Acute Renal Syndrome/Renal Angina

Abstract

Acute kidney injury (AKI) is a widespread problem in the intensive care unit (ICU) that heralds increased morbidity, mortality, and ICU length and cost of stay, independent of other factors (1–3). Unfortunately, there are few, if any, specific interventions proven to prevent or treat AKI. Renal replacement therapy is a reactionary, supportive therapy that almost by definition is started long after the inciting process and well into the pathophysiologic cascade of AKI. Although renal replacement therapy is effective at treating the sequelae of AKI such as electrolyte, fluid, and acid-base disorders, it does not address the underlying disease and is rather a bridge to hoped-for spontaneous renal recovery. Although many interventions have been studied to treat AKI and prevent its progression (4), nothing has been clearly beneficial, and we are left with the obvious yet nonspecific interventions: Maintain renal perfusion, avoid nephrotoxic drugs, and correct the underlying process (sepsis, hypovolemia). Many have suggested that at least one reason for the futility of interventions for AKI is late disease detection using conventional markers of renal function (4–7). That is, by the time azotemia and its sequelae are detected, renal injury is well established and may be outside the window for mitigation by an intervention (8). Part of the problem is that in contrast to many other acute disease states in which patients present with acute symptoms, patients with AKI are relatively asymptomatic until the disease is advanced. For example, in the case of acute myocardial infarction, patients typically present with symptoms of disease (chest pain, …