Nephrology — MCQs
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Which of the following statements about contrast-induced acute kidney injury is true?
A patient presents with hematuria of several days and dysmorphic red blood cell casts in the urine. What is the most likely site of origin for the bleeding?
What is the appropriate infusion time for the dialysate in a 38-year-old patient with chronic renal failure?
Which syndrome is characterized by proteinuria, hematuria, and hypertension?
A 48-year-old woman with chronic renal failure has bilaterally enlarged kidneys with multiple cysts on renal scan. She experienced a sudden onset of severe headache. A cerebral angiogram showed marked narrowing of cerebral artery branches near the base of the brain, consistent with vasospasm, and no intraparenchymal hemorrhage. Which of the following conditions MOST likely produced these findings?
Which of the following is a common feature of NSAID-induced allergic interstitial nephritis?
A patient with chronic renal failure reports pruritus. Which instruction should be included in this patient’s teaching plan?
Which of the following are characteristic features of medullary sponge kidney?
What is seen in Bartter syndrome?
A 29-year-old female with a history of Sjogren's syndrome presents with a 2-day episode of watery diarrhea. Physical examination is unremarkable. Considering her history, the physician checks her urine electrolytes, which show: K = 31 mEq/L, Na = 100 mEq/L, Cl = 105 mEq/L. What is her current diagnosis?
Nephrology Indian Medical PG Practice Questions and MCQs
Question 571: Which of the following statements about contrast-induced acute kidney injury is true?
- A. Serum creatinine rises after 12 hours.
- B. Peak serum creatinine occurs within 2 weeks.
- C. Dialysis requirement is usually uncommon. (Correct Answer)
- D. High fractional excretion of sodium is a common finding.
Explanation: **Explanation:** Contrast-Induced Acute Kidney Injury (CI-AKI) is a form of acute tubular necrosis (ATN) caused by the administration of iodinated contrast media. **Why Option C is correct:** CI-AKI is typically a self-limiting condition. While it causes a transient decline in renal function, the injury is usually mild. **Dialysis is required in less than 1% of cases** in the general population, though the risk increases slightly in patients with pre-existing advanced chronic kidney disease or cardiogenic shock. **Analysis of Incorrect Options:** * **Option A:** Serum creatinine typically begins to rise within **24 to 48 hours** after contrast exposure, not 12 hours. * **Option B:** The peak serum creatinine level is usually reached within **3 to 5 days**, with levels typically returning to baseline within 7 to 10 days. A 2-week timeframe is too long for the peak of CI-AKI. * **Option D:** Unlike most forms of ATN, CI-AKI often presents with a **low fractional excretion of sodium (FeNa < 1%)**. This is due to the intense renal medullary vasoconstriction that precedes tubular injury, mimicking a pre-renal pattern. **Clinical Pearls for NEET-PG:** * **Definition:** An absolute increase in serum creatinine of $\geq$ 0.3 mg/dL or a $\geq$ 50% increase from baseline within 48–72 hours [1]. * **Risk Factors:** Pre-existing CKD (most important), Diabetes Mellitus, heart failure, and volume depletion. * **Prevention:** The most effective preventive strategy is **intravenous hydration** with isotonic saline (0.9% NaCl) before and after the procedure. * **Contrast Type:** Low-osmolar or iso-osmolar contrast agents are preferred to reduce nephrotoxicity.
Question 572: A patient presents with hematuria of several days and dysmorphic red blood cell casts in the urine. What is the most likely site of origin for the bleeding?
- A. Kidney (Correct Answer)
- B. Ureter
- C. Bladder
- D. Urethra
Explanation: **Explanation:** The presence of **dysmorphic red blood cells (RBCs)** and **RBC casts** is a pathognomonic finding for **glomerular bleeding**, indicating that the source of hematuria is the **Kidney** (specifically the renal parenchyma/glomerulus) [1]. 1. **Why Kidney is correct:** When RBCs pass through the damaged glomerular basement membrane (GBM) and travel through the renal tubules, they undergo mechanical trauma and osmotic stress, leading to a "dysmorphic" appearance (e.g., acanthocytes) [1]. Furthermore, RBCs get trapped in a matrix of **Tamm-Horsfall mucoprotein** within the distal convoluted tubule or collecting duct, forming **RBC casts** [1]. The presence of these casts confirms that the bleeding originated within the nephron. 2. **Why other options are incorrect:** * **Ureter, Bladder, and Urethra:** These represent the post-renal or "lower" urinary tract. Bleeding from these sites is typically characterized by **isomorphic (uniform) RBCs** and the **absence of casts**, as the blood enters the urine stream after the site of protein matrix formation in the tubules [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Acanthocytes:** RBCs with "mickey mouse ears" or blebs; if they constitute >5% of the urine RBCs, it is highly specific for glomerular disease [1]. * **Glomerular vs. Non-Glomerular Hematuria:** * **Glomerular:** Smoky/Cola-colored urine, RBC casts, dysmorphic RBCs, and significant proteinuria [1]. * **Non-Glomerular:** Bright red urine, blood clots (never seen in glomerular bleeding), and isomorphic RBCs. * **Common Causes:** Glomerular bleeding is often due to IgA Nephropathy (most common worldwide), Post-Streptococcal Glomerulonephritis (PSGN), or Alport Syndrome.
