Hypertension-induced renal injury is a multifactorial process which plays a crucial role in the development of chronic kidney disease. Multiple studies have demonstrated that interstitial rather than glomerular changes correlate better with renal functional capacity. Recent evidence indicates that mast cells and cell signaling proteins such as fibroblast growth factor-2 may contribute to the progression of interstitial changes under hypertensive conditions. The aim of our study was to determine the localization of mast cells in the renal cortex and report on the changes in their number, to analyze the distribution of fibroblast growth factor-2, to assess the extent of renal fibrosis and to evaluate renal damage and correlate it with the changes in the number of mast cells in a model of hypertension-induced renal injury by comparing two age groups of spontaneously hypertensive rats. We used 6- and 12-month-old animals. A light microscopic study was conducted on sections stained with hematoxylin and eosin, periodic acid-Schiff stain, Mallory’s trichrome method and toluidine blue. For the immunohistochemical study we used monoclonal antibodies against mast cell tryptase and fibroblast growth factor-2 and a polyclonal antibody against c-kit. The expression of fibroblast growth factor-2 was assessed semi-quantitatively. The number of mast cells was evaluated on toluidine blue-, tryptase- and c-kit-stained sections, as well as double-stained sections and a comparative statistical analysis with the Mann-Whitney test was conducted between the two age groups. Our results showed that mast cells were located mainly in the peritubular and perivascular areas and were absent in the region of the renal corpuscles. Their number increased significantly in 12-month-old animals. Immunostaining for tryptase, c-kit and double staining for both molecules yielded identical results. The immunohistochemical expression of fibroblast growth factor-2 increased in the kidneys of older animals, as did the percentage of collagen fibers. In addition, we described more severe renal damage in 12-month-old spontaneously hypertensive rats and noted a positive correlation in both age groups between the number of mast cells on the one hand and glomerular sclerosis index and tubulointerstitial damage index, on the other. The results obtained in the present study support the pivotal role of mast cells in the development of hypertension-induced kidney damage.

高血压引起的肾脏损伤是一个多因素过程，在慢性肾脏疾病的发展中起着至关重要的作用。多项研究表明，肾小球间质性改变而非肾小球性改变与肾功能的相关性更好。最近的证据表明肥大细胞和细胞信号蛋白如成纤维细胞生长因子2可能有助于高血压条件下间质变化的进展。我们的研究目的是确定肥大细胞在肾皮质中的定位并报告其数量的变化，以分析成纤维细胞生长因子2的分布，通过比较两个年龄段的自发性高血压大鼠，评估肾脏纤维化的程度并评估肾脏损害，并将其与肥大细胞的数量相关联，将其与高血压引起的肾脏损害模型相关联。我们使用了6个月和12个月大的动物。对用苏木精和曙红染色，高碘酸-席夫（Schiff）染色，马洛（Mallory）三色法和甲苯胺蓝染色的切片进行光学显微镜研究。对于免疫组织化学研究，我们使用了针对肥大细胞类胰蛋白酶和成纤维细胞生长因子2的单克隆抗体，以及针对c-kit的多克隆抗体。成纤维细胞生长因子2的表达进行了半定量评估。在甲苯胺蓝，胰蛋白酶和c-kit染色的切片上评估肥大细胞的数量，以及双染色切片，并在两个年龄组之间进行了Mann-Whitney检验的比较统计分析。我们的结果表明，肥大细胞主要位于肾小管周围和血管周围区域，而肾小体区域则不存在。在12个月大的动物中，它们的数量显着增加。胰蛋白酶的免疫染色，c-kit和两个分子的双重染色均产生相同的结果。在成年动物的肾脏中，成纤维细胞生长因子2的免疫组织化学表达增加，胶原纤维的百分比也增加。此外，我们描述了在12个月大的自发性高血压大鼠中更为严重的肾脏损害，并注意到两个年龄组中一方面肥大细胞数量与另一方面的肾小球硬化指数和肾小管间质损害指数之间呈正相关。在本研究中获得的结果支持肥大细胞在高血压引起的肾脏损害的发展中的关键作用。