USE OF EMPIRICAL DEFLAZACORT TO PRESERVE KIDNEY FUNCTION AND DELAY ONSET OF RENAL REPLACEMENT THERAPY IN PATIENTS WITH CKD OF UNKNOWN ETIOLOGY

Introduction:

Chronic kidney disease (CKD) represents a global public health problem. Over 90% of patients requiring renal replacement therapy (RRT) in India die because of inability to afford care, and even in those who do start RRT, 60% stop for financial reasons. In some cases of CKD, the etiology has been established, while it remains unexplained in many parts of the world, being therefore termed chronic kidney disease of unknown origin (CKDu) or alternatively chronic interstitial nephritis in developing countries.

Methods:

This is a retrospective, observational, single tertiary care center study done in 60 patients of CKD, with non-biopsiable kidneys, hence unknown etiology, who received empiric deflazacort. Inclusion criteria was patients of CKD, non-biopsable kidneys on ultrasonography with unknown etiology who have not been treated with steroids earlier.

Aims: 1) Analysis of kidney function estimated by eGFR (CKD-EPI) at initiation and 3 months after initiating deflazacort. 2)Comparison of onset of RRT in responders and non-responders groups.

All 60 patients received deflazacort starting with dose of 30 mg and tapered to 6 mg within 3 to 6 months of initiation based on clinical response.

Responders–Improvement in eGFR by 25% from baseline in first 3 months after initiation of empiric deflazacort.

Non-responders–No improvement or worsening of eGFR from baseline in first 3 months of initiation of empiric deflazacort. 

Results:

Out of 60 patients we observed that 37 (62%) patients responded to treatment and 23 (38%) were non-responders. Median (IQR) age at onset of disease was 43.5 (32.8, 51.3) years and 27 (45%) were men. Median (IQR) serum creatinine at diagnosis was 4.98 (4.10, 6.19) mg/dL in responders versus 7.45 (6.12, 8.90) mg/dL in non-responders and was statistically significant (P=0.002). The median (IQR) eGFR at diagnosis in responders was 12 (10, 16) mL/min/1.73m2 and in non-responders was 8 (6, 10) mL/min/1.73m2 which changed to 18 (16, 24) mL/min/1.73m2 and 7 (6, 10) mL/min/1.732 respectively after treatment with deflazacort indicating that lower the initial eGFR, poorer is the improvement. Treatment initiated within 1 year of diagnosis was significantly associated with response to deflazacort (68% responders versus 13% non-responders, P<0.001). In non-responders 9 (39%) patients ended up in end stage kidney disease (ESKD) requiring start of renal replacement therapy (RRT)—dialysis or kidney transplant, whereas only 6 (16%) of responders required RRT (P<0.046). Mean (IQR) duration to ESKD or last follow-up if not reached ESKD was 11 (6, 24) months in responders group while 3 (3, 4) months in non-responder group indicating the beneficial effect of empiric deflazacort in delaying the need of RRT. Serious side effects of steroid were not seen in any of the patients.

Conclusions:

In our study, eGFR at diagnosis >10 mL/min/1.73m2, early start of empirical deflazacort were the positive predictors of response to treatment and hence delay in the initiation of RRT. Use of empiric deflazacort in patients with CKD of unknown etiology showed improvement in kidney function and delayed the need of RRT without any serious adverse effects of steroid. Limitations of the study were small sample size and retrospective study. Larger future studies are required

I have no potential conflict of interest to disclose.

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