Nephrology Practice Questions

Q: All of the following are associated with polyuria except?

Rapidly progressive glomerulonephritis. **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].

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

Post-streptococcal glomerulonephritis. 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.

Q: A 35-year-old man with AML and WBC of 100,000 cells/µl is treated with chemotherapy and develops oliguric renal failure. His urine is acidic and numerous crystals are noted in the urine. What is the most likely diagnosis?

Urate nephropathy. The clinical scenario describes **Acute Urate Nephropathy**, a classic manifestation of **Tumor Lysis Syndrome (TLS)**. In patients with high-grade hematologic malignancies (like AML) and a high tumor burden (WBC >100,000/µl), rapid cell lysis following chemotherapy releases massive amounts of intracellular purines. These are metabolized into **uric acid**. [2] 1. **Why Urate Nephropathy is correct:** Uric acid is poorly soluble in the acidic environment of the distal tubules and collecting ducts. This leads to the precipitation of uric acid crystals, causing intrarenal obstruction and oliguric acute kidney injury (AKI). [1] The presence of **acidic urine** and **numerous crystals** is pathognomonic. [2] 2. **Why other options are incorrect:** * **Nephrocalcinosis:** This involves calcium phosphate deposition in the renal parenchyma, usually seen in chronic hypercalcemic states or distal RTA, not typically presenting as acute oliguric failure post-chemotherapy. * **Leukemic infiltration:** While it can cause renal enlargement, it rarely causes sudden, acute oliguric renal failure immediately following the initiation of chemotherapy. * **Acute Tubular Necrosis (ATN):** While some chemo agents are nephrotoxic, the specific mention of high WBC count, acidic urine, and crystals points specifically to urate crystal-induced obstruction rather than direct tubular cell death. **High-Yield Clinical Pearls for NEET-PG:** * **Uric Acid/Creatinine Ratio:** In acute urate nephropathy, the ratio is typically **>1.0**, whereas in other causes of AKI, it is 7.0) increases uric acid solubility but is now controversial as it may promote calcium phosphate precipitation.

Q: A 64-year-old woman presents with metabolic alkalosis and a bicarbonate level of 34 mEq/L. Which of the following is the most likely cause?

Diuretic use. **Explanation:** **Metabolic alkalosis** is characterized by an increase in plasma bicarbonate ($HCO_3^-$) and an increase in pH. The correct answer is **Diuretic use** (specifically loop and thiazide diuretics), which is a classic cause of "contraction alkalosis." 1. **Why Diuretic Use is Correct:** * **Volume Contraction:** Diuretics cause loss of $NaCl$ and water, leading to extracellular fluid (ECF) volume depletion. This activates the Renin-Angiotensin-Aldosterone System (RAAS). * **Aldosterone Effect:** Increased aldosterone promotes $Na^+$ reabsorption in exchange for $H^+$ and $K^+$ secretion in the distal tubule. The loss of $H^+$ leads to "new" $HCO_3^-$ generation. * **Chloride Depletion:** Diuretics cause chloride loss; low chloride levels impair the $HCO_3^-/Cl^-$ exchanger in the collecting duct, preventing the excretion of excess bicarbonate. 2. **Why Other Options are Incorrect:** * **Hyperkalemia:** Acidosis causes hyperkalemia (as $H^+$ moves intracellularly and $K^+$ moves out). Conversely, **hypokalemia** causes alkalosis. * **Mineralocorticoid Deficiency (e.g., Addison’s):** A lack of aldosterone leads to $H^+$ retention, resulting in **Normal Anion Gap Metabolic Acidosis (RTA Type 4)**, not alkalosis. * **Diarrhea:** Lower GI secretions are rich in $HCO_3^-$. Loss of these fluids leads to **Metabolic Acidosis**. **High-Yield Clinical Pearls for NEET-PG:** * **Saline Responsiveness:** Metabolic alkalosis due to diuretics or vomiting is "Saline Responsive" (Urinary $Cl^- 20$ mEq/L). * **The "H" Rule:** In alkalosis, look for the "Low's": Hypovolemia, Hypochloremia, and Hypokalemia.

Q: Which of the following has no role in the management of acute onset hyperkalemia?

