Nephrology — MCQs

A 13-year-old boy is referred for evaluation of nocturnal enuresis and short stature. His blood pressure is normal. The hemoglobin level is 8 g/dL, urea 112 mg/dL, creatinine 6 mg/dL, sodium 119 mEq/dL, potassium 4 mEq/L, calcium 7 mg/dL, phosphate 6 mg/dL, and alkaline phosphatase 300 U/L. Urinalysis shows trace proteinuria with hyaline casts; no red and white cells are seen. Ultrasound shows bilateral small kidneys, and the micturating cystourethrogram is normal. What is the most likely diagnosis?

Q559Easy

What is the most common cause of end-stage renal disease?

Q560Easy

What is a common symptom of medullary sponge kidney disease?

Nephrology Indian Medical PG Practice Questions and MCQs

Question 551: A patient presents with oliguria. Investigations reveal the following: Urine osmolality 620 mosm/kg, Urine sodium 12 mmol/L, and Urine/plasma urea ratio 13:1. What is the most likely diagnosis?

A. Prerenal acute kidney injury (Correct Answer)
B. Acute tubular necrosis
C. Acute cortical necrosis
D. Urinary tract obstruction

Explanation: ### Explanation The clinical presentation and biochemical parameters point towards **Prerenal Acute Kidney Injury (AKI)** [1]. In prerenal states, the kidneys are structurally intact but respond to decreased renal perfusion by maximizing water and sodium reabsorption [2]. **1. Why Prerenal AKI is correct:** * **Urine Osmolality (>500 mOsm/kg):** High osmolality indicates that the renal tubules are functioning correctly and are concentrating the urine in response to ADH to conserve water. * **Urine Sodium (<20 mmol/L):** Low urinary sodium is a hallmark of prerenal AKI. The kidneys activate the Renin-Angiotensin-Aldosterone System (RAAS) to aggressively reabsorb sodium to restore effective circulating volume [2]. * **Urine/Plasma Urea Ratio (>8:1):** A high ratio indicates significant urea reabsorption and concentrated urine, typical of prerenal azotemia. **2. Why other options are incorrect:** * **Acute Tubular Necrosis (ATN):** This is an intrinsic renal injury where the tubules lose their concentrating ability. Expected findings include low urine osmolality (<350 mOsm/kg), high urine sodium (>40 mmol/L), and a fractional excretion of sodium (FeNa) >2%. * **Acute Cortical Necrosis:** This is a severe form of intrinsic injury (often post-obstetric complications) leading to permanent renal failure and anuria; the biochemical indices would reflect intrinsic damage, not conservation. * **Urinary Tract Obstruction (Post-renal):** Initially, indices may mimic prerenal AKI, but as pressure builds, tubular damage occurs, leading to an inability to concentrate urine (isosthenuria). **High-Yield Clinical Pearls for NEET-PG:** * **FeNa (Fractional Excretion of Sodium):** The most reliable differentiator. **<1%** suggests Prerenal; **>2%** suggests ATN. * **BUN/Creatinine Ratio:** In prerenal AKI, the ratio is typically **>20:1** because urea is reabsorbed along with sodium/water, while creatinine is not. * **Urinary Sediment:** Prerenal AKI shows **hyaline casts**, whereas ATN shows **"muddy brown" granular casts**.

Question 552: Dialysis disequilibrium syndrome occurs due to:

A. Cerebral edema (Correct Answer)
B. Hypertension
C. Aluminum toxicity
D. Amyloid deposition

Explanation: Explanation: Dialysis Disequilibrium Syndrome (DDS) is a clinical phenomenon characterized by neurological symptoms occurring during or shortly after hemodialysis, particularly in patients with high baseline urea levels (first-time dialysis). Why Cerebral Edema is the correct answer: The underlying mechanism is the "Reverse Osmotic Effect." During hemodialysis, urea is rapidly cleared from the intravascular compartment. However, urea moves slowly out of the brain cells due to the blood-brain barrier. This creates an osmotic gradient where the brain becomes hyperosmolar relative to the plasma. Consequently, water shifts from the plasma into the brain cells to equalize the concentration, leading to cerebral edema and increased intracranial pressure [1]. Why the other options are incorrect: * Hypertension: While blood pressure may fluctuate during dialysis, it is not the primary cause of DDS. In fact, DDS can sometimes present with hypotension or normal BP. * Aluminum Toxicity: This is associated with "Dialysis Dementia" (a chronic progressive encephalopathy), not the acute symptoms of DDS. * Amyloid Deposition: This refers to Dialysis-Related Amyloidosis (DRA), caused by $\beta_2$-microglobulin accumulation, leading to carpal tunnel syndrome and bone cysts over years of treatment. High-Yield Clinical Pearls for NEET-PG: * Risk Factors: High BUN (>150 mg/dL), first dialysis session, and metabolic acidosis. * Clinical Features: Headache, nausea, vomiting, restlessness, and in severe cases, seizures or coma. * Prevention: The most effective strategy is to use a slow blood flow rate and shorter duration for the initial dialysis sessions to prevent rapid shifts in osmolality. * Management: If DDS occurs, the dialysis should be slowed or stopped, and hypertonic saline or mannitol may be used to reduce cerebral edema [1].

