Contributions to nephrology
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Septic acute kidney injury (AKI) is the most common form of AKI seen in critically ill patients in developed countries. Its pathogenesis has been traditionally attributed to ischemia secondary to decreased cardiac output and hypotension, which trigger sustained renal vasoconstriction and in turn exacerbate and sustain the ischemia. ⋯ Furthermore, the induction of prolonged severe subtotal ischemia by acute occlusion of the renal artery does not seem to trigger subsequent renal vasoconstriction and, finally, experimental studies suggest that immune-mediated injury may be a more likely cause of tubular cell dysfunction than ischemia. These lines of evidence suggest that the pathogenesis of AKI is complex, does not simply involve ischemia, and may differ according to the etiological trigger.
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Acute kidney injury (AKI) is frequently encountered in the intensive care unit, and from its inception, morbidity and mortality increase in these patients compared to those without AKI. Despite numerous clinical trials and newer pharmacological agents, very little progress has been made to reduce the deaths that occur in this population. ⋯ This critical loss of balance of these mediators appears to be due both to a reduction in clearance and increase in production as demonstrated by experimental studies of bilateral nephrectomy and ischemia-reperfusion, respectively. The evidence and mechanisms for distant organ injury following AKI will be discussed.
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Acute heart failure (HF) and acute kidney injury (AKI) are common. These syndromes are each associated with considerable morbidity, mortality, and health resource utilization and are increasingly encountered. Fluid accumulation and overload are common themes in the pathophysiology and clinical course of both HF and AKI. ⋯ To date, the impact of fluid balance in both of these syndromes, more so with AKI, has likely been underappreciated. There is little to no data specifically on fluid balance in the cardiorenal syndrome, where acute/chronic heart disease can directly contribute to acute/chronic worsening of kidney function that likely exacerbates fluid homeostasis. Additional investigations are needed.
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The correct selection of anticoagulation in acute blood purification is crucial for avoiding exacerbation of bleeding in critical care patients with acute renal failure, as these patients frequently exhibit hemorrhagic complications. The mode of acute blood purification is determined mainly by the patient's hemodynamic stability, and continuous renal replacement therapies (CRRTs) have been extensively performed for patients with hemodynamic instability. Unfractionated heparin, low molecular weight heparin and nafamostat mesilate (nafamostat) are available in acute blood purification for the patients. ⋯ This is especially the case with patients of small stature, which is the case for many Japanese people. Nafamostat can be used safely in CRRT for critical care patients with acute renal failure and bleeding risks, because it acts as a regional anticoagulant due to its pharmacological characteristics. Nafamostat has been widely used in acute blood purification at critical care units in Japan.
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Acute kidney injury (AKI) requiring dialysis occurs frequently, and its pathogenesis involves multiple pathways within which hemodynamic, inflammatory and nephrotoxic factors overlap. Several studies have tried to assess the risk factors leading to AKI, and found, among other factors, that preoperative renal dysfunction is important. Currently, it is uncertain when dialysis therapy should start. However, AKI after cardiac surgery should be treated early by continuous hemodialysis.