Risk of adrenal insufficiency with steroid maintenance therapy in renal transplantation

Boots, Johannes M. M.; Ham, E.C.H. van den; Christiaans, Maarten H. L.; Hooff, J. P. van

doi:10.1016/s0041-1345(02)02987-1

Cited by 20 publications

(12 citation statements)

References 7 publications

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“…In addition, there seemed to be a dose‐dependent effect of prednisolone, with lower endogenous glucocorticoid production in RTR treated with a higher daily prednisolone dose. This is in line with previous studies showing that chronic prednisolone treatment suppresses endogenous glucocorticoid production after kidney transplantation . Interestingly, we found that there was considerable variation in endogenous glucocorticoid production within groups of RTR who were treated with the same daily prednisolone dose.…”

Section: Discussionsupporting

confidence: 93%

“…The most often used corticosteroids after kidney transplantation are prednisone and prednisolone. A well‐known effect of chronic treatment with these drugs is suppression of the hypothalamus‐pituitary‐adrenal (HPA) axis, leading to reduced endogenous cortisol synthesis by the adrenal gland (Figure ). The HPA axis is the central stress response system.…”

Section: Introductionmentioning

confidence: 99%

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Endogenous urinary glucocorticoid metabolites and mortality in prednisolone‐treated renal transplant recipients

Vulto

Minovíc

Vries

et al. 2020

Clinical Transplantation

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Background: Chronic corticosteroid treatment suppresses HPA-axis activity and might alter activity of 11β hydroxysteroid dehydrogenases (11β-HSD). We aimed to investigate whether the endogenous glucocorticoid production and 11β-HSD activities are altered in prednisolone-treated renal transplant recipients (RTR) compared with healthy controls and whether this has implications for long-term survival in RTR. Methods: In a longitudinal cohort of 693 stable RTR and 275 healthy controls, 24-hour urinary cortisol, cortisone, tetrahydrocorisol (THF), allotetrahydrocortisol (alloTHF), and tetrahydrocortisone (THE) were measured using liquid chromatography tandemmass spectrometry. Twenty-four-hour urinary excretion of cortisol and metabolites were used as measures of endogenous glucocorticoid production; (THF + alloTHF)/ THE and cortisol/cortisone ratios were used as measures of 11β-HSD activity.Results: Urinary cortisol and metabolite excretion were significantly lower in RTR compared with healthy controls (P < .001), whereas (THF + alloTHF)/THE and cortisol/cortisone ratios were significantly higher (P < .001 and P = .002). Lower total urinary metabolite excretion and higher urinary (THF + alloTHF)/THE ratios were associated with increased risk of mortality, independent of age, sex, estimated glomerular filtration rate, C-reactive protein, body surface area, and daily prednisolone dose, respectively. Conclusions: Endogenous glucocorticoid production and 11β-HSD activities are altered in prednisolone-treated RTR. Decreased total urinary endogenous glucocorticoid metabolite excretion and increased urinary (THF + alloTHF)/THE ratios are associated with increased risk of mortality. K E Y W O R D S 11βHSD, cortisol, mortality, prednisolone, renal transplant recipients S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section. How to cite this article: Vulto A, Minović I, de Vries LV, et al. Endogenous urinary glucocorticoid metabolites and mortality in prednisolone-treated renal transplant recipients. Clin

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Endogenous urinary glucocorticoid metabolites and mortality in prednisolone‐treated renal transplant recipients

Vulto

Minovíc

Vries

et al. 2020

Clinical Transplantation

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“…A summary of these groups is presented in Table 1 , while a condensed version of the data extraction table can be seen in Supplementary File 3 . There were thirteen RCTs [19] , [22] , [23] , [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] with random allocation and blinding maintained throughout; the remaining 60 studies were classified as observational studies [12] , [13] , [14] , [15] , [34] , [35] , [36] , [37] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] , [46] , [47] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] , [57] , [58] , [59] , [60] , [61] , [62] , [63] , [64] , [65] , [66] , [67] , [68] , [69] , [70] , [71] , [72] , [73] , [74] , [75] , [76] , [77] , [78] , [79] , [80] , [81] …”

Section: Resultsmentioning

confidence: 99%

Systemic glucocorticoid therapy and adrenal insufficiency in adults: A systematic review

Joseph

Hunter

Ray

et al. 2016

Seminars in Arthritis and Rheumatism

140

119

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ObjectivesThe aim of this systematic literature review was to summarize the current knowledge regarding the prevalence of, time to recovery from, and influence of glucocorticoid dose and duration on glucocorticoid-induced adrenal insufficiency (AI).MethodsEligible studies were original research articles, which included adult patients with an indication for glucocorticoids and measured adrenal function following exposure to systemic glucocorticoids. Searches were performed in Web of Science and MEDLINE, with further articles identified from reference lists. Screening was performed in duplicate. Data were extracted for each group of glucocorticoid-exposed patients within eligible studies. The reported proportion of patients with AI was summarized as median and inter-quartile range. Results were then stratified by daily dose, cumulative dose, duration of exposure and time since last glucocorticoid use. The risk of bias within and across studies was considered: for randomised controlled trials risk of bias was assessed using the tool developed by the Cochrane Collaboration.ResultsOverall, 73 eligible studies were identified out of 673 screened. The percentage of patients with AI ranged from 0% to 100% with a median (IQR) = 37.4% (13–63%). Studies were small—median (IQR) group size 16 (9–38)—and heterogeneous in methodology. AI persisted in 15% of patients retested 3 years after glucocorticoid withdrawal. Results remained widely distributed following stratification. AI was demonstrated at <5 mg prednisolone equivalent dose/day, <4 weeks of exposure, cumulative dose <0.5 g, and following tapered withdrawal.ConclusionsThe heterogeneity of studies and variability in results make it difficult to answer the research questions with confidence based on the current literature. There is evidence of AI following low doses and short durations of glucocorticoids. Hence, clinicians should be vigilant for adrenal insufficiency at all degrees of glucocorticoid exposure.

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“…With removal of the offending agent from the body, a reduction in the inflammatory host response may result as Gd has been seen in tissues long after the exposure. Thakral et al (12) reported a patient with NSF in whom Gd deposits were found in affected areas more than 3 years since Gd exposure. As bone is a Gd reservoir, it can continually release Gd into the blood stream, which can subsequently result in tissue deposition in patients with kidney disease who are unable to normally excrete this metal (13).…”

Section: Mandip Panesar and Rabi Yacoubmentioning

confidence: 99%

“…Once prednisone dose is at 5 mg daily, further dose reductions should be at a rate of 1 mg/day per month until off. This results in a tapering of steroids over approximately 6 months and appears to allow restoration of adrenal secretory function and avoid symptoms (12,13). If at the time of allograft failure, the patient was being treated for acute rejection with large steroid doses, a more rapid steroid taper to 10 mg guided by clinical judgment is appropriate.…”

mentioning

confidence: 99%

When and how should immunosuppression be tapered for the failed renal allograft?

Formica¹

2011

Seminars in Dialysis

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Risk of adrenal insufficiency with steroid maintenance therapy in renal transplantation

Cited by 20 publications

References 7 publications

Endogenous urinary glucocorticoid metabolites and mortality in prednisolone‐treated renal transplant recipients

Endogenous urinary glucocorticoid metabolites and mortality in prednisolone‐treated renal transplant recipients

Systemic glucocorticoid therapy and adrenal insufficiency in adults: A systematic review

When and how should immunosuppression be tapered for the failed renal allograft?

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