Pituitary-Adrenocortical Function in Chronic Renal Failure: Studies of Episodic Secretion of Cortisol and Dexamethasone Suppressibility*

Wallace, Eleanor Z.; Rosman, Paul M.; Toshav, Nina; Sacerdote, Alan; Balthazar, Adriana

doi:10.1210/jcem-50-1-46

Cited by 103 publications

(69 citation statements)

References 15 publications

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“…Increased plasma levels of immunoreactive glucagon/proglucagon are frequently present in CRF (22), but at nonpharmacologic concentrations glucagon does not appear to change skeletal muscle metabolism (17). Although parathyroid hormone may affect skeletal muscle metabolism in normal rats, muscle ofuremic rats appears to be resistant to its catabolic effects (23 (24,25). The present results extend these reports by showing that CRF increases glucocorticoid excretion independently of metabolic acidosis.…”

Section: Discussionsupporting

confidence: 78%

Mechanisms for defects in muscle protein metabolism in rats with chronic uremia. Influence of metabolic acidosis.

May¹,

Kelly²,

Mitch³

1987

J. Clin. Invest.

313

193

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Chronic renal failure (CRF) is associated with metabolic acidosis and abnormal muscle protein metabolism. As we have shown that acidosis by itself stimulates muscle protein degradation by a glucocorticoid-dependent mechanism, we assessed the contribution of acidosis to changes in muscle protein turnover in CRF. A stable model of uremia was achieved in partially nephrectomized rats (plasma urea nitrogen, 100-120 mg/dl, blood bicarbonate < 21 meq/liter). CRF rats excreted 22% more nitrogen than pair-fed controls (P < 0.005), so muscle protein synthesis and degradation were measured in perfused hindquarters. CRF rats had a 90% increase in net protein degradation (P < 0.001); this was corrected by dietary bicarbonate. Correction of acidosis did not reduce the elevated corticosterone excretion rate of CRF rats, nor did it improve a second defect in muscle protein turnover, a 34% lower rate of insulin-stimulated protein synthesis. Thus, abnormal nitrogen production in CRF is due to accelerated muscle proteolysis caused by acidosis and an acidosis-independent inhibition of insulin-stimulated muscle protein synthesis.

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Section: Discussionsupporting

confidence: 78%

Mechanisms for defects in muscle protein metabolism in rats with chronic uremia. Influence of metabolic acidosis.

May¹,

Kelly²,

Mitch³

1987

J. Clin. Invest.

313

193

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“…Uremia could constitute a stress condition where ACTH secretion is increased thus causing an increase in plasma Estrone. Cortisol levels too are found to be higher in uremic men [15].…”

Section: Discussionmentioning

confidence: 84%

Prolactin, Gonadotropins, Testosterone, and Estrogens in Uremic Men Undergoing Periodic Hemodialysis

Mastrogiacomo

Feghali

Besi

et al. 1982

Archives of Andrology

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Forty-five uremic men, aged 20 to 68 years, undergoing periodic hemodialysis were investigated regarding their plasma testosterone ('I') and human prolactin (hPRL); in 25 of those. plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), estrone ( E l ) and 17-p estradiol (EJ were also measured by radioirnmunoassay (RIA). Means -+ standard deviations were: T = 379 k 157 ng/dl; hPRL = 24 2 30 ng/ml; LH = 49 c 48 rnlU/ml; FSH = 10 ? 8 mlU1 ml; E l = 108 2 35 pg/ml; and E, = 10 t 6 pg/ml. Twenty percent had hyperprolactinemia, and 24% had hypotestosteronemia. LH was elevated in 95% of men, while FSH was higher than normal in only three cases (12%). E, was tentatively low in ME6, while El was elevated in 76% of men. Hyperprolactinemia could be due to hemodilution, reduced renal excretion. stress, or hypothalamic-pituitary disregulation; it cannot be accounted for by E, induction, since E2 was low in 6 4 % of patients. Low T can be explained by a local toxic effect of uremia on the testis. and high LH would be the result of decreased negative feed-back. FSH is normal indicating that inhibin production by the testis was unaltered. Low EZ can be explained by testicular damage and/or reduced T. The increase in El. mainly of adrenocortical origin, may be due to increased adrenocorticotropic hormone (ACTH) as a result of stress conditions imposed by chronic renal failure and periodic hemodialysis.

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“…Dexamethasone suppression tests have been reported to be unchanged by some [3]and blunted by others [4, 5, 6, 7, 8]in patients on chronic hemodialysis. This lack of suppressibility has been attributed to various factors.…”

Section: Introductionmentioning

confidence: 99%

Paper Chromatography prior to Cortisol RIA Allows for Accurate Use of the Dexamethasone Suppression Test in Chronic Renal Failure

Herle

Birnbaum

Slomowitz

et al. 1998

Nephron

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The assessment of the hypothalamic-pituitary-adrenal axis in patients with chronic renal failure (CRF) on hemodialysis is often hampered by abnormal responses to the standard 1-mg dexamethasone suppression test. Various mechanisms have been proposed to explain this lack of suppressibility. The present study was designed to look into the mechanisms possible for these findings in patients with CRF. We studied 6 patients with CRF on hemodialysis and 5 healthy subjects utilizing the 1-mg dexamethasone suppression test as well as the 50-mg hydrocortisone suppression test. Samples were assayed for dexamethasone, adrenocorticotropic hormone, corticosterone, and cortisol by both direct radioimmunoassay (RIA) and RIA after paper chromatography. Utilizing the direct cortisol RIA, 4 of 6 patients with CRF exhibited blunted dexamethasone suppression, while all 6 patients showed normal suppressibility after dexamethasone when cortisol was measured after paper chromatography. In contrast, all controls showed normal suppressibility regardless of the cortisol assay procedure used. The hydrocortisone suppression test was unreliable in the setting of CRF. Mean dexamethasone levels were similar in both groups. Plasma adrenocorticotropic hormone levels were significantly higher in the CRF patients, possibly indicative of an underlying hypothalamic-pituitary-adrenal axis abnormality. Abnormalities in dexamethasone suppression testing in patients with CRF may be explained by the overestimation of cortisol levels by direct RIA rather than by alteration of dexamethasone absorption or metabolism. Measurement of cortisol after paper chromatography is superior to direct RIA of cortisol in patients with CRF.

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Pituitary-Adrenocortical Function in Chronic Renal Failure: Studies of Episodic Secretion of Cortisol and Dexamethasone Suppressibility*

Cited by 103 publications

References 15 publications

Mechanisms for defects in muscle protein metabolism in rats with chronic uremia. Influence of metabolic acidosis.

Mechanisms for defects in muscle protein metabolism in rats with chronic uremia. Influence of metabolic acidosis.

Prolactin, Gonadotropins, Testosterone, and Estrogens in Uremic Men Undergoing Periodic Hemodialysis

Paper Chromatography prior to Cortisol RIA Allows for Accurate Use of the Dexamethasone Suppression Test in Chronic Renal Failure

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