mg/m2/hr
B. greater than 40 mg/m2/hr (Correct Answer)
C. greater than 2 gm/m2/24hrs
D. greater than 4 gm/m2/24hrs

Explanation: **Explanation:** In pediatric nephrology, defining the severity of proteinuria is crucial for diagnosing Nephrotic Syndrome. The hallmark of this condition is "massive" or **nephrotic-range proteinuria**, which leads to hypoalbuminemia and subsequent edema. **Why Option B is correct:** The standard definition for nephrotic-range proteinuria in children is a protein excretion rate of **>40 mg/m²/hr**. This value is derived from timed urine collections and is the most precise metric used in clinical guidelines (such as ISPN and KDIGO) to differentiate nephrotic syndrome from milder forms of glomerular injury. **Analysis of Incorrect Options:** * **Option A (>30 mg/m²/hr):** This is a sub-nephrotic range. While abnormal, it does not meet the diagnostic threshold for Nephrotic Syndrome. * **Option C (>2 gm/m²/24hrs):** While 1 gram/m²/24hrs is sometimes used as a threshold for "heavy" proteinuria, the specific diagnostic cutoff for nephrotic range is generally cited as **>1 gram/m²/day** or more accurately **>50 mg/kg/day**. 2 grams is an arbitrary figure in this context. * **Option D (>4 gm/m²/24hrs):** This value is excessively high and far exceeds the minimum diagnostic criteria. **High-Yield Clinical Pearls for NEET-PG:** * **Spot Urine Protein/Creatinine Ratio (uPCR):** In clinical practice, a ratio of **>2 mg/mg** (or >200 mg/mmol) is considered nephrotic range. * **Dipstick Grading:** Nephrotic syndrome typically shows **3+ or 4+** on a urine dipstick. * **Definition of Nephrotic Syndrome:** It is a clinical triad of Nephrotic-range proteinuria, Hypoalbuminemia (<2.5 g/dL), and Edema. Hyperlipidemia is a frequent association but not always required for diagnosis. * **Normal Proteinuria:** In children, normal protein excretion is **<4 mg/m²/hr**.

Question 176: Which of the following is NOT true about Bartter syndrome?

A. Hyperkalemic metabolic alkalosis (Correct Answer)
B. Presentation in neonates with ototoxicity and Barttin gene mutation
C. Decreased potassium absorption from the thick ascending limb of the loop of Henle
D. Autosomal recessive inheritance

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, mimicking the effect of chronic loop diuretic (furosemide) use. **1. Why Option A is the correct answer (The False Statement):** The hallmark of Bartter syndrome is **Hypokalemic metabolic alkalosis**, not hyperkalemic. The defect in the TAL leads to failure of sodium, chloride, and potassium reabsorption. The resulting increased sodium delivery to the distal tubule triggers aldosterone secretion, which promotes potassium and hydrogen ion excretion in the collecting duct, leading to hypokalemia and metabolic alkalosis. **2. Analysis of Incorrect Options (True Statements):** * **Option B:** Antenatal/Neonatal Bartter syndrome (Type IV) is caused by mutations in the **BSND gene (encoding Barttin)**. This type is uniquely associated with sensorineural deafness (ototoxicity) because Barttin is essential for chloride channels in both the kidney and the inner ear. * **Option C:** The primary pathophysiology involves a defect in the **NKCC2 transporter**, ROMK channel, or ClC-Kb channel, all of which result in decreased potassium and solute reabsorption in the TAL. * **Option D:** Most forms of Bartter syndrome (Types I-IV) follow an **autosomal recessive** inheritance pattern. **High-Yield Clinical Pearls for NEET-PG:** * **Bartter vs. Gitelman:** Bartter presents early (infancy) with **hypercalciuria** (stones), whereas Gitelman presents later (adolescence) with **hypocalciuria** and hypomagnesemia. * **Mnemonic:** **B**artter is like **B**loop (Loop diuretics); **G**itelman is like **G**thiazide (Thiazide diuretics). * **Clinical Features:** Polyhydramnios (antenatal), failure to thrive, and "floppy baby" due to hypokalemia.

