Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 241: In a patient with a low serum anion gap, what is the most likely metabolic disorder?

A. Metabolic acidosis (Correct Answer)
B. Metabolic alkalosis
C. Respiratory acidosis
D. Respiratory alkalosis

Explanation: The **Serum Anion Gap (SAG)** is calculated as $[Na^+] - ([Cl^-] + [HCO_3^-])$. A normal gap is typically $12 \pm 4$ mEq/L. While we usually focus on a *high* anion gap, a **low serum anion gap (<6 mEq/L)** is a significant clinical finding often associated with specific types of **Metabolic Acidosis** [1]. **Why Metabolic Acidosis is correct:** A low anion gap occurs when there is an increase in unmeasured cations or a decrease in unmeasured anions. In the context of acid-base disorders, certain forms of metabolic acidosis—specifically those associated with **Multiple Myeloma**—result in a low SAG. In myeloma, the accumulation of cationic IgG paraproteins (unmeasured cations) reduces the gap. Additionally, **Bromide ingestion** (which causes a false elevation in measured chloride) can lead to a metabolic acidosis picture with a characteristically low or even negative anion gap. **Why other options are incorrect:** * **Metabolic Alkalosis:** Typically presents with a normal or slightly elevated anion gap due to increased negative charges on albumin [2]. * **Respiratory Acidosis & Alkalosis:** These are primary respiratory disturbances [3]. While they may cause compensatory changes in bicarbonate levels, they do not characteristically lower the serum anion gap. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most common cause of Low SAG:** Hypoalbuminemia (Albumin is the primary unmeasured anion; for every 1 g/dL drop in albumin, the SAG drops by ~2.5 mEq/L). 2. **Differential for Low SAG:** Multiple Myeloma (IgG), Hypermagnesemia, Hypercalcemia, Lithium toxicity, and Bromide/Iodide intoxication. 3. **Formula for Adjusted Anion Gap:** $Observed\ AG + 2.5 \times (Normal\ Albumin - Patient\ Albumin)$.

Question 242: Hyponatremia is associated with all of the following EXCEPT:

A. SIADH
B. CRF
C. Nephrotic syndrome
D. Lithium therapy (Correct Answer)

Explanation: **Explanation:** The core concept in this question is understanding which conditions cause water retention (leading to hyponatremia) versus those that cause water loss or resistance to ADH (leading to hypernatremia) [1]. **Why Lithium therapy is the correct answer:** Lithium is the classic cause of **Nephrogenic Diabetes Insipidus (NDI)**. It enters the principal cells of the collecting duct through ENaC channels and interferes with the action of Antidiuretic Hormone (ADH). This results in an inability to concentrate urine, leading to polyuria and the loss of free water. When free water is lost in excess of electrolytes, the serum sodium concentration rises, leading to **hypernatremia**, not hyponatremia. **Analysis of incorrect options:** * **SIADH (Option A):** Characterized by excessive ADH secretion, leading to inappropriate water reabsorption in the collecting ducts [1]. This causes dilutional **hyponatremia** with concentrated urine [2]. * **CRF (Chronic Renal Failure - Option B):** In advanced renal failure, the kidneys lose the ability to excrete free water due to a reduced glomerular filtration rate (GFR) and impaired tubular function, commonly resulting in hypervolemic **hyponatremia** [2]. * **Nephrotic Syndrome (Option C):** This is a state of "decreased effective arterial blood volume" due to low oncotic pressure (hypoalbuminemia). This triggers ADH release and the RAAS pathway, leading to water retention and hypervolemic **hyponatremia** [2]. **Clinical Pearls for NEET-PG:** * **Lithium Side Effects:** Remember the mnemonic **LITH**: **L**eukocytosis, **I**nsipidus (Nephrogenic), **T**remors/Teratogenicity (Ebstein’s anomaly), **H**ypothyroidism. * **Drug of Choice:** Amiloride is used to treat Lithium-induced NDI because it blocks the ENaC channels, preventing Lithium from entering the tubular cells. * **Hyponatremia Rule:** Always differentiate between Euvolemic (SIADH), Hypovolemic (Diuretics/Vomiting), and Hypervolemic (CHF/Cirrhosis/Nephrotic) states [2].