Intravenous bicarbonate. Explanation: The management of acute hyperkalemia focuses on three goals: stabilizing the cardiac membrane, shifting potassium into cells, and eliminating potassium from the body [1]. **1. Why Intravenous Bicarbonate is the Correct Answer:** Current clinical guidelines (including KDIGO and AHA) state that **intravenous sodium bicarbonate** has no role in the *acute* management of hyperkalemia, especially when not associated with metabolic acidosis. While it was historically used to shift potassium into cells, evidence shows it is ineffective as a bolus and works too slowly to be useful in an emergency. It may only be considered in cases of severe pre-existing metabolic acidosis (pH < 7.1). **2. Analysis of Other Options:** * **Calcium chloride (Option C):** This is the **first-line** treatment for hyperkalemia with ECG changes [1]. It antagonizes the membrane-excitability effects of potassium, stabilizing the cardiac myocyte membrane to prevent arrhythmias [1]. It does *not* lower serum potassium levels. * **Intravenous regular insulin (Option D):** Usually given with 25-50g of Dextrose, insulin stimulates the Na+/K+-ATPase pump, shifting potassium into the intracellular compartment. It is the most reliable agent for rapid potassium reduction. * **Nebulization with salbutamol (Option B):** Beta-2 agonists also stimulate the Na+/K+-ATPase pump to shift potassium intracellularly. It acts synergistically with insulin. **High-Yield Clinical Pearls for NEET-PG:** * **Fastest onset of action:** Calcium gluconate/chloride (1-3 mins) – but it is **cardioprotective only.** [1] * **Most effective for shifting K+:** Insulin + Dextrose. * **Calcium Gluconate vs. Chloride:** Calcium chloride contains 3x more elemental calcium than gluconate but is more irritating to peripheral veins. * **Definitive treatment:** Hemodialysis is the most effective method for potassium removal if medical therapy fails or in renal failure.

Q: Which of the following is NOT a component of dialysate in hemodialysis?

Aluminium. **Explanation:** The goal of hemodialysis is to mimic the filtration function of the kidney by removing metabolic waste products and excess electrolytes while maintaining physiological balance [1]. **Why Aluminium is the correct answer:** Aluminium is **not** a component of dialysate; in fact, its presence is strictly avoided. Historically, aluminium toxicity was a major complication in dialysis patients (leading to **Dialysis Encephalopathy**, osteomalacia, and microcytic anemia) due to its presence in untreated tap water used for dialysate or the use of aluminium-containing phosphate binders [2]. Modern dialysis requires highly purified water (via Reverse Osmosis) to ensure aluminium levels are negligible. **Why the other options are incorrect:** * **Sodium (A):** Dialysate sodium is typically kept at 135–145 mEq/L. It is essential to maintain serum osmolality and prevent "Dialysis Disequilibrium Syndrome." * **Potassium (B):** Potassium is a vital component, usually kept at 0–4 mEq/L. The concentration is adjusted based on the patient's pre-dialysis serum potassium levels to facilitate the removal of excess potassium via a concentration gradient [1]. * **Glucose (D):** Glucose is added to the dialysate (typically 100–200 mg/dL) to prevent hypoglycemia during the procedure and to provide a small osmotic gradient to assist in fluid removal. **High-Yield Clinical Pearls for NEET-PG:** * **Dialysis Encephalopathy:** Characterized by speech disturbances, seizures, and progressive dementia due to aluminium toxicity. * **Water Purification:** Reverse Osmosis (RO) is the gold standard for preparing water for dialysate to remove contaminants like aluminium, copper, and chloramines. * **Bicarbonate:** Modern dialysate uses bicarbonate as a buffering agent instead of acetate to correct metabolic acidosis.

Q: Hypokalemic hypertension is a feature of which condition?

