
Population Risk Predictors of Major Adverse Kidney Events Attributed to FSGS from the CURE-CKD Registry
Topics: Nephrology FSGS Non-product CURE-CKD RWE Publication Summary
Nicholas S, Kornowske L, Jones C et al.
10.1186/s12882-025-04334-6
Summary
An analysis of the Center for Kidney Disease Research, Education, and
Hope (CURE-CKD) registry identifies predictors of major adverse kidney events (MAKE) in focal segmental glomerulosclerosis (FSGS)1
Background
Focal segmental glomerulosclerosis (FSGS) is the leading cause of nephrotic syndrome in adults in the United States and a major contributor to kidney failure.2 The heterogeneous presentation of FSGS can cause difficulty in the identification of patient characteristics that can be used to predict outcomes and treatment response.1
While clinical markers such as proteinuria and reduced estimated glomerular filtration rate (eGFR) are recognized predictors of kidney function decline, population-level evidence on FSGS risk factors specific for major adverse kidney events (MAKE) is lacking.1-3
Aim
The aim of this study was to identify both traditional clinical and unique non-clinical predictors of MAKE in adults with FSGS using real-world data from the Center for Kidney Disease Research, Education, and Hope (CURE-CKD) registry.1
Approach
This retrospective cohort study utilized data from the Providence and University of California, Los Angeles (UCLA) Health Systems’ records within the CURE-CKD registry (2016-2022).1 FSGS was identified in adult patients by International Classification of Diseases (ICD) 9/ICD 10 diagnostic codes.1 Patients were excluded from the study if they experienced kidney failure or kidney replacement therapy, which was defined by a baseline eGFR <15 mL/min/1.73 m² or a diagnosis/procedure code indicative of kidney failure, transplant, or dialysis.1
Clinical and non-clinical variables were evaluated as predictors of MAKE, defined as ≥40% eGFR decline, kidney failure, dialysis/transplant, or death.1
Findings
Baseline characteristics of FSGS total cohort (N=629)1:
- Mean age (SD), years: 53 (17)
- Male: 54%
- Mean eGFR: 60 mL/min/1.73 m²
- Median urine albumin-creatinine ratio (UACR): 1,430 mg/g
- Median urine protein-creatinine ratio (UPCR): 1.6 g/g
MAKE were common among adults with FSGS in the CURE-CKD registry1
The incidence of MAKE was 42% over a median follow-up of 2.9 years; 51% had ≥40% eGFR decline as first event
Predictors of higher MAKE hazard included1:
- UACR ≥1,430 mg/g or UPCR ≥1.6 g/g: Hazard ratio (HR)=3.46 (95% confidence interval [CI]: 2.28 to 5.23)
- Non-corticosteroid immunomodulator prescription: HR=1.87 (95% CI: 1.32 to 2.65)
- Non-commercial health insurance: HR=1.78 (95% CI: 1.36 to 2.33)
- Lower eGFR per 10 mL/min/1.73 m²: HR=1.25 (95% CI: 1.18 to 1.32)
- More outpatient visits: HR=1.03 (95% CI: 1.01 to 1.05)
- Hospitalization: HR=1.64 (95% CI: 1.25 to 2.15)
Older age was suggested to be a protective factor (HR=0.89; 95% CI: 0.82 to 0.98).1
Key takeaway
In this large diverse cohort of adult patients with FSGS, risk factors for MAKE included not only known clinical markers (i.e. low eGFR, high albuminuria/proteinuria) but also healthcare access and utilization variables such as insurance type and hospitalization history.1 Integrating these predictors into risk models may enable more timely interventions and personalized management strategies for patients with FSGS.1
Footnotes
Support for this study was provided by an investigator-initiated grant from Travere Therapeutics Inc. Please see the publication for the full list of disclosures.
CI, confidence interval; CURE-CKD, Center for Kidney Disease Research, Education, and Hope Registry; eGFR, estimated glomerular filtration rate; FSGS, focal segmental glomerulosclerosis; HR, hazard ratio; ICD, International Classification of Diseases; MAKE, major adverse kidney event; SD, standard deviation; UACR, urine albumin-creatinine ratio; UPCR, urine protein-creatinine ratio; UCLA, University of California, Los Angeles.
- Nicholas SB et al. BMC Nephrol. 2025;26(1):403.
- Rosenberg AZ et al. Clin J Am Soc Nephrol. 2017;12(3):502-517.
- He HG et al. BMC Nephrol. 2019;20(1):328.
MA-DS-25-0088 | September 2025