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Kai-Uwe Eckardt, Carsten Willam, Ulrich Frei, Severe hypophosphataemia in paracetamol-induced oliguric renal failure, Nephrology Dialysis Transplantation, Volume 14, Issue 8, August 1999, Pages 2013–2014, https://doi.org/10.1093/ndt/14.8.2013
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Introduction
Since the first reports of paracetamol overdose, acute renal failure has often been noted as a complication of fulminant hepatic failure [1]. A similar frequency of renal impairment in paracetamol intoxications and other causes of acute liver damage suggested that this association is not due to a specific nephrotoxic effect of paracetamol [2]. Subsequently, however, retrospective analysis of two large patient series revealed that approximately 1% of patients admitted after paracetamol overdose develop acute renal failure in the absence of fulminant liver damage [3,4]. In addition, single cases were reported in whom renal failure occurred in the absence of any clinical or biochemical evidence of liver damage [4,5].
Hypophosphataemia is another recognized feature of paracetamol poisoning. Its incidence and severity correlate with the extent of hepatic damage, but it was also found in the absence of clinical or biochemical evidence of liver toxicity [6]. Jones et al. [6] concluded, from a significant correlation between the serum phosphate concentration and renal phosphate threshold concentration, that the hypophosphataemia associated with paracetamol intoxication is due to phosphaturia rather than intracellular redistribution. Here we report a case of severe hypophosphataemia in a patient with paracetamol intoxication, who was oliguric, which argues strongly against renal phosphate loss as the underlying mechanism.
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