Question 177: What is the daily water requirement for a child weighing 30 kg, with a height of 123 cm, and a body surface area (BSA) of 1 m²?

A. 1300 ml
B. 1700 ml (Correct Answer)
C. 2000 ml
D. 2500 ml

Explanation: The daily water requirement in pediatrics is calculated using two primary methods: the **Holliday-Segar formula** (based on weight) and the **Body Surface Area (BSA) method**. ### 1. Why 1700 ml is Correct For children weighing more than 10–20 kg, the BSA method is often preferred for calculating maintenance fluids as it more accurately reflects metabolic needs and insensible water loss. * **Standard Formula:** Maintenance fluid = **1500 ml/m²/day**. * **Calculation:** $1500 \text{ ml} \times 1 \text{ m}^2 (\text{BSA}) = 1500 \text{ ml}$. * **Insensible Losses & Activity:** In a clinical setting, requirements often range between **1500–1700 ml/m²/day** to account for standard physical activity and urinary concentration. Among the given options, **1700 ml** is the most appropriate clinical estimate for a child of this size. If using the **Holliday-Segar Formula** (Weight-based): * First 10 kg: 1000 ml * Next 10 kg: 500 ml * Remaining 10 kg (at 20 ml/kg): 200 ml * **Total:** $1000 + 500 + 200 = 1700 \text{ ml}$. Both methods converge on 1700 ml, making it the definitive answer. ### 2. Why Other Options are Incorrect * **A (1300 ml):** This underestimates the requirement for a 30 kg child (only ~43 ml/kg), which would lead to dehydration. * **C (2000 ml):** This exceeds the maintenance requirement ($>65 \text{ ml/kg}$) and is typically reserved for children with increased losses (e.g., fever or phototherapy). * **D (2500 ml):** This is the average requirement for an adult or a child with severe polyuria/dehydration. ### 3. High-Yield Clinical Pearls for NEET-PG * **Holliday-Segar Rule:** 100 ml/kg (first 10 kg), 50 ml/kg (next 10 kg), 20 ml/kg (thereafter). * **Neonatal Exception:** This formula is **not** used for neonates <14 days old. * **Insensible Water Loss (IWL):** Approximately **400 ml/m²/day**. It increases by 10–12% for every 1°C rise in body temperature. * **BSA Calculation:** If not provided, use Mosteller’s formula: $\sqrt{\frac{\text{Height (cm)} \times \text{Weight (kg)}}{3600}}$.

Question 178: A newborn male presents with urinary retention, lethargy and a distended bladder. Antenatal ultrasound showed a "keyhole sign" with a thickened bladder wall. Which of the following is the most likely diagnosis?

A. Posterior urethral valves (Correct Answer)
B. Hypospadias
C. Vesicoureteral reflux
D. Neurogenic bladder

Explanation: ***Posterior urethral valves***- The **"keyhole sign"** seen on antenatal ultrasound, characterized by a dilated posterior urethra and a thickened, distended bladder, is highly specific for **posterior urethral valves (PUV)**.- PUV is the most common cause of severe **lower urinary tract obstruction** in male newborns, leading directly to symptoms like lethargy, a palpable **distended bladder**, and urinary retention.*Hypospadias*- *Hypospadias* is an abnormal location of the **urethral meatus** on the ventral aspect of the penis.- It does not cause the severe **obstructive uropathy** (like urinary retention and bladder distension) or the **keyhole sign** observed in this patient.*Vesicoureteral reflux*- *Vesicoureteral reflux* (VUR) involves the reflux of urine from the bladder back up to the ureters and is typically a **non-obstructive** cause of hydronephrosis and UTIs.- While VUR can coexist with PUV, it is the secondary phenomenon, and VUR itself does not cause the primary **urethral obstruction** or the characteristic **keyhole appearance**.*Neurogenic bladder*- A *neurogenic bladder* results from impaired nerve supply, often due to conditions like **spina bifida**, leading to poor bladder emptying.- While it can cause retention, the unique finding of the **keyhole sign** points specifically to a fixed, **anatomical obstruction** in the posterior urethra, which is not characteristic of neurological issues.

