Stress steroids are not required for patients receiving a renal allograft and undergoing operation

It is commonly believed that patients receiving exogenous glucocorticoids have hypothalamic-pituitary-adrenal (HPA) axis suppression and require exogenous, supplemental, high-dose stress glucocorticoids to meet the demands of operative or other stress. Several recent reports suggest both that clinically important HPA axis suppression is extremely uncommon and that the levels of glucocorticoids required for stress are much lower than previously believed. In addition, the high doses of steroids currently used for stress prophylaxis may actually increase morbidity and mortality.

To test the need for stress steroids, a prospective study of 52 recipients of a renal allograft who underwent 58 operative procedures was conducted. No patient received stress steroids but only baseline, immunosuppressive doses of glucocorticoids. Clinical (hypotension, myalgias, arthralgias, ileus, and fever) and laboratory (serum sodium, eosinophil count, and 24-hour urinary-free cortisol from perioperative and nonstressed time periods) data were obtained to document evidence for adrenocortical insufficiency.

There was no clinical or laboratory evidence for adrenocortical insufficiency in any of the patients. Twenty-four hour urinary-free cortisol levels showed that all patients had endogenous adrenocortical function and, combined with clinical outcome, this function was sufficient to meet the demands of stress.

Adrenocortical insufficiency is much less common in recipients of a renal allograft than previously thought. Supplemental exogenous stress glucocorticoids are not required to meet the demands of operative stress in these patients. While biochemical testing of HPA axis function may sometimes reveal evidence for adrenal insufficiency, these tests do not predict clinical outcome and are far too sensitive to guide therapy.