MD - Doctor of Medicine Renal and Urinary Systems Questions and Answers

Question 1

A 65-year-old male with a long-standing history of type 2 diabetes and hypertension presents with fatigue, lower extremity edema, and a metallic taste in his mouth. Laboratory results show a GFR of 25 mL/min/1.73 m², serum potassium of 5.8 mEq/L, and BUN of 80 mg/dL. Which of the following medications that acts on the renal system is most likely contributing to his hyperkalemia?

Accepted Answer

Lisinopril

Answer

Lisinopril, an ACE inhibitor, is a common cause of hyperkalemia in patients with chronic kidney disease (CKD). ACE inhibitors block the conversion of angiotensin I to angiotensin II, leading to decreased aldosterone secretion. Aldosterone is responsible for potassium excretion in the distal tubules, so its inhibition leads to potassium retention. Furosemide (a loop diuretic) and hydrochlorothiazide (a thiazide diuretic) both increase potassium excretion. Amlodipine, a calcium channel blocker, does not significantly affect potassium levels.

Question 2

A 45-year-old female is diagnosed with Autosomal Dominant Polycystic Kidney Disease (ADPKD) after an incidental finding of multiple bilateral renal cysts on an abdominal ultrasound. Which of the following is the most accurate description of the underlying pathophysiology of this condition?

Accepted Answer

Mutations in PKD1 or PKD2 genes, leading to abnormal ciliary function, altered tubular cell proliferation, and fluid secretion into cysts.

Answer

ADPKD is primarily caused by mutations in the PKD1 (encoding polycystin-1) or PKD2 (encoding polycystin-2) genes. These proteins are crucial for the normal function of renal tubular cilia, which act as mechanosensors. Dysfunction of these cilia leads to abnormal intracellular signaling (e.g., increased cAMP), resulting in increased cell proliferation, fluid secretion, and the progressive formation and enlargement of renal cysts.

Question 3

A 22-year-old male is brought to the emergency department after being found unconscious at a rave. He is diagnosed with rhabdomyolysis secondary to MDMA (ecstasy) use. Which of the following is the primary mechanism by which rhabdomyolysis causes acute kidney injury (AKI)?

Accepted Answer

Renal tubular obstruction by myoglobin casts and direct cytotoxicity of myoglobin.

Answer

In rhabdomyolysis, massive breakdown of skeletal muscle releases large amounts of myoglobin into the circulation. This myoglobin is filtered by the glomeruli but can precipitate in the renal tubules, especially in the setting of dehydration and acidic urine, forming casts that cause physical obstruction. Additionally, the heme component of myoglobin is directly toxic to renal tubular epithelial cells, causing acute tubular necrosis.

Question 4

A 7-year-old boy presents with a palpable purpuric rash on his lower extremities, arthralgia, and abdominal pain. A urinalysis reveals microscopic hematuria and proteinuria. These findings are most consistent with which of the following conditions?

Accepted Answer

Henoch-Schönlein Purpura (HSP) Nephritis

Answer

The clinical triad of a palpable purpuric rash (without thrombocytopenia), arthritis, and abdominal pain is characteristic of Henoch-Schönlein Purpura (HSP), an IgA-mediated small-vessel vasculitis. Renal involvement (HSP Nephritis) is common, occurring in up to 50% of patients, and typically manifests as hematuria and proteinuria due to glomerular inflammation.

Question 5

A 58-year-old patient with type 2 diabetes and chronic kidney disease (stage 3) is started on an SGLT2 inhibitor. Which of the following best describes the primary renal mechanism by which this class of medication provides renoprotection?

Accepted Answer

Reducing proximal tubular sodium and glucose reabsorption, which restores tubuloglomerular feedback and reduces glomerular hyperfiltration.

Answer

SGLT2 inhibitors block the sodium-glucose cotransporter 2 in the proximal convoluted tubule, increasing urinary excretion of glucose and sodium. The increased sodium delivery to the macula densa restores tubuloglomerular feedback, leading to afferent arteriolar vasoconstriction. This action reduces intraglomerular pressure and corrects the glomerular hyperfiltration that is a key driver of diabetic kidney disease progression.

MD - Doctor of Medicine Practice Test

MD - Doctor of Medicine Practice Test

MD - Doctor of Medicine Renal and Urinary Systems Questions and Answers