Question 553: Which of the following is NOT a feature of hepato-renal syndrome?

A. Normal GFR (Correct Answer)
B. Normal urinary sediments
C. Low Na+ in urine
D. Normal renal biopsy

Explanation: Explanation: Hepatorenal Syndrome (HRS) is a form of functional renal failure that occurs in patients with advanced liver disease (cirrhosis or fulminant hepatic failure) [1]. The core pathophysiology involves intense splanchnic vasodilation, which leads to systemic hypotension and a compensatory, profound renal vasoconstriction [1]. 1. Why "Normal GFR" is the correct answer: By definition, HRS is a state of progressive renal failure. Therefore, the Glomerular Filtration Rate (GFR) is always significantly reduced (typically <40 mL/min or a doubling of serum creatinine) [1]. A "Normal GFR" is incompatible with a diagnosis of HRS. 2. Why the other options are incorrect (Features of HRS): * Normal Urinary Sediments: Since HRS is a functional failure (hemodynamic) rather than structural damage to the nephrons, the urine microscopy is characteristically "bland" or normal, without casts or hematuria [1]. * Low Na+ in Urine: Due to the activation of the Renin-Angiotensin-Aldosterone System (RAAS) in response to perceived hypovolemia, the kidneys aggressively reabsorb sodium. Urinary sodium is typically <10–15 mEq/L [1]. * Normal Renal Biopsy: Because the kidneys are histologically intact and the failure is purely functional, a biopsy would show normal architecture. Clinical Pearls for NEET-PG: * Diagnosis of Exclusion: You must first rule out shock, nephrotoxic drugs, and organic kidney disease [1]. * Key Diagnostic Criteria: No improvement in serum creatinine (to <1.5 mg/dL) after at least 2 days of diuretic withdrawal and volume expansion with Albumin (1g/kg/day) [1]. * Treatment of Choice: Vasoconstrictors (Terlipressin is preferred) plus Albumin [1]. The definitive treatment is a Liver Transplant.

Question 554: Mutations in the epithelial sodium channel (ENaC) are associated with which of the following conditions?

A. Liddle syndrome (Correct Answer)
B. Gordon syndrome
C. Baer syndrome
D. Gitelman syndrome

Explanation: Liddle syndrome is an autosomal dominant disorder caused by **gain-of-function mutations** in the genes encoding the subunits ($\beta$ or $\gamma$) of the **Epithelial Sodium Channel (ENaC)** located in the collecting duct. These mutations prevent the degradation of ENaC, leading to its persistent expression on the apical membrane. This results in excessive sodium reabsorption and potassium secretion, manifesting as early-onset hypertension, hypokalemia, and metabolic alkalosis. Crucially, because the volume expansion suppresses the renin-angiotensin system, patients present with **low renin and low aldosterone** levels (pseudohyperaldosteronism) [1]. **Incorrect Options:** * **Gordon Syndrome (Pseudohypoaldosteronism Type II):** Caused by mutations in WNK kinases (WNK1/WNK4), leading to increased activity of the Na-Cl cotransporter (NCC). It presents with hypertension and **hyperkalemia**. * **Bartter Syndrome:** Involves mutations in transporters in the **Thick Ascending Limb** (e.g., NKCC2, ROMK), presenting like loop diuretic use (hypotension, hypokalemia). * **Gitelman Syndrome:** Caused by loss-of-function mutations in the **NCC** in the distal convoluted tubule, mimicking thiazide diuretic use (hypotension, hypocalciuria, hypomagnesemia). **High-Yield Clinical Pearls for NEET-PG:** * **Treatment Choice:** Liddle syndrome does **not** respond to Spironolactone (as the defect is distal to the mineralocorticoid receptor). It is treated with ENaC blockers like **Amiloride** or **Triamterene**. * **Triad:** Hypertension + Hypokalemia + Low Renin/Aldosterone = Think Liddle Syndrome [1]. * **Inheritance:** Most primary tubulopathies (Bartter, Gitelman) are autosomal recessive, but **Liddle syndrome is autosomal dominant**.

