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Serum catalytic iron and progression of chronic kidney disease: findings from the ICKD study
Ashok K Yadav1, Arpita Ghosh2, Smita Divyaveer3
1Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and Research, Chandigarh.
Insights
Serum catalytic iron (SCI) is linked to worse outcomes in chronic kidney disease (CKD) patients. Higher SCI levels independently predict major kidney events, suggesting its potential as a risk marker and therapeutic target.
Area of Science:
- Nephrology
- Biochemistry
- Clinical Medicine
Background:
- Non-transferrin bound iron, a catalytic iron moiety, generates reactive oxygen species and is linked to adverse health outcomes.
- Serum catalytic iron (SCI) is hypothesized to correlate with the progression of chronic kidney disease (CKD).
Purpose of the Study:
- To investigate the association between serum catalytic iron (SCI) and the progression of chronic kidney disease (CKD).
Main Methods:
- Serum samples from Indian CKD participants were analyzed for iron parameters, including SCI, using the bleomycin-detectable iron assay.
- The incidence of major adverse kidney endpoints (MAKE) was assessed using Cox proportional hazards models, adjusted for relevant covariates.
Main Results:
- In 2002 participants, higher SCI levels were independently associated with a 78% increased hazard of MAKE after adjusting for age and sex.
- Further adjustments for various risk factors confirmed SCI's independent association with MAKE and kidney failure in mild to moderate CKD patients.
Conclusions:
- Serum catalytic iron (SCI) is a strong, independent predictor of major adverse kidney events in CKD patients.
- SCI may serve as a valuable risk marker and potential therapeutic target for managing CKD progression.
Background:
The non-transferrin bound catalytic iron moiety catalyses production of toxic reactive oxygen species and is associated with adverse outcomes. We hypothesized that serum catalytic iron (SCI) is associated with progression of chronic kidney disease (CKD).
Methods:
Baseline samples of the Indian Chronic Kidney Disease participants with at least one follow up visit were tested for total iron, iron binding capacity, transferrin saturation, SCI, ferritin and hepcidin. SCI was measured using the bleomycin-detectable iron assay that detects biologically active iron. Association with the incidence of major kidney endpoints, (MAKE, a composite of kidney death, kidney failure or > 40% loss of eGFR) was examined using Cox proportional hazards model adjusted for sex and age.
Results:
2002 subjects (49.9 ± 11.6 years, 68.1% males, baseline eGFR 41.01 ml/min/1.73m2) were enrolled. After a median follow up of 12.6 (12.2, 16.7) months, the composite MAKE occurred in 280 (14%). After adjusting for age and sex, increase from 25th to 75th percentile in SCI, transferrin saturation, ferritin and hepcidin were associated with 78% (43-122%), 34% (10-62%), 57% (24-100%) and 74% (35-124%) increase in hazard of MAKE, respectively. SCI was associated with MAKE and kidney failure after adjustment for occupational exposure, hypertension, diabetes, tobacco, alcohol use, history of AKI, baseline eGFR, uACR, and allowing baseline hazard to vary by centre.
Conclusions:
SCI is strongly and independently associated with composite MAKE in patients with mild to moderate CKD. Confirmation in other studies will allow consideration of SCI as a risk marker and treatment target.
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