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Combined therapy with dialysis and glucocorticoids in critically ill renal failure patients.

Sepsis syndrome is a significant cause of mortality in the dialysis population, accounting for more than 75% of all deaths from infection [1]. During many acute illnesses, including sepsis, an increase in serum levels of cortisol is an important physiological response that is protective against injury. This response is secondary to increased production of corticotropin-releasing hormone and corticotropin, as well as to a reduction in negative feedback from cortisol [2]. However, in addition to the well-known effect that pre-existing conditions have on the hypothalamic-pituitary-adrenal axis, it has recently been reported that cortisol deficiency occurs during the course of acute illness [3]. This blunting of the physiological response results from elevated cytokine levels, which induce systemic or tissue-specific corticosteroid resistance [4]. Cortisol deficiency in intensive care patients can be difficult to discern clinically, as clinical indicators of the diagnosis are frequently non-specific [3]. In addition, some laboratory findings accompanying this condition in the dialysis population, such as hyperkalaemia and hyponatraemia, can be misleading. In dialysis patients, the persistence of these disturbances even after the initiation of efficient dialysis treatment should raise the suspicion of cortisol deficiency, and more specific laboratory tests should be performed. In this report, we describe four cases of sepsis syndrome in renal failure patients that, despite dialysis treatment in our intensive care unit, presented persistent hyperkalaemia, hyponatraemia, or both. We found these alterations to be related to cortisol deficiency, confirming that this phenomenon can occur even in the presence of renal failure and showing that aldosterone can act in all cells, mainly in intestinal cells.