Nephrology — MCQs

A 4-year-old boy develops a large erythematous rash around the site of a mosquito bite. One month later, he is taken to a pediatrician due to a puffy face and swollen ankles. The scanty urine sample has a reddish-brown hue and contains both red blood cells and protein. Which of the following distinctive features would be most likely to be seen on renal biopsy?

Q98Easy

In children, what is the definition of acute kidney injury in terms of urine output?

Q99Easy

In hemolytic uremic syndrome, which of the following is characteristic?

Q100Medium

A 9-year-old boy presents with decreased urine output, cola-colored urine, and swelling of the face and hands for 2 days. He is hypertensive, has a puffy face, and pitting edema of the lower limbs. Four weeks prior, he had skin lesions. A diagnosis of post-streptococcal glomerulonephritis is made. If an antibiotic is to be used to limit the spread of nephritogenic organisms, what is the drug of choice?

Nephrology Indian Medical PG Practice Questions and MCQs

Question 91: All are features of Alport syndrome, except?

A. Hematuria
B. Sensorineural hearing loss
C. Lenticonus
D. Hypertelorism (Correct Answer)

Explanation: **Explanation:** Alport Syndrome is a hereditary disorder of basement membranes caused by mutations in the genes encoding the **alpha-3, alpha-4, or alpha-5 chains of Type IV collagen**. This collagen is a crucial structural component of the glomerular basement membrane (GBM), the cochlea, and the eye. **Why Hypertelorism is the Correct Answer:** * **Hypertelorism (Option D):** This refers to an abnormally increased distance between the eyes. It is a craniofacial dysmorphism seen in syndromes like Apert or Noonan syndrome, but it is **not** a feature of Alport syndrome. Alport syndrome primarily affects the kidneys, ears, and eyes due to the specific distribution of Type IV collagen. **Why the other options are incorrect (Features of Alport Syndrome):** * **Hematuria (Option A):** This is the most common and earliest sign. Patients typically present with persistent microscopic hematuria or episodes of gross hematuria triggered by upper respiratory infections. * **Sensorineural Hearing Loss (Option B):** This is a classic extra-renal manifestation. It is bilateral, progressive, and usually affects high-frequency sounds, typically manifesting in late childhood or adolescence. * **Lenticonus (Option C):** Anterior lenticonus (conical protrusion of the lens) is a **pathognomonic** sign of Alport syndrome. Other ocular findings include "fleck retina" (perimacular whitish-yellow dots). **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most common is **X-linked Dominant** (COL4A5 mutation), followed by Autosomal Recessive. * **Electron Microscopy (Gold Standard):** Shows characteristic **"Basket-weave appearance"** (irregular thinning and thickening/lamellation of the GBM). * **Diagnosis:** Often suspected in a child with hematuria and a family history of renal failure or deafness. * **Management:** ACE inhibitors are used to delay the progression to End-Stage Renal Disease (ESRD). Post-transplant, some patients may develop **Anti-GBM disease (Goodpasture-like syndrome)**.

Question 92: What is the most common cause of persistent hypertension in a child with intrinsic renal disease?

A. Chronic glomerulonephritis
B. Chronic pyelonephritis (Correct Answer)
C. Obstructive uropathy
D. Renal tumor

Explanation: **Explanation:** **Chronic pyelonephritis** (often associated with vesicoureteral reflux and renal scarring) is the most common cause of persistent hypertension in children with intrinsic renal disease. The underlying mechanism involves **segmental renal scarring**, which leads to localized ischemia. This ischemia triggers the **Renin-Angiotensin-Aldosterone System (RAAS)**, resulting in sustained elevation of blood pressure. In pediatric practice, any child with a history of recurrent urinary tract infections (UTIs) and hypertension must be evaluated for reflux nephropathy. **Analysis of Incorrect Options:** * **Chronic Glomerulonephritis (A):** While a common cause of acute hypertension (e.g., PSGN), it is less frequently the cause of *persistent* hypertension compared to the structural scarring seen in chronic pyelonephritis. * **Obstructive Uropathy (C):** This can lead to chronic kidney disease and hypertension, but it usually manifests as hypertension *after* significant renal parenchymal damage or secondary infection (pyelonephritis) has occurred. * **Renal Tumor (D):** While Wilms' tumor can cause hypertension due to renin production or renal artery compression, it is a rare cause compared to inflammatory/infectious parenchymal diseases. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of hypertension in children (overall):** Renal parenchymal disease (specifically chronic pyelonephritis/scarring). * **Most common cause of acute hypertension in children:** Acute Post-Streptococcal Glomerulonephritis (PSGN). * **Most common cause of renovascular hypertension in children:** Fibromuscular dysplasia (unlike atherosclerosis in adults). * **Gold standard for detecting renal scars:** DMSA Scan.

