Prevalence, risk factors, and the screening value of basal cortisol for adrenal insufficiency after corticosteroid therapy in children with idiopathic nephrotic syndrome.

Abstract

Background: Children with idiopathic nephrotic syndrome (INS) receive prolonged glucocorticoids that can suppress the hypothalamic-pituitary-adrenal (HPA) axis and cause adrenal insufficiency (AI). We estimated the prevalence, risk factors, and basal-cortisol screening performance of biochemical AI in children with INS in remission and off corticosteroids.

Methods: In this single-centre cross-sectional study, 138 children with INS, off corticosteroids for ≥3 months after ≥2 weeks of full-dose prednisolone, underwent a standard-dose ACTH stimulation test (25 IU intramuscular Acton Prolongatum). Peak cortisol <500 nmol/L (18 µg/dL) defined AI.

Results: Biochemical AI occurred in 26/138 children (18.8%). Low basal cortisol (< 138 nmol/L) occurred in 18 (13.0%) but captured only 12 of 26 cases. Suppression did not differ by NS subtype (p = 0.392). Suppressed children were older at enrolment (median 129 vs 97 months; p = 0.044) and had ≈31% lower basal cortisol (159.0 vs 230.5 nmol/L; p < 0.001). Basal cortisol moderately discriminated AI (AUC 0.798; negative predictive value 92.9% at an exploratory cut-off of 186.5 nmol/L). Prevalence declined with time off steroids (23.1%, 21.2%, and 13.2% at 3-6, 6-12, and >12 months; p = 0.400). Exploratory multivariable analysis, limited by few events, identified no significant predictors. All five children with peritonitis-related hypotension had AI.

Conclusions: Biochemical AI affects one in five children with INS after prolonged corticosteroid therapy and may persist beyond one year. Basal morning cortisol may serve as an initial screen, but this exploratory threshold requires validation in independent cohorts. Dynamic testing and stress-dose preparedness remain important.