Given the following laboratory and urinalysis results: K+: 5.5 mmol/L; Ca2+: 3.00 mmol/L; Phosphate: 1.60 mmol/L; Urea: 9.3 mmol/L; Ammonium: 70 µmol/L; Triglycerides: 2.4 mmol/L; Serum osmolality: 340 mOsm/kg; Urine albumin: 140 mg/L; Glucose: POS; Renal tubular epithelial cells: PRESENT; Broad casts: PRESENT; Waxy casts: PRESENT; Hyaline casts: 5-10/hpf. What is the suspected diagnosis?

Prepare for the CAMLPR Chemistry Test. Enhance your understanding with interactive quizzes, flashcards, and detailed explanations. Boost your confidence and readiness for exam success!

Multiple Choice

Given the following laboratory and urinalysis results: K+: 5.5 mmol/L; Ca2+: 3.00 mmol/L; Phosphate: 1.60 mmol/L; Urea: 9.3 mmol/L; Ammonium: 70 µmol/L; Triglycerides: 2.4 mmol/L; Serum osmolality: 340 mOsm/kg; Urine albumin: 140 mg/L; Glucose: POS; Renal tubular epithelial cells: PRESENT; Broad casts: PRESENT; Waxy casts: PRESENT; Hyaline casts: 5-10/hpf. What is the suspected diagnosis?

The key idea is that the urine sediment and casts point to long-standing, severe kidney damage rather than an acute, reversibly damaged kidney. Broad casts are a hallmark of advanced chronic kidney disease because they form in severely dilated, chronically injured tubules and reflect slow flow and tubular degeneration. Waxed casts strengthen that impression, indicating a high degree of chronicity and tubular/glomerular disruption. The appearance of renal tubular epithelial cells also signals tubular injury, which fits with long-term renal failure. Together with rising potassium and elevated urea, these findings align with end-stage renal disease, where GFR is markedly reduced and the kidney can no longer maintain electrolyte and nitrogen waste balance. Prerenal azotemia would typically show relatively benign urinalysis with few abnormal casts and would improve with hydration, not the chronic, degenerative sediment pattern seen here. Acute tubular necrosis would more commonly show granular (muddy brown) casts rather than predominantly broad/waxy casts, and its onset is acute rather than progressive to end-stage disease. Nephrotic syndrome would emphasize heavy proteinuria, hypoalbuminemia, and hyperlipidemia with edema, rather than a sediment dominated by broad and waxy casts indicating chronic repair and scarring.

The key idea is that the urine sediment and casts point to long-standing, severe kidney damage rather than an acute, reversibly damaged kidney. Broad casts are a hallmark of advanced chronic kidney disease because they form in severely dilated, chronically injured tubules and reflect slow flow and tubular degeneration. Waxed casts strengthen that impression, indicating a high degree of chronicity and tubular/glomerular disruption. The appearance of renal tubular epithelial cells also signals tubular injury, which fits with long-term renal failure. Together with rising potassium and elevated urea, these findings align with end-stage renal disease, where GFR is markedly reduced and the kidney can no longer maintain electrolyte and nitrogen waste balance.

Prerenal azotemia would typically show relatively benign urinalysis with few abnormal casts and would improve with hydration, not the chronic, degenerative sediment pattern seen here. Acute tubular necrosis would more commonly show granular (muddy brown) casts rather than predominantly broad/waxy casts, and its onset is acute rather than progressive to end-stage disease. Nephrotic syndrome would emphasize heavy proteinuria, hypoalbuminemia, and hyperlipidemia with edema, rather than a sediment dominated by broad and waxy casts indicating chronic repair and scarring.

More practice questions