What Is the Best Means of Preventing Perioperative Renal Injury?

INTRODUCTION

Perioperative acute kidney injury (AKI) is defined as a new onset of AKI within 7 days after surgery according to the Kidney Diseases: Improving Global Outcomes (KDIGO) criteria. It is associated with substantial short- and long-term complications, including, but not limited to, an increased risk for dying, a longer hospital stay, progression to chronic kidney disease (CKD), and considerably increased health care costs. Like all types of AKI, perioperative AKI represents a clinical syndrome rather than a single disease. The risk depends on acute and chronic comorbidities, urgency and type of surgery, and anesthetic-related factors.

PATHOGENESIS

In health, the kidneys receive 20% of the cardiac output. Renal blood flow is tightly maintained throughout a wide range of perfusion pressures via complex interactions between the sympathetic nervous system, vasodilators (i.e., nitric oxide, prostaglandin E2), and vasoconstrictors, such as endothelin, angiotensin II, and adenosine. During surgery, the kidneys are particularly vulnerable through exposure to a variety of insults, and the majority of perioperative AKI is multifactorial in cause.

Hemodynamic Instability

Intraoperative hypotension is a risk factor for postoperative AKI. In a large retrospective analysis of more than 30,000 noncardiac surgeries, intraoperative hypotension (defined as a mean arterial pressure [MAP] <55 mm Hg) was an independent risk factor for AKI. The risk increased with duration of hypotension and was significant for episodes as short as 1 to 5 minutes. A separate analysis of 57,000 patients showed that even brief periods of a MAP less than 65 mm Hg for a few minutes increased the risk for AKI. Certain types of surgery are particularly associated with renal hypoperfusion, such as vascular surgery procedures. ^, Similarly, in the setting of cardiac surgery, nonpulsatile flow during cardiopulmonary bypass (CPB) and hemodilution may contribute to AKI, together with systemic inflammation and release of free hemoglobin.

Microcirculatory Dysfunction

The intrarenal microcirculation is essential to kidney function. Microcirculatory dysfunction, as often seen in sepsis, results in heterogeneous flow and may lead to patchy areas of hypoperfusion next to regions with preserved tissue oxygenation. These alterations of microcirculatory flow can develop even when systemic hemodynamics appear adequate.

Tubular Cell Injury

Tubular cells are very vulnerable to hypoperfusion. By nature, they also are at the frontline of filtered substances, including drug metabolites and inflammatory mediators. For instance, during cardiac surgery with CPB, free hemoglobin may be released and cause tubular damage through direct toxicity and through intratubular crystal formation.

Renal Venous Congestion

Kidneys are encapsulated organs. Elevated central venous pressure and the resultant increased pressure along the renal vascular tree can lead to renal congestion with compression of tubules and reduction in glomerular filtration rate. Most evidence stems from patients with congestive heart failure, but clamping of the renal vein has also been shown to cause kidney injury.

Intraabdominal Hypertension

Although a transient increase of intraabdominal pressure during laparoscopic surgery with a reduction of urinary output is not predictive for postoperative AKI, longer periods of elevated intraabdominal pressure can cause compression of the renal vasculature and subsequent AKI.

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