Hyperreninemic Hypoaldosteronism in the Critically 111: A New Entity*

Zipser, Robert D.; Davenport, Mark W.; Martin, Keith L.; Tuck, Michael L.; Warner, Nicholas P.; Swinney, Robert; Davis, Curtis L..; Horton, Richard

doi:10.1210/jcem-53-4-867

Cited by 130 publications

(68 citation statements)

References 32 publications

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“…These alterations have been described also in critically ill and hypotensive patients 37 . Total body water expansion and potassium depletion (vomiting, diarrhea, urinary potassium loss) may act as potent blocks to aldosterone secretion by adrenal glands in kala-azar patients.…”

Section: Discussionmentioning

confidence: 78%

Hyponatremia in visceral leishmaniasis

Verde

Veronese

et al. 2010

Rev. Inst. Med. trop. S. Paulo

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SUMMARYThere are few reports linking hyponatremia and visceral leishmaniasis (kala-azar). This is a study of 55 consecutive kala-azar patients and 20 normal individuals as a control group. Hyponatremia and serum hypo-osmolality were detected in 100% of kalaazar patients. High first morning urine osmolality (750.0 ± 52.0 vs. 894.5 ± 30.0mOsm/kg H 2 O, p < 0.05), and high 24-hour urine osmolality (426.0 ± 167.0 vs. 514.6 ± 132.0 mOsm/kg H 2 O, p < 0.05) demonstrated persistent antidiuretic hormone secretion. Urinary sodium was high (82.3 ± 44.2 vs.110.3 ± 34.7 mEq/L, p < 0.05). Low seric uric acid occurred in 61.8% of patients and increased fractional urinary uric acid excretion was detected in 74.5% of them. Increased glomerular filtration rate was present in 25.4% of patients. There was no evidence of extracellular volume depletion. Normal plasma ADH levels were observed in kala-azar patients. No endocrine or renal dysfunction was detected. It is possible that most hyponatremic kala-azar patients present the syndrome of inappropriate antidiuretic hormone secretion.

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Section: Discussionmentioning

confidence: 78%

Hyponatremia in visceral leishmaniasis

Verde

Veronese

et al. 2010

Rev. Inst. Med. trop. S. Paulo

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“…Renin and angiotensin are the strongest stimulators for aldosterone release (and not the hypothalamus and pituitary gland). Incapacity to increase aldosterone levels is also related to increased morbidity and mortality (10).…”

Section: Physiopathology Of Adrenal Insufficiency In Critical Care Pamentioning

confidence: 99%

Diagnosis of adrenal failure in critically ill patients

Moraes

Czepielewski

Friedman

et al. 2011

Arq Bras Endocrinol Metab

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SUMMARYIn the last two decades there was important evolution on the knowledge of the function of the hypothalamic-pituitary-adrenal axis. In the last decade, the expression "relative adrenal insufficiency" (RAI) was created, and more recently "critical illness-related corticosteroid insufficiency" (CIRCI) was used to designate those patients in which cortisol production was not sufficiently increased in stress situations. Patients with CIRCI have elevated hospital morbidity and mortality. Currently, there is a wide discussion about diagnostic criteria for this dysfunction. Besides basal cortisol, some publications now study the role of other tests, such as cortrosyn test − either in low (1 μg) or high doses (250 μg); free cortisol, salivary cortisol, metyrapone test and others. With this review, we aimed at summarizing the results of the most influent papers that intended to define diagnostic criteria for CIRCI. We also suggest an approach for CIRCI diagnosis and make it clear that the decision about steroid therapy in septic shock patients is matter apart from RAI. Arq Bras Endocrinol Metab. 2011;55(5):295-302 Keywords Adrenal insufficiency; sepsis; septic shock; cortrosyn; steroid therapy; CIRCI (critical illness-related corticosteroid insufficiency); RAI (relative adrenal insufficiency) SUMÁRIO Nas últimas décadas, houve uma importante evolução no conhecimento sobre a função do eixo hipotálamo-pituitária-adrenal. Na última década, foi cunhada a expressão "insuficiência adrenal relativa" (IAR) e, mais recentemente, a expressão "insuficiência adrenal relacionada à doença grave" (CIRCI) foi utilizada para designar aqueles pacientes nos quais a produção de cortisol não era suficientemente elevada em situações de estresse. Pacientes com CIRCI apresentam elevada morbidade e mortalidade em hospitais. Atualmente, há uma ampla discussão sobre os critérios de diagnóstico para essa desordem. Além do cortisol basal, algumas publicações analisaram o papel de outros testes, tais como o teste de estímulo com ACTH (cortrosina), com doses baixas (1 mg) ou altas (250 mg), cortisol livre, cortisol salivar, teste da metirapona e outros. O objetivo desta revisão foi resumir os resultados dos artigos mais importantes que buscaram definir os critérios de diagnóstico para a CIRCI. Também sugerimos uma abordagem para o diagnóstico da CIRCI e deixamos claro que a decisão sobre a terapia com esteroides em pacientes em choque séptico é uma questão separada da IAR. Arq Bras Endocrinol Metab. 2011;55(5):295-302 Descritores Insuficiência adrenal; sepse; choque séptico; cortrosina; terapia com esteroides; CIRCI (insuficiência adrenal relacionada à doença grave); IAR (insuficiência adrenal relativa)

