Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 10-year-old boy with glucose-6-phosphate dehydrogenase deficiency developed acute renal failure during the icteric phase of non-fulminant hepatitis A infection. He needed peritoneal dialysis for 54 days. Acute tubular necrosis was confirmed by percutaneous renal biopsy. He had complete recovery of his renal function when he was discharged.
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PMID:Acute viral hepatitis, glucose-6-phosphate dehydrogenase deficiency and prolonged acute renal failure: a case report. 853 46

We report two children with hemolytic anemia during the course of hepatitis A infection. On admission, the patients had high blood urea nitrogen, creatinine, and uric acid levels, as well as anemia, leucocytosis, and direct and indirect hyperbilirubinemia. Both patients had a glucose-6-phosphate dehydrogenase deficiency (G6PD) and autoimmune antibodies. They were given vitamin K on admission. Inadvertent administration of vitamin K could have been related to an acute reduction in hemoglobin concentration. To prevent renal damage, plasmapheresis with fresh frozen plasma was done to clear bilirubin and plasma hemoglobin. The hyperbilirubinemia responded to plasmapheresis. However, acute tubular necrosis complicated the clinical course in one patient, and several sessions of hemodialysis were required. In conclusion, intravascular hemolysis should be considered in patients with hepatitis A infection, marked hyperbilirubinemia, and anemia. Although hepatitis A vaccination is not yet recommended for routine administration, high-risk patients, including those with a G6PD deficiency, should be vaccinated against hepatitis A.
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PMID:Etiology of hemolysis in two patients with hepatitis A infection: glucose-6-phosphate dehydrogenase deficiency or autoimmune hemolytic anemia. 1832 Feb 20

Acute kidney injury (AKI) with evidence of hemolysis is associated with tropical infections. However, pigment-induced AKI can happen with relatively uncommon genetic causes of hemolytic anemia, i.e., glucose 6-phosphate deficiency (G6PD). We share our experience of three such patients whose clinical presentation was similar to jaundice, AKI with hemolysis with suspicion of thrombotic microangiopathy. On evaluation, all had a history of usage of anti-malarial and with G6PD estimation revealing deficient status even during the episode while other tests such as Coomb's test and bone marrow biopsy was normal in all three patients. The kidney biopsy revealed acute tubular necrosis with red blood cell casts and pigments in all the cases. All patients were managed conservatively and showed complete recovery. Thus in tropical countries G6PD deficiency although is not common, should be considered among patients who have received antimalarial drugs presenting as AKI and a detailed hemolytic work-up needs to be carried out as an important cause of preventable recurrent AKI in tropical countries.
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PMID:G6PD deficiency is not an uncommon cause of pigment nephropathy. 3058 69

Rasburicase is a recombinant urate-oxidase enzyme and is a very important medication for tumor lysis syndrome. Methemoglobinemia and hemolysis are known side effects of rasburicase that result from oxidative stress caused by hydrogen peroxide, a byproduct generated during the breakdown of uric acid to allantoin. Patients with G6PD deficiency have a decreased tolerance to oxidative stress and are therefore at a greater risk of hemolysis and methemoglobinemia with rasburicase. Our patient is a 56-year-old Caucasian male with a recent diagnosis of grade 2-3a non-Hodgkin's lymphoma who presented to our emergency department with shortness of breath and dark discoloration of urine. Patient was discharged 36 hours ago from our hospital after he was given a first course of R-CHOP regimen and a dose of rasburicase. On further evaluation, patient was found to have severe anemia with hemolytic picture, hyperkalemia and acute kidney injury. He also had a discrepancy of the transcutaneous saturation (75%) and the saturation in an arterial blood gas value (99%). His methemoglobin level was found to be 11.9%. We were aware that methylene blue is a contraindication in patients with G6PD deficiency but considering patient being Caucasian and low risk for it and his deteriorating respiratory condition, it was decided to offer the treatment and patient received 1 dose of methylene blue which failed to improve his methemoglobinemia. He was also given vitamin C and 8 units of packed red blood cell throughout his stay in the hospital. Patient's hospital course was complicated by ARDS needed to be on mechanical ventilation support for 4 days and acute renal failure secondary to pigment nephropathy and acute tubular necrosis which required a hemodialysis support. Even if rasburicase induced methemoglobinemia and hemolysis are not very common complications, clinicians who prescribe and follow patients should detect this serious complication early and manage it accordingly. Our case can be used as a reminder that patients should be followed closely and given the right instructions on discharge to treat these complications which are associated with severe consequences. It is also vital to assume a diagnosis of G6PD deficiency until proven otherwise in a patient who presents with rasburicase induced hemolysis and avoid administration of methylene blue even if the patient is from a low risk ethnicity for G6PD as in our patient.
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PMID:Rasburicase induced severe hemolysis and methemoglobinemia in a Caucasian patient complicated by acute renal failure and ARDS. 3060 5