smoothened br Conflict of interest br Introduction Acute kid

Conflict of interest
Introduction Acute kidney injury in patients who are receiving anti-cancer treatments is an uncommon but serious complication. Such injury is often induced by nephrotoxic agents or urinary tract obstruction by space-occupying lesions. Among the many possible causes for renal function impairment in cancer patients, oxalate nephropathy is a rare but irreversible etiology. Oxalate nephropathy is associated with surgery, smoothened glycol poisoning, inflammatory bowel disease, or food ingestion. Nephrolithiasis, nephrocalcinosis, progressive chronic kidney disease, and end-stage kidney disease are the most common clinical presentations. Herein, we report a 65-year old man with gallbladder cancer who developed progressive renal function deterioration several months after Roux-en-Y hepaticojejunostomy. Subsequently, oxalate nephropathy was confirmed by renal biopsy.
Case report A 65-year-old man was diagnosed to have gallbladder cancer with common bile duct invasion. In an effort to cure the underlying cancer, the patient underwent cholecystectomy, hilar lymph node dissection and Roux-en Y hepaticojejunostomy. However, local recurrence over the liver was later identified and he received a partial hepatectomy six months thereafter. In all, the patient received a total of 12 cycles of chemotherapy with cisplatin and 5-FU after surgery. His serum creatinine at baseline was 1.07 mg/dL (normal: 0.7–1.4). After the 12 cycles of chemotherapy were completed, the patient\'s medical team fortuitously noted deteriorated renal function (serum creatinine: 5.69 mg/d). The patient showed no signs of hematuria or proteinuria, but did have a history of gouty arthritis. Abdominal ultrasonography revealed multiple stones over the left kidney without hydronephrosis; the length of the right and left kidneys was 9.5 and 9.1 cm, respectively. Initially, platinum-associated renal function impairment was considered, which halted additional chemotherapy. One month later, however, his serum creatinine level had elevated to 14.77 mg/dL. A routine urine test showed only mild proteinuria and glucosuria, and arterial blood gas analysis indicated metabolic acidosis. Hyperuricemia (12.8 mg/dL; normal: 2.4–7.2 mg/dL) was also noted. Immunological examinations showed negative ANA, ANCA, and anti-GBM antibody which essentially excluded the possibility of Goodpasture\'s disease and vasculitis associated renal function impairment. Thereafter, a renal biopsy was performed on the patient due to his unexplained acute kidney injury. The histological examination showed oxalate crystal deposition over the tubular lumina, resulting in tubular dilation, tubular cell injury and focal tubular basement membrane destruction (Fig. 1). Besides, increased leukocyte infiltration, composed of mononuclear cells, and a small number of eosinophils with focal edematous change was found over the interstitium. This pathological presentation was consistent with oxalate nephropathy. This patient denied a history of ethylene glycol ingestion, excessive dietary ingestion, or high vitamin C intake. Thereafter, he initiated regular hemodialysis because of irreversible renal function impairment.
Discussion Oxalate is an endogenous end product of amino acid metabolism absorbed by the gastrointestinal tract and excreted in the urine. Increased absorption of oxalate attributable to inflammatory bowel disease, ileal resection, bariatric surgery, Averrhoa carambola (star fruit), Averrhoa bilimbi (cucumber tree fruit), rhubarb, peanuts and black tea are the possible causes of enteric hyperoxaluria. Additionally, increased intestinal absorption of oxalate due to malabsorption is the pathophysiology of hyperoxaluria in patients with non-excessive ingestion. Hyperoxaluria due to malabsorption of fatty acid also could be caused by a deficiency of pyridoxine or vitamin B6, leading to the accumulation of peroxisomal glyoxylate which oxidizes to oxalate in the liver.