Question 573: What is the appropriate infusion time for the dialysate in a 38-year-old patient with chronic renal failure?
- A. 15 minutes (Correct Answer)
- B. 30 minutes
- C. 1 hour
- D. 2 to 3 hours
Explanation: ### Explanation In Peritoneal Dialysis (PD), the procedure is divided into three distinct phases collectively known as an **"Exchange."** These phases are: 1. **Inflow (Fill):** The dialysate is introduced into the peritoneal cavity [1]. 2. **Dwell:** The fluid remains in the cavity for diffusion and osmosis to occur [1]. 3. **Drain:** The used fluid is removed. The correct answer is **15 minutes** because the standard clinical protocol for the **Inflow phase** typically ranges from **10 to 20 minutes** (averaging 15 minutes). This duration is sufficient to allow the fluid to enter by gravity without causing sudden intra-abdominal pressure discomfort, while remaining efficient enough to maximize the subsequent dwell time. #### Analysis of Incorrect Options: * **30 minutes (B):** This is unnecessarily slow for an inflow phase and would reduce the overall efficiency of the dialysis session. * **1 hour (C):** This duration is far too long for simple infusion and is more characteristic of a short dwell time in specific rapid-exchange protocols. * **2 to 3 hours (D):** This represents the typical **Dwell Time**, not the infusion time [1]. During this period, metabolic wastes (urea, creatinine) and excess water move from the blood into the dialysate. #### NEET-PG High-Yield Pearls: * **Peritoneal Membrane:** Acts as the semi-permeable membrane. The most common complication of PD is **Peritonitis** (look for cloudy effluent and a cell count >100/µL with >50% neutrophils). * **Standard Volume:** Usually 2 liters of dialysate per exchange in adults. * **Contraindication:** Absolute contraindications include loss of peritoneal surface area (extensive adhesions) or unrepairable abdominal wall hernias. * **Glucose:** The primary osmotic agent used in standard dialysate to pull fluid across the membrane [1].
Question 574: Which syndrome is characterized by proteinuria, hematuria, and hypertension?
- A. Nephrotic syndrome
- B. Acute nephritis (Correct Answer)
- C. Renal cell carcinoma
- D. Nephrocalcinosis
Explanation: **Explanation:** The correct answer is **Acute Nephritis** (also known as Nephritic Syndrome). This clinical entity is defined by a specific constellation of symptoms resulting from acute glomerular inflammation. **1. Why Acute Nephritis is correct:** The hallmark of nephritic syndrome is the **"Nephritic Triad"**: * **Hematuria:** Often presenting as "cola-colored" or smoky urine due to RBC casts and dysmorphic RBCs leaking through an inflamed glomerular basement membrane [1]. * **Hypertension:** Caused by fluid retention and impaired sodium excretion [1], [3]. * **Proteinuria:** Usually in the sub-nephrotic range (<3.5 g/day). Additionally, patients often present with **Oliguria** and **Azotemia** (elevated Cr/BUN) [2]. **2. Why other options are incorrect:** * **Nephrotic Syndrome:** Characterized by massive proteinuria (>3.5 g/day), hypoalbuminemia, and generalized edema [1]. While it involves proteinuria, hematuria and hypertension are typically absent or minimal. * **Renal Cell Carcinoma (RCC):** Classically presents with the triad of flank pain, hematuria, and a palpable abdominal mass. It does not typically cause systemic hypertension or significant proteinuria. * **Nephrocalcinosis:** Refers to the deposition of calcium salts in the renal parenchyma. It is usually asymptomatic in early stages or presents with features of the underlying metabolic disorder (e.g., hyperparathyroidism) rather than an acute nephritic picture. **NEET-PG High-Yield Pearls:** * **Most common cause:** Post-Streptococcal Glomerulonephritis (PSGN) is the classic prototype of acute nephritis in children [3]. * **Pathognomonic finding:** The presence of **RBC casts** in urine sediment is the most specific indicator of glomerular bleeding (nephritis). * **Differentiating Proteinuria:** Nephritic (<3.5 g/day) vs. Nephrotic (>3.5 g/day) [1].
