MO154: Enteric Budesonide in IGAN Nephropathy: A Real World Clinical Practice

Abstract

Abstract BACKGROUND AND AIMS The gut–kidney axis seems to have a principal role in immunoglobulin A nephropathy (IgAN) development [1], leading to new treatment approaches. Enteric budesonide, a glucocorticosteroid that release the active drug in the distal ileum, has proved proteinuria reduction and estimated glomerular filtration rate (eGFR) benefit [1, 2]. Moreover, systemic steroid therapy implies severe adverse events that budesonide seems to avoid [1, 3]. Therefore, we aim to evaluate the effect of budesonide treatment in our cohort of patients affected by IgAN. METHOD We retrospectively selected 17 patients, from 19 to 74 years, which were treated with enteric budesonide. All of them, except for a patient with Henoch-Schönlein purpura and microhaematuria, had a renal biopsy-confirmed primary IgAN. Twelve were patients with native kidney disease and five were patients with kidney transplant. Three with native kidney disease were excluded due to the lack of therapeutic compliance. The median dose of budesonide was 9 mg/day for the whole period of treatment. Twelve were already treated with renin-angiotensin system (RAS) blockade, which was continued throughout the follow-up period. During the follow-up (maximum 2 years), creatinine, proteinuria measured as change in urine protein creatinine ratio (UPCR) and haematuria were assessed. RESULTS Baseline characteristics are shown in Table 1. Overall, the median reductions of UPCR at 3, 6, 12 and 24 months were of 33.08%, 54.62%, 15.38% and 15.38%, respectively. At 6 months, the median UPCR was reduced from baseline 1.3 g/g [IQ range (25%–75%): –0.58 to –4.22] to 0.59 g/g [IQ range (25%–75%): –0.17 to –0.85], P = .028. The creatinine remained stable at 6 months, with baseline median 1.57 mg/dL [IQ range (25%–75%): –1.03 to to 2.03], and creatinine at 6 months with median 1.42 mg/dL [IQ range (25%–75%): –1.01 to –1.93]. Five patients (35.7%) did not have haematuria when budesonide was started, which remained stable at 6 months. No corticosteroid-related side effects were observed. No differences were found between patients with native disease or transplant kidney. CONCLUSION Enteric budesonide reduced proteinuria in patients with IgAN nephropathy. Our results suggest that enteric budesonide may represent a new approach to treatment of IgAN in both patients with native and kidney transplant.