Acute Aluminum Neurotoxicity Secondary To Treatment Of Severe Hyperphosphatemia Of Acute Renal Failure And The K/DOQI Guidelines: A Case Report And Review Of The Literature

摘要

Despite the efficacy of aluminum based compounds to bind phosphate from the gastrointestinal tract in the treatment of hyperphosphatemia associated with renal failure, their use is limited by their potential for multi-system toxicity. The current K/DOQI guidelines recommend their use be limited, both in terms of their indications for use as well as duration of therapy, to prevent the development of such side effects. We report a case of a patient with renal failure after orthotopic liver transplantation that developed acute encephalopathy from aluminum intoxication following aluminum hydroxide phosphate binder therapy despite its use being limited and within the guidelines set by the current K/DOQI recommendations. We propose an even more cautious use of these agents and a proactive approach to neurological complications arising amongst patients on this therapy. Introduction Despite the efficacy of aluminum based compounds to bind phosphate from the gastrointestinal tract in the treatment of hyperphosphatemia associated with renal failure, their use is limited by their potential for multi-system toxicity. The current United States Kidney/Dialysis Outcomes Quality Initiative (K/DOQI) guidelines updated in 2004 recommend their use be limited, both in terms of their indications as well as duration of therapy, to prevent the development of such side effects[1]. We report a case of a patient with renal failure after orthotopic liver transplantation that developed acute encephalopathy from aluminum intoxication following aluminum hydroxide phosphate binder therapy despite its use being limited and within the guidelines set by the current K/DOQI recommendations. We propose an even more cautious use of these agents and a proactive approach to neurological complications arising amongst patients on this therapy. Case Report A 50 yr old white male was admitted via the emergency department of our hospital in July 2004 with an acute decompensation of liver function secondary to recurrent Hepatitis C in an allograft received 8 years earlier. An expedited work-up resulted in a successful re-transplantation 2 days later but the immediate postoperative period was complicated by the development of acute anuric renal failure and severe hyperphosphatemia (see table). His renal failure was thought to be from acute tubular necrosis for which supportive therapies were instituted. Within 24hours he became non-oliguric, and his serum creatinine peaked at 5.3mg/dL (468.5mmol/L) so that he never required dialysis. However, his hyperphosphatemia worsened further and peaked at 12.2 mg/dl (3.94mmol/L). Nephrological consultation on the 3 rd postoperative day recommended a time and dose limited trial of aluminum hydroxide (Amphogel ? USA) at 45 ml orally thrice a day for a maximum period of 4 weeks. His nasogatric tube feeds were modified to a low Phosphate formulation (Nepro ? USA). By the 9 th postoperative day, his Amphogel dose was reduced to 20 ml thrice a day in view of improving renal function and serum phosphate level.