Question 575: A 48-year-old woman with chronic renal failure has bilaterally enlarged kidneys with multiple cysts on renal scan. She experienced a sudden onset of severe headache. A cerebral angiogram showed marked narrowing of cerebral artery branches near the base of the brain, consistent with vasospasm, and no intraparenchymal hemorrhage. Which of the following conditions MOST likely produced these findings?
- A. Bacterial meningitis
- B. Severe atherosclerosis
- C. Malignant hypertension
- D. Subarachnoid hemorrhage (Correct Answer)
Explanation: **Explanation:** **1. Why Subarachnoid Hemorrhage (SAH) is Correct:** The clinical presentation describes a patient with **Autosomal Dominant Polycystic Kidney Disease (ADPKD)**, characterized by chronic renal failure and bilaterally enlarged cystic kidneys [3]. ADPKD is strongly associated with **berry (saccular) aneurysms** in the Circle of Willis (occurring in ~10% of patients). The "sudden onset of severe headache" (thunderclap headache) is the classic presentation of a ruptured berry aneurysm leading to **Subarachnoid Hemorrhage** [1]. A key complication of SAH, typically occurring 3–14 days post-bleed, is **reactive vasospasm** caused by the release of endothelin and other spasmogenic substances from broken-down blood products [2]. This explains the "marked narrowing of cerebral artery branches" seen on the angiogram. **2. Why Other Options are Incorrect:** * **Bacterial Meningitis:** While it causes headache and meningeal signs [1], it does not typically cause focal arterial narrowing (vasospasm) on an angiogram or correlate with ADPKD. * **Severe Atherosclerosis:** This causes chronic, irregular narrowing or occlusion of vessels but does not present with a sudden-onset severe headache or the specific systemic association with cystic kidneys [1]. * **Malignant Hypertension:** Though common in renal failure, it usually presents with encephalopathy, papilledema, and intraparenchymal changes rather than isolated cerebral vasospasm. **3. NEET-PG High-Yield Pearls:** * **ADPKD Associations:** Berry aneurysms (most common extra-renal manifestation), hepatic cysts (most common overall), mitral valve prolapse, and diverticulosis [3]. * **Vasospasm Management:** Nimodipine (a calcium channel blocker) is the drug of choice to reduce ischemic neurological deficits following SAH [2]. * **Diagnosis:** Non-contrast CT is the initial investigation of choice for SAH; if negative but suspicion is high, perform a Lumbar Puncture (look for xanthochromia) [1], [2].
Question 576: Which of the following is a common feature of NSAID-induced allergic interstitial nephritis?
- A. Fever
- B. Rash
- C. Eosinophilia
- D. Heavy proteinuria (Correct Answer)
Explanation: ### Explanation **Correct Option: D (Heavy proteinuria)** NSAID-induced **Acute Interstitial Nephritis (AIN)** is a unique clinical entity that differs significantly from classic drug-induced AIN (e.g., caused by Penicillins or Sulfonamides). The hallmark of NSAID-induced AIN is the frequent association with **Minimal Change Disease (MCD)** or Membranous Nephropathy, leading to **nephrotic-range proteinuria (>3.5g/day)** [1]. This occurs because NSAIDs inhibit cyclooxygenase, diverting arachidonic acid metabolism toward the lipoxygenase pathway. This results in an overproduction of leukotrienes, which can alter glomerular permeability and cause podocyte foot process effacement. **Why other options are incorrect:** * **A, B, and C (Fever, Rash, Eosinophilia):** These constitute the "classic triad" of drug-induced AIN. While common in hypersensitivity reactions to antibiotics (like Methicillin), this triad is **notoriously absent** in NSAID-induced cases. Patients typically present months after starting the drug, often lacking systemic allergic features [1]. **High-Yield Clinical Pearls for NEET-PG:** * **The "Classic Triad":** Fever, rash, and eosinophilia are seen in only **10–15%** of all AIN cases; their absence does not rule out the diagnosis [1]. * **Latency Period:** Unlike most drugs which cause AIN within days, NSAID-induced AIN can occur after **months** of chronic use. * **Urinalysis:** Look for "sterile pyuria" (WBCs without bacteria) and WBC casts. Eosinophiluria (Hansel’s stain) is suggestive but not pathognomonic [1]. * **Management:** The first step is the immediate cessation of the offending NSAID. Corticosteroids may be used if renal function does not improve.
