Kidney Disease Center, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China; Kidney Disease Immunology Laboratory, The Third Grade Laboratory, State Administration of Traditional Chinese Medicine of China, Hangzhou, China; Key Laboratory of Multiple Organ Transplantation, Ministry of Health of China, Hangzhou, China; Key Laboratory of Nephropathy of Zhejiang Province, Hangzhou, China.
Nephrology (Carlton). 2014 Jun;19(6):307-17. doi: 10.1111/nep.12225.
Serum- and glucocorticoid-inducible kinase SGK1 functions as an important regulator of transepithelial sodium transport by activating epithelial sodium channel in renal tubules. Considerable evidence demonstrated that SGK1 was associated with hypertension and fibrosing diseases, such as diabetic nephropathy and glomerulonephritis. The present study was performed to evaluate the role of SGK1 played in immunoglobulin A (IgA) nephropathy.
Seventy-six patients of biopsy-proven IgA nephropathy and 33 healthy volunteers were enrolled in this study. All patients and healthy volunteers' urinary and serum samples were tested for SGK1 expression by indirect enzyme-linked immunosorbent assay. Meanwhile all patients' renal tissues were semi-quantified for SGK1 expression by immunohistochemistry assay. The relationships between SGK1 expressions and clinical or pathological parameters were also assessed.
SGK1 expression was upregulated in urine and renal tubules in patients of Oxford classification T1 and T2, whereas its expression in serum did not increase significantly. Relationship analysis indicated that urinary and tissue SGK1 expressions were associated with heavy proteinuria and renal insufficiency in patients with IgA nephropathy. On the other hand, RAS blockades would reduce the SGK1 levels both in urine and renal tissues.
These results suggested that urinary SGK1 should be a good indicator of tubulointerstitial damage in patients of IgA nephropathy. SGK1 expressions in urine and renal tissues were associated with the activity of renin-angiotensin-aldosterone system.
血清和糖皮质激素诱导激酶 SGK1 通过激活肾脏小管中的上皮钠通道，作为跨上皮钠转运的重要调节剂发挥作用。大量证据表明，SGK1 与高血压和纤维化疾病有关，如糖尿病肾病和肾小球肾炎。本研究旨在评估 SGK1 在免疫球蛋白 A（IgA）肾病中的作用。
本研究纳入了 76 名经活检证实的 IgA 肾病患者和 33 名健康志愿者。通过间接酶联免疫吸附试验检测所有患者和健康志愿者的尿液和血清中 SGK1 的表达。同时，通过免疫组织化学法对半定量检测所有患者的肾组织中 SGK1 的表达。还评估了 SGK1 表达与临床或病理参数之间的关系。
在牛津分类 T1 和 T2 的患者中，SGK1 在尿液和肾小管中的表达上调，而其在血清中的表达没有显著增加。相关性分析表明，IgA 肾病患者的尿和组织 SGK1 表达与大量蛋白尿和肾功能不全有关。另一方面，RAS 阻断剂会降低尿和肾组织中的 SGK1 水平。
这些结果表明，尿 SGK1 应该是 IgA 肾病患者肾小管间质损伤的一个良好指标。尿和肾组织中的 SGK1 表达与肾素-血管紧张素-醛固酮系统的活性有关。
