Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 171: In chronic renal failure, what is the typical change in anion gap?

A. Decrease in anion gap
B. Normal anion gap
C. Increase in anion gap (Correct Answer)
D. Metabolic alkalosis

Explanation: **Explanation:** In Chronic Renal Failure (CRF), the primary acid-base disturbance is a **High Anion Gap Metabolic Acidosis (HAGMA)**. This occurs because, as the Glomerular Filtration Rate (GFR) declines (typically below 20–25 mL/min), the kidneys lose the ability to excrete "fixed" organic and inorganic acids [1]. These unmeasured anions—primarily **phosphates, sulfates, and organic acids**—accumulate in the blood, displacing bicarbonate and increasing the anion gap. **Analysis of Options:** * **Option C (Correct):** The retention of acid anions (phosphates/sulfates) that are not measured in the standard electrolyte panel leads to an increased anion gap. * **Option A:** A decreased anion gap is rare and usually associated with hypoalbuminemia, lithium toxicity, or multiple myeloma, but not CRF. * **Option B:** While early-stage Chronic Kidney Disease (CKD) can present with a Normal Anion Gap Metabolic Acidosis (due to impaired ammoniagenesis) [4], the **typical** and classic presentation of advanced CRF/Uremia is an increased anion gap [2]. * **Option D:** Metabolic alkalosis occurs with acid loss (e.g., vomiting) or bicarbonate gain, which is the opposite of the pathophysiology in renal failure. **High Yield Pearls for NEET-PG:** 1. **The "MUDPILES" Mnemonic:** Remember that **'U' stands for Uremia** (CRF) as a classic cause of High Anion Gap Metabolic Acidosis. 2. **Bicarbonate levels:** In CRF, the serum bicarbonate typically stabilizes between 12–20 mEq/L; a level below 10 mEq/L suggests an additional acute process. 3. **Early vs. Late CKD:** Early CKD (Stage 1-3) often shows a Normal Anion Gap (Hyperchloremic) Acidosis [4], but as it progresses to CRF (Stage 4-5), it converts to a High Anion Gap Acidosis [3].

Question 172: All of the following conditions are associated with hypokalemia, except?

A. Adrenal tumor
B. Thiazide
C. Diarrhea
D. Acute renal failure (Correct Answer)

Explanation: The correct answer is **Acute Renal Failure (ARF)**. In ARF, particularly during the **oliguric phase**, the kidneys are unable to effectively excrete potassium due to a drastic reduction in the Glomerular Filtration Rate (GFR). This leads to **hyperkalemia**, which is one of the most life-threatening complications of renal failure [1]. **Why the other options are incorrect:** * **Adrenal Tumor:** Specifically, an aldosterone-secreting tumor (Conn’s Syndrome) causes primary hyperaldosteronism. Aldosterone acts on the distal tubules to reabsorb sodium and water while secreting potassium into the urine, leading to **hypokalemia** [1]. * **Thiazide Diuretics:** These inhibit the Na-Cl symporter in the distal convoluted tubule. The increased delivery of sodium to the collecting ducts stimulates sodium reabsorption in exchange for potassium secretion, resulting in **hypokalemia**. * **Diarrhea:** Lower gastrointestinal fluids are rich in potassium and bicarbonate. Excessive loss of these fluids leads to direct potassium depletion and metabolic acidosis (or contraction alkalosis in some cases), causing **hypokalemia** [1]. **NEET-PG High-Yield Pearls:** 1. **Phase Matters:** While the oliguric phase of ARF causes hyperkalemia, the **recovery (polyuric) phase** of ARF can actually cause hypokalemia due to osmotic diuresis. 2. **ECG in Hyperkalemia:** Look for tall "tented" T-waves, PR prolongation, and widening of the QRS complex (Sine wave pattern) [1]. 3. **Liddle’s Syndrome:** A rare genetic cause of hypokalemia that mimics hyperaldosteronism but with low renin and low aldosterone levels. 4. **Hypomagnesemia:** Always check magnesium levels in refractory hypokalemia, as potassium cannot be corrected until magnesium is replenished [1].

Question 173: Normal to increased kidney size is seen in all of the following conditions except?

