Abstract
Hydroxyethylstarch (HES) 200/0.5 is associated with renal failure. Several studies have suggested that renal function is affected but the subsequent arguments leave the clinician in no man's land. A recent study in Critical Care by Simon and colleagues using a two hit animal model of shock demonstrates that the use of a higher molecular weight starch, HES 200/0.5, is associated with impaired renal function when compared with ringers acetate, gelatin or a lower molecular weight starch, HES 130/0.42. The authors conclude that both the lower molecular weight starch and the ringers acetate 'preserve renal function and attenuate tubular damage better than 10% hydroxyethylstarch 200/0.5 in saline'. Added to the previous evidence, the renal effects of HES200/0.5 are probably real. Many clinicians have already moved to the lower molecular weight starches on the basis of doubt rather than certainty, but this study tips the balance. The cause remains elusive and the lack of a mechanism should be seen as a problem.
Highlights
The paradox that using higher molecular weight starches to prevent organ failure might cause it has been an anxiety
The evidence included the presence of the same osmotic nephrosis lesions that were seen with Dextran 40 and functional changes
The functional changes were first described when HES 220/0.6 given to renal donors was associated with impaired renal function in the subsequent recipients, this was contentious [6,7]
Summary
The paradox that using higher molecular weight starches to prevent organ failure might cause it has been an anxiety. The authors of a recent paper in Critical Care are to be congratulated for trying to nail the issue of whether hydroxyethylstarch (HES) 200/0.5 is associated with renal failure [1]. Colloids such as Dextran 40 have been implicated but the culprit, this time, is allegedly the hyperoncotic higher molecular weight HES 200/0.5 [2].
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