Renal hemodynamics, function and oxygenation in critically ill patients and after major surgery

The present review outlines the available data from the work of our group on renal hemodynamics, function and oxygenation in critically ill patients with acute renal dysfunction such as in postoperative acute kidney injury, early clinical septic shock, in patients undergoing cardiac surgery with cardiopulmonary bypass or in patients undergoing liver transplantation. We also provide information on renal hemodynamics, function and oxygenation in patients with chronic renal impairment due to congestive heart failure. This review will argue that the common denominator, for these groups of patients, is that renal oxygenation is impaired in all groups caused by a lower renal oxygen delivery or a pronounced increase in renal oxygen consumption.

The Relation Of Intraoperative Renal Oxygen Saturation Change With Postoperative Acute Kidney Injury

Objective: Acute kidney injury seen in 25-30 % of the cases after open heart surgery where cardiopulmonary bypass was performed, is one of the most important factors that affect the success of the on- pump open heart surgery by increasing the rates of postoperative morbidity, and mortality. Near infrared spectroscopy (NIRS) is a noninvasive monitoring that frequently used method that allows correction of imbalances in oxygen supply to the brain and vital organs. We aimed to investigate the relationship between renal oxygen saturation values and postoperative acute kidney injury. Method: Fifty patients who underwent on- pump open heart surgery between July 2020 and January 2021 by using cardiopulmonary bypass were included in the study. Demographic data included age, gender, body mass index (BMI), hypertension, diabetes mellitus, chronic obstructive pulmonary disease, other chronic diseases and left ventricular ejection fraction. The definition of acute kidney injury was defined according to the criteria of KDIGO. At the end of the postoperative 48th hour the relationship between intraoperative renal rSO2 changes in patients with or without acute kidney injury was evaluated. Results: Fifty patients were included in the current study. The median (IQR) age of 50 patients was 62 (54.3-66.5), and mostly male patients constituted the study populatio,. When we evaluated the intraoperative data, there were statistically significant differences in changes in renal rSO2 values in patients who had and had not developed postoperative acute kidney injury (-12%, -3%, respectively) (p: 0.001). In the multivariate logistic regression analysis, the change in rSO2 values in the intraoperative period [(from - 10% to 0.5%), OR: 0.18 (0.04-0.76) p: 0.03] were found to be an independent predictor of postoperative acute kidney injury. Conclusion: We found that the decrease of renal rSO2 measurements during surgery may predict the development of acute kidney injury in the postoperative period. We think that renal oxygen saturation monitoring with NIRS is a very effective method for predicting postoperative renal dysfunction, because it is both noninvasive and reflects simultaneous data.

CONDITION OF RENAL OXYGENATION IN PRETERM INFANTS WITH HEMODINAMICALLY SIGNIFICANT PATENT DUCTUS ARTERIOSUS

The aim: To study the condition of renal oxygenation (RrSO2) and fractional tissue oxygen extraction (FTOE) in the kidneys of premature infants with HSPDA. Materials and methods: 74 preterm newborns (gestational age 29-36 weeks) were divided into three groups: І – 40 children with HSPDA, ІІ – 17 children with patent ductus arteriosus (PDA) without hemodynamic disorders, ІІІ – 17 children with closed ductus arteriosus. Renal oxygen saturation (RrSO2) was assessed during the whole day on the first, third and tenth day of life with near-infrared spectroscopy. FTOE was calculated according to the formula: FTOE = (SpO2 – RrSO2)/SpO2. Results: With HSPDA on the first and third days of life, there was a significant decrease in RrSO2 and a significant increase in FTOE by the kidney tissue in comparison with children with PDA without hemodynamic disorders and children with a closed ductus arteriosus. The results obtained can be explained by the “phenomenon of the systemic circulation stealing” and the development of hypoperfusion, ischemia of the kidney tissues, which leads to an increase in the need for oxygen in the parenchyma.On the tenth day of life, premature infants who had HSPDA on the first day showed an increase in RrSO2 and a decrease in FTOE. Conclusions: Non-invasive monitoring of renal oxygenation using can be used as a screening tool to identify the phenomenon of “ductal stealing” in HSPDA.

