Podocytes are the key target cells for injury across the spectrum of primary and secondary proteinuric kidney disorders, which account for up to 90% of cases of kidney failure worldwide. Seminal experimental and clinical studies have established a causative link between podocyte depletion and the magnitude of proteinuria in progressive glomerular disease. However, no substantial advances have been made in glomerular disease therapies, and the standard of care for podocytopathies relies on repurposed immunosuppressive drugs. The past two decades have seen a remarkable expansion in understanding of the mechanistic basis of podocyte injury, with prospects increasing for precision-based treatment approaches. Dozens of disease-causing genes with roles in the pathogenesis of clinical podocytopathies have been identified, as well as a number of putative glomerular permeability factors. These achievements, together with the identification of novel targets of podocyte injury, the development of potential approaches to harness the endogenous podocyte regenerative potential of progenitor cell populations, ongoing clinical trials of podocyte-specific pharmacological agents and the development of podocyte-directed drug delivery systems, contribute to an optimistic outlook for the future of glomerular disease therapy.

足细胞是原发性和继发性蛋白尿肾病损伤的关键靶细胞，这些疾病占全球肾衰竭病例的 90%。开创性的实验和临床研究已经确定了进行性肾小球疾病中足细胞耗竭与蛋白尿程度之间的因果关系。然而，肾小球疾病的治疗尚未取得实质性进展，足细胞病的护理标准依赖于重新调整用途的免疫抑制药物。在过去的二十年里，人们对足细胞损伤机制基础的理解有了显着的扩展，基于精确治疗方法的前景也越来越大。已鉴定出数十种在临床足细胞病发病机制中发挥作用的致病基因，以及一些假定的肾小球通透性因子。这些成就，以及足细胞损伤新靶点的确定、利用祖细胞群内源性足细胞再生潜力的潜在方法的开发、足细胞特异性药物制剂的持续临床试验以及足细胞定向药物递送系统的开发，有助于对肾小球疾病治疗的未来持乐观态度。