A patient returns from her initial hemodialysis treatment with nausea, confusion, twitching and jerking. The pathophysiologic mechanism of dialysis responsible for these manifestations is a

Correct Answer: C

Rationale: Disequilibrium syndrome from rapid solute removal creates a brain osmotic gradient, causing edema and neurological symptoms not heparin (bleeding), volume loss (hypotension), or sodium (electrolyte). This distinguishes dialysis complications, key for patient monitoring, contrasting with fluid dynamics.

Correct Answer: D

Rationale: Mesangial cells contract to reduce GFR area and phagocytose debris not produce systemic angiotensin II (juxtaglomerular cells). 'A and C' are true, distinguishing mesangial roles, critical for filtration regulation, contrasting with renin-angiotensin.

Correct Answer: B

Rationale: Renal threshold (~180 mg/dL or mg%) is the plasma glucose level where reabsorption saturates, spilling into urine not rate (mg/min) or higher values. This distinguishes glucose homeostasis, critical for diabetes, contrasting with saturation definitions.

Correct Answer: B

Rationale: Renin comes from juxtaglomerular cells (afferent arteriole), not efferent macula densa (DCT), fenestrated capillaries (glomerulus), and collecting tubules (rays) are correct. This distinguishes renin's source, key for RAAS, contrasting with vascular misplacement.

Correct Answer: A

Rationale: In sarcoidosis, hypercalciuria stems from absorptive hypercalciuria excess vitamin D from granulomas increases gut calcium absorption, spilling into urine. Renal hypercalciuria involves kidney leak, not primary in sarcoidosis absorption drives it. Low calcium intake reduces, not raises, urinary calcium opposite effect. Reduced oxalate excretion is unrelated oxalate binds calcium, not source here. Absorptive mechanism distinguishes sarcoidosis' systemic etiology, key to its stone risk, unlike renal, dietary, or oxalate factors.