2003
DOI: 10.1007/s00134-003-1986-6
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Hyperreninemic hypoaldosteronism: a possible etiological factor of septic shock-induced acute renal failure

Abstract: Transient hyperreninemic hypoaldosteronism is common in patients with septic shock. These abnormal aldosterone levels are associated with greater sodium and fluid depletion and are followed by enhanced incidence of acute renal failure requiring renal replacement therapy and prolonged length of stay in ICU.

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Cited by 72 publications
(48 citation statements)
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“…Our findings provide in vivo evidence that increases in aldosterone and cortisol secretion result from independent mechanisms. This is consistent with previous studies involving critically ill patients with (17) or wi thout (18) sepsis. Therefore, patients with septic shock may exhibit insufficient glucocorticoid production without concomitant deficiency of mineralocorticoid synthesis, and vice versa.…”
Section: Discussionsupporting
confidence: 93%
“…Our findings provide in vivo evidence that increases in aldosterone and cortisol secretion result from independent mechanisms. This is consistent with previous studies involving critically ill patients with (17) or wi thout (18) sepsis. Therefore, patients with septic shock may exhibit insufficient glucocorticoid production without concomitant deficiency of mineralocorticoid synthesis, and vice versa.…”
Section: Discussionsupporting
confidence: 93%
“…Our results confirm previous observations of a lack of association between sepsis and DHEA and S-DHEA deficiency [23]. Previous observations of sepsis which showed dissociation between aldosterone levels and renin activity [24,25] are not in contradiction with our findings of intact zona glomerulosa. In fact, these findings together suggest that aldosterone regulation is shifted from renin to ACTH and/or cytokine command.…”
Section: Discussionsupporting
confidence: 64%
“…Despite the high angiotensin II plasma levels, pronounced hypotension, associated with a reduced vasopressor effect of angiotensin II, has been reported [17]. Moreover, RAS activation contributes to oxidative stress and endothelial dysfunction [24], which has been associated with development of kidney [33] and pulmonary [25,26] injury and with the severity of organ dysfunction [19].…”
Section: Angiotensin II Receptorsmentioning
confidence: 99%