Nephrology — MCQs

Nephrology Indian Medical PG Practice Questions and MCQs

Question 751: In a patient with chronic kidney disease, what is the primary reason for choosing an ARB over an ACE inhibitor for managing proteinuria?

A. ARB; lower risk of adverse effects in renal impairment
B. ACE inhibitor; more effective at reducing proteinuria in all patients
C. ARB; better tolerated in patients with renal impairment (Correct Answer)
D. ACE inhibitor; reduces blood pressure more effectively in chronic kidney disease

Explanation: ARB; better tolerated in patients with renal impairment - Angiotensin receptor blockers (ARBs) are often preferred in patients with chronic kidney disease (CKD) due to a lower incidence of side effects, particularly chronic cough, compared to ACE inhibitors [1]. - This improved tolerability often leads to better patient adherence and sustained treatment for proteinuria management, which is crucial in CKD. ARB; lower risk of adverse effects in renal impairment - While ARBs have a lower incidence of certain side effects like cough compared to ACE inhibitors, both drug classes carry similar risks for other adverse effects in renal impairment, such as hyperkalemia and acute kidney injury [2]. - The primary differentiator is often the prevention of cough and angioedema, leading to better overall tolerability rather than a universally lower risk of *all* adverse effects. ACE inhibitor; more effective at reducing proteinuria in all patients - ACE inhibitors and ARBs are considered equally effective at reducing proteinuria in most patients with CKD by blocking the renin-angiotensin-aldosterone system (RAAS) [2]. - The choice between them in CKD is often driven by tolerability issues rather than superior antiproteinuric efficacy of one over the other [1]. ACE inhibitor; reduces blood pressure more effectively in chronic kidney disease - Both ACE inhibitors and ARBs are highly effective at reducing blood pressure in patients with CKD, which is a critical aspect of kidney protection [2]. - There is no substantial evidence to suggest that ACE inhibitors are inherently more effective than ARBs at lowering blood pressure in this patient population.

Question 752: A 65-year-old male with chronic kidney disease presents with persistent fatigue and a hemoglobin level of 9 g/dL. Despite optimal dialysis and iron supplementation, his hemoglobin remains low. What is the most appropriate next step in managing his anemia?

A. Administer blood transfusion
B. Prescribe oral folic acid
C. Start erythropoiesis-stimulating agents (ESAs) (Correct Answer)
D. Administer intravenous vitamin B12

Explanation: ***Start erythropoiesis-stimulating agents (ESAs)*** - **Anemia of chronic kidney disease (CKD)** is primarily due to insufficient erythropoietin production by the kidneys [1]. - Since iron stores are replete and other causes of anemia have been ruled out, ESAs are indicated to **stimulate red blood cell production** [2]. *Administer blood transfusion* - Blood transfusions provide temporary relief for severe anemia but come with risks like **transfusion reactions**, **iron overload**, and **alloimmunization**, which can complicate future transplantation. - They are generally reserved for cases of **symptomatic anemia** or **acute blood loss**, where immediate hemoglobin elevation is necessary, not for chronic management of CKD-related anemia first-line. *Prescribe oral folic acid* - Folic acid supplementation is crucial for **DNA synthesis** and red blood cell maturation, but there is no indication of **folate deficiency** in this patient. - While important for patients on dialysis due to increased losses, it will not address the primary issue of **erythropoietin deficiency**. *Administer intravenous vitamin B12* - Vitamin B12 is essential for red blood cell production, and a deficiency can lead to **macrocytic anemia**. - However, there is no evidence presented to suggest **vitamin B12 deficiency**, and supplementation would not correct the underlying problem of **insufficient erythropoietin** in CKD.

Question 753: A 35-year-old woman with systemic lupus erythematosus (SLE) presents with worsening proteinuria and edema. A kidney biopsy reveals diffuse proliferative glomerulonephritis. Which combination of therapies would be the most effective?

