Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 841: A 7-year-old girl was brought with complaints of generalized swelling of the body. Urinary examination reveals grade 3 proteinuria and the presence of hyaline and fatty casts. She has no history of hematuria. Which of the following statements about her condition is true?

A. No IgG deposits or C3 deposition on renal biopsy (Correct Answer)
B. Her C3 levels will be low
C. IgA Nephropathy is the likely diagnosis
D. Minimal change disease is characterized by the absence of hematuria and significant proteinuria.

Explanation: ***No IgG deposits or C3 deposition on renal biopsy*** - This finding is characteristic of **minimal change disease**, which is common in children and typically presents with **nephrotic syndrome** features [1]. - The absence of **IgG** and **C3** indicates that it is not associated with **immune complex-mediated diseases**. *IgA Nephropathy* - Usually presents with **hematuria** and **IgA deposition**, which are not seen in this case [2]. - In IgA nephropathy, **proteinuria** is typically less than nephrotic levels, contrary to the patient's **grade 3 proteinuria**. *Alpo's syndrome* - There is no such recognized syndrome related to the symptoms described; it likely refers to a misunderstanding or misnomer. - Conditions leading to nephrotic syndrome in children do not include this as a diagnosis. *Her C3 levels will be low* - In minimal change disease, **C3 levels** are typically normal, unlike in **glomerulonephritis** where low levels may be observed [3]. - This condition is not associated with **systemic disease** that would affect complement levels.

Question 842: Uremic complications typically arise during which of the following phases of renal failure?

A. Initiation
B. Maintenance (Correct Answer)
C. Diuretic Phase
D. Recovery Phase

Explanation: ***Maintenance*** - During the **maintenance phase**, renal function is severely impaired, leading to the accumulation of **uremic toxins** and metabolic waste products. - This prolonged period of reduced kidney function is when **uremic complications** such as pericarditis, encephalopathy, and coagulopathy typically manifest. *Initiation* - The **initiation phase** is characterized by the initial insult to the kidneys and the onset of reduced glomerular filtration, but significant uremic complications are usually not yet apparent. - It is a period of evolving injury, and the body's compensatory mechanisms may still be able to mitigate acute toxicity. *Diuretic Phase* - The **diuretic phase** is a period of gradual improvement from renal failure, where urine output increases, but the kidneys may still have impaired ability to concentrate urine or fully excrete waste. - While electrolyte imbalances can occur, severe uremic complications are less common as renal function starts to recover. *Recovery Phase* - In the **recovery phase**, renal function gradually normalizes, and the kidneys regain their ability to excrete waste products effectively. - Uremic complications would typically be resolving, not arising, during this phase as **renal repair** takes place.

Question 843: Which of the following causes metabolic acidosis?

A. Thiazide diuretic therapy
B. Recurrent vomiting
C. Mineralocorticoid deficiency (Correct Answer)
D. Bartter's syndrome

Explanation: ***Mineralocorticoid deficiency*** - **Mineralocorticoid deficiency**, such as in **Addison's disease**, leads to impaired aldosterone production. - This results in reduced **potassium excretion** and **sodium reabsorption**, causing **hyperkalemia** and metabolic acidosis due to decreased hydrogen ion secretion [1]. *Bartter's syndrome* - **Bartter's syndrome** is a genetic disorder affecting the **thick ascending limb of the loop of Henle**, leading to excessive losses of sodium, chloride, and potassium. - This condition typically results in **metabolic alkalosis** due to increased hydrogen ion secretion and volume contraction rather than acidosis. *Thiazide diuretic therapy* - **Thiazide diuretics** inhibit the **sodium-chloride cotransporter** in the **distal convoluted tubule**, promoting sodium and chloride excretion. - This can lead to **hypokalemia** and **metabolic alkalosis** due to volume contraction and increased hydrogen ion secretion, not acidosis. *Recurrent vomiting* - **Recurrent vomiting** causes the loss of **gastric acid (HCl)**, leading to a decrease in hydrogen ions in the body [1]. - This condition characteristically results in **metabolic alkalosis** due to the loss of acid and compensatory renal mechanisms, not acidosis [1].

Question 844: What is the most common cause of chronic renal failure?

