Systemic effects of targeted-release budesonide in patients with IgA nephropathy

Jonathan Briggs; Katharine Lazarus; Laura Palmer; Siane Simioni; Thomas Cairns; Marie Condon; Jeremy Levy; Liz Lightstone; Lina Nikolopoulou; Maria Prendecki; Tabitha Turner-Stokes; Stephen McAdoo; Karim Meeran; Megan Griffith

doi:10.1530/endoabs.117.P32

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Endocrine Abstracts (2026) 117 P32 | DOI: 10.1530/endoabs.117.P32

SFEBES2026 Poster Presentations Adrenal and Cardiovascular (54 abstracts)

Systemic effects of targeted-release budesonide in patients with IgA nephropathy

Jonathan Briggs , Katharine Lazarus , Laura Palmer , Siane Simioni , Thomas Cairns , Marie Condon , Jeremy Levy , Liz Lightstone , Lina Nikolopoulou , Maria Prendecki , Tabitha Turner-Stokes , Stephen McAdoo , Karim Meeran & Megan Griffith

Author affiliations

Imperial College Healthcare NHS Trust, London, United Kingdom

Background: Targeted-release formulation budesonide (TRf-budesonide) delivers budesonide to the distal ileum/ proximal colon where it acts on Peyer’s patches to reduce the production of Gd-IgA1, improving proteinuria and preserving eGFR in patients with IgA nephropathy. Budesonide is a highly potent glucocorticoid; 16 mg is equivalent to oral prednisolone 213 mg. After extensive first pass metabolism (via CYP3A4), systemic bioavailability of budesonide is 10%, equating to a daily dose of prednisolone 20 mg. Concern remains over the side effects of systemic absorption of TRf-budesonide. We aimed to evaluate this in our patient cohort.

Methods: Retrospective study evaluating glucocorticoid-related adverse effects in patients treated with TRf-budesonide at a single glomerulonephritis clinic.

Results: To date, 16 patients remain on treatment; 13 patients have completed a >9-month course of treatment (full dose: n = 9; reduced dose: n = 4). Glucocorticoid-induced adverse effects were common. 14/29 (48.3%) patients experienced a median weight gain of 3.8 kg (1.5 – 8.6) on treatment. 8/29 (27.6%) patients developed acne, 6/29 (20.7%) patients developed an infection requiring antibiotics, two patients required inpatient treatment. 12/29 (41.3%) patients required a dose increase or new antihypertensive medication during the treatment period. All patients with pre-diabetes (n = 3) and T2D (n = 1) at the start of treatment had a mean increase in HbA1c of 4.75mmol/mol during the treatment period. A further two patients developed pre-diabetes. Morning serum cortisol was measured in 19 patients whilst on treatment. Levels were undetectable (<28nmol/l) in 9/19 (47.3%) of patients. Only five patients had a morning cortisol greater than 150nmol/l.

Conclusion: Nearly half of patients demonstrated systemic absorption with suppressed endogenous cortisol production. Glucocorticoid-induced adverse effects were frequent, as was an increased need for antihypertensive medication and an observed deterioration in glycaemia. Future work is required to evaluate the longer-term effects of TRf-budesonide, including its effect on the hypothalamic-pituitary-adrenal axis and burden of glucocorticoid associated morbidity.