Update on Diabetic Kidney Disease (DKD): Focus on Non-Albuminuric DKD and Cardiovascular Risk.
Diabetic kidney disease is increasingly recognised as heterogeneous, with a non-albuminuric phenotype (reduced eGFR without albuminuria) now common; cohort evidence on whether it carries higher cardiovascular risk than albuminuric forms is conflicting, and phenotype-specific treatment guidance is still lacking.
Background
The classic model of diabetic kidney disease describes progressive glomerular hyperfiltration, microalbuminuria, proteinuria, and declining eGFR leading to dialysis. Large studies have challenged this paradigm by showing that eGFR can decline independently of albuminuria, defining a non-albuminuric phenotype with eGFR below 60 and absence of albuminuria whose pathogenesis remains unknown.
Key recommendations
The review notes that the leading hypothesis for non-albuminuric diabetic kidney disease is an acute kidney injury-to-chronic kidney disease transition with predominantly tubular rather than glomerular damage. Which phenotype carries higher cardiovascular risk is debated, given contrasting results in the literature; some cohorts associate the non-albuminuric phenotype with elevated cardiovascular and heart-failure risk, while others find its prognosis is not uniformly worse and is strongly influenced by coexisting macrovascular disease.
Clinical implications
Although several drug classes benefit diabetic kidney disease, there is a lack of studies analysing their differential effects across phenotypes, so no specific therapy guidelines exist for one phenotype versus another. The review argues for assessing both eGFR and albuminuria to characterise phenotype and improve cardiovascular and renal risk stratification in diabetic patients with chronic kidney disease.
Category
Research
Source
Biomolecules
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