OUTCOME OF USE OF ENTERIC RELEASED BUDESONIDE IN IGA NEPHROPATHY PATIENTS WITH NEPHROTIC AND SUBNEPHROTIC PROTEINURIA PRESENTATIONS: PROSPECTIVE COMPARATIVE STUDY IN TERTIARY CARE CENTRE

Introduction:

Biopsy proven IgA Nephropathy patients with persistent proteinuria (>1gm) even after 3 months of conservative management with optimized BP control using RAS inhibition, immunosuppressive therapy in form of systemic steroid (oral prednisolone) and enteric released budesonide are considered.  In this study, efficacy and safety of enteric release formulation of oral budesonide is compared between patients of nephrotic proteinuria presentation (after achieving subnephrotic proteinuria on systemic steroids) to patients with sub nephrotic proteinuria presentation

Methods:

Adult biopsy proven IgA Nephropathy patients with persistent proteinuria>1g after 3 months of RAS inhibition were started on either prednisolone or enteric released budesonide depending on initial presentation being nephrotic range proteinuria, AONS ( Arm A) or sub nephrotic proteinuria, SNP (Arm B) respectively. Patients with age<18 years, eGFR<30, crescentic presentation and IFTA>50 were excluded. Patients with nephrotic range proteinuria received oral prednisolone in dose of 1mg/kg for 6 months including tapering. Patients who were either non responsive or intolerant or relapse on tapering/stopping prednisolone were switched to enteric released budesonide (9 mg BD). The patients with sub nephrotic proteinuria presentation were directly started on budesonide (9 mg BD). In both arms, the complete remission(CR) was labelled as proteinuria <1 gm while the partial remission(PR) as proteinuria <50% of the baseline & less than 2 gm/day.  The patients on budesonide were evaluated at 3,6,9 months for efficacy & safety with comparison between two arms through SPSS software version 21.(CR-1, PR-2, NR-3)

Results:

37 arm B patients (mean proteinuria 1.83 gm/day) received oral budesonide, and 15 patients of Arm A achieving PR (mean proteinuria of 2.23gm/day) recieved budesonide after mean duration of 3 months.  At 3,6 and 9 months of budesonide treatment, 3/15 (20%) , 4/15(26%), 5/15( 33%) patients of Arm A respectively achieved CR whereas 19/37 (50%),[p=0.03] ,28/37 patients (75%)[p=0.004], 30/37 patients(81%)[ p= 0.032] in arm B achieved CR. The results suggest enteric release budesonide may better address the IgAN group with subnephrotic proteinuria. At 9 months of treatment, mean eGFR improvement was 17.86 in nephrotic arm and 29.08 in subnephrotic arm being statistically significant(p =0.016). 

Of 15 patients in arm A, 1 each had worsening of hypertension, GI intolerance,  cushingoid facies and cataract. 25% patients developed  side effects but none required hospital admission. Of 37 patients of arm B, 7 required escalation of antihypertensives, 1 each developed infection, dysglycemia, menstrual irregularity ,4 each GI intolerance and cushingoid facies, 2 developed rash,  thus 56% of patients developed side effects but none requiring hospital admission. The comparison of adverse effects between two arms were statistically insignificant.

Conclusions:

This study highlights enteric budesonide release therapy may be safe and efficacious in SNP group ( Arm B) , but may not be as efficacious in AONS ( Arm A), highlighting the pathogenesis may not be the same in both.

I have no potential conflict of interest to disclose.

I did not use generative AI and AI-assisted technologies in the writing process.