A. Corticosteroids and mycophenolate mofetil (Correct Answer)
B. NSAIDs and angiotensin receptor blockers
C. Cyclophosphamide and methotrexate
D. Plasmapheresis and intravenous immunoglobulin

Explanation: Corticosteroids and mycophenolate mofetil - This combination is often used for treating **diffuse proliferative glomerulonephritis** in SLE, targeting the **immune-mediated inflammation** effectively. - **Corticosteroids** reduce inflammation quickly, while **mycophenolate mofetil** helps in long-term disease management by inhibiting lymphocyte proliferation. [1] *NSAIDs and angiotensin receptor blockers* - NSAIDs can be used for pain in SLE but are **not effective** for addressing significant glomerulonephritis or proteinuria. [1] - Angiotensin receptor blockers help with hypertension and may reduce proteinuria, but do not modify the underlying immune pathogenesis. [1] *Plasmapheresis and intravenous immunoglobulin* - Plasmapheresis is utilized in severe cases but is not the first-line therapy for **routine diffuse glomerulonephritis** in SLE. - Intravenous immunoglobulin is supportive but does not specifically target the underlying disease process as effectively as corticosteroids and mycophenolate mofetil. *Cyclophosphamide and methotrexate* - Cyclophosphamide is a strong immunosuppressant but has significant **toxicity** and is usually reserved for severe cases or those not responsive to other therapies. - Methotrexate is less effective for **severe renal manifestations** compared to corticosteroids and mycophenolate mofetil. [1]

Question 754: A 60-year-old woman with a history of smoking presents with hematuria. What is the most appropriate initial investigation?

A. CT urogram
B. Ultrasound
C. Cystoscopy
D. Urinalysis (Correct Answer)

Explanation: ***Urinalysis*** - A **urinalysis** is the most appropriate initial investigation for hematuria [1] to confirm the presence of red blood cells, rule out pseudobloody urine, and identify potential causes like infection or proteinuria [1]. - It helps differentiate between glomerular and non-glomerular hematuria and can guide further imaging or invasive procedures [1]. *Cystoscopy* - While cystoscopy is crucial for directly visualizing the bladder and prostatic urethra in cases of confirmed hematuria, it is an **invasive procedure** and not typically the first step. - It is often performed after initial urinalysis and imaging have been completed and a source of bleeding is still unclear or to confirm a bladder lesion. *CT urogram* - A **CT urogram** is an excellent imaging modality for evaluating the entire urinary tract (kidneys, ureters, bladder) in cases of confirmed hematuria, especially when malignancy is suspected [1]. - However, it should be performed after urinalysis confirms true hematuria and provides context for the imaging findings. *Ultrasound* - **Ultrasound** is a non-invasive imaging technique that can assess the kidneys and bladder for structural abnormalities, stones, or masses [2]. - It is a good initial imaging study but follows urinalysis and may not fully evaluate the *entire* urinary tract or subtle lesions as effectively as a CT urogram.

Question 755: What is the primary concern in a patient with an electrolyte imbalance characterized by hyponatremia?

A. Neurological disturbances (Correct Answer)
B. Cardiac arrhythmias
C. Renal failure
D. Respiratory distress

Explanation: ***Neurological disturbances*** - **Hyponatremia** leads to **osmotic shifts** causing cerebral edema, which manifests as confusion, seizures, or even coma [1]. - The brain's sensitivity to rapid fluid shifts makes neurological complications the most immediate and severe concern [3]. *Cardiac arrhythmias* - While severe electrolyte imbalances can affect cardiac function, **hyponatremia** directly impacts the central nervous system more profoundly than cardiac rhythm in its initial stages. - **Hyperkalemia** or severe **hypokalemia** are more commonly associated with life-threatening cardiac arrhythmias. *Renal failure* - **Hyponatremia** is often a *symptom* or can be *caused by* underlying renal dysfunction, but it does not directly *cause* acute renal failure as its primary and most immediate concern [2]. - Conditions like **severe hypovolemia** can lead to prerenal azotemia and acute kidney injury, which might be associated with hyponatremia. *Respiratory distress* - Respiratory distress can occur in severe hyponatremia due to **pulmonary edema** if fluid overload is present, but it is not the primary and most direct concern compared to neurological impairment. - Conditions like **acidosis** or primary **respiratory diseases** are more direct causes of respiratory distress.

Question 756: A 70-year-old male with chronic kidney disease stage 4 presents with uremic pericarditis. What is the next best step in management?

