Studies on cortisol metabolism during haemodialysis in man

Deck, K. A.; Fischer, Bernard M.; Hillen, H.F.P.

doi:10.1111/j.1365-2362.1979.tb00924.x

Cited by 14 publications

(7 citation statements)

References 11 publications

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“…Deck et al were not sure about the exact cause of the increased plasma clearance rate of cortisol. An increased metabolism during HD due to increased protein binding or a change in the cortisol metabolism itself were discussed [ 21 ].…”

Section: Resultsmentioning

confidence: 99%

“… unknown n.a. HD Akmal M, 1977 [ 26 ] case-control study 17 11 6 5 (46%) unknown 47.8 29.6 HD Deck KA, 1979 [ 21 ] observational study 7 7 0 2 (29%) n.a. 28–38 n.a.…”

Section: Resultsmentioning

confidence: 99%

“…The ACTH test takes over 1 hour, which the patient must spend in the hospital in addition to his time on HD. However, results of Deck et al regarding plasma clearance rate indicate that false low cortisol levels may occur during HD, thus potentially leading to an overdiagnosing of AI [ 21 ]. Further studies are required to specifically verify the reliability of an ACTH test or other tests during HD.…”

Section: Discussionmentioning

confidence: 99%

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Adrenal function testing in dialysis patients – a review of the literature

et al. 2021

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Background Secondary adrenal insufficiency is a frequent issue in patients with renal replacement therapy. There are concerns about metabolism and clearance for adrenocorticotropic hormone (ACTH) and cortisol in addition to hemoconcentration as confounding factors during hemodialysis (HD). Therefore, ACTH testing is currently performed before or in between HD sessions. This review of the literature aims to evaluate the current evidence for validity of testing for adrenal insufficiency in patients on chronic renal replacement therapy. Methods A literature search of PubMed database for interventional and observational clinical trials was performed. Case reports and reviews were excluded. The search included all articles published until July 2020. Results Of 218 potentially eligible articles, 16 studies involving 381 participants were included. Seven studies performed an ACTH test before HD or in between HD sessions. There was no data available regarding ACTH testing during HD. But there was evidence of decreased cortisol levels during HD as compared to afterwards. All included 16 studies measured basal cortisol, and seven studies performed an ACTH test. Seven trials had comparable data of baseline cortisol for a quantitative analysis. Standardized mean difference of overall cortisol was 0.18 nmol/l (95%CI − 0.08 to 0.44) in the case group. Conclusions In patients undergoing renal replacement therapy, basal serum cortisol values are comparable to healthy volunteers. There is limited data on the validity of stimulated cortisol in these patients, especially during HD. Trial registration Registration no. CRD42020199245.

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Section: Resultsmentioning

confidence: 99%

“… unknown n.a. HD Akmal M, 1977 [ 26 ] case-control study 17 11 6 5 (46%) unknown 47.8 29.6 HD Deck KA, 1979 [ 21 ] observational study 7 7 0 2 (29%) n.a. 28–38 n.a.…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Adrenal function testing in dialysis patients – a review of the literature

et al. 2021

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“…Adrenal failure was finally very severe in our case. Upon admission, cortisol production must have been virtually absent because plasma cortisol was undetectable despite the cortisol metabolism is depressed in haemodialysis patients [ 6 ]. However, the patient presented with only hypoglycaemic coma and mild hypothermia, but not with circulatory collapse or electrolyte abnormalities.…”

Section: Discussionmentioning

confidence: 99%

Hypoglycaemic coma due to adrenal failure in a chronic haemodialysis patient

Tanaka

Suganuma

Funase

et al. 2010

Clinical Kidney Journal

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A 62-year-old man, receiving chronic haemodialysis and suffering from alcoholic liver cirrhosis and chronic pancreatitis, presented with hypoglycaemic coma. Plasma cortisol was undetectable (< 5.5 nmol/L) with suppressed adrenocorticotropic hormone (ACTH), which established a diagnosis of adrenal failure due to ACTH deficiency. Twenty-five milligrams of oral hydrocortisone eradicated hypoglycaemia. Presentation of adrenal failure in this patient was atypical because he was hypertensive, serum electrolytes including sodium were normal and anaemia was unremarkable, which were all due to end-stage renal disease and its treatment with haemodialysis. As far as we are aware, this is the first case report of hypoglycaemic coma due to adrenal failure in a chronic haemodialysis patient.

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“…Little research has directly investigated hepatic metabolism of glucocorticoids in CKD. A study by Deck et al provides some evidence that the accumulation of THF, 5a-THF and THE (the end products of hepatic cortisol metabolism) may attenuate hepatic inactivation and metabolic clearance of cortisol (66). Clearance of cortisol in patients with end-stage renal failure was higher during dialysis than after dialysis, but the dialytic removal of cortisol itself accounted only for 20-35% of the difference.…”

Section: Hpa Axis Regulation Of Cortisol Secretion In Ckdmentioning

confidence: 99%

Cortisol excess in chronic kidney disease – A review of changes and impact on mortality

2023

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Chronic kidney disease (CKD) describes the long-term condition of impaired kidney function from any cause. CKD is common and associated with a wide array of complications including higher mortality, cardiovascular disease, hypertension, insulin resistance, dyslipidemia, sarcopenia, osteoporosis, aberrant immune function, cognitive impairment, mood disturbances and poor sleep quality. Glucocorticoids are endogenous pleiotropic steroid hormones and their excess produces a pattern of morbidity that possesses considerable overlap with CKD. Circulating levels of cortisol, the major active glucocorticoid in humans, are determined by a complex interplay between several processes. The hypothalamic-pituitary-adrenal axis (HPA) regulates cortisol synthesis and release, 11β-hydroxysteroid dehydrogenase enzymes mediate metabolic interconversion between active and inactive forms, and clearance from the circulation depends on irreversible metabolic inactivation in the liver followed by urinary excretion. Chronic stress, inflammatory states and other aspects of CKD can disturb these processes, enhancing cortisol secretion via the HPA axis and inducing tissue-resident amplification of glucocorticoid signals. Progressive renal impairment can further impact on cortisol metabolism and urinary clearance of cortisol metabolites. Consequently, significant interest exists to precisely understand the dysregulation of cortisol in CKD and its significance for adverse clinical outcomes. In this review, we summarize the latest literature on alterations in endogenous glucocorticoid regulation in adults with CKD and evaluate the available evidence on cortisol as a mechanistic driver of excess mortality and morbidity. The emerging picture is one of subclinical hypercortisolism with blunted diurnal decline of cortisol levels, impaired negative feedback regulation and reduced cortisol clearance. An association between cortisol and adjusted all-cause mortality has been reported in observational studies for patients with end-stage renal failure, but further research is required to assess links between cortisol and clinical outcomes in CKD. We propose recommendations for future research, including therapeutic strategies that aim to reduce complications of CKD by correcting or reversing dysregulation of cortisol.

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Studies on cortisol metabolism during haemodialysis in man

Cited by 14 publications

References 11 publications

Adrenal function testing in dialysis patients – a review of the literature

Adrenal function testing in dialysis patients – a review of the literature

Hypoglycaemic coma due to adrenal failure in a chronic haemodialysis patient

Cortisol excess in chronic kidney disease – A review of changes and impact on mortality

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