Acute kidney injury (AKI) is the leading cause of nephrology consultation and is associated with high mortality rates. The primary causes of AKI include ischemia, hypoxia or nephrotoxicity. An underlying feature is a rapid decline in GFR usually associated with decreases in renal blood flow. Inflammation represents an important additional component of AKI leading to the extension phase of injury, which may be associated with insensitivity to vasodilator therapy. It is suggested that targeting the extension phase represents an area potential of treatment with the greatest possible impact. The underlying basis of renal injury appears to be impaired energetics of the highly metabolically active nephron segments (i.e., proximal tubules and thick ascending limb) in the renal outer medulla, which can trigger conversion from transient hypoxia to intrinsic renal failure. Injury to kidney cells can be lethal or sublethal. Sublethal injury represents an important component in AKI, as it may profoundly influence GFR and renal blood flow. The nature of the recovery response is mediated by the degree to which sublethal cells can restore normal function and promote regeneration. The successful recovery from AKI depends on the degree to which these repair processes ensue and these may be compromised in elderly or CKD patients. Recent data suggest that AKI represents a potential link to CKD in surviving patients. Finally, earlier diagnosis of AKI represents an important area in treating patients with AKI that has spawned increased awareness of the potential that biomarkers of AKI may play in the future.

/pdf/pathophysiology-of-acute-kidney-injury-57ami3f8ia.pdf

Pathophysiology of Acute Kidney Injury

Acute renal failure (ARF), classically defined as an abrupt decrease in kidney function that leads to accumulation of nitrogenous wastes such as blood urea nitrogen and creatinine, is a common clinical problem with increasing incidence, serious consequences, unsatisfactory therapeutic options, and

/pdf/update-on-mechanisms-of-ischemic-acute-kidney-injury-1ype1s84nf.pdf

Update on mechanisms of ischemic acute kidney injury.

Ischemic acute renal failure: an inflammatory disease?

As covered in the preceding sections, acute renal failure (ARF) is a syndrome associated with high mortality in humans. Current therapy is limited to supportive measures and preventive strategies, none of which have been definitively shown to alter mortality. Ischemic ARF is often associated with

Recent Advances in the Pathophysiology of Ischemic Acute Renal Failure

Acute renal failure (ARF), characterized by sudden loss of the ability of the kidneys to excrete wastes, concentrate urine, conserve electrolytes, and maintain fluid balance, is a frequent clinical problem, particularly in the intensive care unit, where it is associated with a mortality of between 50% and 80%. In this review, the epidemiology and pathophysiology of ARF are discussed, including the vascular, tubular, and inflammatory perturbations. The clinical evaluation of ARF and implications for potential future therapies to decrease the high mortality are described.

/pdf/acute-renal-failure-definitions-diagnosis-pathogenesis-and-5fxrujaoc0.pdf

Acute renal failure: definitions, diagnosis, pathogenesis, and therapy

There is accumulating circumstantial evidence suggesting that endothelial cell dysfunction contributes to the “no-reflow” phenomenon in postischemic kidneys. Here, we demonstrated the vulnerability...

Endothelial dysfunction in ischemic acute renal failure: rescue by transplanted endothelial cells

There have been developed several types of experimental techniques for evaluation of renal microcirculation. Although each methodology possesses excellent and unique characteristics, it requires substantial artificial manipulation that might alter the renal microvascular responsiveness. To circumvent such limitations of previous ex vivo or in vitro approaches to glomerular microcirculation, we have developed a pencil lens probe CCD intravital videomicroscopic system that allows us to evaluate both systemic hemodynamics and renal microcirculation. Furthermore, real time images of afferent and efferent arterioles as well as glomeruli can be continuously assessed, which would facilitate the functional characterization of these microvessels in vivo. Finally, the tapered nature of the CCD probe of this videomicroscopy may allow direct observation of the renal microvasculature in small animals. In conclusion, this novel technique is a valuable tool for unveiling the in vivo, in situ, and intact renal microvascular behavior, and may provide further approaches to the understanding of renal microcirculation.

Direct in vivo visualization of glomerular microcirculation by intravital pencil lens-probe CCD videomicroscopy.

special communication Intravital videomicroscopy of peritubular capillaries in renal ischemia

The recent refinement and computerization of intravital microscopy have permitted us to monitor microcirculation in vivo with minimal invasion. Here, we report on the first findings made with the use of a pencil-lens intravital microscope as applied to the ischemic rat kidney. Peritubular capillary and glomerular blood flow were monitored under basal conditions, during renal artery occlusion, and immediately after release of the clamp. Erythrocyte velocity was calculated as an angle in consecutive spatiotemporal images. Intravital videomicroscopy during the reperfusion period showed intermittent cessation and partial recovery of blood flow in both peritubular and glomerular capillaries. Blood flow was uniformly orthograde under control conditions; however, the retrograde flow occurred on reperfusion. The patency of peritubular capillaries was partially compromised during the early reperfusion period but rapidly recovered. The recovery of glomerular microcirculation occurred faster than that of peritubular capillaries. We suggest that a functional vasculopathy develops very early in the course of ischemia-reperfusion in superficial cortical microvasculature and is more pronounced in peritubular capillaries, thus accounting for the development of patchy injury of tubular epithelia.

https://www.physiology.org/doi/pdf/10.1152/ajprenal.00310.2001

Intravital videomicroscopy of peritubular capillaries in renal ischemia

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Endothelial dysfunction in ischemic acute renal failure: rescue by transplanted endothelial cells

Direct in vivo visualization of glomerular microcirculation by intravital pencil lens-probe CCD videomicroscopy.

special communication Intravital videomicroscopy of peritubular capillaries in renal ischemia

Intravital videomicroscopy of peritubular capillaries in renal ischemia