Question 93: All are features of Bartter syndrome EXCEPT?

A. Hypokalemia
B. Metabolic alkalosis
C. Hypocalciuria (Correct Answer)
D. Salt wasting

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 (Furosemide)**. **Why Hypocalciuria is the correct answer:** In Bartter syndrome, the defect in the NKCC2 transporter (or related channels) leads to a loss of the positive transepithelial potential. This potential is normally the driving force for the paracellular reabsorption of Calcium and Magnesium. Consequently, patients experience **Hypercalciuria** (increased urinary calcium), which often leads to nephrocalcinosis. **Hypocalciuria** is actually a hallmark feature of **Gitelman syndrome** (which mimics Thiazide diuretics). **Analysis of incorrect options:** * **Hypokalemia:** Impaired sodium reabsorption in the TAL increases sodium delivery to the distal tubule. This stimulates aldosterone, which promotes potassium excretion in exchange for sodium, leading to profound hypokalemia. * **Metabolic Alkalosis:** Increased distal delivery of sodium and high aldosterone levels also promote hydrogen ion secretion, resulting in hypokalemic metabolic alkalosis. * **Salt Wasting:** Since the TAL is responsible for reabsorbing ~25% of filtered sodium, a defect here leads to significant urinary salt loss, polyuria, and secondary activation of the Renin-Angiotensin-Aldosterone System (RAAS). **NEET-PG High-Yield Pearls:** * **Bartter vs. Gitelman:** Bartter presents early (infancy/childhood) with polyhydramnios and hypercalciuria. Gitelman presents later (adolescence) with hypocalciuria and hypomagnesemia. * **Mnemonic:** **B**artter = **B**ig (Loop of Henle/Loop diuretics); **G**itelman = **G**ritty (Distal tubule/Thiazides). * **Clinical Sign:** Patients often have a "triangular face" and large ears.

Question 94: An 11-year-old child presents with failure to thrive and metabolic acidosis with an increased anion gap. Which of the following is NOT a likely diagnosis in the differential diagnosis?

A. Insulin dependent diabetes mellitus
B. Chronic renal failure
C. Renal tubular acidosis (Correct Answer)
D. Inborn errors of metabolism

Explanation: The core of this question lies in distinguishing between the types of metabolic acidosis based on the **Anion Gap (AG)**. ### **Explanation of the Correct Answer** **Option C (Renal Tubular Acidosis)** is the correct answer because it is a classic cause of **Normal Anion Gap Metabolic Acidosis (NAGMA)**, also known as hyperchloremic metabolic acidosis. In RTA, the pathology involves either a failure to reclaim bicarbonate (Proximal/Type 2) or a failure to excrete hydrogen ions (Distal/Type 1). Since the loss of bicarbonate is compensated by a reciprocal increase in serum chloride to maintain electroneutrality, the anion gap remains within the normal range (8–12 mEq/L). ### **Analysis of Incorrect Options (Causes of High Anion Gap Metabolic Acidosis - HAGMA)** * **A. Insulin Dependent Diabetes Mellitus:** Leads to Diabetic Ketoacidosis (DKA). The accumulation of unmeasured anions (acetoacetate and beta-hydroxybutyrate) increases the anion gap. * **B. Chronic Renal Failure:** In advanced stages, the kidneys fail to excrete organic acids (phosphates, sulfates, and urates). These "fixed acids" accumulate, leading to HAGMA. * **D. Inborn Errors of Metabolism (IEM):** Conditions like Organic Acidemias (e.g., Methylmalonic acidemia) result in the accumulation of organic acids, which are unmeasured anions, thus causing HAGMA. ### **High-Yield Clinical Pearls for NEET-PG** * **Mnemonic for HAGMA (MUDPILES):** **M**ethanol, **U**remia (CRF), **D**KA, **P**araldehyde, **I**NH/Iron, **L**actic acidosis, **E**thylene glycol, **S**alicylates/Starvation. * **Mnemonic for NAGMA (USED CARP):** **U**retero-sigmoidostomy, **S**aline infusion, **E**ndocrine (Addison’s), **D**iarrhea, **C**arbonic anhydrase inhibitors, **A**mmonium chloride, **R**enal Tubular Acidosis (**RTA**), **P**ancreatic fistula. * **RTA & Growth:** While all types of RTA cause failure to thrive (FTT), **Distal RTA (Type 1)** is most frequently associated with nephrocalcinosis and rickets in pediatric exams.

