Last update:
21-Jul-2000

Arch Hellen Med, 16(6), November-December 1999, 569–573

BRIEF REVIEW

Pathogenesis of acute renal failure in the sepsis syndrome

C. IATROU,¹ N. KAPERONIS^2
1Department of Nephrology, General Hospital of Athens “G. Gennimatas”
²Department of Nephrology, “Hippokration” General Hospital of Athens, Greece

The sepsis syndrome or systemic inflammatory response syndrome (SIRS) is a clinically recognized phenomenon which occurs in patients with acute infections. SIRS may also develop in patients with a variety of other conditions such as multiple trauma, malignancy, acute pancreatitis and hepatitis, burn injury, acute transplant rejection etc. In the case of infections the terms sepsis and SIRS are synonymous. The syndrome is characterized by an abnormal inflammatory reaction in organs remote from the initial insult, due to interaction between proinflammatory and anti-inflammatory mediators. Acute renal failure is often a component of the sepsis syndrome and complicates the disease course in 15% of patients in the intensive care units. This dysfunction results from renal vasoconstriction and reduction in glomerular filtration rate and precedes systemic hypotension. Hemodynamic (systemic, renal) and nonhemodynamic (humoral, cellular) factors all participate in the pathogenesis of acute renal failure during SIRS. Cytokines, such as tumor necrosis factor (TNF) and interleukin-1 (IL-1) and other mediators, such as platelet-activating factor (PAF) probably play a major role, but endothelin, nitric oxide (NO), thromboxane A₂, leukotrienes, interleukins 8 and 6 (IL-8, IL-6) and bradykinin are involved as well. In addition neutrophils, as a cellular factor, play a key role in the pathogenesis of acute renal failure in the sepsis syndrome.

Kew words: Acute renal failure, Multiple organ dysfunction, Sepsis, Systemic inflammatory response.