Hyperkalemia tacrolimus nephrotox

Long-term follow-up (mean of 93 months) of tacroU-mus-based immunosuppression has been reported in 121 adult patients with liver transplants (10). Infections were the most common causes of deaths (17 patients out of 42), and half of them occurred during the first year after transplantation. Cardiovascular events (seven patients) or de novo malignancies (three patients) were also important causes of death. End-stage renal disease related to tacrolimus nephrotoxicity was noted in two patients who required renal transplantation At 7 years, other important adverse effects included hyperkalemia (30%) or... 

Tacrolimus can be administered orally or intravenously. The half-life of the intravenous form is approximately 9-12 hours. Like cyclosporine, tacrolimus is metabolized primarily by P450 enzymes in the liver, and there is potential for drug interactions. The dosage is determined by trough blood level at steady state. Its toxic effects are similar to those of cyclosporine and include nephrotoxicity, neurotoxicity, hyperglycemia, hypertension, hyperkalemia, and gastrointestinal complaints. 

Nephrotoxicity, neurotoxicity (tremor, headache, motor disturbances, seizures), G1 complaints, hypertension, hyperkalemia, hyperglycemia, and diabetes are all associated with tacrolimus use. As with cyclosporine, nephrotoxicity is limiting. Tacrolimus has a negative effect on pancreatic islet beta cells, and glucose intolerance and diabetes melli-tus are well-recognized complications of tacrolimus-based immunosuppression. As with other immunosuppressive agents, there is an increased risk of secondary tumors and opportunistic infections. Notably, tacrolimus does not adversely affect uric acid or LDL cholesterol. 

Nephrotoxicity, neurotoxicity (tremor, headache, motor disturbances, seizures), GI complaints, hypertension, hyperkalemia, hyperglycemia, and diabetes are all associated with tacrolimus use. 

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