Question 95: Which of the following is NOT a clinical feature of minimal change glomerulonephritis?

A. Hypertension (Correct Answer)
B. Edema
C. Selective proteinuria
D. Fever

Explanation: **Explanation:** Minimal Change Disease (MCD) is the most common cause of Nephrotic Syndrome in children (80-90% of cases). The hallmark of MCD is the effacement of podocyte foot processes, leading to a loss of the glomerular polyanionic charge barrier. **Why Hypertension is the Correct Answer:** In MCD, the glomerular basement membrane remains structurally intact, and there is no significant inflammatory cell infiltration or endocapillary proliferation. Consequently, the Glomerular Filtration Rate (GFR) is usually preserved. **Hypertension and Hematuria** are "nephritic" features and are characteristically **absent** in MCD. Their presence should prompt a clinician to consider alternative diagnoses like Focal Segmental Glomerulosclerosis (FSGS) or Membranoproliferative Glomerulonephritis (MPGN). **Analysis of Other Options:** * **Edema:** This is the most common presenting feature. Severe hypoalbuminemia (due to massive proteinuria) leads to decreased oncotic pressure, resulting in salt and water retention and pedal/periorbital edema. * **Selective Proteinuria:** MCD is characterized by "selective" proteinuria, meaning mainly **Albumin** is lost in the urine. This occurs because only the charge barrier is lost, while the size barrier remains relatively intact. * **Fever:** While not a direct feature of the pathology, children with MCD are highly prone to infections (like Spontaneous Bacterial Peritonitis) due to the loss of immunoglobulins and complement factors in the urine. Fever is a common clinical finding during relapses triggered by infections. **High-Yield Clinical Pearls for NEET-PG:** * **Light Microscopy:** Appears normal (hence "Minimal Change"). * **Electron Microscopy (Gold Standard):** Shows effacement/fusion of podocyte foot processes. * **Immunofluorescence:** Negative (No immune deposits). * **Treatment:** Corticosteroids (Prednisolone) are the first-line treatment; MCD is highly steroid-responsive. * **Most common complication:** Infections (specifically *Streptococcus pneumoniae*).

Question 96: A 7-year-old girl presents with generalized body swelling. Urinalysis shows grade 3 proteinuria and the presence of hyaline and fatty casts. She has no history of hematuria. Which of the following statements about her condition is true?

A. No IgG deposits or C3 deposition on renal biopsy (Correct Answer)
B. C3 level will be low
C. IgA nephropathy is the likely diagnosis
D. Alport's syndrome is the likely diagnosis

Explanation: The clinical presentation of generalized body swelling (edema) and heavy proteinuria (Grade 3) in a 7-year-old child, in the absence of hematuria, is the classic hallmark of **Minimal Change Disease (MCD)**. MCD is the most common cause of Nephrotic Syndrome in children (approx. 80% of cases). ### **Why Option A is Correct** In Minimal Change Disease, **Immunofluorescence (IF) microscopy** typically shows **no deposits** (negative for IgG, IgA, IgM, and C3). The primary pathology is seen only on Electron Microscopy, which reveals the **effacement (fusion) of podocyte foot processes**. Light microscopy usually appears normal, hence the name "Minimal Change." ### **Why Other Options are Incorrect** * **Option B (Low C3):** MCD is characterized by normal serum complement levels. Low C3 levels are seen in "nephritic" conditions like Post-Streptococcal Glomerulonephritis (PSGN), Membranoproliferative Glomerulonephritis (MPGN), or Systemic Lupus Erythematosus (SLE). * **Option C (IgA Nephropathy):** This typically presents as asymptomatic microscopic hematuria or gross hematuria following an upper respiratory tract infection (synpharyngitic hematuria), not pure nephrotic syndrome. * **Option D (Alport’s Syndrome):** This is a hereditary collagen disorder presenting with hematuria, progressive renal failure, sensorineural hearing loss, and ocular defects (lenticonus). ### **High-Yield NEET-PG Pearls** * **Most common cause of Nephrotic Syndrome in children:** Minimal Change Disease. * **Most common cause in adults:** Focal Segmental Glomerulosclerosis (FSGS) or Membranous Nephropathy. * **Hallmark finding:** Effacement of foot processes on Electron Microscopy. * **Treatment of choice:** Corticosteroids (Prednisolone). MCD is highly steroid-responsive. * **Selectivity:** Proteinuria in MCD is typically "highly selective" (mainly albumin).

