Zamami Ryo, Kohagura Kentaro, Miyagi Tsuyoshi, Kinjyo Takanori, Shiota Kazutaka, Ohya Yusuke
aDialysis Unit, University Hospital of the Ryukyus bDepartment of Cardiovascular Medicine, Nephrology and Neurology, University of the Ryukyus School of Medicine, Nishihara-cho, Japan.
J Hypertens. 2016 Nov;34(11):2274-9. doi: 10.1097/HJH.0000000000001091.
Morphological analysis suggests that afferent arteriole hyalinosis reflects disturbed autoregulation of glomerular hemodynamics. However, the effect of arteriolar hyalinosis on the correlation between blood pressure (BP) levels and proteinuria is unknown in patients with chronic kidney disease (CKD). Therefore, we conducted a cross-sectional study to determine this correlation.
A total of 109 patients with nonnephrotic CKD (55 men and 54 women) who underwent renal biopsy were recruited. Arteriolar hyalinosis was semiquantitatively assessed via arteriole grading. We examined the correlation between BP and urine protein levels (g/gCr) according to the presence of arteriolar hyalinosis.
Patients had a mean age, BP, estimated glomerular filtration rate, and urine protein level of 40 years, 126/75 mmHg, 86 ml/min per 1.73 m, and 1.3 g/gCr, respectively. Patients with hyalinosis (n = 59) exhibited significant increases in median proteinuria (g/gCr) because the SBP increased (<130, 130-140, and ≥140 mmHg: 1.0, 1.3, and 2.3, respectively; P = 0.045); however, median proteinuria was comparable in patients without hyalinosis (n = 50), regardless of SBP. Multiple logistic analysis revealed that combined high BP and hyalinosis were significantly associated with increased proteinuria, defined as equal to or greater than the median value (odds ratio: 5.99, 95% confidence interval: 1.13-31.70, P < 0.05 vs. high BP-/hyalinosis-). Moreover, this combination was associated with the largest glomerular diameter.
Renal arteriolar hyalinosis may potentiate susceptibility to BP-related glomerular damage in patients with nonnephrotic CKD. Dysregulated afferent arteriolar resistance via arteriolar sclerosis may affect hypertensive renal damage.
形态学分析表明,入球小动脉玻璃样变性反映了肾小球血流动力学自身调节紊乱。然而,在慢性肾脏病(CKD)患者中,小动脉玻璃样变性对血压(BP)水平与蛋白尿之间相关性的影响尚不清楚。因此,我们进行了一项横断面研究以确定这种相关性。
共纳入109例接受肾活检的非肾病性CKD患者(55例男性和54例女性)。通过小动脉分级对小动脉玻璃样变性进行半定量评估。我们根据小动脉玻璃样变性的存在情况检查了血压与尿蛋白水平(g/gCr)之间的相关性。
患者的平均年龄、血压、估计肾小球滤过率和尿蛋白水平分别为40岁、126/75 mmHg、86 ml/min per 1.73 m²和1.3 g/gCr。玻璃样变性患者(n = 59)的蛋白尿中位数(g/gCr)显著增加,因为收缩压升高(<130、130 - 140和≥140 mmHg:分别为1.0、1.3和2.三,分别为;P = 0.045);然而,无玻璃样变性的患者(n = 50)的蛋白尿中位数无论收缩压如何均相当。多因素逻辑分析显示,高血压合并玻璃样变性与蛋白尿增加显著相关,蛋白尿定义为等于或大于中位数(比值比:5.99,95%置信区间:1.13 - 31.70,与高血压阴性/玻璃样变性阴性相比P < 0.05)。此外,这种组合与最大的肾小球直径相关。
肾小动脉玻璃样变性可能增强非肾病性CKD患者对血压相关肾小球损伤的易感性。通过小动脉硬化导致的入球小动脉阻力失调可能影响高血压肾损伤。