Perioperative Renoprotection: Clinical Implications

Khaschayar Saadat-Gilani, MD; Alexander Zarbock, MD; Melanie Meersch, MD

Disclosures

Anesth Analg. 2020;131(6):1667-1678. 

In This Article

Pathophysiology

The pathophysiology of AKI is complex and multifactorial. A mismatch of oxygen delivery and demand is mainly responsible for renal dysfunction. This insufficient delivery is usually due to impaired renal blood flow or impaired microcirculation. That way, hypoperfusion and inflammation are the 2 main factors for acute renal dysfunction.

Under normal circumstances, the kidneys have intrinsic (myogenic and juxtaglomerular feedback mechanisms) and extrinsic (sympathetic nervous system, renin–angiotensin–aldosterone system) autoregulatory properties. In the perioperative period, renal hypoperfusion occurs frequently through hypovolemia-associated reduction of mean arterial pressure (MAP). Initially, perfusion pressure and GFR can be maintained through the activation of the autoregulatory systems, especially the sympathetic nervous system, which results in the release of angiotensin II and antidiuretic hormone through renin. However, persistent hypoperfusion causes a decrease in GFR secondary to vasoconstriction of the afferent and efferent arterioles. The compensatory effects depend highly on the autoregulatory capabilities of the kidneys. For instance, in patients with chronic kidney disease, these mechanisms are altered.[37]

Systemic inflammation as second major factor for the development of AKI leads to tubular injury resulting in renal damage through microcirculatory dysfunction, leukocyte migration, and endothelial dysfunction.[38,39]

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