Nephrology Practice Questions

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

Increase in anion gap. **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].

Q: A 19-year-old girl develops sudden-onset non-bloody diarrhea. She was previously well and is not taking any medications or traveled anywhere recently. Her abdomen is soft and nontender on examination, and the anion gap is normal. For the above patient with new symptoms, select the most likely acid-base disorder.

Metabolic acidosis. **Explanation:** The patient presents with sudden-onset diarrhea and a normal anion gap. The correct answer is **Metabolic Acidosis** (specifically, Normal Anion Gap Metabolic Acidosis or NAGMA) [1]. **1. Why Metabolic Acidosis is Correct:** Diarrhea is a classic cause of NAGMA [2]. Intestinal secretions (below the stomach) are rich in bicarbonate ($HCO_3^-$). In profuse diarrhea, the body loses large amounts of bicarbonate. According to the principle of electroneutrality, as bicarbonate is lost, the kidneys retain chloride ($Cl^-$) to maintain electrical balance, leading to **hyperchloremic metabolic acidosis** [3]. Because the decrease in $HCO_3^-$ is offset by an increase in $Cl^-$, the Anion Gap ($Na^+ - [Cl^- + HCO_3^-]$) remains within the normal range (8–12 mEq/L) [3]. **2. Why Incorrect Options are Wrong:** * **Metabolic Alkalosis:** This occurs with the loss of acid (e.g., persistent vomiting or nasogastric suction) or the use of diuretics [4]. Diarrhea causes base loss, not acid loss. * **Respiratory Acidosis:** This is caused by alveolar hypoventilation (e.g., COPD, opioid overdose), leading to $CO_2$ retention [5]. It is not a primary result of GI losses. * **Respiratory Alkalosis:** This results from hyperventilation (e.g., anxiety, high altitude, pulmonary embolism), leading to excessive $CO_2$ washout [5]. **Clinical Pearls for NEET-PG:** * **NAGMA Mnemonic (USED CARP):** **U**reterosigmoidostomy, **S**aline infusion, **E**ndocrine (Addison’s), **D**iarrhea, **C**arbonic anhydrase inhibitors (Acetazolamide), **A**mmonium chloride, **R**enal tubular acidosis (RTA), **P**ancreatic fistula. * **Urine Anion Gap (UAG):** In NAGMA, UAG helps differentiate GI loss (negative UAG) from RTA (positive UAG) [3]. * **High Anion Gap Metabolic Acidosis (HAGMA):** Remember the mnemonic **MUDPILES** (Methanol, Uremia, DKA, Propylene glycol, Iron/INH, Lactate, Ethylene glycol, Salicylates).

Q: Isoosmolar urine is seen in which of the following conditions?

Acute tubular necrosis (ATN). **Explanation:** The correct answer is **Acute Tubular Necrosis (ATN)**. **1. Why ATN is correct:** In ATN, the tubular epithelial cells are damaged, leading to a loss of the kidney's ability to concentrate or dilute urine. The kidneys cannot maintain the medullary osmotic gradient or respond to ADH. Consequently, the urine osmolality becomes fixed at the same osmolality as plasma (approximately **290–300 mOsm/kg**), a condition known as **Isosthenuria**. The Urine Specific Gravity typically remains fixed at **1.010**. **2. Why other options are incorrect:** * **Severe Dehydration:** In a healthy physiological response to dehydration, ADH levels rise, causing the kidneys to reabsorb water. This results in **hyperosmolar (concentrated) urine** (typically >500 mOsm/kg). * **Diabetes Insipidus (DI):** Whether central or nephrogenic, DI is characterized by an inability to reabsorb water in the collecting ducts. This leads to the excretion of large volumes of **hypoosmolar (dilute) urine** (typically <200 mOsm/kg). * **Polycystic Kidney Disease (PCKD):** While chronic kidney diseases eventually lead to a loss of concentrating ability, in the early to mid-stages, the urine is not characteristically isoosmolar in the same acute, diagnostic fashion as seen in ATN. **3. High-Yield Clinical Pearls for NEET-PG:** * **Isosthenuria:** Urine Specific Gravity of **1.010** is the hallmark of ATN. * **Fractional Excretion of Sodium (FeNa):** In ATN, FeNa is typically **>2%** (due to tubular damage), whereas in Pre-renal Azotemia, it is **<1%** (tubules are intact and conserving sodium). * **Urinary Casts:** Look for **"Muddy brown granular casts"** in the urine sediment, which are pathognomonic for ATN.

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

Chronic glomerulonephritis. 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].

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

Membranous nephropathy, Lupus nephritis, Renal amyloidosis. 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].

Q: Which of the following is not a feature of acute renal failure?

