Nephrology Practice Questions

Q: Acute renal failure most commonly results in which of the following electrolyte and acid-base disturbances?

Hyperkalemia with metabolic acidosis. **Explanation:** In Acute Renal Failure (ARF), now commonly termed Acute Kidney Injury (AKI), the sudden decline in GFR leads to the accumulation of metabolic waste products and the failure of homeostatic mechanisms. **Why Hyperkalemia and Metabolic Acidosis occur:** 1. **Hyperkalemia:** The kidneys are the primary route for potassium excretion. In ARF, the reduced distal delivery of sodium and decreased GFR impair the secretion of $K^+$ in the collecting ducts. Additionally, the associated acidosis causes an intracellular-to-extracellular shift of $K^+$ (as $H^+$ ions enter cells, $K^+$ exits to maintain electroneutrality). 2. **Metabolic Acidosis:** The kidneys fail to excrete "fixed" non-volatile acids (like phosphates and sulfates) produced by daily metabolism. Furthermore, there is a failure to reabsorb filtered $HCO_3^-$ and a defect in ammonia production ($NH_3$), which is essential for buffering $H^+$ ions in the urine. This results in a **High Anion Gap Metabolic Acidosis (HAGMA)**. **Analysis of Incorrect Options:** * **Options A & B (Metabolic Alkalosis):** Alkalosis is rare in ARF. It typically occurs with massive vomiting or excessive diuretic use, whereas renal failure inherently causes acid retention. * **Options B & D (Hypokalemia):** Hypokalemia is not a feature of the maintenance phase of ARF. It is more commonly seen in the **recovery (diuretic) phase** of AKI or in specific conditions like Renal Tubular Acidosis (RTA). **NEET-PG High-Yield Pearls:** * **ECG in Hyperkalemia:** Look for tall "tented" T-waves, widened QRS, and loss of P-waves. * **Exception:** In AKI caused by aminoglycosides or cisplatin, patients may occasionally present with hypokalemia due to tubular wasting. * **Anion Gap:** AKI typically causes a High Anion Gap Metabolic Acidosis due to the retention of unmeasured anions (sulfates, phosphates).

Q: All are indicated in a patient with cystinuria with multiple renal stones except?

Cysteamine. **Explanation:** **Cystinuria** is an autosomal recessive disorder characterized by a defect in the COAL transporter (Cystine, Ornithine, Arginine, Lysine) in the proximal renal tubule. This leads to high urinary cystine levels, which are poorly soluble in acidic urine, resulting in recurrent hexagonal radiolucent stones. **Why Cysteamine is the correct answer (the "Except"):** Cysteamine is the treatment of choice for **Cystinosis** (a lysosomal storage disorder), not Cystinuria. In Cystinosis, cysteamine enters lysosomes and reacts with cystine to form a cysteine-cysteamine complex that can exit the lysosome. It has no role in preventing or dissolving renal stones in Cystinuria. **Analysis of other options:** * **Increase fluid intake:** This is the first-line management. Maintaining a high urine output (typically >3L/day) decreases the concentration of cystine below its solubility limit. * **Alkalinization of urine:** Cystine solubility increases significantly at a pH >7.5. Potassium citrate or sodium bicarbonate are used to maintain alkaline urine to prevent stone formation. * **Penicillamine:** This is a chelating agent used when conservative measures fail [1]. It reacts with cystine to form a cysteine-penicillamine disulfide complex, which is 50 times more soluble than cystine itself. (Tiopronin is another similar drug used). **NEET-PG High-Yield Pearls:** * **Pathognomonic sign:** Hexagonal (benzene ring-shaped) crystals on urine microscopy. * **Diagnosis:** Positive **Cyanide-Nitroprusside test** (urine turns cherry red). * **Stone Radiopacity:** Cystine stones are "faintly radiopaque" due to their sulfur content (often described as having a "ground-glass" appearance). * **Mnemonic for Transporter:** **COAL** (Cystine, Ornithine, Arginine, Lysine).

Q: All of the following are used to remove potassium in hyperkalemia except?