A. Start high-dose corticosteroids
B. Immediate hemodialysis without heparin (Correct Answer)
C. Administer intravenous antibiotics
D. Perform pericardiocentesis

Explanation: **Immediate hemodialysis without heparin** - **Hemodialysis** is the definitive treatment for **uremic pericarditis** as it removes metabolic toxins and creatinine that accumulate in end-stage renal disease (ESRD) [1]. - **Heparin** should be avoided during dialysis in this setting to prevent the worsening of pericardial bleeding, which can lead to **cardiac tamponade**. *Start high-dose corticosteroids* - **Corticosteroids** are generally not indicated as the primary treatment for uremic pericarditis and may carry risks, especially in patients with chronic kidney disease. - The underlying cause, **uremia**, requires removal of toxins, which corticosteroids cannot achieve. *Administer intravenous antibiotics* - **Antibiotics** target bacterial infections, but **uremic pericarditis** is an inflammatory condition resulting from metabolic waste accumulation, not an infection. - Giving antibiotics would not address the root cause and is thus ineffective. *Perform pericardiocentesis* - **Pericardiocentesis** is reserved for cases where there is evidence of **cardiac tamponade** or a large, symptomatic **pericardial effusion** not responsive to dialysis. - Since the question does not mention signs of tamponade, it is not the initial best step, as addressing the uremia is paramount.

Question 757: Evaluating a patient with metabolic acidosis, which test would best determine the anion gap?

A. Serum electrolyte panel (Correct Answer)
B. Arterial blood gas (ABG)
C. Urine ketone test
D. Serum osmolality

Explanation: ***Serum electrolyte panel*** - The **anion gap** is calculated using concentrations of measured cations (primarily **sodium**) and anions (primarily **chloride** and **bicarbonate**), all of which are included in a standard serum electrolyte panel [1]. - The formula for anion gap is: **Na+ - (Cl- + HCO3-)**. *Arterial blood gas (ABG)* - An ABG measures **pH**, **PCO2**, and **bicarbonate** (HCO3-), which are crucial for diagnosing acid-base disorders but do not provide the full electrolyte profile needed to calculate the anion gap directly [1]. - While bicarbonate from an ABG can be used in the anion gap formula, an ABG alone does not provide the **sodium** and **chloride** values necessary for its calculation. *Urine ketone test* - This test detects the presence of **ketone bodies** in the urine, which are indicative of ketoacidosis (a type of high anion gap metabolic acidosis). - However, it does not directly provide the electrolyte concentrations needed to calculate the **anion gap**. *Serum osmolality* - Serum osmolality measures the concentration of chemical particles in the blood and is used to calculate the **osmolal gap**, which can indicate the presence of unmeasured osmoles like alcohols. - It does not provide the specific electrolyte values required for the **anion gap** calculation.

Question 758: Which antihypertensive drug class is recommended as first-line therapy for a patient with diabetes and proteinuria?

A. Beta-blockers
B. Diuretics
C. ACE inhibitors (Correct Answer)
D. Calcium channel blockers

Explanation: ***ACE inhibitors*** - **ACE inhibitors** are first-line for patients with diabetes and proteinuria due to their **nephroprotective effects**, which reduce intraglomerular pressure and decrease albumin excretion. - They uniquely block the conversion of **angiotensin I to angiotensin II**, thereby reducing vasoconstriction and aldosterone secretion. *Beta-blockers* - While effective for hypertension, **beta-blockers** do not offer the same **renoprotective benefits** as ACE inhibitors in patients with diabetes and proteinuria. - They can also mask the symptoms of **hypoglycemia** in diabetic patients, which is a significant concern. *Diuretics* - **Diuretics** primarily reduce volume and therefore blood pressure but do not directly address the **proteinuria** or provide the same **renal protection** as ACE inhibitors. - They can sometimes worsen **glucose control** and electrolyte imbalances in diabetic patients. *Calcium channel blockers* - **Calcium channel blockers** are suitable for blood pressure control but do not offer significant **renoprotective effects** or reduction in **proteinuria** in diabetic patients. - Some types, particularly dihydropyridines, can cause **peripheral edema**, a side effect that might be undesirable in some patients.

Question 759: A 45-year-old man presents with hematuria, hypertension, and pedal edema. Laboratory results show proteinuria and hypoalbuminemia. What is the most likely diagnosis?