Question 179: What is the recommended treatment for nephrotic syndrome in children?

A. ACE inhibitors
B. Cyclophosphamide
C. Steroids and cyclophosphamide
D. Steroids (Correct Answer)

Explanation: ***Steroids***- **Corticosteroids** (typically Prednisone/Prednisolone) are the recommended **first-line therapy** for pediatric nephrotic syndrome, as *minimal change disease* (**MCD**) is the most common cause (90% of cases).- The vast majority of children with MCD are **steroid-sensitive**, exhibiting remission (proteinuria cessation) within 2-4 weeks of high-dose treatment.*Steroids and cyclophosphamide*- Combination therapy including **cyclophosphamide** is typically reserved for children who show **steroid dependence** or **frequent relapses**, not for initial therapy.- Adding cyclophosphamide as a first-line agent is unnecessary due to its potential for significant **gonadal toxicity** and other systemic side effects.*Cyclophosphamide*- **Cyclophosphamide** is a powerful **second-line immunosuppressive agent** used primarily for children who are steroid-dependent or **steroid-resistant**.- Using it as initial monotherapy is inappropriate because children with MCD usually respond well to steroids alone, avoiding risks like **myelosuppression**.*ACE inhibitors*- **Angiotensin-converting enzyme (ACE) inhibitors** are used primarily to reduce **proteinuria** by lowering **glomerular hydrostatic pressure**.- Their role is generally adjunctive management for resistant proteinuria or for treating associated **hypertension**, not as the primary agent to induce remission.

Question 180: Following urine microscopy and examination, a child is found to have hematuria and RBC casts in the urine. What is the probable cause for this?

A. Focal segmental glomerulosclerosis (FSGS)
B. Membranoproliferative glomerulonephritis (MPGN)
C. Minimal change disease
D. Post-streptococcal glomerulonephritis (PSGN) (Correct Answer)

Explanation: ***Post-streptococcal glomerulonephritis (PSGN)***- RBC casts are highly indicative of **active glomerulonephritis**, demonstrating that red blood cells have leaked through damaged glomeruli and aggregated in the renal tubules.- **PSGN** is the most common cause of acute nephritic syndrome in children, typically following a *Streptococcal* infection, characterized by **hematuria**, hypertension, and mild proteinuria.*Focal segmental glomerulosclerosis (FSGS)*- FSGS almost universally presents as **nephrotic syndrome**, characterized by heavy **proteinuria**, profound edema, and hypoalbuminemia.- While microscopic hematuria may be present, the finding of **RBC casts** is highly uncommon and points away from a primary diagnosis of FSGS.*Membranoproliferative glomerulonephritis (MPGN)*- MPGN often presents with a **mixed nephrotic and nephritic picture**, including hematuria, but is less common acutely than PSGN in children.- PSGN presents with a very typical acute onset of **nephritic features** (hematuria, casts, hypertension) following infection, making it the more probable cause.*Minimal change disease*- This is the leading cause of **nephrotic syndrome** in children, defined by massive **proteinuria** with minimal to no damage visible on light microscopy.- **Minimal change disease** classically presents without significant hematuria and **RBC casts** are virtually absent.

Practice by Chapter

Urinary Tract Infections

Practice Questions

Vesicoureteral Reflux

Practice Questions

Glomerulonephritis

Practice Questions

Nephrotic Syndrome

Practice Questions

Acute Kidney Injury

Practice Questions

Chronic Kidney Disease

Practice Questions

Renal Tubular Disorders

Practice Questions

Congenital Anomalies of the Kidney

Practice Questions

Hydronephrosis

Practice Questions

Hypertension in Children

Practice Questions

Hemolytic Uremic Syndrome

Practice Questions

Renal Replacement Therapy in Children

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?