The effect of hemodilution during normothermic cardiac surgery on renal physiology and function: a review

Perfusion ◽  
2008 ◽  
Vol 23 (6) ◽  
pp. 329-338 ◽  
Author(s):  
H Vermeer ◽  
S Teerenstra ◽  
RGL de Sévaux ◽  
HA van Swieten ◽  
PW Weerwind

Although the definitions of renal dysfunction vary, loss of renal function is a common complication following cardiac surgery using cardiopulmonary bypass (CPB). When postoperative dialysis is required, mortality is approximately 50%. CPB-accompanied hemodilution is a major contributing factor to renal damage as it notably reduces oxygen delivery by reducing the oxygen transport capacity of the blood as well as disturbing the microcirculation. To minimize hypoxemic damage during CPB, lowering of body temperature is applied to reduce the patient’s metabolic rate. At present, however, temperature management during elective adult cardiac surgery is shifting from moderate hypothermia to normothermia. To determine whether the currently accepted levels of hemodilution during CPB can suffice the normothermic patient’s high oxygen demand, we focused this study on renal physiology and postoperative renal function. Hemodilution reduces the capillary density through a diminished capillary viscosity, thereby, redistributing blood from the renal medulla to the renal cortex. As the physiology of the renal medulla makes it a hypoxic environment, this part of the kidney appears to be especially at risk for hypoxic damage caused by a hemodilution-induced lowered oxygen transport and oxygen delivery. In addition, hemodilution is also likely to disturb the hormonal systems regulating renal blood distribution. Clinical studies, mostly of retrospective or observational nature, show that perioperative nadir hematocrit levels lower than approximately 24% are associated with an increased risk to develop postoperative renal failure. A better comprehension of the cause-and-effect relation between low perioperative hematocrits and loss of postoperative renal function may enable more effective renal protective strategies.

2018 ◽  
Vol 33 (6) ◽  
pp. 316-321 ◽  
Author(s):  
Steven C. Mitchell ◽  
Anirudh Vinnakota ◽  
Salil V. Deo ◽  
Alan H. Markowitz ◽  
Basar Sareyyupoglu ◽  
...  

2005 ◽  
Vol 53 (S 01) ◽  
Author(s):  
U Fischer ◽  
P Tossios ◽  
R Raji ◽  
K Hekmat ◽  
H Geissler ◽  
...  

2010 ◽  
Vol 5 (1) ◽  
pp. 104
Author(s):  
Daniel S Menees ◽  
Eric R Bates ◽  
◽  

Coronary artery disease (CAD) affects millions of US citizens. As the population ages, an increasing number of people with CAD are undergoing non-cardiac surgery and face significant peri-operative cardiac morbidity and mortality. Risk-prediction models can be used to help identify those patients at increased risk of peri-operative cardiovascular complications. Risk-reduction strategies utilising pharmacotherapy with beta blockade and statins have shown the most promise. Importantly, the benefit of prophylactic coronary revascularisation has not been demonstrated. The weight of evidence suggests reserving either percutaneous or surgical revascularisation in the pre-operative setting for those patients who would otherwise meet independent revascularisation criteria.


Author(s):  
John R. Prowle ◽  
Lui G. Forni ◽  
Max Bell ◽  
Michelle S. Chew ◽  
Mark Edwards ◽  
...  

AbstractPostoperative acute kidney injury (PO-AKI) is a common complication of major surgery that is strongly associated with short-term surgical complications and long-term adverse outcomes, including increased risk of chronic kidney disease, cardiovascular events and death. Risk factors for PO-AKI include older age and comorbid diseases such as chronic kidney disease and diabetes mellitus. PO-AKI is best defined as AKI occurring within 7 days of an operative intervention using the Kidney Disease Improving Global Outcomes (KDIGO) definition of AKI; however, additional prognostic information may be gained from detailed clinical assessment and other diagnostic investigations in the form of a focused kidney health assessment (KHA). Prevention of PO-AKI is largely based on identification of high baseline risk, monitoring and reduction of nephrotoxic insults, whereas treatment involves the application of a bundle of interventions to avoid secondary kidney injury and mitigate the severity of AKI. As PO-AKI is strongly associated with long-term adverse outcomes, some form of follow-up KHA is essential; however, the form and location of this will be dictated by the nature and severity of the AKI. In this Consensus Statement, we provide graded recommendations for AKI after non-cardiac surgery and highlight priorities for future research.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 839.1-839
Author(s):  
Y. J. Oh ◽  
K. W. Moon

