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Published on: October 26, 2020
Kidney Function Decline in Sickle Cell Disease: Associations with Renin-Angiotensin System Inhibitors
Kabir O Olaniran1, Alecia C Nero1, Orson W Moe1,2,3
1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Renin-angiotensin system inhibitors (RASi) did not slow estimated glomerular filtration rate (eGFR) decline in adults with sickle cell disease (SCD). Further research is needed to find effective therapies for kidney disease in SCD patients.
Area of Science:
- Nephrology
- Hematology
- Pharmacology
Background:
- Sickle cell disease (SCD) is linked to rapid kidney function decline.
- Effective therapies to slow this decline are lacking.
- The role of renin-angiotensin system inhibitors (RASi) in SCD kidney disease is unclear.
Purpose of the Study:
- To investigate the association between RASi treatment and estimated glomerular filtration rate (eGFR) decline in adult patients with SCD.
- To compare eGFR changes in patients initiating RASi versus those not receiving treatment.
Main Methods:
- A 2-center observational study using electronic health records from 2010-2024.
- Adult Black patients with SCD and at least one year of follow-up were included.
- Propensity score matching created 1:1 cohorts of RASi users and non-users, balancing covariates.
- Linear mixed models analyzed chronic eGFR slopes (≥90 days post-index).
Main Results:
- Primary analysis included 358 matched patients; sensitivity analyses excluded missing albuminuria data (262 patients) or low-dose RASi (270 patients).
- No significant difference in annual eGFR decline was observed between RASi users and the reference group in any cohort.
- RASi use was not associated with slowed eGFR decline (primary cohort: -0.15 mL/min/year; p=0.84).
Conclusions:
- RASi treatment was not associated with preserved kidney function in this real-world SCD cohort.
- These observational findings highlight the need for prospective clinical trials.
- Urgent research is required to identify effective GFR-preserving therapies for SCD.
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