Acute kidney injury overview: From basic findings to new prevention and therapy strategies

Abstract

Acute kidney injury (AKI) is defined as a decrease in kidney function within hours, which encompasses both injury and impairment of renal function. AKI is not considered a pathological condition of single organ failure, but a syndrome in which the kidney plays an active role in the progression of multi-organ dysfunction. The incidence rate of AKI is increasing and becoming a common (8-16% of hospital admissions) and serious disease (four-fold increased hospital mortality) affecting public health costs worldwide. AKI also affects the young and previously healthy individuals affected by infectious diseases in Latin America. Because of the multifactorial pathophysiological mechanisms, there is no effective pharmacological therapy that prevents the evolution or reverses the injury once established; therefore, renal replacement therapy is the only current alternative available for renal patients. The awareness of an accurate and prompt recognition of AKI underlying the various clinical phenotypes is an urgent need for more effective therapeutic interventions to diminish mortality and socio-economic impacts of AKI. The use of biomarkers as an indicator of the initial stage of the disease is critical and the cornerstone to fulfill the gaps in the field. This review discusses emerging strategies from basic science toward the anticipation of features, treatment of AKI, and new treatments using pharmacological and stem cell therapies. We will also highlight bioartificial kidney studies, addressing the limitations of the development of this innovative technology.

Keywords: Acute kidney injury; Ischemia; Renal physiology; Reperfusion.

Figure 1.. The hallmarks of acute kidney injury (AKI).

The figure represents a schematic view of the main pathophysiological mechanisms of AKI. The inner circle indicates the four altered processes in the kidney that trigger AKI. The outer circle represents the main events encountered in the clinical practice that alter at least one of the four processes depicted in the inner circle. Independently or together, those alterations will contribute to the gradual decrease in GFR. Late diagnosis and/or non-adequate treatment culminate in ERSD. ROS: reactive oxygen species; ER: endoplasmic reticulum; ATN: acute tubular necrosis; EM: epithelial/mesenchymal; GFR: glomerular filtration rates; ESRD: end stage of renal disease.