Adrenal insufficiency in pediatric kidney transplantation recipients

Author:

Chae Hyunwoong Harry1ORCID,Ahmed Azim1ORCID,Bone Jeffrey N.2ORCID,Abdulhussein Fatema S.23ORCID,Amed Shazhan23ORCID,Patel Trisha23ORCID,Blydt‐Hansen Tom D.24ORCID

Affiliation:

1. Faculty of Medicine University of British Columbia Vancouver British Columbia Canada

2. BC Children's Hospital Research Institute Vancouver British Columbia Canada

3. Division of Endocrinology, Department of Pediatrics, BC Children's Hospital University of British Columbia Vancouver British Columbia Canada

4. Division of Nephrology, Department of Pediatrics, BC Children's Hospital University of British Columbia Vancouver British Columbia Canada

Abstract

AbstractBackgroundImmunosuppression of pediatric kidney transplant (PKT) recipients often includes corticosteroids. Prolonged corticosteroid exposure has been associated with secondary adrenal insufficiency (AI); however, little is known about its impact on PKT recipients.MethodsThis was a retrospective cohort review of PKT recipients to evaluate AI prevalence, risk factors, and adverse effects. AI risk was assessed using morning cortisol (MC) and diagnosis confirmed by an ACTH stimulation test. Potential risk factors and adverse effects were tested for associations with MC levels and AI diagnosis.ResultsFifty‐one patients (60.8% male, age 7.4 (IQR 3.8, 13.1) years; 1 patient counted twice for repeat transplant) were included. Patients at risk for AI (MC < 240 nmol/L) underwent definitive ACTH stimulation testing, confirming AI in 13/51 (25.5%) patients. Identified risk factors for AI included current prednisone dosage (p = .001), 6‐month prednisone exposure (p = .02), daily prednisone administration (p = .002), and rejection episodes since transplant (p = .001). MC level (2.5 years (IQR 1.1, 5.1) post‐transplant) was associated with current prednisone dosage (p < .001), 6‐month prednisone exposure (p = .001), daily prednisone administration (p = .006), rejection episodes since transplant (p = .003), greater number of medications (β = −16.3, p < .001), 6‐month hospitalization days (β = −3.3, p = .013), creatinine variability (β = −2.4, p = .025), and occurrence of acute kidney injury (β = −70.6, p = .01).ConclusionGreater corticosteroid exposure was associated with a lower MC level and confirmatory diagnosis of AI noted with an ACTH stimulation test. Adverse clinical findings with AI included greater medical complexity and kidney function lability. These data support systematic clinical surveillance for AI in PKT recipients treated with corticosteroids.

Funder

Faculty of Medicine, University of British Columbia

Publisher

Wiley

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