Liddle syndrome. **Explanation:** The combination of **hypokalemia and hypertension** is a classic indicator of mineralocorticoid excess (or a state that mimics it). **1. Why Liddle Syndrome is Correct:** Liddle syndrome is an autosomal dominant disorder characterized by a "gain-of-function" mutation in the genes encoding the **ENaC (Epithelial Sodium Channel)** in the distal nephron. This leads to constitutive activation of the channels, causing excessive sodium reabsorption and potassium excretion [1]. Clinically, it mimics primary hyperaldosteronism (hypertension, hypokalemia, metabolic alkalosis) but is unique because **renin and aldosterone levels are both low** (pseudohyperaldosteronism) [1]. **2. Why the Other Options are Incorrect:** * **Bartter and Gitelman Syndromes:** These are "salt-wasting" nephropathies. While they both present with hypokalemia and metabolic alkalosis, they are characterized by **normotension or hypotension** due to chronic volume depletion and secondary hyperaldosteronism. * **Graves' Disease:** This is a form of hyperthyroidism. While it can cause systolic hypertension (due to increased cardiac output) and occasionally hypokalemic periodic paralysis, it is not a primary cause of chronic hypokalemic hypertension. **3. NEET-PG Clinical Pearls:** * **Treatment of Liddle Syndrome:** Unlike primary aldosteronism, it does **not** respond to Spironolactone. It is treated with ENaC blockers like **Amiloride or Triamterene**. * **Differential Diagnosis of Hypokalemic Hypertension:** * *High Aldosterone, Low Renin:* Conn’s Syndrome (Primary Aldosteronism) [1]. * *Low Aldosterone, Low Renin:* Liddle Syndrome, Cushing Syndrome, or Licorice ingestion [1]. * *High Aldosterone, High Renin:* Renal Artery Stenosis or Reninoma.

Q: A mother brought her 14-year-old boy with the complaint of cough with blood in sputum and red colored urine. On examination, his BP was 140/90 mmHg. Investigations showed his hemoglobin is 10 mg/dl and hematocrit is 31%. His urinalysis is suggestive of hematuria and proteinuria. Which of the following is the probable diagnosis?

Goodpasture syndrome. ### Explanation The clinical presentation of **hemoptysis** (cough with blood) and **hematuria** (red-colored urine) in a patient with hypertension and anemia points toward a **Pulmonary-Renal Syndrome**. **1. Why Goodpasture Syndrome is Correct:** Goodpasture syndrome is characterized by the presence of circulating **anti-glomerular basement membrane (anti-GBM) antibodies**. These antibodies attack the α3 chain of Type IV collagen found in both the alveolar basement membrane of the lungs and the glomerular basement membrane of the kidneys. This leads to: * **Diffuse Alveolar Hemorrhage:** Presenting as hemoptysis and iron-deficiency anemia (Hb 10 mg/dl). * **Rapidly Progressive Glomerulonephritis (RPGN):** Presenting as hematuria, proteinuria, and hypertension. **2. Why the Other Options are Incorrect:** * **Hemolytic-uremic syndrome (HUS):** Typically presents with a triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury, usually following bloody diarrhea. It does not cause pulmonary hemorrhage. * **Poststreptococcal glomerulonephritis (PSGN):** A common cause of nephritic syndrome in children (hematuria, hypertension, edema) following a throat or skin infection. However, it does not involve the lungs or cause hemoptysis. * **Nephrotic syndrome:** Characterized by massive proteinuria (>3.5g/day), hypoalbuminemia, and generalized edema. Hemoptysis is not a feature, and hematuria is uncommon. **Clinical Pearls for NEET-PG:** * **Diagnosis:** Confirmed by linear immunofluorescence (IF) showing IgG deposits along the GBM. * **Demographics:** Bimodal distribution (young males in their 20s and older females in their 60s). * **Treatment:** Plasmapheresis (to remove antibodies), corticosteroids, and cyclophosphamide. * **Differential for Pulmonary-Renal Syndrome:** Goodpasture syndrome, GPA (Wegener's), and SLE.

Q: A 57-year-old man presents with a serum sodium of 125 mEq/L. On examination, he has pitting edema and elevated neck veins. His urine sodium is 10 mEq/L and urine osmolality is 350 mOsm/kg. What is the most likely diagnosis for this patient's hyponatremia?

