Acute Renal Failure in the Aged

Abstract

Acute Renal Failure: Its Definition and PhysiopathologyAcute renal failure (ARF) the generic term for an abrupt and sustained decrease in renal function resulting in inability to maintain the equilibrium of the internal milieu. Despite the absence of a universal definition, it is reasonable to define ARF as an acute and sustained increase in serum creatinine of 0.5 mg/dL if the baseline is less than 2.5 mg/dL, or an increase in serum creatinine by more than 20% if the baseline is more than 2.5 mg/dL [1].Three mechanisms are involved in the appearance of ARF: diminution of the renal blood flow with preservation of renal parenchymal integrity (prerenal ARF), acute lesions of the renal parenchyma (intrinsic renal ARF), and obstruction of the urinary flow (post-renal ARF) [2]. Pre-renal ARF can be induced by the following situations: intravascular volume depletion, decreased cardiac output, renal vasoconstriction, and impaired autoregulation induced by drugs. Intrinsic ARF can be caused by the compromise of renal vasculature, glomeruli, acute tubular necrosis (ATN), or tubulointerstitial damage.The pathophysiology of ATN can be divided into three phases: initial, maintenance, and recovery. The initial phase of ischemic ATN refers to a hypothetical period of time during which renal perfusion is compromised to the extent that precipitates intrarenal events that are responsible for persistence of renal dysfunction long after the original cause has been resolved. Maintenance refers to the period of ongoing renal failure that is usually followed by a recovery phase during which the renal injury is repaired and baseline renal function is re-established [3]. Although many of the theories that explain the reduction of GFR in ARF have been known for 50 years, the exact pathogenesis of this syndrome, especially the means by which oligoanuria is sustained, remains unresolved; however, it is clearly multifactorial [4,5]. The current consensus opinion is that three major factors contribute to the profound reduction in GFR that characterizes ATN: tubule injury, hemodynamic abnormalities, and intrarenal inflammation. Tubular injury leads to insufficiency by causing "back-leakage" of glomerular filtrate and intratubular obstruction. Intrarenal vasoconstriction and reduction of the ultrafiltration coefficient (Kf) can also directly impair GFR. Most of our knowledge about these factors has been derived from experimental models of ARF, mainly in rodents. These models can be divided into two groups: the hemodynamic models, 385