A. Acute kidney injury
B. Chronic kidney disease
C. Nephrotic syndrome (Correct Answer)
D. Urinary tract infection

Explanation: ***Nephrotic syndrome*** - The combination of **hematuria, hypertension, pedal edema, proteinuria**, and **hypoalbuminemia** is classic for **nephrotic syndrome** [3]. - **Proteinuria** (>3.5 g/24h in adults), associated with **hypoalbuminemia**, causes reduced oncotic pressure, leading to **edema** [2]. *Acute kidney injury* - Characterized by a **sudden decline in kidney function**, leading to retention of waste products. - While it can cause fluid retention and potentially hypertension, **significant proteinuria and hypoalbuminemia** are not primary features. *Chronic kidney disease* - Involves **progressive, irreversible loss of kidney function** over months or years. - While it may involve proteinuria and edema in later stages, the sudden onset implied by the presentation and the classic nephrotic features point away from this. *Urinary tract infection* - Primarily presents with **dysuria, frequency, urgency**, and sometimes hematuria [1]. - It does not typically cause **hypertension, pedal edema**, or significant **proteinuria and hypoalbuminemia**.

Question 760: A 60-year-old male with chronic kidney disease has metabolic acidosis, hyperkalemia, high creatinine, and low bicarbonate. What is the most likely explanation?

A. Decreased renal ammonium excretion and reduced renal bicarbonate reabsorption (Correct Answer)
B. Increased renal potassium reabsorption and enhanced acid production
C. Decreased renal sodium reabsorption and reduced gluconeogenesis
D. Increased gastrointestinal potassium absorption and decreased renal perfusion

Explanation: ***Decreased renal ammonium excretion and reduced renal bicarbonate reabsorption*** - In **chronic kidney disease (CKD)**, the damaged kidneys lose their ability to excrete **ammonium** (a major mechanism for acid elimination) and **reabsorb bicarbonate** (essential for buffering acids) [2]. - This impaired acid-base regulation leads to the accumulation of acid, causing **metabolic acidosis** and **hyperkalemia** due to reduced potassium excretion by the failing kidneys [3]. Patients with deteriorating renal function may exhibit deep respirations as a clinical sign of this metabolic acidosis [1]. *Increased renal potassium reabsorption and enhanced acid production* - **Increased renal potassium reabsorption** would generally exacerbate hyperkalemia; however, the primary issue in CKD is **decreased potassium excretion**, not increased reabsorption as a cause of hyperkalemia. - While there might be some **enhanced acid production** from metabolism, the main mechanism for metabolic acidosis in CKD is the kidney's *inability to excrete* the normal acid load [3]. *Decreased renal sodium reabsorption and reduced gluconeogenesis* - **Decreased renal sodium reabsorption** typically leads to sodium wasting and potentially hypotension, which is not the primary cause of the constellation of symptoms (acidosis, hyperkalemia, high creatinine) in this scenario. - **Reduced gluconeogenesis** can occur in CKD, contributing to hypoglycemia, but it is not directly linked to the development of metabolic acidosis or hyperkalemia. *Increased gastrointestinal potassium absorption and decreased renal perfusion* - While **decreased renal perfusion** can worsen kidney function and contribute to acidosis and hyperkalemia [1] by reducing glomerular filtration, it doesn't fully explain the primary mechanism of **metabolic acidosis in CKD**, which is related to impaired acid excretion and bicarbonate reabsorption. - **Increased gastrointestinal potassium absorption** is not typically a primary driver of hyperkalemia in CKD unless there is excessive dietary intake or specific conditions affecting GI absorption; the kidney's inability to excrete potassium is paramount.

Practice by Chapter

Acute Kidney Injury

Practice Questions

Chronic Kidney Disease

Practice Questions

Glomerular Diseases

Practice Questions

Tubulointerstitial Diseases

Practice Questions

Nephrotic and Nephritic Syndromes

Practice Questions

Urinary Tract Infections

Practice Questions

Renal Replacement Therapy

Practice Questions

Fluid and Electrolyte Disorders

Practice Questions

Acid-Base Disorders

Practice Questions

Kidney in Systemic Diseases

Practice Questions

Kidney Stones and Obstructive Uropathy

Practice Questions

Hypertension in Kidney Disease

Practice Questions

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Nephrology — MCQs

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