The kidney vasculature has a unique and complex architecture that is central for the kidney to exert its multiple and essential physiological functions with the ultimate goal of maintaining homeostasis. An appropriate development and coordinated assembly of the different vascular cell types and their association with the corresponding nephrons is crucial for the generation of a functioning kidney. In this review we provide an overview of the renal vascular anatomy, histology, and current knowledge of the embryological origin and molecular pathways involved in its development. Understanding the cellular and molecular mechanisms involved in renal vascular development is the first step to advance the field of regenerative medicine.

Juxtaglomerular cells are crucial for blood pressure and fluid-electrolyte homeostasis. The factors that maintain the life of renin cells are unknown. In vivo, renin cells receive constant cell-to-cell, mechanical, and neurohumoral stimulation that maintain their identity and function. Whether the presence of this niche is crucial for the vitality of the juxtaglomerular cells is unknown. Integrins are the largest family of cell adhesion molecules that mediate cell-to-cell and cell-to-matrix interactions. Of those, β1-integrin is the most abundant in juxtaglomerular cells. However, its role in renin cell identity and function has not been ascertained. To test the hypothesis that cell-matrix interactions are fundamental not only to maintain the identity and function of juxtaglomerular cells but also to keep them alive, we deleted β1-integrin in vivo in cells of the renin lineage. In mutant mice, renin cells died by apoptosis, resulting in decreased circulating renin, hypotension, severe renal-vascular abnormalities, and renal failure. Results indicate that cell-to-cell and cell-to-matrix interactions via β1-integrin is essential for juxtaglomerular cells survival, suggesting that the juxtaglomerular niche is crucial not only for the tight regulation of renin release but also for juxtaglomerular cell survival—a sine qua non condition to maintain homeostasis.

Objective: To describe 3 different standardized approaches to improving neonatal acute kidney injury (AKI) identification and the impact on AKI identification, incidence, and nephrology consultation and referral.Study Design: Retrospective cohort study in three academic NICUs. We compared AKI identification, AKI incidence, nephrology consultation and nephrology follow-up before and after implantation of local protocols to standardized neonatal AKI identification.Result: Neonatal AKI identification improved in all three NICUs following protocol implementation (26% to 85%, P<0.0001). Each center also saw increases in nephrology consultation (15% to 83%, P<0.0001) and nephrology follow-up (7% to 73%, P<0.0001). AKI incidence decreased significantly (21% to 12%, P<0.0001). Conclusion:Multiple strategies can be successfully operationalized to improve neonatal AKI identification. While different in approach, each strategy resulted in increased AKI identification and nephrology involvement. This study emphasizes the importance of local standardized approaches to AKI to improve AKI identification and nephrology involvement in the NICU.

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