A. Diabetic nephropathy
B. Polycystic kidney disease
C. AIDS-related nephropathy
D. Chronic glomerulonephritis (Correct Answer)

Explanation: In clinical nephrology, the progression of Chronic Kidney Disease (CKD) typically leads to **bilateral small, shrunken kidneys** due to progressive fibrosis and loss of nephrons. However, certain conditions are classic exceptions where kidney size remains normal or becomes enlarged despite renal failure. **Why Option D is Correct:** **Chronic Glomerulonephritis (CGN)** is the prototypical cause of small, shrunken kidneys [1]. Long-standing inflammation leads to extensive glomerular scarring, tubular atrophy, and interstitial fibrosis, resulting in a significant reduction in renal cortical thickness and overall kidney size [1]. **Why Incorrect Options are Wrong:** * **Diabetic Nephropathy (A):** This is the most common cause of CKD with enlarged kidneys. Hyperfiltration, cellular hypertrophy, and the accumulation of extracellular matrix (Kimmelstiel-Wilson nodules) lead to increased renal volume. * **Polycystic Kidney Disease (B):** Autosomal Dominant PKD (ADPKD) causes massive bilateral kidney enlargement due to the progressive growth of thousands of fluid-filled cysts. * **AIDS-related Nephropathy (C):** HIV-associated nephropathy (HIVAN) typically presents with large, echogenic kidneys on ultrasound due to profound tubulointerstitial inflammation and "collapsing" focal segmental glomerulosclerosis. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Large Kidneys in CKD:** "SHAPE" * **S** – Systemic Amyloidosis * **H** – HIV-associated nephropathy * **A** – Autosomal Dominant Polycystic Kidney Disease * **P** – Progressive Diabetic Nephropathy * **E** – End-stage Multiple Myeloma (due to light chain deposition) * **Other causes:** Renal vein thrombosis, Hydronephrosis, and Acute Glomerulonephritis (due to edema). * **Ultrasound Tip:** A kidney size of **<9 cm** is generally indicative of irreversible chronic renal failure [1].

Question 174: All of the following are true about oliguric acute renal failure EXCEPT:

A. Anemia
B. Metabolic Acidosis
C. Uremia
D. Hypercalcemia (Correct Answer)

Explanation: In **Oliguric Acute Renal Failure (ARF)**, the sudden decline in glomerular filtration rate (GFR) leads to the accumulation of nitrogenous waste and electrolyte imbalances [1]. **Why Hypercalcemia is the Correct Answer (The Exception):** In the acute phase of renal failure, **Hypocalcemia** is the classic finding, not hypercalcemia. This occurs due to: 1. **Hyperphosphatemia:** Impaired phosphate excretion leads to phosphate binding with ionized calcium (metastatic calcification). 2. **Vitamin D Deficiency:** Reduced conversion of 25-OH Vitamin D to its active form (1,25-(OH)₂D₃) by the kidneys. 3. **Skeletal Resistance:** The bones become resistant to the action of Parathyroid Hormone (PTH). *Note: Hypercalcemia may only occur during the recovery (diuretic) phase if there is mobilization of calcium from tissues or underlying rhabdomyolysis.* **Explanation of Incorrect Options:** * **Anemia:** Common in ARF due to decreased erythropoietin production, hemodilution, and a shortened red cell life span caused by the uremic environment [2]. * **Metabolic Acidosis:** The kidney fails to excrete fixed acids (H⁺ ions) and cannot regenerate bicarbonate, leading to a High Anion Gap Metabolic Acidosis (HAGMA) [2]. * **Uremia:** The hallmark of ARF is the retention of nitrogenous waste products (Azotemia), which manifests clinically as Uremia (nausea, vomiting, encephalopathy) [2]. **NEET-PG High-Yield Pearls:** * **Most common electrolyte abnormality in ARF:** Hyperkalemia (Life-threatening). * **Fractional Excretion of Sodium (FeNa):** <1% in Prerenal Azotemia; >2% in Acute Tubular Necrosis (ATN). * **Urinary Sediments:** "Muddy brown granular casts" are pathognomonic for ATN.

Question 175: Which of the following conditions can cause renal vein thrombosis?

