Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
The year 2015 has seen great progress in the renal fibrosis field, as key studies began to build a consensus on the importance of epithelial-to-mesenchymal transition, cell cycle arrest, and defective metabolism in the pathogenesis of kidney fibrosis. New findings also point to a role of developmental signalling in renal fibrogenesis.
2015 saw the publication of several important studies in the renal stem cell and developmental biology fields. Key studies provided insights into the ageing of nephron progenitors and optimal conditions to stimulate the expansion of nephron progenitors, and reported the in vitro generation of kidney organoids.
Podocyte biologists can boast of some important advances in 2015. Some of the key developments include defining the transcriptional targets of the Wilms' tumour protein on a genome-wide scale, the identification of new mitochondria-centred pathways for maintaining podocyte homeostasis, and new insights into the regulation and pathogenic activation of TRPC6.
Combination therapy with optimal doses of multiple antihypertensive drugs fails to achieve blood pressure (BP) control in up to 15% of hypertensive patients. Key studies in 2015 highlighted the risks of uncontrolled hypertension and evaluated new therapeutic modalities designed to achieve satisfactory BP control in patients with treatment-resistant hypertension.
Numerous studies in 2015 focused on therapeutic immune modulation and immunosuppression. Trials of budenoside in patients with IgA nephropathy who are unresponsive to supportive therapy, and of low-dose IL-2 to enforce regulatory T-cell-mediated immunosuppression in autoimmune disease all produced promising results.
Knowledge of the pathogenesis of glomerular disease and approaches to therapy continued to advance in 2014. Key studies identified thrombospondin type-1 domain-containing protein 7A as an antigenic target in primary membranous nephropathy, and demonstrated efficacy of rituximab as maintenance therapy in relapsing or steroid-dependent nephrotic syndrome and antineutrophil cytoplasmic antibody-associated vasculitis.
In 2014, key articles in the field of acute kidney injury highlighted the importance of tubular homeostasis in renal regeneration. Cell cycle regulators, inflammatory signals and progenitors were identified as important factors that mediate the balance between inflammation and tubular regeneration necessary for renal repair.
