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.

Blood Pressure and Oxygen Targets on Kidney Injury After Cardiac Arrest

“…13 Kidney blood flow is mainly controlled by autoregulation influencing preglomerular resistance and intraglomerular capillary pressure, which ensures consistent glomerular perfusion at variable MAP at wide ranges. 14 Impaired kidney autoregulation incites glomerular and tubular injury and, thus, dysfunction that may be further augmented by PCAS. 14 Only a few studies have assessed kidney outcomes in relation to specific targets of blood pressure in patients with OHCA.…”

“…14 Impaired kidney autoregulation incites glomerular and tubular injury and, thus, dysfunction that may be further augmented by PCAS. 14 Only a few studies have assessed kidney outcomes in relation to specific targets of blood pressure in patients with OHCA. In a post hoc analysis of 851 patients from the TTM trial (Target Temperature Management After Cardiac Arrest), authors found decreasing MAP values to be associated with lower estimated glomerular filtration rate and increased need for CKRT during targeted temperature management therapy.…”

“…14 Impaired kidney autoregulation incites glomerular and tubular injury and, thus, dysfunction that may be further augmented by PCAS. 14…”

“…The BOX study was an investigator-initiated, randomized trial. In a 2-by-2 factorial design, comatose patients with OHCA were allocated to 1 of 2 targets of blood pressure (MAP, 63 mm Hg or 77 mm Hg) and open-label restrictive (9-10 kPa) or liberal (13)(14) target of a partial pressure of arterial oxygen (Pao 2 ). Furthermore, patients were randomly assigned to device-based temperature control targeting 36 °C for 24 hours followed by device-based fever prevention, targeting 37 °C for either 12 or 48 hours.…”

Early warning value of urinary oxygen tension monitoring for paediatric intensive care unit sepsis-associated acute kidney injury: a retrospective study

“…The kidney receives 1/4 of the cardiac output, but the kidney itself is vulnerable to hypoxia [11,12]. Early studies suggested that the maintenance of renal function depended on renal perfusion with su cient renal blood ow, and renal underperfusion was considered the key to the occurrence of SA-AKI.…”