Hypokalemia. In Acute Kidney Injury (AKI), the sudden decline in GFR leads to the accumulation of metabolic waste products and electrolytes that are normally excreted by the kidney [1]. **Why Hypokalemia is the Correct Answer:** The hallmark of AKI is **Hyperkalemia**, not hypokalemia. As GFR drops, the kidney's ability to excrete potassium is severely impaired. Additionally, the associated metabolic acidosis causes a shift of potassium from the intracellular to the extracellular compartment (H+/K+ exchange), further raising serum potassium levels. Hypokalemia is generally only seen in specific scenarios like the recovery (diuretic) phase of ATN or in specific types of drug-induced nephrotoxicity (e.g., Amphotericin B). **Explanation of Incorrect Options:** * **Hyperphosphatemia:** Reduced renal excretion of phosphate leads to its accumulation in the blood [2]. * **Hypocalcemia:** This occurs due to two main reasons: (1) Hyperphosphatemia causes calcium-phosphate precipitation in soft tissues, and (2) Decreased production of 1,25-dihydroxyvitamin D by the injured kidneys leads to reduced intestinal calcium absorption. Modest hypocalcaemia is common in these patients [2]. * **Metabolic Acidosis:** The kidneys fail to excrete fixed acids (like sulfates and phosphates) and cannot regenerate sufficient bicarbonate, resulting in a **High Anion Gap Metabolic Acidosis (HAGMA)**. **High-Yield Clinical Pearls for NEET-PG:** 1. **ECG in AKI:** Always look for tall tented T-waves (earliest sign of hyperkalemia). 2. **Fractional Excretion of Sodium (FeNa):** 2% suggests Acute Tubular Necrosis (ATN). 3. **Indications for Urgent Dialysis (AEIOU):** **A**cidosis (refractory), **E**lectrolytes (Hyperkalemia), **I**ntoxications, **O**verload (Fluid), **U**remia (Pericarditis/Encephalopathy).

Q: What is the primary treatment for hyperphosphatemia?

Sevelamer. Self-study of hyperphosphatemia management focuses on clinical interventions. **Explanation:** **1. Why Sevelamer is Correct:** Sevelamer is a **non-absorbable phosphate binder** used primarily in patients with Chronic Kidney Disease (CKD) on dialysis [1, 5]. It works by binding to dietary phosphate within the gastrointestinal tract, preventing its absorption and promoting excretion in the feces. Unlike older binders (like Calcium carbonate), Sevelamer is **calcium-free**, which is a significant advantage as it reduces the risk of iatrogenic hypercalcemia and subsequent metastatic vascular calcification [2]. **2. Why Other Options are Incorrect:** * **A. Calcitonin:** This hormone inhibits bone resorption and increases renal calcium excretion. It is used for hypercalcemia and Paget’s disease, not as a primary treatment for hyperphosphatemia. * **C. Magnesium hydroxide:** While magnesium can bind phosphate, it is not a primary treatment. Its use is limited by the risk of magnesium toxicity (hypermagnesemia) and its potent laxative effect. * **D. Diuretics:** While some diuretics (like Acetazolamide) can increase phosphate excretion, they are ineffective in CKD patients with failing kidneys—the population most commonly requiring treatment for hyperphosphatemia. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Sevelamer is a cross-linked polymer that acts like an ion-exchange resin. * **Pleiotropic Effects:** Beyond lowering phosphate, Sevelamer also lowers LDL cholesterol and uric acid levels. * **Other Binders:** **Lanthanum carbonate** is another non-calcium binder. **Aluminum hydroxide** is the most potent binder but is avoided long-term due to aluminum toxicity (encephalopathy and osteomalacia) [2]. * **First-line:** In CKD, the first step is dietary restriction, followed by phosphate binders taken **with meals** to maximize binding of dietary phosphorus [1].

Question 1

A patient presents with the following blood biochemical values: Calcium 6 mg/dL; Uric acid 13 mg/dL; Phosphorus 12 mg/dL; Creatinine 6 mg/dL. Which of the following is a possible diagnosis?

Accepted Answer

Uric acid nephropathy

Answer

Krait bite

Answer

Hypercalcemic nephropathy

Answer

Rickets

Question 2

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

Accepted Answer

Increase in anion gap

Answer

Decrease in anion gap

Answer

Normal anion gap

Answer

Metabolic alkalosis

Question 3

A 19-year-old girl develops sudden-onset non-bloody diarrhea. She was previously well and is not taking any medications or traveled anywhere recently. Her abdomen is soft and nontender on examination, and the anion gap is normal. For the above patient with new symptoms, select the most likely acid-base disorder.

Accepted Answer

Metabolic acidosis

Answer

Metabolic alkalosis

Answer

Respiratory acidosis

Answer

Respiratory alkalosis

Question 4

Isoosmolar urine is seen in which of the following conditions?

Accepted Answer

Acute tubular necrosis (ATN)

Answer

Severe dehydration

Answer

Diabetes insipidus

Answer

Polycystic kidney disease (PCKD)

Question 5

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

Accepted Answer

Chronic glomerulonephritis

Answer

Diabetic nephropathy

Answer

Polycystic kidney disease

Answer

AIDS-related nephropathy

Question 6

Which of the following conditions can cause renal vein thrombosis?

Accepted Answer

Membranous nephropathy, Lupus nephritis, Renal amyloidosis

Answer

Membranous nephropathy, Lupus nephritis, Post-streptococcal glomerulonephritis

Answer

Membranoproliferative glomerulonephritis, Post-streptococcal glomerulonephritis, Renal amyloidosis

Answer

Membranous nephropathy, Post-streptococcal glomerulonephritis, Renal amyloidosis

Question 7

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

Accepted Answer

Sodium Restriction

Answer

Protein Restriction

Answer

Fluid Intake Increase

Answer

All of the above

Question 8

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?

Accepted Answer

Essential mixed cryoglobulinemia

Answer

Post-streptococcal glomerulonephritis (PSGN)

Answer

Membranoproliferative glomerulonephritis

Answer

Focal segmental glomerulosclerosis

Question 9

Which of the following is not a feature of acute renal failure?

Accepted Answer

Hypokalemia

Answer

Hyperphosphatemia

Answer

Hypocalcemia

Answer

Metabolic acidosis

Question 10

What is the primary treatment for hyperphosphatemia?

Accepted Answer

Sevelamer

Answer

Calcitonin

Answer

Magnesium hydroxide

Answer

Diuretics

Nephrology — MCQs

Nephrology — MCQs

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