Kidney Microcirculation as a Target for Innovative Therapies in AKI

Abstract

Acute kidney injury (AKI) is a serious multifactorial conditions accompanied by the loss of function and damage. The renal microcirculation plays a crucial role in maintaining the kidney's functional and structural integrity for oxygen and nutrient supply and waste product removal. However, alterations in microcirculation and oxygenation due to renal perfusion defects, hypoxia, renal tubular, and endothelial damage can result in AKI and the loss of renal function regardless of systemic hemodynamic changes. The unique structural organization of the renal microvasculature and the presence of autoregulation make it difficult to understand the mechanisms and the occurrence of AKI following disorders such as septic, hemorrhagic, or cardiogenic shock; ischemia/reperfusion; chronic heart failure; cardiorenal syndrome; and hemodilution. In this review, we describe the organization of microcirculation, autoregulation, and pathophysiological alterations leading to AKI. We then suggest innovative therapies focused on the protection of the renal microcirculation and oxygenation to prevent AKI.

Keywords: acute kidney injury; innovative therapies; microcirculation; oxygenation.

Figure 1

Direct observation using hand-held video microscopy (HVM) of the microcirculatory structure and cortical tubule organization in the kidney. Figures were obtained from automated microcirculatory measurement software (MicroTools) [18]. The white arrow indicates the cortical tubules, and the black arrow shows peritubular vessels around the tubules (A). (B) represents the vessel border drawn by MicroTools in the renal cortex.

Figure 2

The effects of the sympathetic and renal autoregulatory systems on renal microcirculation. ABP: arterial blood pressure; Na⁺: sodium; Art: artery; Af-Art: afferent arteriole; Ef-Art: efferent arteriole; ↑: high; ↓: low.

Figure 3

The endothelial cell and glycocalyx structure.