Pathophysiology Crystal-induced kidney injury

晶体可以以许多不同的方式诱导肾损伤，例如在胆固醇栓塞期间、小管内结晶或在尿石症期间。在之前的项目中，我们能够生成关于草酸钙晶体诱导的肾脏炎症的重要数据。在这里，我们提出了一个系统的研究肾免疫和非免疫细胞的激活和损伤引起的各种临床相关的晶体。此外，我们将探索肾脏胆固醇栓塞和尿酸盐肾病的创新疾病模型。此外，我们将探讨晶体肉芽肿形成的分子机制。通过系统的研究，本项目将揭示结晶性肾病的分子病理生理学。

Crystals can induce kidney injury in many different ways, e.g. during cholesterol embolism, intratubular crystallization or during urolithiasis. In the previous project we were able to generate important data on calcium oxalate crystal-induced kidney inflammation. Here we propose systematic studies on the activation and injury of renal immune and non-immune cells induced by a great variety of clinically relevant crystals. In addition, we will explore innovate disease models of cholesterol embolism of the kidney and urate nephropathy. Furthermore, we will explore the molecular mechanisms of crystal granuloma formation. By the help of systematic studies this project will unravel the molecular pathophysiology of crystal nephropathies.