Background:Gout is the most common inflammatory arthritis resulting from a chronic deposition of MSU crystals in the joints and other soft tissues. After the process of repeated tissue damage and repair due to gout, tophi could be formed around the affected joints. Intra-articular tophi may sometimes result in bone destruction, joint deformities, and dysfunction which can adversely affect the patient’s quality of life. Furthermore, early-onset tophaceous gout patients are more likely to develop renal dysfunction, however, few studies have investigated if the presence of tophi is related with the progression of renal dysfunction in gout patients.Objectives:We aimed to compare clinical characteristics of patients with and without tophi at the time of the diagnosis of gout and investigate the effect of tophi on the renal function in gout patients.Methods:Data of 257 patients who were first diagnosed with gout at the Kangwon National University Hospital from January 2012 to December 2018 were retrospectively studied. Patients were divided into 2 groups according to the presence of tophi at the diagnosis. We compared clinical characteristics and the progression of renal dysfunction between the two groups.Results:Of all patients, 66 (25.5%) initially presented with tophi. Patients with tophi were older, had a longer duration of symptoms, and had a higher prevalence of multiple joint involvement than those without tophi. The decline in the eGFR was more prominent in patients with tophi than in those without (-4.8±14.5 ml/min/1.73m2vs. -0.7±11.9 ml/min/1.73m2, respectively; P=0.039). In multivariate logistic regression analysis, a prolonged symptom duration (odds ratio [OR], 1.010; 95% confidence interval [CI], 1.004–1.017; P=0.001) and multiple joint involvement (OR, 3.027; 95% CI, 1.831–5.004; P<0.001) were significantly associated with increased risk of formation of tophi. The presence of tophi was significantly associated with a rapid decline in the eGFR (β=-0.141; P=0.035).Conclusion:A prolonged symptom duration and multiple joint involvement were independent risk factors for tophi as the presenting symptom in gout patients. The presence of tophi was associated with a declining renal function. Therefore, an early diagnosis and active treatment are important in tophaceous gout.References:[1]Bardin T, Richette P. Definition of hyperuricemia and gouty conditions. Curr Opin Rheumatol 2014;26:186-91.[2]Liu F, Du GL, Song N, Ma YT, Li XM, Gao XM, et al. Hyperuricemia and its association with adiposity and dyslipidemia in Northwest China: results from cardiovascular risk survey in Xinjiang (CRS 2008-2012). Lipids Health Dis 2020;19:58.[3]Dalbeth N, Merriman TR, Stamp LK. Gout. Lancet 2016;388:2039-52.[4]Ruoff G, Edwards NL. Overview of Serum Uric Acid Treatment Targets in Gout: Why Less Than 6 mg/dL? Postgrad Med 2016;128:706-15.[5]Bieber A, Schlesinger N, Fawaz A, Mader R. Chronic tophaceous gout as the first manifestation of gout in two cases and a review of the literature. Semin Arthritis Rheum 2018;47:843-8.Disclosure of Interests:None declared.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A51-A51
Author(s):  
Huan Yang ◽  
Michael Vazquez ◽  
Monika Haack ◽  
Janet Mullington

Abstract Introduction Insufficient sleep is associated with an increased risk of hypertension. It is well established that long-term BP regulation is modulated by the renin-angiotensin-aldosterone system (RAAS) and chronic kidney disease is a strong independent risk factor for development of cardiovascular disease. This study investigated the biomarkers of RAAS and renal function during repetitive exposures to controlled, experimental sleep restriction (SR). We hypothesized an upregulation of RAAS and increased markers of impaired renal function. Methods Twenty-one healthy participants (11 women, average age 31±2 years) completed the 22-day in-hospital SR protocol: permitted 4h of sleep/night from 0300-0700 for 3 nights followed by a recovery sleep, repeated 4 times. Blood samples were collected and plasma renin activity (PRA) was assessed in the morning (7:05am) and in the evening before bedtime (22:45pm) at baseline, experimental days (3rd day of each of the 4 blocks), and recovery. Urinary albumin to creatinine ratio (ACR) was measured from 24-h urinary collection at baseline, first and fourth SR blocks. Estimated glomerulus filtration rate (eGFR) was calculated based on the serum cystatin C levels at baseline and last block of SR. Results Percent change of evening PRA significantly increased during 4 blocks of SR and recovery (SR effect p=0.039), but not morning PRA (SR effect p=0.34). Specifically, evening PRA increased up to 98.4% in the first (p&lt;0.01), 61.3% in the second (p=0.04) SR blocks, and 57.5% (p=0.05) in recovery. Urinary ACR showed no significant changes during first or fourth SR blocks (SR effect p=0.28). In addition, eGFR did not change in the fourth SR block compared to BL (paired t-test, p=0.27). Conclusion We did not see increased markers of impaired renal function (ACR or eGFR). Rather, short-term repetitive exposures to SR significantly increased percent change of PRA measured before bedtime, and evening PRA did not return to BL level during recovery. Our results suggested that sleep deficiency may contribute to hypertension through upregulation of RAAS during wake time. Support (if any) SRSF (CDA to Huan Yang), NIH (R01HL106782 to Dr. Janet Mullington), Harvard Catalyst, Harvard Clinical and Translational Science Center (UL1TR001102).


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