A. Glomerulonephritis (acute to chronic)
B. Chronic pyelonephritis
C. Diabetes mellitus (Correct Answer)
D. Hypertensive renal disease

Explanation: ***Diabetes mellitus*** - **Diabetes mellitus** is the leading cause of **chronic renal failure (CRF)**, responsible for approximately 45-50% of all cases [2]. - Both type 1 and type 2 diabetes can lead to **diabetic nephropathy**, a progressive kidney disease that ultimately results in end-stage renal disease (ESRD) [1], [2]. *Glomerulonephritis (acute to chronic)* - While various forms of **glomerulonephritis** can cause chronic renal failure, they collectively account for a smaller percentage compared to diabetes. - The progression from acute to chronic glomerulonephritis is not as prevalent as diabetic nephropathy in the overall etiology of CRF. *Chronic pyelonephritis* - **Chronic pyelonephritis**, an infection-related kidney scarring, is a cause of CRF but is less common than diabetes and hypertension as primary drivers. - It often results from recurrent **urinary tract infections (UTIs)** and **vesicoureteral reflux**. *Hypertensive renal disease* - **Hypertension** is the second most common cause of CRF, often co-occurring with diabetes or contributing independently to renal damage [1], [2]. - Untreated or poorly controlled hypertension leads to **nephrosclerosis**, a hardening of the small arteries in the kidneys, impairing their function over time.

Question 845: Which of the following diseases is MOST likely to present with proteinuria?

A. Aneurysms
B. Polycystic kidney disease
C. Diabetic nephropathy (Correct Answer)
D. Glomerulonephritis

Explanation: ***Glomerulonephritis*** [1], [2] - It is characterized by **inflammation of the glomeruli**, leading to significant **proteinuria** due to increased permeability [1]. - Commonly associated with **hematuria** and **edema**, which further supports its presence in renal pathology [1], [2]. *Polycystic kidney disease* - Mainly presents with **renal cysts** and may have **hematuria** but does not typically cause significant proteinuria early on. - Proteinuria can occur later due to renal insufficiency, but is not a hallmark feature of the disease. *Pyelonephritis* - This condition primarily causes **inflammatory changes** in the kidney due to infection, leading to **fever** and **flank pain**, rather than proteinuria. - While mild proteinuria may occur, it is usually characterized by **white blood cells** and bacteria in the urine rather than significant protein loss. *Ateriitis* - Typically refers to **inflammation of the arteries**, which does not involve kidney structures directly related to proteinuria [3]. - This condition is associated with other systemic symptoms but rarely presents with notable **urinary protein loss** [3].

Question 846: Which of the following is a cause of metabolic acidosis with a normal anion gap?

A. Diabetic ketoacidosis
B. Aspirin poisoning
C. Renal tubular acidosis (Correct Answer)
D. Lactic acidosis

Explanation: ***Renal tubular acidosis*** - **Renal tubular acidosis (RTA)** is characterized by a defect in renal acid excretion or bicarbonate reabsorption, leading to **metabolic acidosis** with a **normal anion gap** [1]. - The deficiency in net acid excretion results in the retention of chloride ions to maintain electroneutrality, hence it's also known as **hyperchloremic metabolic acidosis** [1]. *Diabetic ketoacidosis* - **Diabetic ketoacidosis (DKA)** is a high anion gap metabolic acidosis caused by the accumulation of **ketoacids** (beta-hydroxybutyrate, acetoacetate). - These unmeasured anions increase the anion gap, distinguishing it from normal anion gap acidosis. *Aspirin poisoning* - **Aspirin (salicylate) poisoning** typically causes a **mixed acid-base disorder** with both metabolic acidosis and respiratory alkalosis [1]. - The metabolic acidosis component is a **high anion gap acidosis** due to the accumulation of salicylates and their metabolites. *Lactic acidosis* - **Lactic acidosis** is a common cause of **high anion gap metabolic acidosis**, resulting from the overproduction or decreased clearance of **lactate** [1]. - The increased concentration of lactate, an unmeasured anion, leads to the widening of the anion gap.

Question 847: Acute anuria may occur in all of the following except:

A. Use of furosemide in patients receiving cephalosporin
B. Acute pancreatitis
C. Performing intravenous urogram in patient with multiple myeloma
D. Use of intravenous dextran in anemic patients (Correct Answer)

Explanation: ***Use of intravenous dextran in anemic patients*** - **Dextran** is a plasma volume expander and does not directly cause renal failure or anuria in anemic patients. - While large amounts of dextran can rarely cause **osmotic nephrosis**, it's not typically associated with acute anuria, especially compared to the other options. *Acute pancreatitis* - Severe acute pancreatitis can lead to **prerenal acute kidney injury** due to **hypovolemia** from fluid sequestration and systemic inflammation [1]. - This can progress to **acute tubular necrosis** and anuria if not promptly managed [1]. *Performing intravenous urogram in patient with multiple myeloma* - Patients with **multiple myeloma** are highly susceptible to **contrast-induced nephropathy** due to their pre-existing renal damage from light chain deposition [1]. - This can severely worsen kidney function and lead to acute anuria [1]. *Use of furosemide in patients receiving cephalosporin* - The combination of **furosemide** (a loop diuretic) and **cephalosporins** (nephrotoxic antibiotics like cephaloridine) can cause **additive nephrotoxicity** [1]. - This interaction can lead to **acute kidney injury** and ultimately anuria, especially in susceptible individuals [1].

