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The following is a summary of “Lipid abnormality in diabetic kidney disease and potential treatment advancements,” published in the March 2025 issue of Frontiers in Endocrinology by Tu et al.
Studies have correlated dyslipidemia to a higher risk of atherosclerotic cardiovascular disease (ASCVD) and the progression of diabetic kidney disease (DKD), with early lipid management potentially preserving renal function.
Researchers conducted a retrospective study to investigate dyslipidemia’s clinical features, lipid-induced renal injury mechanisms, and advancements in lipid-lowering therapy in DKD.
They searched the literature in PubMed, Web of Science, and EMBASE, using specific keywords, including “diabetic kidney disease,” “diabetic nephropathy,” “diabetes,” “dyslipidemia,” “kidney,” “cardiovascular disease,” and “lipid therapy” (PubMed, Web of Science, EMBASE).
The results showed that high triglyceride (TG) and low high-density lipoprotein (HDL) levels were linked to higher risks of albuminuria and estimated glomerular filtration rate (eGFR) decline. Abnormal lipid metabolism contributed to glomerular podocyte and renal tubular epithelial cell damage through ectopic lipid deposition, impairing filtration and increasing urinary albumin excretion. Lipid-lowering therapies helped reduce lipid accumulation, suppress inflammatory mediators, and mitigate renal fibrosis. Fibrates and statins lowered albuminuria and slowed eGFR decline in early DKD, though the long-term effects on renal outcomes remained uncertain. Pro-protein convertase subtilisin/kexin 9 (PCSK9)-targeted treatments had fewer renal side effects and were more effective in reducing inflammation and improving kidney function than statins and fibrates.
Investigators concluded that LDL apheresis (LDL-A) and double filtration plasmapheresis (DFPP) exhibited potential as valuable clinical interventions for patients with diabetes experiencing severe hypercholesterolemia or intolerance to lipid-lowering medications.
Source: frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2025.1503711/full
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