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A transdermal patch formulation of a non-steroidal anti-inflammatory drug (NSAID) used by a 44-year-old man resulted in acute interstitial nephritis and acute tubular injury. This patient also had a history of mild kidney dysfunction and osteoporosis. The NSAID patch had been prescribed after a traffic accident. He was also receiving a vitamin D analog and taking over-the-counter calcium supplements. Two months later, renal dysfunction and hypercalcemia were discovered. A renal biopsy showed acute interstitial nephritis and acute tubular injury. Once these agents were withdrawn, the renal function recovered. This is the first reported occurrence of biopsy-proven acute interstitial nephritis attributable to NSAID patch usage.

Background: Panitumumab is the first human combinatorial antibody for the treatment of metastatic colorectal carcinoma. Dermatologic toxicity of all grades occurs in more than 90% of patients. However, there are few reports of purpura induced by anti-epidermal growth factor receptor antibody. Renal failure is also uncommon as an adverse event of anti-epidermal growth factor receptor antibody., Case Presentation: A 67-year-old Japanese man with advanced colon cancer received monotherapy with panitumumab. General malaise, bilateral edema of his legs, and bilateral purpura of his forearms developed 2 days after the second cycle of panitumumab. A skin biopsy was performed to evaluate the purpuric lesions on his left leg and leukocytoclastic vasculitis was diagnosed. Blood tests showed grade III acute renal failure with a blood urea nitrogen level of 33.8 mg/dL and a creatinine level of 3.10 mg/dL., Conclusions: This is the first reported case of leukocytoclastic vasculitis followed by purpura and acute renal failure associated with panitumumab.

Acute kidney injury (AKI) is caused by diverse pathologies, although it may occasionally result from concurrent renal efflux disturbances. We herein describe a case of AKI in a patient complicated by renal cell carcinoma (RCC) with renal vein and inferior vena cava (IVC) involvement. A neoplastic thrombus which disrupted the blood flow in the renal vein appeared to play a role in the rapid decline in the renal function. Such a scenario has rarely been mentioned in the previous literature describing the cases of RCC complicated by AKI. Concerns regarding the diagnostic and therapeutic strategies for RCC are also discussed.

We report 2 cases with a good recovery from acute kidney injury (AKI) due to exercise-induced AKI associated with renal hypouricemia. Case 1 involves a 20-yearold man who had a similar episode 1 year earlier. He complained of nausea, vomiting and loin pain after playing football. On admission, his serum creatinine was 3.27 mg/dl and he was treated with intravenous fluid infusion (2 l/d). His renal function deteriorated and creatinine rose to 9.82 mg/dl. A renal hemodynamic evaluation using duplex Doppler ultrasound showed a high arterial resistance index (RI). After we changed his treatment to intravenous continuous infusion of 2 µg/kg/min dopamine, RI decreased sequentially and creatinine decreased without hemodialysis. A renal biopsy performed 7 days after dopamine infusion showed no changes in glomeruli and tubules, suggesting the absence of acute tubular necrosis, and no uric acid crystals or myoglobin casts in tubules. Case 2 involves a 42-year-old man who complained of loin pain after riding a motorcycle. On admission, his creatinine and creatine phosphokinase (CPK) were 3.93 mg/dl and 59 mU/ml, respectively. His RI was also high and he was treated immediately with an intravenous continuous infusion of 2 µg/kg/min dopamine. RI and creatinine decreased sequentially. Both cases suggest the effectiveness of dopamine infusion for AKI due to renal hypouricemia in which the RI of the renal arteries is high.