Question 243: Increased anion gap acidosis is seen in which of the following conditions?

A. Acute renal failure
B. Alcoholic ketoacidosis (Correct Answer)
C. Diabetic ketoacidosis
D. Ethylene glycol poisoning

Explanation: High Anion Gap Metabolic Acidosis (HAGMA) occurs when there is an accumulation of unmeasured organic acids in the blood [1]. The classic mnemonic used for these conditions is **MUDPILES** (Methanol, Uremia, DKA, Paraldehyde, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates) [3]. **Why Alcoholic Ketoacidosis (AKA) is the correct answer:** In AKA, chronic alcohol consumption combined with starvation leads to the accumulation of **beta-hydroxybutyrate** and **acetoacetate** [2]. These ketoacids increase the anion gap. While DKA and Ethylene glycol also cause HAGMA [4], in the context of this specific question format (often seen in older NEET-PG/AIIMS patterns), AKA is highlighted as a classic example of profound ketoacidosis. **Analysis of Options:** * **Diabetic Ketoacidosis (C) & Ethylene Glycol (D):** Both are technically correct causes of HAGMA. Ethylene glycol toxicity leads to metabolic acidosis via metabolites like glycolic acid [4]. However, in single-best-answer exams, if the question implies a specific clinical scenario or if it is a "multiple correct" type question (common in PGI/AIIMS), all three (B, C, D) would be right. In a standard NEET-PG single-choice format, this question may be considered "faulty" or "all of the above" should have been an option. * **Acute Renal Failure (A):** This causes HAGMA only when it reaches the stage of **Uremia** (accumulation of phosphates and sulfates). Early or non-uremic renal failure may present with a normal anion gap [3]. **High-Yield Clinical Pearls for NEET-PG:** 1. **GOLD MARK:** The updated mnemonic for HAGMA (Glycols, Oxoproline, L-lactate, D-lactate, Methanol, Aspirin, Renal failure, Ketoacidosis). 2. **Osmolar Gap:** If HAGMA is present with an increased osmolar gap, suspect **Methanol** or **Ethylene glycol** poisoning [4]. 3. **Normal Anion Gap (NAGMA):** Remember **HARDUPS** (Hyperalimentation, Acetazolamide, Renal Tubular Acidosis, Diarrhea, Uretero-sigmoidostomy, Pancreatic fistula) [3]. Diarrhea is the most common cause of NAGMA.

Question 244: Which of the following is seen in hemolytic uremic syndrome?

A. Spherocytes
B. Schistocytes (Correct Answer)
C. Target cells
D. Heinz bodies

Explanation: **Explanation:** **Hemolytic Uremic Syndrome (HUS)** is characterized by the classic triad of Microangiopathic Hemolytic Anemia (MAHA), thrombocytopenia, and acute kidney injury [1], [2]. The hallmark of HUS is the formation of microthrombi within small blood vessels (capillaries and arterioles). As red blood cells (RBCs) attempt to pass through these partially occluded vessels, they are mechanically shredded by fibrin strands [1]. These fragmented RBCs are known as **Schistocytes** (or helmet cells). Their presence on a peripheral blood smear is diagnostic of MAHA. **Analysis of Incorrect Options:** * **A. Spherocytes:** These are small, round RBCs lacking central pallor, typically seen in **Hereditary Spherocytosis** [3] or **Autoimmune Hemolytic Anemia (AIHA)**. In AIHA, the hemolysis is immune-mediated, not mechanical. * **C. Target cells (Codocytes):** These have a "bullseye" appearance and are characteristic of **Thalassemia**, hemoglobinopathies (HbC), or obstructive liver disease. * **D. Heinz bodies:** These are inclusions of denatured hemoglobin seen in **G6PD deficiency**. They are visualized with supravital stains and lead to "bite cells" when removed by splenic macrophages. **High-Yield Clinical Pearls for NEET-PG:** * **Etiology:** Most commonly caused by Shiga toxin-producing *E. coli* (**STEC**, O157:H7) following a prodrome of bloody diarrhea [1]. * **Atypical HUS:** Caused by uncontrolled activation of the alternative complement pathway (mutations in Factor H). * **Key Lab Findings:** Increased LDH, decreased haptoglobin, and a **negative Direct Coombs Test** (distinguishes it from AIHA). * **Management:** Primarily supportive; antibiotics and anti-motility agents are generally avoided in STEC-HUS as they may worsen toxin release.