Beta 2 agonists. To manage hyperkalemia, treatments are categorized into three mechanisms: **membrane stabilization** (Calcium gluconate), **intracellular shifting**, and **actual removal** of potassium from the body. [1] ### **Explanation of the Correct Answer** **Option C (Beta 2 agonists)** is the correct answer because it does **not** remove potassium from the body. Instead, it works by **intracellular shifting**. [2] Beta-2 agonists (like Albuterol/Salbutamol) stimulate the Na+/K+-ATPase pump, driving potassium from the extracellular fluid into the cells. [2] While this rapidly lowers serum potassium levels, the total body potassium remains unchanged. [2] ### **Analysis of Incorrect Options (Methods that REMOVE Potassium)** * **A. Cation exchange resins:** (e.g., Sodium Polystyrene Sulfonate, Patiromer) These work in the gastrointestinal tract by exchanging sodium or calcium for potassium ions, which are then excreted in the feces. * **B. Diuretics:** Loop diuretics (e.g., Furosemide) and Thiazides increase potassium excretion through the kidneys by inhibiting sodium reabsorption and increasing distal tubular flow. [3] * **D. Dialysis:** Hemodialysis is the most definitive and rapid method for the physical removal of potassium from the blood, typically reserved for refractory or life-threatening hyperkalemia. ### **NEET-PG High-Yield Pearls** * **The "Shift" Agents:** Insulin (with glucose) and Beta-2 agonists are the mainstays for shifting potassium intracellularly. [2] * **First Step in Management:** If ECG changes (like peaked T-waves) are present, the first step is **Calcium Gluconate** to stabilize the cardiac membrane (it does not lower K+ levels). [1] * **Definitive Treatment:** Dialysis is the "gold standard" for potassium removal in patients with renal failure. * **Caution:** Avoid Beta-2 agonists in patients with active coronary ischemia as they can cause tachycardia.

Q: Lactic acidosis is not seen in which of the following conditions or substances?

Tolbutamide. **Explanation:** Lactic acidosis is a form of high anion gap metabolic acidosis (HAGMA) caused by the accumulation of lactate, typically due to tissue hypoxia or impaired metabolism of lactic acid. **Why Tolbutamide is the correct answer:** Tolbutamide is a first-generation sulfonylurea used in the treatment of Type 2 Diabetes. Unlike **Biguanides (e.g., Phenformin and Metformin)**, which inhibit mitochondrial respiration and gluconeogenesis leading to lactate accumulation, sulfonylureas work by stimulating insulin release from pancreatic beta cells. They do not interfere with lactate metabolism and, therefore, do not cause lactic acidosis. **Analysis of Incorrect Options:** * **Methanol Poisoning:** Methanol metabolism produces formic acid, which inhibits mitochondrial cytochrome c oxidase. This disrupts the electron transport chain, leading to anaerobic glycolysis and subsequent lactic acidosis. * **Respiratory Failure:** Severe respiratory failure leads to hypoxemia. In the absence of adequate oxygen, cells shift from aerobic metabolism to anaerobic glycolysis, producing excess lactic acid (Type A Lactic Acidosis). * **Circulatory Failure:** Conditions like shock or heart failure cause systemic hypoperfusion. This leads to inadequate oxygen delivery to tissues, resulting in profound Type A lactic acidosis. **NEET-PG High-Yield Pearls:** * **Classification:** Lactic acidosis is divided into **Type A** (Hypoxic: shock, anemia, heart failure) and **Type B** (Non-hypoxic: drugs like Metformin, Linezolid, or metabolic diseases). * **Drug-Induced:** Phenformin was withdrawn globally due to a high risk of lactic acidosis; Metformin carries a much lower risk but is contraindicated in renal failure. * **Mnemonic for HAGMA:** **MUDPILES** (Methanol, Uremia, DKA, Propylene glycol, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates).

Q: Which of the following is NOT true about Bartter syndrome?

Causes hypokalemic alkalosis. The correct answer is **A (Causes hypokalemic alkalosis)** because the question asks for the statement that is **NOT** true. This is a "negative" question; while Bartter syndrome *does* cause hypokalemic metabolic alkalosis, the statement itself is a true clinical feature, making it a "wrong" choice for a "NOT true" question. ### **Explanation of Options** * **Option A (Incorrect Statement for this question):** Bartter syndrome is characterized by **hypokalemic metabolic alkalosis** with normal to low blood pressure [1]. This occurs because the defect in the Thick Ascending Limb (TAL) mimics a permanent "loop diuretic" effect, leading to increased distal delivery of sodium and subsequent potassium/hydrogen ion secretion. * **Option B (False Statement/Correct Answer):** This is the "NOT true" statement. While Bartter Syndrome Type IV (caused by **BSND gene** mutations) presents with neonatal salt wasting and **sensorineural deafness**, there is no such entity as a "BSNDM2" gene mutation. * **Option C (True Statement):** The primary defect in Bartter syndrome is the failure of the **NKCC2 transporter** (or related channels like ROMK) in the TAL. Since the TAL is responsible for roughly 25-30% of sodium and potassium reabsorption, a defect here significantly decreases potassium absorption. * **Option D (True Statement):** Most forms of Bartter syndrome (Types I-IV) are inherited in an **autosomal recessive** pattern. ### **Clinical Pearls for NEET-PG** * **Bartter vs. Gitelman:** Bartter syndrome mimics **Loop Diuretics** (TAL defect, hypercalciuria); Gitelman syndrome mimics **Thiazides** (Distal Tubule defect, hypocalciuria). * **Hypercalciuria:** A key differentiator for Bartter is increased urinary calcium, which can lead to nephrocalcinosis. * **Antenatal Bartter:** Often presents with polyhydramnios and premature delivery.

