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INTRODUCTION The incidence of acute kidney injury in patients with acute pancreatitis carries a poor prognosis. Hemolytic-uremic syndrome (HUS) is characterized by nonimmune hemolytic anemia, thrombocytopenia, and renal failure caused by platelet thrombi in the microcirculation of the kidney. HUS as a result of alcoholic pancreatitis is scarcely reported.[1] We report a case of alcoholic pancreatitis complicated with renal dysfunction followed by HUS, successfully managed with plasmapheresis after early recognition. CASE REPORT A 32-year-old male was admitted to hospital with complaints of abdominal pain, distension, vomiting, and reduce urine output. He had consumed alcohol in a substantial amount at a party, night before the onset of symptoms. He was a known hypertensive, controlled on low-dose amlodipine, otherwise healthy. On examination, the patient was afebrile, pale, dehydrated with tender, distended abdomen, and hypoactive bowel sounds. Ultrasonography of the abdomen revealed mild fatty liver and mild ascites with pancreas obscured by overlying gas-filled loops. Over the next 2 days, he became jaundiced and oliguric. Renal functions deteriorated with increase in urea and creatinine. He had an abrupt decrease in hemoglobin and platelet count and increased in serum bilirubin [Table 1]. Further evaluation revealed raised levels of procalcitonin, normal coagulation profile, and negative stool for occult blood. His peripheral blood film revealed numerous fragmented red cells and schistocytes. Table 1 Laboratory investigations during hospitalization

CASE REPORT A 32-year-old male was admitted to hospital with complaints of abdominal pain, distension, vomiting, and reduce urine output. He had consumed alcohol in a substantial amount at a party, night before the onset of symptoms. He was a known hypertensive, controlled on low-dose amlodipine, otherwise healthy. On examination, the patient was afebrile, pale, dehydrated with tender, distended abdomen, and hypoactive bowel sounds. Ultrasonography of the abdomen revealed mild fatty liver and mild ascites with pancreas obscured by overlying gas-filled loops. Over the next 2 days, he became jaundiced and oliguric. Renal functions deteriorated with increase in urea and creatinine. He had an abrupt decrease in hemoglobin and platelet count and increased in serum bilirubin [Table 1]. Further evaluation revealed raised levels of procalcitonin, normal coagulation profile, and negative stool for occult blood. His peripheral blood film revealed numerous fragmented red cells and schistocytes. Table 1 Laboratory investigations during hospitalization In view of Coombs-negative hemolytic anemia, thrombocytopenia, and acute renal failure with schistocytes on blood smear, a diagnosis of HUS was made complicating acute pancreatitis. On the 3rd day, he was initiated on plasmapheresis: 2 L of plasma exchange per cycle (30 ml/kg) supplemented with albumin and fresh frozen plasma product transfusions as replacement fluids. In due course, three sessions of hemodialysis and four sessions of plasmapheresis were provided to him on alternate days, also requiring additional two units of blood transfusions. He was managed with empirical intravenous antibiotics and total parenteral nutrition (TPN) for initial 5 days. Culture (blood and urine) reports were sterile.

e sessions of hemodialysis and four sessions of plasmapheresis were provided to him on alternate days, also requiring additional two units of blood transfusions. He was managed with empirical intravenous antibiotics and total parenteral nutrition (TPN) for initial 5 days. Culture (blood and urine) reports were sterile. By the 7th day, there was substantial improvement in clinical condition with significant increase in urine output. Laboratory parameters improved with hemoglobin, increased platelet count, reduction in urea, creatinine, and total bilirubin level. By the 10th day, the patient was shifted out to wards and was discharged in stable condition by the 14th day on oral antibiotics. DISCUSSION HUS and thrombotic thrombocytopenic purpura (TTP) are classified into a group of disorders called thrombotic microangiopathies.[2] The term “HUS” was coined by Gasser et al. in 1955 and describes an illness consisting of acute renal failure accompanied by nonimmune hemolytic anemia and thrombocytopenia.[3] HUS is most commonly seen in children, but cases among adults have also been increasingly described in association with infections, transplants, autoimmune diseases, drugs, and neoplasms. It is divided as typical HUS (Shiga-like toxin-associated HUS) and atypical HUS (non-Shiga-like toxin-associated HUS). Atypical HUS is further subclassified as familial due to complement dysregulation and sporadic due to Streptococcus pneumoniae infection.[456]

s, transplants, autoimmune diseases, drugs, and neoplasms. It is divided as typical HUS (Shiga-like toxin-associated HUS) and atypical HUS (non-Shiga-like toxin-associated HUS). Atypical HUS is further subclassified as familial due to complement dysregulation and sporadic due to Streptococcus pneumoniae infection.[456] The etiology of HUS following pancreatitis is not clearly understood as there are only few cases reported in the literature. Swisher et al. described patients who were diagnosed with acute pancreatitis and then subsequently developed an acute episode of TTP-HUS.[1] Several hypotheses have proposed the role of inflammatory mediators, tumor necrosis factor and interleukin (IL)-1, that can induce widespread vascular endothelial injury.[7] Circulating pancreatic proteases interact with a number of components of the coagulation system. They induce clotting factor activation precipitating disseminated intravascular coagulation and also proteolyse the fibrinogen resulting in dysfibrinogenemia. It is proposed that in cases of HUS-TTP secondary to pancreatitis, circulating proteases may modify circulating von Willebrand factor (vWF) molecules enabling spontaneous binding to platelet membrane glycoproteins with subsequent platelet aggregation.[8] Serum estimation of vWF-cleaving protease (ADAMTS-13) has been used to differentiate between TTP and HUS as patients with TTP have deficient ADAMTS-13 activity in plasma compared to patients with HUS.[9] However, in our patient, levels could not be measured due to unavailability of test at center.

telet aggregation.[8] Serum estimation of vWF-cleaving protease (ADAMTS-13) has been used to differentiate between TTP and HUS as patients with TTP have deficient ADAMTS-13 activity in plasma compared to patients with HUS.[9] However, in our patient, levels could not be measured due to unavailability of test at center. The treatment of HUS following acute pancreatitis is primarily supportive. Exchange plasmapheresis has been reported to be an effective treatment with a response rate of 79%.[10] Rituximab (anti-CD20 antibody) is an alternative treatment option in refractory or relapsing HUS.[11] CRRT/SLED is the preferred treatment for acute kidney injury in intensive care units. It removes metabolic waste products and eliminates inflammatory mediators such as IL-1, IL-6, and IL-8 which contributes to early recovery, as in our case.[1213] In conclusion, it is important that physicians recognize thrombotic microangiopathy (HUS/TTP) as one of the potential causes of acute renal failure among adult patients with acute pancreatitis, especially in the setting of anemia and thrombocytopenia. Till date, a total of 22 cases have been described to develop HUS/TTP following pancreatitis of varied etiology. Our patient had an excellent response to hemodialysis and plasma exchange with complete resolution of his microangiopathy and recovery of renal function. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.