Mitochondrial DNA copy number in peripheral blood of IgA nephropathy: a cross-sectional study

被引:5
作者
Liu, Jiaqi [1 ,2 ,3 ]
Wang, Rong [1 ,2 ,3 ]
Luo, Ning [1 ,2 ,3 ]
Li, Zhibin [4 ]
Mao, Haiping [1 ,2 ,3 ]
Zhou, Yi [1 ,2 ,3 ]
机构
[1] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Nephrol, Guangzhou, Peoples R China
[2] Sun Yat Sen Univ, NHC Key Lab Clin Nephrol, Guangzhou, Peoples R China
[3] Guangdong Prov Key Lab Nephrol, Guangzhou, Peoples R China
[4] Xiamen Univ, Epidemiol Res Unit, Affiliated Hosp 1, Xiamen, Peoples R China
基金
中国国家自然科学基金;
关键词
IgA nephropathy; mitochondrial DNA; renal function; renal pathology; Oxford classification; ASSOCIATION; DISEASE; RISK;
D O I
10.1080/0886022X.2023.2182133
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Mitochondrial DNA (mtDNA) copy number (CN) is a biomarker of mitochondrial function and has been reported associated with kidney disease. However, its association with IgA nephropathy (IgAN), the most common cause of glomerulonephritis (GN), has not been evaluated. We included 664 patients with biopsy-proven IgAN and measured mtDNA-CN in peripheral blood by multiplexed real-time quantitative polymerase chain reaction (RT-qPCR). We examined the associations between mtDNA-CN and clinical variables and found that patients with higher mtDNA-CN had higher estimated glomerular filtration rate (eGFR) (r = 0.1009, p = .0092) and lower serum creatinine (SCr), blood urea nitrogen (BUN), and uric acid (UA) (r=-0.1101, -0.1023, -0.07806, respectively, all p values <.05). In terms of pathological injury, mtDNA-CN was higher in patients with less mesangial hypercellularity (p = .0385, M0 vs. M1 score by Oxford classification). Multivariable logistic regression analyses also showed that mtDNA-CN was lower for patients with moderate to severe renal impairment (defined as eGFR < 60 mL/min/1.73 m(2)) vs. mild renal impairment, with the odds ratio of 0.757 (95% confidence interval: 0.579-0.990, p = .042). In conclusion, mtDNA-CN was correlated with better renal function and less pathological injury in patients with IgAN, proposing that systemic mitochondrial dysfunction may be involved in or reflect the development of IgAN.
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页数:8
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