Question 245: Indications of Continuous renal replacement therapy are all except?

A. Hyperglycemia (Correct Answer)
B. Hyperkalemia
C. Metabolic acidosis
D. Uremic symptoms

Explanation: The indications for initiating Renal Replacement Therapy (RRT), whether intermittent (IHD) or continuous (CRRT), are traditionally remembered by the mnemonic **AEIOU**. [1] **1. Why Hyperglycemia is the Correct Answer:** Hyperglycemia is **not** an indication for dialysis. It is managed medically with insulin protocols and fluid resuscitation. While severe hyperglycemia can lead to osmotic diuresis or Diabetic Ketoacidosis (DKA), the primary treatment is biochemical correction, not extracorporeal removal. **2. Analysis of Incorrect Options (Indications for CRRT):** * **Hyperkalemia (Option B):** Refractory hyperkalemia (typically K+ >6.5 mEq/L) or rapidly rising levels despite medical management is a life-threatening emergency requiring urgent RRT to prevent cardiac arrhythmias. * **Metabolic Acidosis (Option C):** Severe metabolic acidosis (typically pH <7.1) that is unresponsive to medical therapy (like bicarbonate) is a standard indication for RRT. * **Uremic Symptoms (Option D):** Clinical signs of uremia, such as uremic encephalopathy, pericarditis, or neuropathy, are absolute indications for starting dialysis regardless of the absolute BUN/Creatinine levels. **3. Clinical Pearls for NEET-PG:** * **The AEIOU Mnemonic:** * **A:** Acidosis (Refractory metabolic acidosis) * **E:** Electrolytes (Refractory Hyperkalemia) * **I:** Ingestions (Salicylates, Lithium, Isopropyl alcohol, Magnesium, Ethylene glycol) [1] * **O:** Overload (Fluid overload refractory to diuretics) * **U:** Uremia (Pericarditis, Encephalopathy, Asterixis) * **CRRT vs. IHD:** CRRT is specifically preferred over Intermittent Hemodialysis (IHD) in **hemodynamically unstable patients** (e.g., septic shock) because it allows for slower, more gradual fluid and solute removal. [1] * **High-Yield Fact:** The most common cause of death in patients with Acute Kidney Injury (AKI) is **infection/sepsis**, not the renal failure itself.

Question 246: A young adult normotensive patient presents with painless gross hematuria. What is the most likely diagnosis?

A. Minimal change disease
B. IgA nephropathy (Correct Answer)
C. Crescentic glomerulonephritis
D. Membranoproliferative glomerulonephritis

Explanation: **Explanation:** **IgA Nephropathy (Berger’s Disease)** is the most common cause of primary glomerulonephritis worldwide. The classic presentation is a young adult presenting with **episodic, painless gross hematuria**, often triggered by an upper respiratory tract infection (synpharyngitic hematuria) [1]. Unlike other nephritic syndromes, patients are frequently **normotensive** in the early stages and lack significant edema [1]. The underlying pathology involves the deposition of IgA in the glomerular mesangium [3]. **Why other options are incorrect:** * **Minimal Change Disease:** This is the most common cause of Nephrotic Syndrome in children. It typically presents with massive proteinuria and generalized edema (anasarca), not gross hematuria [2]. * **Crescentic Glomerulonephritis (RPGN):** This is a clinical emergency characterized by a rapid decline in renal function (rising creatinine) and is often associated with systemic symptoms, hypertension, and significant oliguria, rather than isolated painless hematuria [3]. * **Membranoproliferative Glomerulonephritis (MPGN):** This typically presents with a mixed nephritic-nephrotic picture. Patients often have persistent low complement levels (C3) and are more likely to be hypertensive [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Synpharyngitic Hematuria:** Hematuria occurs simultaneously or within 1-2 days of an infection in IgA Nephropathy [1]. (Contrast this with **PSGN**, where hematuria occurs 1-3 weeks *after* a sore throat [2]). * **Diagnosis:** Gold standard is Renal Biopsy showing **mesangial IgA deposits** on Immunofluorescence [3]. * **Prognosis:** The most reliable predictor of poor prognosis is the degree of persistent proteinuria and hypertension. * **Association:** Often associated with Celiac disease and Henoch-Schönlein Purpura (HSP).

