
Population-Level Risk Factors for Kidney Outcomes in IgA Nephropathy: The CURE-CKD Registry
Topics: Nephrology IgAN CURE-CKD RWE Publication Summary
Tuttle K, Kornowske L, Jones C et al.
10.1016/j.xkme.2025.100981
Summary
Population-level data from the Center for Kidney Disease Research,Education, and Hope (CURE-CKD) Registry were used to identify IgA nephropathy risk factors of major adverse kidney events (MAKE)1
Background
IgA nephropathy is a glomerular disease found in populations worldwide.2 Low estimated glomerular filtration rate (eGFR), proteinuria, and histologic findings are established prognostic markers, while other IgA nephropathy risk factors such as population-level variables like health insurance status and healthcare utilization have not been explored.1,3
Aim
The aim of this study is to assess the impact of demographic, clinical, and population-level characteristics on the risk of major adverse kidney events (MAKE) in adults with IgA nephropathy using the Center for Kidney Disease Research, Education, and Hope (CURE-CKD) registry.1
Approach
A longitudinal, real-world cohort study was conducted between 2016 and 2022, using data from 2,571 adults with IgA nephropathy from Providence and University of California Los Angeles (UCLA) Health Systems’ records within the CURE-CKD registry.1
Predictors included:
- Age
- Gender
- Race
- eGFR
- Urine albumin-creatinine ratio (UACR)
- Urine protein-creatinine ratio (UPCR)
- Diabetes
- Hypertension
- Medications
- Health insurance type
- Hospitalization
- Outpatient visit frequency
Outcomes included time to first MAKE, defined as ≥40% eGFR decline, eGFR <15 mL/min/1.73 m2, kidney failure, dialysis/transplant, or death.1
Findings
The majority of the full cohort with IgA nephropathy was from the Providence health system (74%, 1,905/2,571)1
- Gender: 50% (1,277/2,571) women1
- Mean age (± SD): 58 ± 18 years old at baseline1
- Asian race: 13% (325/2,571)1
- 53% (1,354/2,571) had commercial health insurance as the primary payer
- Comorbidities1
- Diabetes was present in 28% (708/2,571)
- Hypertension was present in 75% (1,919/2,571)
- Treatment modalities1
- Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB) were used by 49% (1,250/2,571)
- Corticosteroids and other immunomodulators were used by 39% (1,006/2,571) and 3% (77/2,571), respectively
Within 3 years (median follow-up 2.8 years), 22% (536/2,571) experienced MAKE1
MAKE was comprised of1:
- 61% (327/536) ≥40% eGFR decline
- 20% (108/536) kidney failure with eGFR <15 mL/min/1.73 m2
- 4% (23/536) dialysis
- 3% (17/536) transplant
- 11% (61/536) all-cause death
Several predictors significantly increased the hazard of MAKE1:
- Hospitalization (HR=2.59; 95% CI, 2.14-3.12)
- Other immunomodulators (HR=1.59; 95% CI, 1.09-2.30)
- Non-commercial health insurance (HR=1.46; 95% CI, 1.19-1.80)
- Low eGFR (HR=1.28; 95% CI, 1.24-1.33)
- Diabetes (HR=1.30; 95% CI, 1.07-1.57)
- ACE inhibitor or ARB use (HR=1.26; 95% CI, 1.04-1.53)
- Outpatient visits (HR=1.01; 95% CI, 1.00-1.03)
Key takeaway
In this large, diverse US cohort, using real-world data, both clinical and non-clinical IgA nephropathy risk factors, including insurance type, hospitalization, and more frequent outpatient encounters, predicted MAKE.1 Incorporating these population-level factors into risk models may help to stratify patients with IgA nephropathy and enable a population health approach within health systems for monitoring and therapeutic interventions to reduce risks.1
Footnotes
This study was funded through an investigator-initiated grant from Travere Therapeutics Inc. Please see the publication for the full list of disclosures.
ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; CI, confidence interval; CURE-CKD, Center for Kidney Disease Research,
Education, and Hope; eGFR, estimated glomerular filtration rate; HR, hazard ratio; MAKE, major adverse kidney event; UACR, albumin-creatinine ratio; UPCR, urine protein-creatinine ratio; UCLA, University of California Los Angeles.
- Tuttle KR, Kornowske LM, Jones CR et al. Kidney Med. 2025;7:100981.
- Rodrigues JC, Haas M, Reich HN. Clin J Am Soc Nephrol. 2017;12(4):677-686.
- Howie AJ, Lalayiannis AD. Kidney360. 2023;4(8):1103-1111.
MA-DS-25-0090 | September 2025