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Acute tubular necrosis, acute interstitial nephritis and cast nephropathy: 8 case reports In a case series, 8 patients including 7 men and 1 woman aged 18–82 years were described, who developed acute tubular necrosis, acute interstitial nephritis or cast nephropathy during treatment with gentamicin, tobramycin, vancomycin or vedolizumab [routes, dosages and durations of treatments to reactions onsets not stated]. Case 1: The 18-year-old man developed acute tubular necrosis and acute renal failure, during treatment with tobramycin. The man was diagnosed with acute lymphocytic leukaemia and received unspecified chemotherapy. Subsequently, he developed fever and urinary tract infection, and started receiving tobramycin. However, 2 days later, he developed acute renal failure (serum creatinine: 10 mg/dL). Light microscopy revealed unremarkable glomeruli, slightly dilated proximal tubules with moderate vacuolization changes in the cytoplasm hematoxylin/eosin stained section and some diminished brush borders on PAS stained section. Proximal tubules stained moderately positive for kidney injury molecule-1 (KIM-1). These findings were consistent with moderate acute tubular injury (acute tubular necrosis). Electron microscopy showed numerous round and dilated lysosomes containing randomly distributed whirling electron dense materials (zebra bodies or myeloid bodies) in proximal tubules. These were also found in some distal tubules. The myeloid bodies were measured ranging from 500–1000nm in sizes. At a one year follow-up, his serum creatinine was noted to be in the normal range. Case 2: The 82-year-old man developed acute tubular necrosis during treatment with gentamicin. The man, who had a medical history of hypertension, developed acute pyelonephritis. He started receiving gentamicin [gentamycin]. However, he developed acute kidney injury with elevated serum creatinine of 7.3 mg/dL, from his baseline of 1.2 mg/dL. A native renal biopsy showed etiology of the acute kidney injury. Light microscopy showed dilated proximal tubules with prominently diminished brush borders consistent with moderate acute tubular injury (acute tubular necrosis). Electron microscopy showed numerous myeloid bodies ranging from 400–1000nm. At a one year follow-up, his serum creatinine remained high at 6.5 mg/dL. The slow recovery was considered to be associated with his hypertension with underline renal damage. Case 3: The 51-year-old man developed acute tubular necrosis and cast nephropathy, during treatment with vancomycin. The man, who had a medical history of alcohol abuse, developed sepsis. He was initiated on treatment with vancomycin for sepsis. However, his serum creatinine level increased to 8.7 mg/dL. Urine analysis revealed 1+ blood, but was negative for protein. Light microscopy showed unremarkable glomeruli, but various degrees of acute tubular injury in proximal tubules and occasional interstitial nephritis components. The bluish casts in the lumina of distal tubules on routinely hematoxylin/eosin stained sections with some dilat