Question 577: A patient with chronic renal failure reports pruritus. Which instruction should be included in this patient’s teaching plan?
- A. Rub the skin vigorously with a towel
- B. Take frequent baths
- C. Apply alcohol-based emollients to the skin
- D. Keep fingernails short and clean (Correct Answer)
Explanation: **Explanation:** **Uremic pruritus** is a common and distressing complication of Chronic Kidney Disease (CKD), particularly in patients with end-stage renal disease (ESRD) [2]. It is thought to be caused by the accumulation of uremic toxins, hyperphosphatemia [3], and secondary hyperparathyroidism. **Why Option D is Correct:** The primary goal in managing pruritus is to prevent secondary complications. Patients often scratch uncontrollably, especially during sleep. Keeping **fingernails short and clean** minimizes skin trauma (excoriations) and reduces the risk of secondary bacterial infections (e.g., *Staphylococcus aureus*), which can lead to cellulitis or sepsis [2] in immunocompromised CKD patients. **Why Other Options are Incorrect:** * **Option A:** Rubbing the skin vigorously increases local irritation and can cause further skin breakdown, exacerbating the itch-scratch cycle. * **Option B:** Frequent baths, especially with hot water, strip the skin of natural oils, leading to xerosis (dry skin), which significantly worsens uremic pruritus. * **Option C:** Alcohol-based products have a drying effect on the skin. Patients should instead use **water-based or oil-based emollients** to maintain skin hydration [1]. **NEET-PG High-Yield Pearls:** * **First-line Medical Management:** Optimization of dialysis and control of serum phosphorus (using phosphate binders). * **Topical Therapy:** Emollients and capsaicin cream. * **Systemic Therapy:** Gabapentin or Pregabalin are highly effective for uremic pruritus. * **Phototherapy:** Narrowband UVB (NB-UVB) is the most effective non-pharmacological treatment for refractory cases. * **Key Lab Finding:** Often associated with high Calcium-Phosphate (Ca x P) product [3].
Question 578: Which of the following are characteristic features of medullary sponge kidney?
- A. Autosomal dominant, Nephrocalcinosis, and More common in females
- B. Autosomal dominant, Nephrocalcinosis, and Minimal proteinuria
- C. Autosomal dominant, Nephrocalcinosis, and Minimal proteinuria (Correct Answer)
- D. Autosomal dominant and Nephrocalcinosis
Explanation: **Medullary Sponge Kidney (MSK)** is a congenital malformation characterized by the cystic dilatation of the collecting ducts in the renal papillae [1]. While most cases are sporadic, a significant number of cases show an **Autosomal Dominant** inheritance pattern, often associated with mutations in the *RET* proto-oncogene or *GDNF*. ### **Why Option C is Correct:** 1. **Autosomal Dominant:** Recent studies indicate a strong familial clustering with dominant inheritance in many patients. 2. **Nephrocalcinosis:** This is a hallmark feature. Urinary stasis in the dilated collecting ducts, combined with associated hypercalciuria and distal renal tubular acidosis (dRTA), leads to the formation of calcium phosphate/oxalate stones (nephrocalcinosis and nephrolithiasis) [1]. 3. **Minimal Proteinuria:** Since MSK primarily affects the medullary collecting ducts and not the glomeruli, glomerular filtration remains intact. Proteinuria, if present, is typically minimal (<500 mg/day). ### **Analysis of Incorrect Options:** * **Option A:** MSK does not show a female predilection; it affects both sexes equally, though it is often diagnosed earlier in females due to a higher frequency of symptomatic urinary tract infections. * **Option B & D:** While these contain correct elements, Option C is the most comprehensive answer, encompassing the triad of inheritance, classic imaging findings (nephrocalcinosis), and the absence of significant glomerular damage (minimal proteinuria). ### **High-Yield Clinical Pearls for NEET-PG:** * **Imaging Gold Standard:** Intravenous Urogram (IVU) showing the **"Paintbrush" appearance** [1] or "bouquet of flowers" due to contrast filling the dilated ducts. * **Associated Conditions:** Often linked with **Beckwith-Wiedemann Syndrome** and **Caroli’s Disease**. * **Complications:** Recurrent calcium stones [1], distal RTA (Type 1), and impaired urinary concentrating ability. * **Prognosis:** Generally excellent; renal failure is rare unless complicated by severe recurrent infections or massive stone burden [1].
Question 579: What is seen in Bartter syndrome?