Question 247: Chronic renal failure is often complicated by all of the following except?

A. Myopathy
B. Hemolytic uremic syndrome (Correct Answer)
C. Peripheral neuropathy
D. Ectopic calcification

Explanation: **Explanation:** The correct answer is **B. Hemolytic Uremic Syndrome (HUS)**. **Why HUS is the correct answer:** Hemolytic Uremic Syndrome is a **cause** of acute kidney injury (AKI), not a complication of Chronic Renal Failure (CRF) [1]. HUS is characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure [1]. While HUS can lead to chronic kidney disease if the initial damage is severe, it does not develop as a secondary consequence of pre-existing CRF. **Analysis of incorrect options (Complications of CRF):** * **Myopathy (A):** Uremic myopathy is common in advanced CRF due to vitamin D deficiency, hyperparathyroidism, malnutrition, and the accumulation of uremic toxins [1]. * **Peripheral Neuropathy (C):** This is a classic "dying-back" neuropathy affecting distal lower limbs [1]. It is caused by the retention of middle-sized molecules (uremic toxins) and usually serves as an indication for starting dialysis. * **Ectopic Calcification (D):** Also known as metastatic calcification, this occurs due to a high **Calcium x Phosphate product** (>55). Secondary hyperparathyroidism leads to calcium deposition in soft tissues, blood vessels (Mönckeberg's sclerosis), and joints [1]. **NEET-PG High-Yield Pearls:** * **Most common cause of CRF:** Diabetes Mellitus (followed by Hypertension) [1]. * **Earliest sign of Uremic Encephalopathy:** Asterixis (flapping tremors). * **Uremic Frost:** A late sign where urea crystals deposit on the skin after sweat evaporates. * **Cardiovascular disease:** The most common cause of death in patients with CRF. * **Anemia in CRF:** Primarily due to decreased Erythropoietin production [1]; it is typically normocytic normochromic.

Question 248: All of the following are causes of acute tubular necrosis (ATN) except?

A. Radiocontrasts
B. Placenta previa (Correct Answer)
C. Amphotericin B
D. Abruptio placentae

Explanation: Acute Tubular Necrosis (ATN) is the most common cause of intrinsic Acute Kidney Injury (AKI), resulting from either **prolonged ischemia** or **direct nephrotoxicity** [1]. **Why Placenta Previa is the correct answer:** Placenta previa refers to the implantation of the placenta over the internal os. While it causes significant painless antepartum hemorrhage, it is typically managed electively or diagnosed early. Unless it leads to massive, uncompensated hemorrhagic shock (which is rare with modern management), it does not characteristically cause ATN. In contrast, **Abruptio placentae** (Option D) is a classic cause of severe, sudden concealed or revealed hemorrhage leading to profound hypotension and is a notorious trigger for both ATN and **Bilateral Renal Cortical Necrosis**. **Analysis of Incorrect Options:** * **Radiocontrasts (Option A):** These are potent **nephrotoxins**. They cause ATN through a combination of direct tubular toxicity and intense intrarenal vasoconstriction (medullary hypoxia). * **Amphotericin B (Option B):** This antifungal is a well-known **nephrotoxin**. It causes ATN by increasing tubular permeability and inducing distal renal tubular acidosis (Type 1 RTA). * **Abruptio placentae (Option D):** As mentioned, this leads to severe **ischemic ATN** due to hypovolemic shock and is a high-yield obstetric cause of acute renal failure [1]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Urinary Findings in ATN:** Muddy brown granular casts are pathognomonic. 2. **Fractional Excretion of Sodium (FeNa):** Typically **>2%** in ATN (distinguishes it from Pre-renal AKI where FeNa is <1%). 3. **Ischemic vs. Toxic ATN:** Ischemic ATN primarily affects the **S3 segment** of the proximal tubule and the thick ascending limb of Henle, whereas toxic ATN primarily affects the **S1 and S2 segments** of the proximal tubule.

