Updates in Acute Kidney Injury With Sepsis in critical Ill Patients

Abstract

Acute kidney injury (AKI) is a common sequel of sepsis in the intensive care unit, it occurs in about 19% of patients with moderate sepsis, 23% with severe sepsis and 51% with septic shock, when blood cultures are positive. The exact pathophysiology of sepsis-induced AKI is not known, however, it is generally accepted that it has a multi-pronged injury pathway as follows: - Apoptosis exists to have a more prominent role than necrosis in the mechanisms that explains the tubular epithelial cell injury in sepsis. - Altration in the renal blood flow : by which renal hyperemia and/or kidney ischemia cause loss of glomerular filtration rate (GFR). The vascular derangement in septic AKI occurs in response to certain substances like nitric oxide (NO), endothlins, tumor necrosis factor and interleukin-1 - Local soluble mediators: as cellular and humoral cytokines which are integral to organ dysfunction in sepsis syndromes with the kidney being especially vulnerable to cytokine mediated injury. - Coagulation cascade: The activation of coagulation and deposition of fibrin in the tissues is a well defined component of the multiple organ failure in sepsis. It is difficult to implement timely preventive strategies for septic acute kidney injury as renal damage may have already occurred before signs of sepsis become overt. Conventional urinary biomarkers such as casts and fractional excretion of sodium have been insensitive and nonspecific for the early recognition of septic AKI. Fortunately, the application of innovative technologies such as functional genomics and proteomics to human and animal models of AKI has uncovered several novel genes and gene products that are emerging as biomarkers. Management of septic AKI starting with adequate and early goal directed therapy as recommended by The surviving sepsis campaign, this is achieved by administration of Crystalloids to maintain central venous pressure at 8 to 12mmHg and keep mixed venous saturation of O2¬ >70%. If main arterial blood pressure <65% and urine excretion <7.1mL/kg Vasopressors were added. Choice of the resuscitating fluid along with timing and amount of fluid administration are also emerging as important determinants of AKI, in clinical the use of crystalloid is preferred because of the higher cost of colloid. To achieve adequate renal perfusion pressure, fluid resuscitation is not enough and patients with sepsis often require vasopressor support. Norepinephrine seems to be the drug of choice when volume and cardiac output have been corrected and significant vasodilation impedes the achievement of an adequate renal perfusion pressure. Treatment with activated protein C (APC) reduced progression to renal failure as well as the need for renal replacement therapy. Tight glycaemic control: The use of aggressive insulin therapy aimed at achieving normoglycemia in critically ill patients has been shown to reduce mortality significantly in critically ill, surgical patients with sepsis. There is also a dramatic reduction in the development of severe AKI that required RRT.