Q: Which disease does not recur in the kidney after renal transplant?

Alport syndrome. **Explanation:** The correct answer is **Alport syndrome**. This is because Alport syndrome is a genetic disorder caused by mutations in the genes encoding the **Type IV collagen** alpha chains (COL4A3, COL4A4, or COL4A5). Since the defect is intrinsic to the patient’s own genetic makeup and basement membrane structure, the transplanted kidney—which comes from a donor with normal collagen genes—will possess a normal glomerular basement membrane (GBM). Therefore, the disease cannot "recur" in the donor tissue. Interestingly, a small percentage of Alport patients may develop **Anti-GBM disease (de novo Goodpasture syndrome)** post-transplant because their immune system recognizes the normal Type IV collagen in the graft as foreign. **Analysis of Incorrect Options:** * **Amyloidosis:** This is a systemic metabolic process. The underlying plasma cell dyscrasia or chronic inflammation continues to produce amyloid proteins, which will eventually deposit in the new graft. * **Goodpasture Syndrome:** This is an autoimmune disease mediated by circulating anti-GBM antibodies. If the transplant is performed while antibody titers are still high, the antibodies will attack the new kidney. * **Diabetic Nephropathy:** As long as the patient remains diabetic, the systemic metabolic environment (hyperglycemia) will eventually cause characteristic histological changes (Kimmelstiel-Wilson nodules) in the transplanted kidney. **High-Yield Clinical Pearls for NEET-PG:** * **Most common disease to recur post-transplant:** MPGN Type II (Dense Deposit Disease) — nearly 100% recurrence. * **Most common cause of graft loss due to recurrence:** FSGS (Focal Segmental Glomerulosclerosis). * **Oxalosis:** High rate of recurrence; often requires a combined liver-kidney transplant. * **IgA Nephropathy:** Frequently recurs histologically, but rarely leads to early graft loss.

Question 1

A patient presents with symptoms suggestive of stage IV kidney disease, including anemia and progressive malnutrition. Which of the following glomerular filtration rate (GFR) ranges would be most consistent with this stage of kidney disease?

Accepted Answer

GFR of 15-29 mL/min per 1.73 m2

Answer

GFR of 60-89 mL/min per 1.73 m2

Answer

GFR of 30-59 mL/min per 1.73 m2

Answer

GFR less than 15 mL/min per 1.73 m2

Question 2

Acute renal failure most commonly results in which of the following electrolyte and acid-base disturbances?

Accepted Answer

Hyperkalemia with metabolic acidosis

Answer

Hyperkalemia with metabolic alkalosis

Answer

Hypokalemia with metabolic alkalosis

Answer

Hypokalemia with metabolic acidosis

Question 3

All are indicated in a patient with cystinuria with multiple renal stones except?

Accepted Answer

Cysteamine

Answer

Increase fluid intake

Answer

Alkalinization of urine

Answer

Penicillamine

Question 4

All of the following are used to remove potassium in hyperkalemia except?

Accepted Answer

Beta 2 agonists

Answer

Cation exchange resins

Answer

Diuretics

Answer

Dialysis

Question 5

Which of the following conditions is NOT typically steroid-resistant?

Accepted Answer

Minimal change glomerulonephritis

Answer

Post-streptococcal glomerulonephritis

Answer

Rapidly progressive glomerulonephritis

Answer

Recurrent hematuria

Question 6

Lactic acidosis is not seen in which of the following conditions or substances?

Accepted Answer

Tolbutamide

Answer

Methanol poisoning

Answer

Respiratory failure

Answer

Circulatory failure

Question 7

Which of the following is NOT true about Bartter syndrome?

Accepted Answer

Causes hypokalemic alkalosis

Answer

Presents in neonates with ototoxicity and has a BSNDM2 gene mutation

Answer

Involves decreased potassium absorption from the thick ascending limb

Answer

Is inherited in an autosomal recessive pattern

Question 8

A client with chronic renal failure who is scheduled for hemodialysis this morning is due to receive a daily dose of enalapril (Vasotec). When should the nurse plan to administer this medication?

Accepted Answer

On return from dialysis

Answer

Just before dialysis

Answer

During dialysis

Answer

The day after dialysis

Question 9

A 24-year-old woman has dipstick-positive results for blood in her urine, which have been repeated twice between menstrual periods and remain positive. Microscopic evaluation reveals RBCs, some of which are deformed and some are in the form of casts. Which of the following is the most likely cause of the hematuria?

Accepted Answer

Glomerulonephritis

Answer

Urinary tract stones

Answer

Trauma

Answer

Benign renal tumor

Question 10

Which disease does not recur in the kidney after renal transplant?

Accepted Answer

Alport syndrome

Answer

Amyloidosis

Answer

Goodpasture syndrome

Answer

Diabetic nephropathy

Nephrology — MCQs

Nephrology — MCQs

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