A. Membranous nephropathy, Lupus nephritis, Post-streptococcal glomerulonephritis
B. Membranous nephropathy, Lupus nephritis, Renal amyloidosis (Correct Answer)
C. Membranoproliferative glomerulonephritis, Post-streptococcal glomerulonephritis, Renal amyloidosis
D. Membranous nephropathy, Post-streptococcal glomerulonephritis, Renal amyloidosis

Explanation: Renal Vein Thrombosis (RVT) is a well-known complication of **Nephrotic Syndrome**. The underlying pathophysiology involves a hypercoagulable state caused by the urinary loss of anticoagulant proteins (like Antithrombin III, Protein C, and S) and a concomitant increase in procoagmatic factors and platelet aggregation. **Why Option B is Correct:** While any cause of nephrotic syndrome can lead to RVT, it is most strongly associated with specific pathologies: 1. **Membranous Nephropathy (MN):** This is the most common cause of RVT in adults (incidence up to 30-50%) [1]. 2. **Membranoproliferative Glomerulonephritis (MPGN):** Also carries a high risk. 3. **Lupus Nephritis:** Particularly Class V (Membranous) lupus nephritis. 4. **Renal Amyloidosis:** A significant cause of heavy proteinuria and subsequent thrombosis. **Why Other Options are Incorrect:** * **Post-streptococcal Glomerulonephritis (PSGN):** This is primarily a **Nephritic Syndrome** [1]. While it involves glomerular injury, it typically does not present with the massive, sustained proteinuria required to create the profound hypercoagulable state seen in RVT. Options A, C, and D are incorrect because they include PSGN. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Investigation:** Selective Renal Venography (though CT Angiography is the preferred initial non-invasive test). * **Clinical Presentation:** Can be acute (flank pain, hematuria, sudden decline in GFR) or chronic (often asymptomatic, discovered during workup for pulmonary embolism). * **Left vs. Right:** The left renal vein is more commonly involved due to its more complex anatomical drainage (e.g., receiving the left gonadal vein). * **Most Common Cause:** Membranous Nephropathy is the single most high-yield association for RVT in exams [1].

Question 176: A patient has had calcium nephrocalcinosis for the past 10 years. Which of the following dietary recommendations should NOT be suggested?

A. Protein Restriction
B. Sodium Restriction (Correct Answer)
C. Fluid Intake Increase
D. All of the above

Explanation: **Explanation:** The goal of managing calcium nephrocalcinosis and recurrent calcium stones is to reduce the supersaturation of calcium salts in the urine. [1] **Why Sodium Restriction is the Correct Answer (The "NOT" recommendation):** In the context of this specific question, **Sodium Restriction** is actually a standard, highly recommended intervention for calcium stones/nephrocalcinosis. However, the question asks which should **NOT** be suggested. There appears to be a clinical paradox or a potential error in the provided key, as standard guidelines (KDIGO/Urological associations) strongly advocate for sodium restriction. Sodium restriction reduces proximal tubule sodium-calcium co-transport, thereby decreasing urinary calcium excretion (hypercalciuria). *Note for NEET-PG:* If the question implies that sodium restriction is "not" suggested, it may be based on an outdated or specific institutional preference, but physiologically, **high sodium intake** is what should be avoided. If we must select why it is "not" suggested, it would be under the premise that the patient has a specific salt-wasting tubulopathy (like Bartter or Gitelman syndrome) where sodium restriction could cause volume depletion. [2] **Analysis of Other Options:** * **Protein Restriction (A):** High animal protein intake increases the acid load, leading to hypercalciuria and hypocitraturia. Restricting protein is a standard recommendation. * **Fluid Intake Increase (C):** This is the most critical intervention. Increasing urine volume to >2.5L/day decreases the concentration of stone-forming ions. [3] **Clinical Pearls for NEET-PG:** 1. **Dietary Calcium:** Never restrict dietary calcium; low calcium intake paradoxically increases oxalate absorption in the gut, leading to hyperoxaluria and more stones. 2. **Thiazides:** These are the diuretics of choice for hypercalciuria as they increase distal tubular calcium reabsorption. 3. **Citrate:** Potassium citrate is used to increase urinary pH and inhibit calcium crystallization.

Question 177: All are new markers for Acute Kidney Injury (AKI) except?