Question 555: Which of the following is NOT true regarding intrinsic renal failure in the context of ischemic acute tubular necrosis (ATN)?

A. Specific gravity < 1.015
B. FENa < 1
C. Urine sodium > 20 mmol/L (Correct Answer)
D. Urine creatinine to plasma creatinine ratio < 20

Explanation: In the context of Acute Kidney Injury (AKI), differentiating between **Prerenal Azotemia** and **Intrinsic Renal Failure (Ischemic ATN)** is a high-yield NEET-PG topic [1]. ### **Explanation of the Correct Answer** The correct answer is **C (Urine sodium > 20 mmol/L)** because this statement is actually **TRUE** for ATN, making it the "incorrect" choice in the context of the question. In ATN, there is structural damage to the tubular epithelial cells. These damaged tubules lose their ability to reabsorb sodium. Consequently, sodium is "wasted" in the urine, leading to a **Urine Sodium > 40 mmol/L** (and definitely > 20 mmol/L). ### **Analysis of Incorrect Options** * **B. FENa < 1:** This is the **NOT true** statement (the actual answer to the question's logic). In intrinsic ATN, the Fractional Excretion of Sodium (FENa) is **> 1%** (often > 2%) because the tubules cannot concentrate urine or retain sodium. A FENa < 1% is characteristic of Prerenal failure, where tubules are intact and responding to hypovolemia by conserving sodium. * **A. Specific gravity < 1.015:** True for ATN. Due to the loss of concentrating ability (isosthenuria), the urine becomes dilute and fixed, typically around 1.010. * **D. Urine/Plasma Creatinine ratio < 20:** True for ATN. Since the tubules cannot reabsorb water effectively, the creatinine in the urine is not concentrated, leading to a low ratio. In prerenal states, this ratio is usually > 40. ### **High-Yield Clinical Pearls for NEET-PG** | Parameter | Prerenal Azotemia | Intrinsic ATN | | :--- | :--- | :--- | | **BUN/Creatinine Ratio** | > 20:1 | < 15:1 | | **Urine Sodium (UNa)** | < 20 mmol/L | **> 40 mmol/L** | | **FENa** | < 1% | **> 2%** | | **Urine Osmolality** | > 500 mOsm/kg | < 350 mOsm/kg | | **Microscopy** | Hyaline casts | **Muddy brown granular casts** | *Note: FENa may be < 1% in certain intrinsic causes like Contrast-induced nephropathy or Pigment-induced AKI (Rhabdomyolysis).*

Question 556: A patient presents with severe hyperkalemia and peaked T waves on ECG. What is the most rapid way to decrease serum potassium level?

A. Calcium gluconate IV
B. Oral resins
C. Insulin + glucose (Correct Answer)
D. Sodium bicarbonate

Explanation: The management of hyperkalemia is a high-yield topic for NEET-PG, categorized into three steps: membrane stabilization, intracellular shifting, and elimination [1]. **Why Insulin + Glucose is correct:** Insulin is the most reliable and rapid-acting agent to **shift potassium from the extracellular to the intracellular compartment**. It stimulates the Na+/K+-ATPase pump in skeletal muscle and liver cells [2]. While the effect begins within 10–20 minutes, glucose (Dextrose 25% or 50%) is co-administered solely to prevent hypoglycemia. **Analysis of Incorrect Options:** * **A. Calcium gluconate:** This is the *first* drug given in hyperkalemia with ECG changes, but it **does not decrease serum potassium levels** [1]. It stabilizes the cardiac myocyte membrane by antagonizing the effect of potassium on the resting membrane potential [1]. * **B. Oral resins (e.g., Kayexalate):** These remove potassium from the body via the GI tract. However, they have a very slow onset of action (hours to days) and are not suitable for emergency management. * **D. Sodium bicarbonate:** This shifts potassium into cells by increasing blood pH. However, its efficacy is inconsistent and slower compared to insulin, and it is generally reserved for patients with concomitant metabolic acidosis. **NEET-PG High-Yield Pearls:** 1. **Fastest onset to lower K+:** Insulin + Glucose (10–20 mins) or Inhaled Salbutamol (30 mins). 2. **Definitive treatment:** Hemodialysis is the most effective way to remove potassium in patients with renal failure. 3. **ECG Sequence:** Peaked T waves → PR prolongation/P wave flattening → QRS widening → Sine wave pattern → Asystole [1].

Question 557: Which type of glomerulonephritis is associated with AIDS?

