Acute Renal Failure after Consumption of Fish Gall Bladder

A case of acute renal failure after consumption of fish gall bladder as traditional medical remedy is reported. The patient fully recovered with conservative treatment. The risk of acute kidney failure and even multiple organ dysfunction syndrome following ingestion of fish gall bladder is highlighted. 1. Introduction In India, especially in Assam, people believe that fish gall bladder can improve vision and treat rheumatism. Chinese populations have a similar view and believe it improves eyesight and cure asthma [1]. Due to frequent consumption of fish gall bladder, fish bile poisoning cases care reported more commonly in China, India, Japan, and other Asian countries [2–4]. There were many reports about fish gall bladder poisoning leading to acute renal failure (ARF), acute liver injury, and therefore increasing mortality [5]. The incidence of ARF in fish bile poisoning is 55%–100%, while the mortality rate accounts 91.7%. Recently, studies have shown that fish gall bladder can also damage the heart, liver, and gastrointestinal tract and lead to multiple organ dysfunction syndrome (MODS) [1]. This is a case of gall bladder poisoning leading to acute renal failure in Chinese patient. This report is a whole new perspective on the pathogenesis of acute renal failure on complements about cases of poisoning in fish guts. This has a positive role in guiding treatment of fish bile poisoning, with obvious effect to improve its prognosis. 2. Case Features A 56-years-old Chinese woman with past medical history of chronic bronchitis presented to a community hospital after consumption of grass carp fish gall bladder. Fish gall bladder was about ？cm. Initial symptoms were nausea, vomiting, abdominal cramps, and watery diarrhea. After the onset of the symptoms she was treated in community level hospital with intravenous infusion for three days which did not improve her condition. After 5 days, she was presented in Tianjin Medical University General Hospital, Emergency Medical Center, for better management. On examination vital signs were stable. However, oliguria or anuria was observed in 24 hours and showed no edema. Blood works revealed the following: WBC: /L, N: 80.91%, and HB: 168？g/L; ABG revealed the following: PH: 7.50, PO2: 153？mmHg, Lac: 1.4？mmol/L, HCO3？: 25.7？mmol/L, and BE: 2.7？mmol/L. Urinanalysis reported: RBC: 0/HPF, WBC: 0/HPF, pathological casts: 0/LPF, specific gravity: 1.005, PH: 6.3; biochemistry reported the following: Cr: 277？umol/L, BUN: 13.31？mmol/L, ALT: 95？U/L, AST: 35？U/L, and TBIL: 85.9？mmol/L. After admission intravenously reduced