Question 848: Acute renal failure in a patient who received an incompatible blood transfusion with a hemolytic reaction is best managed by:

A. 20% Mannitol
B. IV fluids with K+ supplementation
C. Alkalinizing the urine
D. Stopping blood transfusion (Correct Answer)

Explanation: ***Stopping blood transfusion*** - The immediate priority in managing an incompatible blood transfusion reaction is to **halt the transfusion** to prevent further hemolysis and renal damage. - Continuing the transfusion would exacerbate the hemolytic process, leading to increased release of **hemoglobin**, which is nephrotoxic. *20% Mannitol* - While mannitol can be used to induce diuresis and potentially flush cast formation in the renal tubules, it is **not the primary or initial step** in managing an acute hemolytic transfusion reaction causing renal failure. [1] - Administering mannitol without first stopping the source of the hemolytic reaction would be ineffective and potentially harmful. *IV fluids with K+ supplementation* - **IV fluids** are crucial to maintain renal perfusion and prevent acute tubular necrosis, especially after stopping the transfusion. [1] - However, **K+ supplementation** is generally contraindicated in cases of acute renal failure (ARF) due to hemolysis, as ARF often leads to hyperkalemia, not hypokalemia. [2] *Alkalinizing the urine* - **Alkalinization of urine** (e.g., with sodium bicarbonate) can help prevent the precipitation of myoglobin or hemoglobin in the renal tubules, which can exacerbate renal damage. - This is a secondary measure that follows discontinuing the transfusion and initiating fluid resuscitation, and not the immediate first step.

Question 849: Anemia in chronic renal failure is due to.

A. Decreased erythropoietin production (Correct Answer)
B. Iron deficiency
C. Hypoplastic bone marrow
D. Decreased folate levels

Explanation: ### Decreased erythropoietin production - The kidneys are the primary site for **erythropoietin (EPO)** production, a hormone essential for **red blood cell production** in the bone marrow [1]. - In chronic renal failure, damaged kidneys are unable to produce adequate amounts of EPO, leading to **normochromic, normocytic anemia** [1]. *Iron deficiency* - While **iron deficiency** can contribute to anemia in chronic renal failure due to blood loss or poor absorption, it is not the primary cause of anemia associated with **chronic kidney disease (CKD)** itself. - Iron deficiency anemia typically presents as **microcytic, hypochromic anemia**. *Hypoplastic bone marrow* - **Hypoplastic bone marrow** (aplastic anemia) or marrow failure is a rare cause of anemia and is not typically associated with chronic renal failure. - Anemia in chronic kidney disease is due to a lack of EPO stimulation, not necessarily an inherent problem with the bone marrow's ability to produce cells. *Decreased folate levels* - **Folate deficiency** can cause **megaloblastic anemia**, which is characterized by large, immature red blood cells. - While patients with chronic renal failure may have nutritional deficiencies, global decreased folate levels are not the primary or most common cause of anemia in chronic renal failure.

Question 850: Which of the following is the most effective treatment for severe acute hyperkalemia requiring definitive management?

A. Insulin and glucose
B. Dialysis (Correct Answer)
C. Resin therapy
D. Calcium gluconate

Explanation: ***Dialysis*** - **Hemodialysis** is the most effective and rapid method for definitively removing **potassium** from the body in cases of **severe acute hyperkalemia**, especially when other treatments are insufficient or renal function is compromised [2]. - It creates a **concentration gradient** that allows for efficient removal of excess potassium from the blood [2]. *Insulin and glucose* - This treatment promotes the **intracellular shift of potassium**, temporarily lowering serum potassium levels but does not remove potassium from the body. - While effective for acute management, it is not a definitive long-term solution as potassium can shift back out of cells. *Resin therapy* - **Potassium-binding resins** (e.g., sodium polystyrene sulfonate) exchange potassium for another ion (like sodium or calcium) primarily in the **gastrointestinal tract**, leading to potassium excretion. - These therapies work slowly and are generally not suitable for **severe acute hyperkalemia** requiring rapid definitive management. *Calcium gluconate* - **Calcium gluconate** is given to **stabilize the cardiac membrane** and reduce the risk of arrhythmias in hyperkalemia [1]. - It does not lower serum potassium levels but rather antagonizes its cardiac effects, making it an emergent symptomatic treatment, not a definitive potassium-lowering measure [1].

Practice by Chapter

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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