Question 97: A 4-year-old boy develops a large erythematous rash around the site of a mosquito bite. One month later, he is taken to a pediatrician due to a puffy face and swollen ankles. The scanty urine sample has a reddish-brown hue and contains both red blood cells and protein. Which of the following distinctive features would be most likely to be seen on renal biopsy?

A. Fusion of podocyte foot processes
B. IgA in the mesangium
C. Linear IgG deposits
D. Subepithelial electron dense humps (Correct Answer)

Explanation: ### Explanation **Diagnosis: Post-Streptococcal Glomerulonephritis (PSGN)** The clinical presentation of a **4-year-old boy** with a history of a skin infection (the mosquito bite likely became infected with *Streptococcus pyogenes*, causing impetigo), followed by a **latent period** (one month), and presenting with **nephritic syndrome** (edema, hematuria, and proteinuria) is classic for PSGN. **1. Why Option D is Correct:** The hallmark finding on **Electron Microscopy (EM)** for PSGN is the presence of **subepithelial electron-dense "humps."** These represent the deposition of immune complexes (containing Streptococcal antigens like NAPlr or SPEB) between the glomerular basement membrane and the podocytes. On Immunofluorescence (IF), this corresponds to a "starry sky" or "lumpy-bumpy" appearance of IgG and C3. **2. Why Incorrect Options are Wrong:** * **A. Fusion of podocyte foot processes:** This is the characteristic EM finding of **Minimal Change Disease (MCD)**. MCD presents as pure nephrotic syndrome (massive proteinuria, no hematuria) and is not typically preceded by a skin infection. * **B. IgA in the mesangium:** This defines **IgA Nephropathy (Berger’s disease)**. While it causes hematuria, it typically presents as "synpharyngitic" hematuria (occurring within 1-2 days of an upper respiratory infection) without a long latent period. * **C. Linear IgG deposits:** This is characteristic of **Goodpasture Syndrome** (Anti-GBM disease), where antibodies are directed against the Type IV collagen of the basement membrane. **3. NEET-PG High-Yield Pearls:** * **Latent Period:** 1–2 weeks after pharyngitis; 3–6 weeks after skin infection (impetigo). * **Lab Findings:** Low C3 levels (normalized by 6–8 weeks); elevated ASO titer (after pharyngitis) or Anti-DNase B (after skin infection). * **Prognosis:** Excellent in children (>95% recover completely); worse in adults. * **Light Microscopy:** Diffuse proliferative glomerulonephritis with "hypercellular" glomeruli due to leukocyte infiltration.

Question 98: In children, what is the definition of acute kidney injury in terms of urine output?

A. Less than 0.3 ml/kg/hr for more than 6 hours
B. Less than 0.5 ml/kg/hr for more than 6 hours (Correct Answer)
C. Less than 0.8 ml/kg/hr for more than 6 hours
D. Less than 1 ml/kg/hr for more than 6 hours

Explanation: The definition of Acute Kidney Injury (AKI) in children is primarily based on the **pRIFLE** (Pediatric Risk, Injury, Failure, Loss, End-stage renal disease) and **KDIGO** criteria. Both classifications define the earliest stage of AKI (Stage 1 or "Risk") based on a reduction in urine output. ### Why Option B is Correct The standard pediatric threshold for AKI is a urine output of **<0.5 ml/kg/hr for at least 6 to 12 hours**. This value is chosen because it represents a significant deviation from the normal pediatric urine output (which is typically >1 ml/kg/hr) and serves as an early physiological marker of declining glomerular filtration before a significant rise in serum creatinine occurs. ### Analysis of Incorrect Options * **Option A (<0.3 ml/kg/hr):** This threshold is used to define **Stage 2 (Injury)** if it persists for >12 hours, or **Stage 3 (Failure)** if it persists for >24 hours. It is too stringent for the initial definition of AKI. * **Options C & D:** These values are too high. While a child producing 0.8 or 1 ml/kg/hr may be monitored, they do not meet the formal diagnostic criteria for AKI. ### High-Yield Clinical Pearls for NEET-PG * **Creatinine Criteria:** In children, AKI is also defined as an increase in serum creatinine to **≥1.5 times the baseline** or an absolute increase of **≥0.3 mg/dL** within 48 hours. * **pRIFLE vs. KDIGO:** While KDIGO is the global standard, **pRIFLE** is specifically validated for pediatrics and uses "estimated Creatinine Clearance (eCCl)" rather than absolute creatinine values. * **Normal Urine Output:** * Infants: 2 ml/kg/hr * Children: 1–1.5 ml/kg/hr * Adolescents: 0.5–1 ml/kg/hr

Question 99: In hemolytic uremic syndrome, which of the following is characteristic?

