Nephrology Practice Questions

Q: Dialysis disequilibrium syndrome occurs due to:

Cerebral edema. 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].

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

Normal GFR. 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.

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

Liddle syndrome. 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**.

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

Urine sodium > 20 mmol/L. 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%** (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 40. ### **High-Yield Clinical Pearls for NEET-PG** | Parameter | Prerenal Azotemia | Intrinsic ATN | | :--- | :--- | :--- | | **BUN/Creatinine Ratio** | > 20:1 | 40 mmol/L** | | **FENa** | 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).*

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

Insulin + glucose. 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].

Q: 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?

Nephronophthisis. **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.

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

Diabetes. **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).

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

Urinary tract infection. **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.

Question 1

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?

Accepted Answer

Prerenal acute kidney injury

Answer

Acute tubular necrosis

Answer

Acute cortical necrosis

Answer

Urinary tract obstruction

Question 2

Dialysis disequilibrium syndrome occurs due to:

Accepted Answer

Cerebral edema

Answer

Hypertension

Answer

Aluminum toxicity

Answer

Amyloid deposition

Question 3

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

Accepted Answer

Normal GFR

Answer

Normal urinary sediments

Answer

Low Na+ in urine

Answer

Normal renal biopsy

Question 4

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

Accepted Answer

Liddle syndrome

Answer

Gordon syndrome

Answer

Baer syndrome

Answer

Gitelman syndrome

Question 5

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

Accepted Answer

Urine sodium > 20 mmol/L

Answer

Specific gravity < 1.015

Answer

FENa < 1

Answer

Urine creatinine to plasma creatinine ratio < 20

Question 6

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

Accepted Answer

Insulin + glucose

Answer

Calcium gluconate IV

Answer

Oral resins

Answer

Sodium bicarbonate

Question 7

Which type of glomerulonephritis is associated with AIDS?

Accepted Answer

Focal segmental glomerulosclerosis

Answer

Post-streptococcal glomerulonephritis

Answer

Mesangiocapillary glomerulonephritis

Answer

Membranous nephropathy

Question 8

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?

Accepted Answer

Nephronophthisis

Answer

Alport's syndrome

Answer

Medullary sponge kidney

Answer

Chronic glomerulonephritis

Question 9

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

Accepted Answer

Diabetes

Answer

Hypertension

Answer

Chronic glomerulonephritis

Answer

Polycystic kidney disease

Question 10

What is a common symptom of medullary sponge kidney disease?

Accepted Answer

Urinary tract infection

Answer

Nocturia

Answer

Anemia

Answer

Azotemia

Nephrology — MCQs

Nephrology — MCQs

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