A. Focal segmental glomerulosclerosis (Correct Answer)
B. Post-streptococcal glomerulonephritis
C. Mesangiocapillary glomerulonephritis
D. Membranous nephropathy

Explanation: The correct answer is **Focal Segmental Glomerulosclerosis (FSGS)**. Specifically, HIV infection is associated with a unique and aggressive variant known as **HIV-Associated Nephropathy (HIVAN)** [1]. **Why FSGS is correct:** HIVAN typically presents as the **collapsing variant** of FSGS [1]. The pathophysiology involves direct infection of the glomerular visceral epithelial cells (podocytes) by the HIV virus, leading to podocyte proliferation, capillary wall collapse, and severe tubulointerstitial damage. Clinically, it presents with nephrotic-range proteinuria, rapidly progressing renal failure, and "large, echogenic kidneys" on ultrasound, even in advanced stages. It is most commonly seen in patients of African descent due to the presence of **APOL1 gene** risk variants. **Why the other options are incorrect:** * **Post-streptococcal glomerulonephritis (PSGN):** This is a classic nephritic syndrome following a Group A Beta-hemolytic Streptococcal infection (skin or throat) and is mediated by immune-complex deposition, not viral infection [1]. * **Mesangiocapillary (Membranoproliferative) GN:** This is most strongly associated with **Hepatitis C** infection and cryoglobulinemia, characterized by a "tram-track" appearance on light microscopy [1]. * **Membranous Nephropathy:** While it can be secondary to infections, it is classically associated with **Hepatitis B**, Syphilis, Malaria, or solid organ malignancies. **High-Yield Clinical Pearls for NEET-PG:** * **HIVAN Hallmark:** Collapsing FSGS + Microcystic tubular dilatation. * **Treatment:** Highly Active Antiretroviral Therapy (HAART) is the mainstay of treatment and can slow progression. * **Key Distinction:** Unlike most chronic kidney diseases where kidneys shrink, in HIVAN, the kidneys are often **normal or enlarged** in size. * **Other HIV-related renal issues:** Immune Complex Kidney Disease (HIVICK) and drug-induced toxicity (e.g., Tenofovir-induced Fanconi syndrome).

Question 558: A 13-year-old boy is referred for evaluation of nocturnal enuresis and short stature. His blood pressure is normal. The hemoglobin level is 8 g/dL, urea 112 mg/dL, creatinine 6 mg/dL, sodium 119 mEq/dL, potassium 4 mEq/L, calcium 7 mg/dL, phosphate 6 mg/dL, and alkaline phosphatase 300 U/L. Urinalysis shows trace proteinuria with hyaline casts; no red and white cells are seen. Ultrasound shows bilateral small kidneys, and the micturating cystourethrogram is normal. What is the most likely diagnosis?

A. Alport's syndrome
B. Medullary sponge kidney
C. Chronic glomerulonephritis
D. Nephronophthisis (Correct Answer)

Explanation: **Explanation:** The clinical presentation of a child with **short stature, nocturnal enuresis (polyuria), and progressive renal failure** (elevated urea/creatinine) with **bilateral small kidneys** and a bland urinary sediment is classic for **Nephronophthisis (NPHP)**. **Why Nephronophthisis is correct:** NPHP is an autosomal recessive tubulointerstitial cystic kidney disease and the most common genetic cause of End-Stage Renal Disease (ESRD) in children. * **Polyuria/Polydipsia:** Defective urinary concentration leads to nocturnal enuresis. * **Salt Wasting:** The low sodium (119 mEq/dL) reflects the inability of the tubules to conserve salt. * **Bland Sediment:** Unlike glomerulonephritis, NPHP shows minimal proteinuria and no hematuria. * **Imaging:** Small, echogenic kidneys are characteristic (unlike Medullary Cystic Kidney Disease, which presents in adults). **Why other options are incorrect:** * **Alport’s Syndrome:** Typically presents with persistent microscopic hematuria, sensorineural deafness, and ocular defects (lenticonus). * **Medullary Sponge Kidney:** Usually an asymptomatic incidental finding in adults; it is associated with nephrolithiasis and hypercalciuria, not early-onset ESRD or small kidneys. * **Chronic Glomerulonephritis:** Would typically present with significant proteinuria, active urinary sediment (RBC casts), and often hypertension, which is absent here. **NEET-PG High-Yield Pearls:** * **NPHP + Retinitis Pigmentosa** = Senior-Løken Syndrome. * **NPHP + Cerebellar Ataxia** = Joubert Syndrome. * **Key Triad:** Polyuria, growth retardation, and anemia out of proportion to renal failure (due to decreased erythropoietin from interstitial damage). * **Biopsy:** Characterized by the "tubulointerstitial triad": tubular basement membrane thickening/disruption, tubular atrophy, and interstitial fibrosis.

