a Wuxi School of Medicine , Jiangnan University , Wuxi , China.
b Department of Nephrology , The Affiliated Hospital of Jiangnan University , Wuxi , China.
Ren Fail. 2018 Nov;40(1):634-639. doi: 10.1080/0886022X.2018.1518242.
M2 Macrophages could improve tubulointerstitial disease in animal models. HIF-1αpromotes macrophage polarization and is involved in tubular injury. The study aims to observe the clinicopathologic significance of M2 macrophage and HIF-1α in tubulointerstitial injury secondary to primary Sjogren's disease.
Renal tissue samples from patients with tubulointerstitial disease secondary to primary Sjogren's disease (SS, n = 10), chronic tubulointerstitial nephritis secondary to drug (CIN, n = 8) were included in this study. The expression of CD163, CD68 and HIF-1α were examined by immunohistochemistry or immunofluorescence.
(1) Renal involvement was the first manifestation in seven of ten (7/10) patients with pSS, including proteinuria, renal dysfunction, renal tubular acidosis and multiple renal stone; and two patient had intractable hypokalemia. (2) There were numerous CD163- positive cells and CD68- positive cells infiltration in tubulointerstitial injury of pSS, especially in patients with hypokalemia. CD163 positive cells and HIF-1αwere mainly expressed in acute tubulointerstitial injury of pSS, which positively correlated to N-acetyl-β-D-glucosaminidase and β2-microglobulin. (3) Compared with CIN, patients with pSS had higher serum globulin level, erythrocyte sedimentation rate (ESR) and lower urinary osmotic pressure. (4) During follow-up of one year, six patients with pSS and acute tubular injury acquired improved renal function on therapy of steroid and total glucosides of peony. The remaining four patients with pSS had stable renal function.
M2 macrophages are involved in acute tubular injury in patients with primary Sjogren's disease. Early intervention can improve renal function of tubulointerstitial injury secondary to primary Sjogren's disease.
M2 巨噬细胞可改善动物模型中的肾小管间质疾病。HIF-1α 促进巨噬细胞极化,并参与肾小管损伤。本研究旨在观察原发性干燥综合征继发小管间质性损伤中 M2 巨噬细胞和 HIF-1α 的临床病理意义。
纳入原发性干燥综合征继发小管间质性疾病(SS,n=10)和药物相关性慢性间质性肾炎继发小管间质性疾病(CIN,n=8)患者的肾组织标本。通过免疫组化或免疫荧光法检测 CD163、CD68 和 HIF-1α 的表达。
(1)10 例 pSS 患者中,7 例(7/10)以肾脏受累为首发表现,包括蛋白尿、肾功能不全、肾小管酸中毒和多发性肾结石;2 例患者存在难治性低钾血症。(2)pSS 患者的小管间质性损伤中存在大量 CD163 阳性细胞和 CD68 阳性细胞浸润,尤其在低钾血症患者中。CD163 阳性细胞和 HIF-1α 主要在 pSS 的急性肾小管间质性损伤中表达,与 N-乙酰-β-D-氨基葡萄糖苷酶和β2-微球蛋白呈正相关。(3)与 CIN 相比,pSS 患者的血清球蛋白水平、红细胞沉降率(ESR)较高,尿渗透压较低。(4)在为期 1 年的随访中,6 例接受泼尼松龙和白芍总苷治疗的 pSS 伴急性肾小管损伤患者肾功能得到改善,其余 4 例 pSS 患者肾功能稳定。
M2 巨噬细胞参与原发性干燥综合征患者的急性肾小管损伤。早期干预可改善原发性干燥综合征继发小管间质性损伤的肾功能。