Match each patient's clinical presentation and laboratory profile with the most characteristic finding expected on their microscopic urinalysis or urine sediment examination.
- A 52-year-old individual recently treated with pantoprazole for reflux who now presents with an asymptomatic rise in serum creatinine to 2.8 mg/dL.White blood cell casts, eosinophils, and sterile pyuria
- A 71-year-old presenting with generalized fatigue, normocytic anemia, elevated total protein with normal albumin, and a new serum creatinine of 3.1 mg/dL.Dense, brightly eosinophilic, glassy tubular casts with fractured edges
- A 34-year-old evaluated for confusion and tachypnea, found to have an anion gap of 28 mEq/L and an osmolar gap of 18 mOsm/kg H2O.Envelope-shaped (octahedral) and needle-shaped monohydrate crystals
- A 64-year-old with newly diagnosed Burkitt lymphoma who developed acute oliguria 48 hours after receiving the first cycle of systemic chemotherapy.Pleomorphic rhomboid, needle-like, or rosette-shaped yellow-brown crystals
Answer
The correct pairings match proton-pump inhibitor use with WBC casts (AIN); suspected multiple myeloma with glassy, fractured casts (cast nephropathy); ethylene glycol ingestion with envelope-shaped oxalate crystals; and tumor lysis syndrome with rhomboid uric acid crystals.
Each clinical scenario describes a classic etiology of acute kidney injury paired with a pathognomonic urine sediment finding. AIN presents with WBC casts, multiple myeloma cast nephropathy with fractured glassy casts, ethylene glycol toxicity with calcium oxalate crystals, and tumor lysis syndrome with uric acid crystals.
Step-by-Step Solution
Key Concept
Correlation of specific acute kidney injury (AKI) etiologies with their pathognomonic urine sediment findings.