Key result
SDF-1, P-selectin, AOPPs, and mitochondrial dysfunction were directly correlated with significant cerebrovascular alterations in patients with early normoalbuminuric diabetic kidney disease.
Why the study?
The study aimed to establish potential associations of cerebral vessel remodeling and functional impairment with biomarkers of inflammation, oxidative stress, and mitochondrial dysfunction in early-stage DKD in type 2 diabetes patients.
Cohort (n=223)
Biomarkers of inflammation, oxidative stress, and mitochondrial dysfunction are associated with significant cerebrovascular alterations in asymptomatic patients with type 2 diabetes and early diabetic kidney disease.
May link early DKD cerebrovascular changes to shared pathways; leaves open confirmation in prospective studies.
Diabetic kidney disease (DKD) displays a high prevalence of cardiovascular and cerebrovascular disease. Both the kidney and the brain share common pathogenic mechanisms, such as inflammation, endothelial dysfunction, oxidative stress, and mitochondrial dysfunction. The aim of this study was to establish a potential association of cerebral vessel remodeling and its related functional impairment with biomarkers of inflammation, oxidative stress, and mitochondrial dysfunction in the early stages of DKD in type 2 diabetes mellitus (DM) patients. A cohort of 184 patients and 39 healthy controls was assessed concerning serum and urinary stromal cell-derived factor-1 (SDF-1), P-selectin, advanced oxidation protein products (AOPPs), urinary synaptopodin, podocalyxin, kidney injury molecule-1 (KIM-1), and N-acetyl-β-(D)-glucosaminidase (NAG). The quantification of the mitochondrial DNA copy number (mtDNA-CN) and nuclear DNA (nDNA) in urine and peripheral blood was conducted using quantitative reverse transcription polymerase chain reaction (qRT-PCR). Using TaqMan tests, the beta-2 microglobulin nuclear gene (B2M) and the cytochrome b (CYTB) gene, which encodes subunit 2 of NADH dehydrogenase (ND2), were evaluated. The MtDNA-CN is the ratio of mitochondrial DNA to nuclear DNA copies, ascertained through the examination of the CYTB/B2M and ND2/B2M ratios. The intima-media thickness (IMT) measurements of the common carotid arteries (CCAs), along with the pulsatility index (PI) and resistivity index (RI) of the internal carotid arteries (ICAs) and middle cerebral arteries (MCAs), were obtained through cerebral Doppler ultrasonography (US). Additionally, the breath-holding index (BHI) was also measured by cerebral Doppler US. PI-ICAs, PI-MCAs, CCAs-IMT, RI-MCAs, and RI-ICAs demonstrated direct relationships with SDF-1, P-selectin, AOPPs, urine mtDNA, podocalyxin, synaptopodin, NAG, and KIM-1 while showing indirect correlations with serum mtDNA and the eGFR. In contrast, the BHI had negative correlations with SDF-1, P-selectin, AOPPs, urine mtDNA, synaptopodin, podocalyxin, KIM-1, and NAG while showing direct associations with serum mtDNA and the eGFR. In conclusion, a causative association exists among SDF-1, P-selectin, and AOPPs, as well as mitochondrial dysfunction, in early diabetic kidney disease (DKD) and significant cerebrovascular alterations in patients with type 2 diabetes mellitus and normoalbuminuric DKD, with no neurological symptoms.
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Petrică et al. (2025) conducted a cohort in Normoalbuminuric diabetic kidney disease and type 2 diabetes mellitus (n=223). SDF-1, P-selectin, AOPPs, and mitochondrial dysfunction vs. Healthy controls was evaluated on Cerebrovascular alterations (intima-media thickness, pulsatility index, resistivity index, breath-holding index). SDF-1, P-selectin, AOPPs, and mitochondrial dysfunction were directly correlated with significant cerebrovascular alterations in patients with early normoalbuminuric diabetic kidney disease.
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