A. Thrombocytopenia and renal failure
B. Normal coagulative profile
C. Microangiopathic hemolytic anemia
D. All of the above (Correct Answer)

Explanation: **Hemolytic Uremic Syndrome (HUS)** is defined by a classic clinical triad: **Microangiopathic Hemolytic Anemia (MAHA), Thrombocytopenia, and Acute Kidney Injury (AKI).** It is most commonly seen in children following a prodrome of bloody diarrhea caused by Shiga toxin-producing *E. coli* (STEC), specifically serotype O157:H7. ### **Explanation of Options:** * **Microangiopathic Hemolytic Anemia (MAHA):** This is a hallmark of HUS. Endothelial injury leads to the formation of microthrombi in small vessels. As RBCs pass through these partially occluded vessels, they are mechanically shredded, resulting in **schistocytes** (fragmented cells) on a peripheral smear and a negative Coombs test. * **Thrombocytopenia and Renal Failure:** Platelets are consumed during the formation of microthrombi, leading to low platelet counts (usually <150,000/mm³). The renal microvasculature is particularly susceptible, leading to decreased GFR, oliguria, and hematuria. * **Normal Coagulative Profile:** This is a **critical diagnostic differentiator.** Unlike Disseminated Intravascular Coagulation (DIC), the coagulation cascade is not activated in HUS. Therefore, PT, aPTT, and Fibrinogen levels remain **normal**. ### **NEET-PG High-Yield Pearls:** * **Most common cause of AKI in children:** HUS. * **Pathogenesis:** Shiga toxin causes direct endothelial damage, primarily in the glomerulus. * **Atypical HUS:** Caused by uncontrolled activation of the alternative complement pathway (Factor H deficiency); treated with **Eculizumab**. * **Management:** Primarily supportive (fluids, dialysis). **Antibiotics and anti-motility agents are contraindicated** in STEC-HUS as they may increase toxin release and worsen the condition.

Question 100: A 9-year-old boy presents with decreased urine output, cola-colored urine, and swelling of the face and hands for 2 days. He is hypertensive, has a puffy face, and pitting edema of the lower limbs. Four weeks prior, he had skin lesions. A diagnosis of post-streptococcal glomerulonephritis is made. If an antibiotic is to be used to limit the spread of nephritogenic organisms, what is the drug of choice?

A. Cefixime
B. Penicillin (Correct Answer)
C. Meropenem
D. Amoxycillin

Explanation: **Explanation:** The clinical presentation of hematuria (cola-colored urine), hypertension, edema, and a history of skin infection (impetigo) 4 weeks prior is classic for **Post-Streptococcal Glomerulonephritis (PSGN)**. PSGN is a Type III hypersensitivity reaction caused by nephritogenic strains of Group A Beta-Hemolytic Streptococcus (GABS). **1. Why Penicillin is Correct:** While antibiotics do not alter the course of the renal disease or prevent the development of PSGN once the infection has occurred, they are indicated to **eradicate the nephritogenic streptococci** from the patient and the throat/skin. This limits the spread of these specific strains to family members and the community. **Penicillin G (or V)** remains the gold standard and drug of choice for GABS due to its narrow spectrum and continued high sensitivity. **2. Why Other Options are Incorrect:** * **Cefixime (A):** A third-generation cephalosporin. While effective against many bacteria, it is unnecessarily broad-spectrum for GABS and is not the first-line recommendation for streptococcal eradication. * **Meropenem (C):** A carbapenem used for multi-drug resistant systemic infections. It is inappropriate for a simple streptococcal skin or throat infection. * **Amoxycillin (D):** While often used for streptococcal pharyngitis due to better taste and absorption, Penicillin remains the classic "textbook" drug of choice for GABS eradication in the context of post-infectious sequelae. **Clinical Pearls for NEET-PG:** * **Latent Period:** PSGN occurs 1–2 weeks after pharyngitis and 3–6 weeks after skin infections (pyoderma). * **Diagnosis:** Low C3 levels are characteristic (normalize in 6–8 weeks). ASO titers are high after pharyngitis; Anti-DNase B is the most sensitive marker after skin infections. * **Prevention:** Unlike Rheumatic Fever, antibiotics **do not** prevent PSGN. * **Management:** Primarily supportive (fluid restriction, diuretics for edema, and antihypertensives like Nifedipine).

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?