A. Plasma IL-18 (Correct Answer)
B. Urinary IL-18
C. Plasma NGAL
D. Urinary NGAL

Explanation: ### Explanation The correct answer is **A. Plasma IL-18**. In the context of Acute Kidney Injury (AKI), the search for "renal troponins" has led to the discovery of several biomarkers that rise earlier than Serum Creatinine. [1] **1. Why Plasma IL-18 is the correct answer:** Interleukin-18 (IL-18) is a pro-inflammatory cytokine produced in the **proximal tubule** in response to injury. While **Urinary IL-18** is a highly specific and sensitive marker for ischemic acute tubular necrosis (ATN), **Plasma IL-18** is not considered a reliable or standard marker for AKI. Plasma levels of IL-18 are often influenced by systemic inflammatory conditions (like sepsis or liver disease), making it non-specific for primary renal insult. **2. Analysis of Incorrect Options:** * **Urinary IL-18:** It is a validated marker that increases significantly (up to 25-fold) in patients with ATN, typically peaking 12–48 hours before the rise in creatinine. * **NGAL (Neutrophil Gelatinase-Associated Lipocalin):** Often called the "gold standard" of new biomarkers. It is produced by nephrons in response to epithelial damage. * **Urinary NGAL:** Reflects decreased reabsorption and increased production by the distal nephron. * **Plasma NGAL:** Reflects both the systemic response and the "back-leak" from injured nephrons. Both are valid early markers for AKI. **3. High-Yield Clinical Pearls for NEET-PG:** * **Earliest Marker:** NGAL is generally considered the earliest marker to rise (within 2 hours of injury). * **KIM-1 (Kidney Injury Molecule-1):** Another high-yield urinary marker; it is a transmembrane protein specifically expressed in the proximal tubule after ischemic or toxic injury. * **Functional vs. Damage Markers:** Creatinine is a marker of *function* (GFR), whereas NGAL, IL-18, and KIM-1 are markers of *structural damage*. * **Cystatin C:** A marker of GFR that is not affected by muscle mass or age, unlike creatinine. [1]

Question 178: A 60-year-old woman presents with generalized edema, skin ulceration, and hypertension. Urine examination shows subnephrotic proteinuria (<2gm) and microscopic hematuria. Serum complement levels are decreased, and she is positive for anti-hepatitis C antibodies. What is the likely diagnosis?

A. Post-streptococcal glomerulonephritis (PSGN)
B. Essential mixed cryoglobulinemia (Correct Answer)
C. Membranoproliferative glomerulonephritis
D. Focal segmental glomerulosclerosis

Explanation: ### Explanation **Correct Option: B. Essential mixed cryoglobulinemia** The clinical triad of **Hepatitis C (HCV) infection**, **hypocomplementemia**, and **systemic involvement** (skin ulcers/purpura, hypertension, and renal disease) is classic for Mixed Cryoglobulinemia (Type II). * **Pathophysiology:** HCV triggers the production of monoclonal IgM (rheumatoid factor) that binds to polyclonal IgG. These complexes precipitate in small vessels, causing vasculitis. * **Renal Manifestation:** It typically presents as a Membranoproliferative Glomerulonephritis (MPGN) pattern on biopsy, but clinically manifests with hematuria, hypertension, and subnephrotic proteinuria [1]. The presence of skin ulcerations (vasculitis) and low complement (C4 is characteristically very low) strongly points to cryoglobulinemia over primary renal diseases [2]. **Why other options are incorrect:** * **A. PSGN:** Usually occurs in children following a throat or skin infection. While it presents with low complement and hematuria, it is not associated with HCV or chronic skin ulcers [1]. * **C. Membranoproliferative glomerulonephritis (MPGN):** While cryoglobulinemia *causes* an MPGN pattern, "Essential Mixed Cryoglobulinemia" is the more specific diagnosis given the systemic features (skin ulcers) and the direct link to Hepatitis C. * **D. Focal segmental glomerulosclerosis (FSGS):** FSGS typically presents with massive **nephrotic-range** proteinuria (>3.5g), normal complement levels, and is not associated with HCV (it is more commonly linked to HIV or Heroin use) [1]. **High-Yield Pearls for NEET-PG:** * **The "C" Connection:** Hepatitis **C**, **C**ryoglobulinemia, and low **C**omplement (especially **C4**). * **Meltzer’s Triad:** Purpura, arthralgia, and weakness (seen in 25-30% of cryoglobulinemia patients). * **Treatment:** The primary goal is treating the underlying HCV infection (Direct-acting antivirals) and immunosuppression (Rituximab/Plasmapheresis) for severe vasculitis [2].

Question 179: A 20-year-old male presents with features of acute renal failure. Blood examination reveals thrombocytopenia and Hb of 10 gm%. What is the likely cause?

