Focus on Renal Pathology
For this web focus, the first for Laboratory Investigation, the editors have chosen the topic of renal pathology. We have gathered the most persuasive articles published in the last two years, as selected by Associate Editor Agnes B. Fogo, M.D.
Laboratory Investigation is an international journal owned by the United States and Canadian Academy of Pathology, whose prime mission is to publish original manuscripts and review articles in the broad area of translational and basic research as is related to experimental pathology.
Renal parenchymal scarring is the most important indicator of poor prognosis in both immune and non-immune mediated renal diseases. The majority of patients with chronic kidney disease ultimately require renal replacement therapy with either dialysis or kidney transplantation to sustain life. Exploring pathways leading to these relentless injury processes or to repair mechanisms are therefore topics of particular interest. Two of the selected articles focus on such potential mechanisms and shed light on novel markers involved in pathogenesis and progression of chronic renal diseases, exploring the roles of inflammatory cytokines and microRNAs in the kidney (Ichii et al. and Wang et al. respectively). Another article with a similar theme (Zhang et al.) specifically details molecular mechanisms involved in hypercholesterolemia-induced chronic kidney disease, including proinflammatory cytokine production and pericyte transdifferentiation into myofibroblasts, the major source of collagen.
Several interesting animal models have been introduced that shed light on the deleterious effect of low nephron number (Wang et al.), the consequences of excessive oxygen-derived free radicals in glycogen storage disease in the kidney (Yiu et al.), the impact of the Ren2 gene on diabetes (Apelhoff et al.), the relationship between podocyte injury and the TNF-α and NF-κβ signaling pathways (Bruggeman et al.), and the effect of age-related mitochondrial damage (Satoh et al).
Another novel animal model establishes the role of OAT1 and MRP4 transporters in tenofovir nephrotoxicity (Kohler et al.). Another mouse model contributes to our understanding of the kidney-specific effects of glycogen synthase kinase3β (Ge et al.)
Other important themes explored include the role of macrophages and inflammatory stimuli in renal injury (Han et al. and Li et al.), and beneficial effects of blocking the β2-kinin receptor and PPAR-γ agonist with decreased inflammation (Tang et al.). The key role of VEGF in capillary repair (Masuda et al.) is also illuminated.
Several studies are relevant to increase understanding of mechanisms of metabolic and cardiovascular diseases (Kuipers et al). Some studies suggest potential novel targets, such as epimorphin in the repair/ reversal of interstitial fibrosis and PKD-1 inactivation for cardiovascular disease in polycystic kidney disease (Yamada et al. and Hassane et al. respectively).
Laboratory Investigation will continue to publish influential articles in the field of renal pathology. In the coming months, look for papers covering this broad range of topics: an animal model that offers insights into the early development of glomerular nephropathies; a description of how the unfolded protein response in podocytes may lead to nephrotic syndrome; a method devised to allow label-free, in vivo imaging of kidney blood flow; a potential therapeutic agent for treating cisplatin nephrotoxicity; a novel treatment for abrogation of proteinuria in rat nephrotoxic serum nephritis; a mechanism that may allow podocytes to better withstand an adverse high-glucose or angiotensin II-rich environment; and a protocol that employs microvascular density as a predictor of clinical outcome in renal cell carcinoma.