- A. Metabolic acidosis
- B. Hypokalemia (Correct Answer)
- C. Hyperkalemia
- D. Decrease in urinary calcium
Explanation: **Explanation:** **Bartter syndrome** is a group of autosomal recessive genetic disorders characterized by a defect in the thick ascending limb (TAL) of the loop of Henle [3]. It mimics the chronic use of **loop diuretics** (like Furosemide). 1. **Why Hypokalemia is correct:** The primary defect involves the NKCC2 transporter (or related channels like ROMK). This leads to a failure of sodium, chloride, and potassium reabsorption in the TAL. The resulting increased distal delivery of sodium to the collecting duct triggers aldosterone-mediated sodium reabsorption in exchange for potassium and hydrogen ions [1]. This leads to profound **hypokalemia** and metabolic alkalosis [2]. 2. **Why other options are incorrect:** * **Metabolic Acidosis (A):** Bartter syndrome causes **Metabolic Alkalosis** due to increased hydrogen ion secretion in the distal tubule (stimulated by aldosterone and volume depletion) [2]. * **Hyperkalemia (C):** This is the opposite of what occurs; potassium is lost excessively in the urine. * **Decrease in urinary calcium (D):** In the TAL, the reabsorption of Ca²⁺ and Mg²⁺ depends on the positive lumen potential created by potassium recycling. Since this mechanism is defective in Bartter syndrome, calcium is not reabsorbed, leading to **Hypercalciuria** (unlike Gitelman syndrome, which causes hypocalciuria). **High-Yield Clinical Pearls for NEET-PG:** * **Bartter vs. Gitelman:** Bartter mimics **Loop diuretics** (High urinary calcium); Gitelman mimics **Thiazides** (Low urinary calcium). * **Presentation:** Polyuria, polydipsia, and growth retardation in childhood. * **Key Lab Findings:** Hypokalemia, Metabolic Alkalosis, Hypercalciuria, and High Renin/Aldosterone levels with **Normal Blood Pressure**.
Question 580: A 29-year-old female with a history of Sjogren's syndrome presents with a 2-day episode of watery diarrhea. Physical examination is unremarkable. Considering her history, the physician checks her urine electrolytes, which show: K = 31 mEq/L, Na = 100 mEq/L, Cl = 105 mEq/L. What is her current diagnosis?
- A. Renal tubular acidosis (Correct Answer)
- B. Hypochloremic metabolic alkalosis
- C. Malignant hypertension
- D. Respiratory alkalosis
Explanation: ### **Explanation** The correct answer is **Renal Tubular Acidosis (RTA)**. **1. Why it is correct:** The patient has Sjogren’s syndrome, which is classically associated with **Distal (Type 1) RTA**. The key to solving this question lies in calculating the **Urine Anion Gap (UAG)**. * **Formula:** $UAG = (Na^+ + K^+) - Cl^-$ * **Calculation:** $(100 + 31) - 105 = +26\text{ mEq/L}$. A **positive UAG** indicates a failure of the kidneys to excrete ammonium ($NH_4^+$), which is characteristic of RTA [1]. In contrast, patients with diarrhea (extra-renal bicarbonate loss) typically have a negative UAG because their kidneys are functioning normally and increasing $NH_4Cl$ excretion to compensate for the acidosis. **2. Why the other options are wrong:** * **Hypochloremic metabolic alkalosis:** This usually results from vomiting or diuretic use [1]. The patient has diarrhea (which causes metabolic acidosis) and the urine chloride is high, not low. * **Malignant hypertension:** This presents with severely elevated BP (>180/120 mmHg) and end-organ damage (papilledema, encephalopathy), which are absent here. * **Respiratory alkalosis:** This is characterized by a primary decrease in $PCO_2$ (hyperventilation). The clinical context of Sjogren’s and electrolyte imbalances points toward a metabolic/renal pathology. **3. NEET-PG High-Yield Pearls:** * **Urine Anion Gap:** Positive ($>0$) = RTA; Negative ($<0$) = Diarrhea/Extra-renal loss. * **Sjogren’s Syndrome:** Most common renal manifestation is **Type 1 (Distal) RTA** due to lymphocytic infiltration of the tubules. * **Type 1 RTA:** Characterized by inability to secrete $H^+$ in the distal tubule, leading to high urine pH ($>5.5$) and hypokalemia [1]. * **Type 2 RTA:** Associated with Fanconi syndrome; failure to reabsorb $HCO_3^-$ in the proximal tubule. * **Type 4 RTA:** Associated with Diabetes Mellitus and **hyperkalemia**.
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
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