A. Haemolytic uremic syndrome (Correct Answer)
B. Hereditary spherocytosis
C. Haemolytic crises
D. Chronic glomerulonephritis

Explanation: ### Explanation The clinical triad of **Acute Kidney Injury (AKI)**, **Microangiopathic Hemolytic Anemia (MAHA)**, and **Thrombocytopenia** is the hallmark of **Hemolytic Uremic Syndrome (HUS)** [1], [2]. **1. Why Option A is Correct:** In HUS, endothelial injury (often triggered by Shiga toxin from *E. coli* O157:H7) leads to the formation of microthrombi in the renal vasculature [1]. This results in: * **Thrombocytopenia:** Due to the consumption of platelets in these microthrombi [1], [2]. * **Hemolytic Anemia (Hb 10 gm%):** As RBCs pass through narrowed, fibrin-clotted vessels, they are mechanically shredded (forming schistocytes) [1]. * **Acute Renal Failure:** Due to decreased renal perfusion and glomerular damage [2]. **2. Why Other Options are Incorrect:** * **B. Hereditary Spherocytosis:** This is an extravascular hemolytic anemia due to a red cell membrane defect. While it causes anemia and jaundice, it does not typically cause thrombocytopenia or acute renal failure. * **C. Hemolytic Crises:** While this explains the drop in hemoglobin (seen in conditions like G6PD deficiency or Sickle Cell Disease), it does not characteristically present with isolated thrombocytopenia and primary acute renal failure unless complicated by pigment nephropathy (which is less common than the classic HUS presentation). * **D. Chronic Glomerulonephritis (CGN):** CGN presents with features of chronic kidney disease (shrunken kidneys, hypocalcemia, secondary hyperparathyroidism). While anemia is common in CGN (due to low erythropoietin), acute-onset thrombocytopenia is not a standard feature. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Microangiopathic hemolytic anemia (schistocytes on smear), Thrombocytopenia, and AKI [1]. * **Most Common Cause:** Shiga toxin-producing *Escherichia coli* (STEC), specifically serotype **O157:H7** [1]. * **Differentiating Feature:** Unlike DIC (Disseminated Intravascular Coagulation), the coagulation profile (PT, aPTT) in HUS is typically **normal**. * **TTP vs. HUS:** Thrombotic Thrombocytopenic Purpura (TTP) presents similarly but often includes **fever** and **neurological symptoms**, caused by **ADAMTS13** deficiency.

Question 180: All of the following are indications for emergency dialysis, EXCEPT:

A. Uremic encephalopathy
B. Persistent hyperkalemia
C. Refractory volume overload
D. Azotemia (Correct Answer)

Explanation: The indications for emergency dialysis are often remembered by the mnemonic **"AEIOU."** The goal is to treat life-threatening complications of renal failure that do not respond to medical management [1]. ### **Why Azotemia is the Correct Answer** **Azotemia** refers to the biochemical finding of elevated nitrogenous waste products (BUN and Creatinine) in the blood. While it indicates renal impairment, the absolute level of BUN or creatinine is **not** an emergency indication for dialysis. Dialysis is initiated based on the **clinical consequences** of renal failure (uremic symptoms) rather than a specific laboratory number. ### **Explanation of Incorrect Options (Indications for Dialysis)** * **A. Uremic Encephalopathy:** This represents severe "Uremic" complications (the **'U'** in AEIOU). Other uremic emergencies include pericarditis and neuropathy [1]. These are absolute indications for immediate dialysis to prevent permanent neurological damage or cardiac tamponade. Patients with deteriorating renal function may develop muscular twitching, fits, drowsiness and coma [1]. * **B. Persistent Hyperkalemia:** This represents **'E'** (Electrolyte imbalance). Specifically, hyperkalemia (>6.5 mEq/L) that is refractory to medical therapy (insulin/dextrose, calcium gluconate, etc.) is a common cause of sudden cardiac death in renal patients. * **C. Refractory Volume Overload:** This represents **'O'** (Overload). Fluid overload (pulmonary edema) that does not respond to high-dose diuretics is a life-threatening emergency requiring ultrafiltration via dialysis [1]. ### **High-Yield Clinical Pearls for NEET-PG** * **The AEIOU Mnemonic:** * **A:** Refractory Metabolic **A**cidosis (pH < 7.1) * **E:** Refractory **E**lectrolytes (Hyperkalemia) * **I:** **I**ngestions (Toxic alcohols like methanol/ethylene glycol, Lithium, Salicylates, Theophylline) * **O:** Refractory Fluid **O**verload (Pulmonary edema) * **U:** **U**remic complications (Encephalopathy, Pericarditis, GI bleed) * **Note:** In chronic kidney disease (CKD), dialysis is usually considered when the GFR drops below **15 ml/min/1.73m² (Stage 5)**, but emergency dialysis is always driven by clinical urgency.

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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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