Global REACH 2018: renal oxygen delivery is maintained during early acclimatization to 4,330 m

Early acclimatization to high altitude is characterized by various respiratory, hematological, and cardiovascular adaptations that serve to restore oxygen delivery to tissue. However, less is understood about renal function and the role of renal oxygen delivery (RDO2) during high altitude acclimatization. We hypothesized that 1) RDO2 would be reduced after 12 h of high altitude exposure (high altitude day 1) but restored to sea level values after 1 wk (high altitude day 7) and 2) RDO2 would be associated with renal reactivity, an index of acid-base compensation at high altitude. Twenty-four healthy lowlander participants were tested at sea level (344 m, Kelowna, BC, Canada) and on day 1 and day 7 at high altitude (4,330 m, Cerro de Pasco, Peru). Cardiac output, renal blood flow, and arterial and venous blood sampling for renin-angiotensin-aldosterone system hormones and NH2-terminal pro-B-type natriuretic peptides were collected at each time point. Renal reactivity was calculated as follows: (Δarterial bicarbonate)/(Δarterial Pco2) between sea level and high altitude day 1 and sea level and high altitude day 7. The main findings were that 1) RDO2 was initially decreased at high altitude compared with sea level (ΔRDO2: −22 ± 17%, P < 0.001) but was restored to sea level values on high altitude day 7 (ΔRDO2: −6 ± 14%, P = 0.36). The observed improvements in RDO2 resulted from both changes in renal blood flow (Δ from high altitude day 1: +12 ± 11%, P = 0.008) and arterial oxygen content (Δ from high altitude day 1: +44.8 ± 17.7%, P = 0.006) and 2) renal reactivity was positively correlated with RDO2 on high altitude day 7 ( r = 0.70, P < 0.001) but not high altitude day 1 ( r = 0.26, P = 0.29). These findings characterize the temporal responses of renal function during early high altitude acclimatization and the influence of RDO2 in the regulation of acid-base balance.

Pre-treatment with the angiotensin receptor 1 blocker losartan protects renal blood flow and oxygen delivery after propofol-induced hypotension in pigs

Hypotensive events are strongly correlated to the occurrence of perioperative acute kidney injury, but the underlying mechanisms for this are not completely elucidated. We hypothesised that anaesthesia-induced hypotension causes renal vasoconstriction and decreased oxygen delivery via angiotensin II-mediated renal vasoconstriction. Pigs were anaesthetised, surgically prepared and randomised to vehicle/losartan treatment (0.15 mg*kg−1). A deliberate reduction in arterial blood pressure was caused by infusion of propofol (30 mg*kg−1) for 10 min. Renal function and haemodynamics were recorded 60 min before and after hypotension. Propofol induced hypotension in all animals (p < 0.001). Renal blood flow (RBF) and renal oxygen delivery (RDO2) decreased significantly regardless of treatment but more so in vehicle-treated compared to losartan-treated (p = 0.001, p = 0.02, respectively). During recovery RBF and RDO2 improved to a greater extent in the losartan-treated compared to vehicle-treated (+ 28 ml*min−1, 95%CI 8–50 ml*min−1, p = 0.01 and + 3.1 ml*min−1, 95%CI 0.3–5.8 ml*min−1, p = 0.03, respectively). Sixty minutes after hypotension RBF and RDO2 remained depressed in vehicle-treated, as renal vascular resistance was still increased (p < 0.001). In losartan-treated animals RBF and RDO2 had normalised. Pre-treatment with losartan improved recovery of renal blood flow and renal oxygen delivery after propofol-induced hypotension, suggesting pronounced angiotensin II-mediated renal vasoconstriction during blood pressure reductions caused by anaesthesia.

Evolution of altered tubular metabolism and mitochondrial function in sepsis-associated acute kidney injury

Sepsis-associated acute kidney injury (s-AKI) has a staggering impact in patients and lacks any treatment. Incomplete understanding of the pathogenesis of s-AKI is a major barrier to the development of effective therapies. We address the gaps in knowledge regarding renal oxygenation, tubular metabolism, and mitochondrial function in the pathogenesis of s-AKI using the cecal ligation and puncture (CLP) model in mice. At 24 h after CLP, renal oxygen delivery was reduced; however, fractional oxygen extraction was unchanged, suggesting inefficient renal oxygen utilization despite decreased glomerular filtration rate and filtered load. To investigate the underlying mechanisms, we examined temporal changes in mitochondrial function and metabolism at 4 and 24 h after CLP. At 4 h after CLP, markers of mitochondrial content and biogenesis were increased in CLP kidneys, but mitochondrial oxygen consumption rates were suppressed in proximal tubules. Interestingly, at 24 h, proximal tubular mitochondria displayed high respiratory capacity, but with decreased mitochondrial content, biogenesis, fusion, and ATP levels in CLP kidneys, suggesting decreased ATP synthesis efficiency. We further investigated metabolic reprogramming after CLP and observed reduced expression of fatty acid oxidation enzymes but increased expression of glycolytic enzymes at 24 h. However, assessment of functional glycolysis revealed lower glycolytic capacity, glycolytic reserve, and compensatory glycolysis in CLP proximal tubules, which may explain their susceptibility to injury. In conclusion, we demonstrated significant alterations in renal oxygenation, tubular mitochondrial function, and metabolic reprogramming in s-AKI, which may play an important role in the progression of injury and recovery from AKI in sepsis.