Question 559: What is the most common cause of end-stage renal disease?

A. Diabetes (Correct Answer)
B. Hypertension
C. Chronic glomerulonephritis
D. Polycystic kidney disease

Explanation: **Explanation:** **1. Why Diabetes is Correct:** Diabetes Mellitus (specifically Type 2) is globally recognized as the **leading cause of End-Stage Renal Disease (ESRD)**, accounting for approximately 40-50% of all cases [2]. The underlying pathophysiology involves chronic hyperglycemia leading to non-enzymatic glycosylation of the glomerular basement membrane, hyperfiltration injury, and eventual Kimmelstiel-Wilson (nodular) glomerulosclerosis [3]. This progression from microalbuminuria to overt nephropathy is the primary driver of the ESRD burden. **2. Why the Other Options are Incorrect:** * **Hypertension (B):** This is the **second most common cause** of ESRD [2]. It causes hypertensive nephrosclerosis. While highly prevalent, it trails behind diabetes in total incidence of renal replacement therapy (RRT) initiation. * **Chronic Glomerulonephritis (C):** This was historically a leading cause but has been overtaken by metabolic diseases. It remains a significant cause in younger populations and developing regions but is not the "most common" overall. * **Polycystic Kidney Disease (D):** Autosomal Dominant PKD is the most common **hereditary** cause of ESRD, but it accounts for only about 5% of the total ESRD population. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of ESRD:** Diabetes Mellitus [1]. * **Most common cause of Nephrotic Syndrome in adults:** Focal Segmental Glomerulosclerosis (FSGS) (Note: Membranous was previously cited, but FSGS is now more frequent in many registries). * **Earliest clinical sign of Diabetic Nephropathy:** Hyperfiltration (increased GFR) [3]. * **First laboratory sign:** Microalbuminuria (30-300 mg/day) [3]. * **Pathognomonic biopsy finding in Diabetes:** Kimmelstiel-Wilson (KW) nodules [3]. * **Drug of choice to slow progression:** ACE inhibitors or ARBs (and more recently, SGLT2 inhibitors).

Question 560: What is a common symptom of medullary sponge kidney disease?

A. Nocturia
B. Anemia
C. Azotemia
D. Urinary tract infection (Correct Answer)

Explanation: **Explanation:** **Medullary Sponge Kidney (MSK)** is a congenital malformation characterized by cystic dilatation of the collecting ducts in the renal papillae [1]. This structural abnormality leads to urinary stasis and impaired urinary acidification, creating a nidus for complications. 1. **Why Urinary Tract Infection (UTI) is correct:** The primary reason for UTIs in MSK is **urinary stasis** within the dilated pre-calyceal ducts. Additionally, MSK is frequently associated with **nephrocalcinosis** and **recurrent calcium oxalate stones** [1], [2] (due to hypercalciuria and distal renal tubular acidosis). These stones act as a focus for persistent or recurrent bacterial infections. 2. **Why other options are incorrect:** * **Nocturia:** While MSK can cause a mild concentrating defect, nocturia is not a hallmark symptom. It is more characteristic of chronic interstitial nephritis or early-stage polycystic kidney disease. * **Anemia & Azotemia:** MSK is generally a **benign, non-progressive condition**. Unlike Autosomal Dominant Polycystic Kidney Disease (ADPKD), MSK rarely leads to Chronic Kidney Disease (CKD) or renal failure [1]. Therefore, azotemia (elevated urea/creatinine) and anemia of chronic disease are typically absent. **High-Yield Clinical Pearls for NEET-PG:** * **Radiological Sign:** The classic appearance on Intravenous Urogram (IVU) is the **"Bouquet of flowers"** or **"Paintbrush"** appearance due to contrast filling the dilated collecting ducts [1]. * **Association:** MSK is associated with **Beckwith-Wiedemann syndrome** and hemihypertrophy. * **Metabolic Profile:** Patients often present with **Type 1 (Distal) RTA**, hypercalciuria, and hypocitraturia [2]. * **Management:** Focuses on preventing stone formation (increased fluid intake, thiazides) and treating UTIs.

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Acute Kidney Injury

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Chronic Kidney Disease

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Glomerular Diseases

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Tubulointerstitial Diseases

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Nephrotic and Nephritic Syndromes

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Urinary Tract Infections

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Renal Replacement Therapy

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Fluid and Electrolyte Disorders

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Acid-Base Disorders

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Kidney in Systemic Diseases

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Kidney Stones and Obstructive Uropathy

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Hypertension in Kidney Disease

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Nephrology — MCQs

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