Pathophysiology of Acute Kidney Injury

Abstract

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.

Anemia Is a Risk Factor for Acute Kidney Injury and Long-Term Mortality in Critically Ill Patients

“…Additionally, patients with both anemia and AKI had a higher mortality risk than the counterpart groups. This may be because both anemia and AKI aggravate organ dysfunction or delay of organ recovery (Cilley et al 1991;Basile et al 2012). Anemia can have both direct and indirect effects on mortality; in the context of indirect effect, anemia may increase the severity of AKI and worsen the mortality rate.…”

Cafeteria Diet Increases Liquid Intake and Serum Creatinine Levels in Rats

“…We speculate that the duration of the treatment was also insufficient to trigger hypertension in these animals, considering that another study showed a robust increase in systolic blood pressure with animals exposed to cafeteria diet for 10 weeks 29 . The most important function of the kidney is filtration and excretion of nitrogenous compounds from blood 30 . Creatinine is a good parameter for assessing renal function, since its production only depends on the muscle cell metabolism and is almost entirely eliminated by glomerular filtration [30][31][32] , and by poor tubular secretion 33 , that may be considered insignificant.…”

“…The most important function of the kidney is filtration and excretion of nitrogenous compounds from blood 30 . Creatinine is a good parameter for assessing renal function, since its production only depends on the muscle cell metabolism and is almost entirely eliminated by glomerular filtration [30][31][32] , and by poor tubular secretion 33 , that may be considered insignificant. Therefore, the intensity of creatinine excretion corresponds to the rate of glomerular filtration, so if glomerular filtration decreases, its excretion also decreases transiently, increasing its levels in body fluids and plasma until the creatinine excretion returns to normal 34 .…”

Worsening of proteinuria caused by combination therapy of hypertonic saline and low-dose furosemide for treatment of acute decompensated heart failure with overt diabetic nephropathy

“…Tubular injury has a link with reduction of RPF through increasing renal vascular resistance, consequently increasing serum creatinine concentration (Fig. 2) [8,9]. Congestive heart failure (CHF) itself can be a cause of proteinuria.…”