Current concepts of AKI in sepsis indicate that systemic inflammation, microvascular dysregulation, and mitochondrial alteration, leading to cell death may be more important than global renal hypoperfusion.
Urine output and SCr are at best surrogate markers of renal function, but can be “normal” in the presence of renal dysfunction.
Recent studies have identified new biomarkers of renal injury that can diagnose AKI earlier than SCr, but these are still in the primary stages of clinical adoption.
Prevention of contrast-induced AKI focuses on the use of noniodinated contrast media, minimizing contrast-media volume, avoiding repeat exposure to contrast media, and expanding plasma volume before administration of contrast media.
The published literature suggests that periprocedural dialysis has no protective effect against CI-AKI.
Acute kidney injury (AKI) is the sudden decline of renal function resulting in the retention of nitrogenous waste products and the inability to regulate electrolytes and extracellular volume. The development of AKI is associated with increased morbidity and mortality. These patients have an increased hospital length of stay and hospital readmissions, all of which translate into increasing resource utilization. The number of deaths resulting from AKI continues to increase even though the treatment of AKI and care of critically ill patients has improved. The reason for this increase in absolute mortality from AKI is twofold: the incidence of AKI is increasing and patients with AKI are older, with a greater number and severity of comorbid conditions.1 Furthermore, we are pushing the boundaries in medicine; sicker patients who once were untreatable are now undergoing more complex and invasive diagnostic and surgical procedures.
Although the kidneys receive approximately 20% of the total cardiac output, they are still at very high risk for ischemic injury. This dichotomy is explained by the fact that most renal blood flow (80%-90%) is directed toward the renal cortex, where it passes through the glomerulus and is filtered.2 The most metabolically active portion of the kidney, however, is not the cortex but the medulla, which is responsible for creating the osmotic gradient that serves to reabsorb water and concentrate urine. In order to maintain this osmotic gradient, blood flow to the medulla is kept low. In fact, the oxygen tension in the medulla is only approximately 10 mm Hg.2 This lack of luxury perfusion to a metabolically active portion of the kidney predisposes it to ischemic injury. Furthermore, the kidney concentrates toxins that the body is exposed to, thereby amplifying the exposure of renal cells to toxic substances.
The etiology of AKI is traditionally divided into prerenal, intrinsic renal, and postrenal. Prerenal azotemia occurs as a complication of decreased renal perfusion with preservation of the cellular architecture of the renal parenchyma. Direct injury to the kidneys results in renal azotemia, or intrinsic renal injury. Postrenal azotemia occurs as a result of obstruction of the urinary outflow ...