Decrease of Glomerular Filtration Rate may be Attributed to the Microcirculation Damage in Renal Artery Stenosis

• Published in: Chinese medical journal Vol. 128; no. 6; pp. 750 - 754
• Main Authors: Dong, Hao-Jian, Huang, Cheng, Luo, De-Mou, Ye, Jing-Guang, Yang, Jun-Qing, Li, Guang, Luo, Jian-Fang, Zhou, Ying-Ling
• Format: Journal Article
• Language: English
• Published: China Medknow Publications Pvt Ltd 20.03.2015; Medknow Publications and Media Pvt. Ltd; Lippincott Williams & Wilkins Ovid Technologies; Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510100, China; Medknow Publications & Media Pvt Ltd; Wolters Kluwer
• Subjects: Aged; Analysis; Angiogenesis; Artery; Cardiology; Diagnosis; Female; Filtration; Glomerular; Glomerular filtration rate; Glomerular Filtration Rate - physiology; Glomerular Filtration Rate; Renal Artery Stenosis; Renal Microcirculation; Humans; Hypertension; Laboratories; Male; Medical imaging; Microcirculation; Microcirculation - physiology; Middle Aged; Original; Prospective Studies; Rate; Renal; Renal artery obstruction; Renal Artery Obstruction - physiopathology; Retrospective Studies; Rodents; Stenosis; Urine; Veins & arteries; China; Renal Artery Stenosis; Renal Microcirculation; Glomerular Filtration Rate
• ISSN: 0366-6999; 2542-5641
• DOI: 10.4103/0366-6999.152483

Background： The decrease ofglomenllar filtration rate has been theoretically supposed to be the result of low perfusion in renal artery stenosis （RAS）. But the gap between artery stenosis and the glomerular filtration ability is still unclear. Methods： Patients with selective renal artery angiogram were divided by the degree of renal artery narrowing, level of estimated glomerular filtration rate （eGFR）, respectively. The different levels ofeGFR, renal microcirculation markers, and RAS severity were compared with each other, to determine the relationships among them. Results： A total of 215 consecutive patients were enrolled in the prospective cohort study. Concentrations of microcirculation markers had no significant difference between RAS group （RAS ≥ 50%） and no RAS group （RAS 〈 50%） or did not change correspondingly to RAS severity. The value ofeGFR in RAS group was lower than that in the no RAS group, but it did not decline parallel to the progressive severity of RAS. The microcirculation markers presented integral difference if grouped by different eGFR level with negative tendency, especially that plasma cystatin C （cysC） and urinary microalbumin to creatinine ratio （mACR） increased with the deterioration ofeGFR, with strong （r= -0.713, P 〈 0.001 ） and moderate （r = -0.580, P 〈 0.001 ） correlations. In the subgroup analysis of severe RAS （RAS 〉 80%）, the levels of plasma cysC and urinary mACR demonstrated stronger negative associations with eGFR, （r = -0.827, P 〈 0.001） and （r= -0.672, P 〈 0.001 ） correlations, respectively. Conclusions： Severity of RAS could not accurately predict the value of eGFR, whereas microcirculation impairment may substantially contribute to the glomerular filtration loss in patients with RAS.