Abstract

IntroductionAcute kidney injury (AKI), which is a major complication after cardiovascular surgery, is associated with significant morbidity and mortality. Diuretic agents are frequently used to improve urine output and to facilitate fluid management in these patients. Mannitol, an osmotic diuretic, is used in the perioperative setting in the belief that it exerts reno-protective properties. In a recent study on uncomplicated postcardiac-surgery patients with normal renal function, mannitol increased glomerular filtration rate (GFR), possibly by a deswelling effect on tubular cells. Furthermore, experimental studies have previously shown that renal ischemia causes an endothelial cell injury and dysfunction followed by endothelial cell edema. We studied the effects of mannitol on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2), and extraction (RO2Ex) in early, ischemic AKI after cardiac surgery.MethodsEleven patients with AKI were studied during propofol sedation and mechanical ventilation 2 to 6 days after complicated cardiac surgery. All patients had severe heart failure treated with one (100%) or two (73%) inotropic agents and intraaortic balloon pump (36%). Systemic hemodynamics were measured with a pulmonary artery catheter. RBF and renal filtration fraction (FF) were measured by the renal vein thermo-dilution technique and by renal extraction of chromium-51-ethylenediaminetetraacetic acid (51Cr-EDTA), respectively. GFR was calculated as the product of FF and renal plasma flow RBF × (1-hematocrit). RVO2 and RO2Ex were calculated from arterial and renal vein blood samples according to standard formulae. After control measurements, a bolus dose of mannitol, 225 mg/kg, was given, followed by an infusion at a rate of 75 mg/kg/h for two 30-minute periods.ResultsMannitol did not affect cardiac index or cardiac filling pressures. Mannitol increased urine flow by 61% (P < 0.001). This was accompanied by a 12% increase in RBF (P < 0.05) and a 13% decrease in renal vascular resistance (P < 0.05). Mannitol increased the RBF/cardiac output (CO) relation (P = 0.040). Mannitol caused no significant changes in RO2Ext or renal FF.ConclusionsMannitol treatment of postoperative AKI induces a renal vasodilation and redistributes systemic blood flow to the kidneys. Mannitol does not affect filtration fraction or renal oxygenation, suggestive of balanced increases in perfusion/filtration and oxygen demand/supply.

Highlights

  • Acute kidney injury (AKI), which is a major complication after cardiovascular surgery, is associated with significant morbidity and mortality

  • To evaluate in more detail the potential beneficial effects of mannitol for treatment of AKI in the perioperative setting, our aim was to evaluate the effects of mannitol on glomerular filtration rate (GFR), renal blood flow (RBF), renal oxygen consumption (RVO2), and the renal oxygen supply/ demand relation in patients with early, ischemic AKI after complicated cardiac surgery

  • In our previous study in postoperative uncomplicated cardiac patients with normal renal function, by using an identical protocol, we found that mannitol did not affect RBF [22], suggesting that mannitol-induced plasma volume expansion and the consequent cardiac release of renal vasodilatory cardiac peptides is not the main mechanism behind the renal vasodilation, as demonstrated in the present study

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Summary

Introduction

Acute kidney injury (AKI), which is a major complication after cardiovascular surgery, is associated with significant morbidity and mortality. In a recent study on uncomplicated postcardiac-surgery patients with normal renal function, mannitol increased glomerular filtration rate (GFR), possibly by a deswelling effect on tubular cells. We studied the effects of mannitol on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2), and extraction (RO2Ex) in early, ischemic AKI after cardiac surgery. Acute kidney injury (AKI) complicates 15% to 30% of cardiac surgeries and is associated with significant morbidity and mortality [1,2,3,4]. It has been suggested that renal vasoconstriction in AKI is caused by afferent arteriolar vasoconstriction mediated by the tubuloglomerular feedback mechanism, vasoconstrictors (catecholamines, angiotensin II, endothelin), and outer medullary congestion. It would be logical that interventions that alleviate this afferent arteriolar vasoconstriction would be beneficial, as they could potentially increase RBF and GFR

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