Question 249: All of the following are associated with polyuria except?

A. Diabetes insipidus
B. Diabetes mellitus
C. Rapidly progressive glomerulonephritis (Correct Answer)
D. Rapidly progressive glomerulonephritis

Explanation: **Explanation:** Polyuria is defined as a urine output exceeding **3 L/day** in adults. It occurs due to either an osmotic diuresis or a defect in water reabsorption. **Why Rapidly Progressive Glomerulonephritis (RPGN) is the correct answer:** RPGN is a clinical syndrome characterized by a rapid decline in GFR (usually >50% within weeks to months). The hallmark of RPGN is **oliguria** (urine output <400 ml/day) or even anuria, accompanied by an active urinary sediment (hematuria and red cell casts) [1]. Because the glomerular filtration rate drops precipitously, the kidneys cannot produce large volumes of urine, making polyuria clinically inconsistent with this diagnosis. **Analysis of Incorrect Options:** * **Diabetes Insipidus (DI):** This is the classic cause of water diuresis. Whether central (ADH deficiency) or nephrogenic (ADH resistance), the collecting ducts fail to reabsorb water, leading to massive volumes of dilute urine [2]. * **Diabetes Mellitus (DM):** This causes **osmotic diuresis**. High blood glucose levels exceed the renal threshold for reabsorption, leading to glucose in the proximal tubule. This glucose acts as an osmotically active particle, pulling water with it into the urine [2]. **NEET-PG High-Yield Pearls:** * **RPGN Histology:** The pathognomonic finding is **crescent formation** in Bowman’s space (composed of proliferating parietal epithelial cells and macrophages). * **Polyuria vs. Frequency:** Always distinguish polyuria (increased volume) from urinary frequency (increased number of voids with normal total volume). * **Other causes of Polyuria:** Hypercalcemia and Hypokalemia (both cause acquired nephrogenic DI), and the diuretic phase of Acute Tubular Necrosis (ATN). * **Oliguria Definition:** <400 ml/day; **Anuria:** <100 ml/day [1].

Question 250: Which of the following types of glomerulonephritis is least likely to cause chronic renal failure (CRF)?

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

Explanation: The correct answer is **Post-streptococcal glomerulonephritis (PSGN)**. **Why PSGN is the correct answer:** PSGN is an acute nephritic syndrome that typically follows a group A beta-hemolytic streptococcal infection. In the vast majority of cases, especially in children, the prognosis is excellent [1]. More than 95% of patients achieve complete spontaneous recovery with conservative management. While it presents with dramatic symptoms (hematuria, edema, and hypertension), it rarely progresses to chronic renal failure (CRF) and usually resolves spontaneously [1]. Only a very small percentage of adults (<5%) may develop long-term complications like persistent hypertension or chronic kidney disease. **Why the other options are incorrect:** * **Membranous Glomerulonephritis (MGN):** This is a common cause of nephrotic syndrome in adults. It follows the "rule of thirds": one-third remit, one-third persist, and **one-third progress to end-stage renal disease (ESRD)** [2]. * **Membranoproliferative Glomerulonephritis (MPGN):** This is a highly aggressive lesion. Type I and Type II (Dense Deposit Disease) have a poor prognosis, with approximately **50% of patients developing CRF** within 10 years. * **Focal Segmental Glomerulosclerosis (FSGS):** This is a leading cause of nephrotic syndrome in adults and is notorious for its progressive nature [1]. It frequently leads to **ESRD**, and it has a high recurrence rate even after kidney transplantation. **High-Yield Clinical Pearls for NEET-PG:** * **Lumpy-Bumpy Appearance:** Immunofluorescence in PSGN shows granular deposits of IgG and C3. * **Subepithelial Humps:** Characteristic finding on Electron Microscopy in PSGN. * **Low Complement:** C3 levels are characteristically low in the acute phase of PSGN but return to normal within 6–8 weeks. * **Prognosis:** PSGN has the best prognosis among the nephritic syndromes, whereas FSGS and MPGN are among the worst.

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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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