Anatomy, Physiology, and Pathophysiology of Renal Circulation

This chapter covers functional anatomy, physiology, and pathophysiology of the renal circulation. While insights about the anatomy of the renal vasculature have evolved some, the understanding of the physiology has improved substantially. Regarding glomerular filtration rate and renal blood flow, this chapter discusses the three levels of organization that can be recognized in renal physiology: first, principle driving forces of renal blood flow and glomerular filtration (based on the Starling forces); second, autoregulation, the system that stabilizes renal blood flow and glomerular filtration rate upon changes in renal perfusion pressure; and last, the neuroendocrine systems that connect systemic hemodynamics to the regulation of renal blood and glomerular filtration. Regarding pathophysiology, the basic derangements happening in renovascular hypertension, in diabetic nephropathy, in hypertensive renal injury, and in cardiorenal syndrome are described

Selective iNOS inhibition for the treatment of sepsis-induced acute kidney injury.

Contains fulltext : 81592.pdf (publisher's version ) (Closed access)The incidence and mortality of sepsis and the associated development of acute kidney injury (AKI) remain high, despite intense research into potential treatments. Targeting the inflammatory response and/or sepsis-induced alterations in the (micro)circulation are two therapeutic strategies. Another approach could involve modulating the downstream mechanisms that are responsible for organ system dysfunction. Activation of inducible nitric oxide (NO) synthase (iNOS) during sepsis leads to elevated NO levels that influence renal hemodynamics and cause peroxynitrite-related tubular injury through the local generation of reactive nitrogen species. In many organs iNOS is not constitutively expressed; however, it is constitutively expressed in the kidney and, in humans, a relationship between the upregulation of renal iNOS and proximal tubular injury during systemic inflammation has been demonstrated. For these reasons, the selective inhibition of renal iNOS might have important implications for the treatment of sepsis-induced AKI. Various animal studies have demonstrated that selective iNOS inhibition-in contrast to nonselective NOS inhibition-attenuates sepsis-induced renal dysfunction and improves survival, a finding that warrants investigation in clinical trials. In this Review, the selective inhibition of iNOS as a potential novel treatment for sepsis-induced AKI is discussed