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“…In contrast to serum cortisol levels, circulating levels of adrenal androgens such as dehydroepiandrosterone sulphate (DHEAS), which has immunostimulatory effects on Th1-helper cells, are low during prolonged critical illness (85±87). Moreover, despite increased plasma renin activity, paradoxically reduced concentrations of aldosterone are found in protracted critical illness (88). This constellation of effects suggests a shift of pregnenolone metabolism away from both mineralocorticoid and adrenal androgen pathways toward the glucocorticoid pathway, orchestrated by an unknown peripheral driving force.…”

Section: Pituitary±adrenal Axismentioning

confidence: 99%

Novel insights into the neuroendocrinology of critical illness

Berghe

2000

European Journal of Endocrinology

226

104

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An unexplained hallmark of prolonged critical illness is the fact that food does not prevent or reverse protein wasting, while fat is paradoxically accrued. This`wasting syndrome' often persists after the underlying disease has been resolved and thus perpetuates intensive care dependency. Although the crucial role of an intact hypothalamus±pituitary axis for homeostasis during stress is well recognized, the differences between the neuroendocrine changes observed in acute and prolonged critical illness were only recently described. Novel insights in this area are reviewed here.The initial endocrine stress response consists primarily of a peripheral inactivation of anabolic pathways while pituitary activity is essentially ampli®ed or maintained. These responses presumably provide the metabolic substrates and host defense required for survival and to delay anabolism, and thus should be considered as adaptive and bene®cial. Persistence of this acute stress response throughout the course of critical illness was hitherto assumed. This assumption has now been invalidated, since a uniformly reduced pulsatile secretion of ACTH, TSH, LH, prolactin (PRL) and GH has been observed in protracted critical illness, causing diminished stimulation of several target organs. Impaired pulsatile secretion of anterior pituitary hormones in the chronic phase of critical illness seems to have a hypothalamic rather than a pituitary origin, as administration of relevant releasing factors evoked immediate and pronounced pituitary hormone release. A reduced availability of TRH, one of the endogenous ligands of the GH-releasing peptide (GHRP) receptor (such as the recently discovered ghrelin) and, in very long-stay critically ill men, also of GHRH, appear to be involved. This hypothesis was further explored by investigating the effects of continuous i.v. infusion of GHRH, GHRP, TRH and their combinations for several days. Pulsatile secretion of GH, TSH and PRL was re-ampli®ed by relevant combinations of releasing factors which also substantially increased circulating levels of IGF-I, GH-dependent binding proteins, thyroxine and tri-iodothyronine (T3) while avoiding a rise in reverse T3. Active feedback-inhibition loops prevented overstimulation of target organs and metabolic improvement was noted with the combined infusion of GHRP and TRH. Whether this novel endocrine strategy will also enhance clinical recovery from critical illness remains to be explored.

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Hyperreninemic Hypoaldosteronism in the Critically 111: A New Entity*

Cited by 130 publications

References 32 publications

Hyponatremia in visceral leishmaniasis

Hyponatremia in visceral leishmaniasis

Diagnosis of adrenal failure in critically ill patients

Novel insights into the neuroendocrinology of critical illness

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