Congestive heart failure (CHF). ### Explanation The patient presents with **hypovolemic hyponatremia** (Sodium 125 mEq/L) and clinical signs of **volume overload** (pitting edema, elevated neck veins). This combination is the hallmark of hypervolemic hyponatremia [1]. **1. Why Congestive Heart Failure (CHF) is Correct:** In CHF, there is a decrease in "effective arterial blood volume" (EABV) despite an increase in total body water. This triggers the **Renin-Angiotensin-Aldosterone System (RAAS)** and the release of **Antidiuretic Hormone (ADH)** [2]. * **Low Urine Sodium ( 100 mOsm/kg):** ADH causes water reabsorption, concentrating the urine [2]. * **Edema/Elevated JVP:** Reflects the increased total body sodium and water [3]. **2. Why Incorrect Options are Wrong:** * **Extrarenal losses (e.g., vomiting/diarrhea):** These cause *hypovolemic* hyponatremia [1]. While urine sodium would be low ( 40 mEq/L)** because there is no stimulus for aldosterone-mediated sodium retention. * **Polydipsia:** This also causes euvolemic hyponatremia, but the urine would be **maximally dilute** (Urine Osmolality 20):** Think Acute or Chronic Renal Failure (kidneys cannot retain sodium) [1]. * **Key Differentiator:** The presence of edema/JVP separates hypervolemic causes from SIADH [3].

Question 1

All of the following are associated with polyuria except?

Accepted Answer

Rapidly progressive glomerulonephritis

Answer

Diabetes insipidus

Answer

Diabetes mellitus

Question 2

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

Accepted Answer

Post-streptococcal glomerulonephritis

Answer

Membranous glomerulonephritis

Answer

Membranoproliferative glomerulonephritis

Answer

Focal segmental glomerulosclerosis

Question 3

Which of the following is not associated with hyponatremia and normal osmolality?

Accepted Answer

Congestive heart failure (CHF)

Answer

Hyperlipidemia

Answer

Hyperproteinemia

Answer

Irrigation of bladder after TURP

Question 4

A 35-year-old man with AML and WBC of 100,000 cells/µl is treated with chemotherapy and develops oliguric renal failure. His urine is acidic and numerous crystals are noted in the urine. What is the most likely diagnosis?

Accepted Answer

Urate nephropathy

Answer

Nephrocalcinosis

Answer

Leukemic infiltration of the kidneys

Answer

Acute tubular necrosis secondary to a nephrotoxic effect of his chemotherapy

Question 5

A 64-year-old woman presents with metabolic alkalosis and a bicarbonate level of 34 mEq/L. Which of the following is the most likely cause?

Accepted Answer

Diuretic use

Answer

Hyperkalemia

Answer

Mineralocorticoid deficiency

Answer

Diarrhea

Question 6

Which of the following has no role in the management of acute onset hyperkalemia?

Accepted Answer

Intravenous bicarbonate

Answer

Nebulization with salbutamol

Answer

Calcium chloride

Answer

Intravenous regular insulin

Question 7

Which of the following is NOT a component of dialysate in hemodialysis?

Accepted Answer

Aluminium

Answer

Sodium

Answer

Potassium

Answer

Glucose

Question 8

Hypokalemic hypertension is a feature of which condition?

Accepted Answer

Liddle syndrome

Answer

Bartter syndrome

Answer

Gitelman syndrome

Answer

Graves' disease

Question 9

A mother brought her 14-year-old boy with the complaint of cough with blood in sputum and red colored urine. On examination, his BP was 140/90 mmHg. Investigations showed his hemoglobin is 10 mg/dl and hematocrit is 31%. His urinalysis is suggestive of hematuria and proteinuria. Which of the following is the probable diagnosis?

Accepted Answer

Goodpasture syndrome

Answer

Hemolytic-uremic syndrome

Answer

Poststreptococcal glomerulonephritis

Answer

Nephrotic syndrome

Question 10

A 57-year-old man presents with a serum sodium of 125 mEq/L. On examination, he has pitting edema and elevated neck veins. His urine sodium is 10 mEq/L and urine osmolality is 350 mOsm/kg. What is the most likely diagnosis for this patient's hyponatremia?

Accepted Answer

Congestive heart failure (CHF)

Answer

Extrarenal sodium and fluid losses

Answer

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Answer

Polydipsia

Nephrology — MCQs

Nephrology — MCQs

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