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Inflammatory Mechanisms as New Biomarkers and Therapeutic Targets for Diabetic Kidney Disease
Radica Z Alicic1, Emily J Johnson1, Katherine R Tuttle1
1Providence Health Care, Spokane, WA; Kidney Research Institute and Division of Nephrology, Seattle, WA; Institute of Translational Health Sciences, Seattle, WA; and the University of Washington School of Medicine, Seattle, WA.
Insights
Diabetic kidney disease (DKD) is a major complication of diabetes. New research highlights inflammation as a key driver, with targeted therapies showing promise for slowing kidney function decline.
Area of Science:
- Nephrology
- Endocrinology
- Immunology
Background:
- Diabetic kidney disease (DKD) is the primary cause of chronic kidney disease (CKD) and end-stage kidney disease (ESKD) globally.
- DKD affects 30-40% of individuals with diabetes, increasing risks for cardiovascular events, infections, and mortality.
- Current treatments fail to halt DKD progression or manage associated comorbidities.
Purpose of the Study:
- To address the urgent need for effective DKD treatments due to rising diabetes prevalence.
- To explore inflammation as a central mechanism in DKD pathogenesis.
- To identify novel therapeutic targets and biomarkers for DKD.
Main Methods:
- Review of current understanding of DKD pathogenesis.
- Analysis of emerging therapeutic strategies targeting inflammatory pathways.
- Evaluation of preliminary clinical trial data for specific inhibitors.
Main Results:
- Inflammation is recognized as a critical factor in DKD-induced kidney damage.
- Inflammatory mediators show potential as both biomarkers and therapeutic targets.
- Phase 2 trials of chemokine C-C motif-ligand 2 and JAK/STAT pathway inhibitors yielded promising outcomes.
Conclusions:
- Targeting inflammatory pathways represents a promising therapeutic avenue for DKD.
- Further research and clinical trials are warranted to validate these novel treatments.
- Effective DKD therapies are crucial given the escalating global diabetes epidemic.
Abstract:
Diabetic kidney disease (DKD) is the leading cause of CKD and end-stage kidney disease (ESKD) worldwide. Approximately 30-40% of people with diabetes develop this microvascular complication, placing them at high risk of losing kidney function as well as of cardiovascular events, infections, and death. Current therapies are ineffective for arresting kidney disease progression and mitigating risks of comorbidities and death among patients with DKD. As the global count of people with diabetes will soon exceed 400 million, the need for effective and safe treatment options for complications such as DKD becomes ever more urgent. Recently, the understanding of DKD pathogenesis has evolved to recognize inflammation as a major underlying mechanism of kidney damage. In turn, inflammatory mediators have emerged as potential biomarkers and therapeutic targets for DKD. Phase 2 clinical trials testing inhibitors of monocyte-chemotactic protein-1 chemokine C-C motif-ligand 2 and the Janus kinase/signal transducer and activator of transcription pathway, in particular, have produced promising results.
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