scholarly journals Kidney`s functional state assessment when using different regimens of intraoperative fluid therapy

2021 ◽  
pp. 30-33
Author(s):  
Yanina Morozova ◽  
Aleksandr Pavlov
Keyword(s):  
Renal Dysfunction ◽  
Functional State ◽  
Fluid Therapy ◽  
Kidney Injury ◽  
Perioperative Period ◽  
Renal Perfusion ◽  
High Tendency ◽  
Surgical Interventions ◽  
Therapy Regimen ◽  
Stable Coronary Heart Disease

The aim of the research. To study the kidneys functional state when using different regimens of intraoperative fluid therapy in high cardiac risk patients during abdominal surgery. Materials and methods. 142 patients who underwent abdominal surgical interventions mainly for oncoproctological diseases of the gastrointestinal tract, aged over 50 years old and with a history of stable coronary heart disease were divided into four groups depending on the way of intraoperative fluid therapy, which was performed according to two regimens: restrictive (R) and liberal (L). R1 (n=36) with rate of intraoperative fluid therapy 3–5 ml/ kg/ h, R2 (n=35) patients received 5–8 ml/kg/h during surgery, L1 (n=35) with intraoperative fluid rate of 8–11 ml/kg/h and L2 (n=36) – more than 11 ml/kg/h intraoperatively. The study of the functional state of the kidneys included the determination of such indicators as urea, creatinine, diuresis, the degree of AKI according to KDIGO in two stages of the study – before surgery and 18–24 hours after. Results. The greatest tendency to develop acute kidney injury was observed in R1 subgroup with a restrictive intraoperative fluid therapy regimen, and the smallest in L1 subgroup with a relatively liberal regimen. The R2 and L2 subgroups took an intermediate place in the number of renal complications. A high tendency to develop renal dysfunction in patients of R1 subgroup was associated with circulatory hypokinesia and a moderate decrease of renal perfusion. Conclusions. The study found that restriction of infusion in R1 subgroup contributed to the development of renal dysfunction in almost half of the patients. First of all it was associated with a decrease of GFR in conditions of circulatory hypokinesia, which is larger in R1 subgroup and amounted to about 35 %. The safest regimens of intraoperative fluid therapy in relation to renal function in the perioperative period were relatively liberal (subgroup L1) and relatively restrictive (subgroup R2), which provided the least number of complications in patients

scholarly journals Perioperative Doppler measurements of renal perfusion are associated with acute kidney injury in patients undergoing cardiac surgery

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Johan Lyngklip Hermansen ◽  
Gabriela Pettey ◽  
Heidi Tofte Sørensen ◽  
Samantha Nel ◽  
Nqoba Tsabedze ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Doppler Ultrasound ◽  
Heart Surgery ◽  
Open Heart Surgery ◽  
Kidney Injury ◽  
Perioperative Period ◽  
Renal Perfusion ◽  
Doppler Measurement ◽  
Venous Flow

AbstractAcute kidney injury (AKI) is a frequent and severe complication in cardiac surgery. Normal renal function is dependent on adequate renal perfusion, which may be altered in the perioperative period. Renal perfusion can be assessed with Doppler measurement. We aimed to determine the association between Doppler measurements of renal perfusion and the development of AKI. This was a prospective, observational study of 100 patients with ≥ one risk factor for postoperative AKI undergoing open-heart surgery. Doppler ultrasound examinations were performed before surgery and on the first and fourth postoperative day. AKI was defined according to the KDIGO criteria and subdivided into mild (KDIGO stage 1) and severe AKI (KDIGO stage 2 + 3). Thirty-three patients developed AKI, 25 developed mild and eight developed severe AKI. Abnormal renal venous flow pattern on the first postoperative day was significantly associated with the development of severe AKI (OR 8.54 (95% CI 1.01; 72.2), P = 0.046), as were portal pulsatility fraction (OR 1.07 (95% CI 1.02; 1.13), P = 0.005). Point-of-care Doppler ultrasound measurements of renal perfusion are associated with the development of AKI after cardiac surgery. Renal and portal Doppler ultrasonography can be used to identify patients at high risk or very low risk of AKI after cardiac surgery.

scholarly journals Abdominal aorta surgical intervention and acute renal injury

2020 ◽  
Vol 179 (2) ◽  
pp. 20-25
Author(s):  
N. I. Glushkov ◽  
M. A. Ivanov ◽  
K. V. Samko ◽  
P. D. Puzdriak ◽  
P. B. Bondarenko ◽  
...  
Keyword(s):  
Abdominal Aorta ◽  
Kidney Injury ◽  
Perioperative Period ◽  
Hemodynamic Instability ◽  
Arterial Disease ◽  
Surgical Interventions ◽  
Emergency Interventions ◽  
Kidney Insufficiency ◽  
Aortic Interventions ◽  
Peripheral Arterial

The OBJECTIVE of this scientific research was to study risk factors, frequency and consequences of acute kidney injury (AKI) after open surgery on the abdominal aorta.METHODS AND MATERIALS. Outcome of surgical interventions in 65 patients were analyzed. AKI was detected in 11 of them; in rest 54 cases, AKI was not registered. The features of the perioperative period, kidney injury markers (creatinine, diuresis, urine), and the comorbidity were evaluated.RESULTS. The initial changes in renal activity, the emergency of intervention, hemodynamic instability, especially after more than 1000 ml perioperative blood loss, the presence of operations for multilevel peripheral arterial disease (MPAD) negatively affected on the AKI occurrence.CONCLUSION. Post-surgical AKI after infrarenal aortic interventions were observed more often in patients with previous kidney insufficiency, as well as after emergency interventions, in cases of hemodynamic instability.

Copeptin as a novel biomarker for detecting early renal dysfunction after TAVI

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J.S Wolter ◽  
J Reifart ◽  
M Renker ◽  
S.D Kriechbaum ◽  
U Fischer-Rasokat ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Serum Creatinine ◽  
Renal Dysfunction ◽  
Venous Blood ◽  
Kidney Injury ◽  
Blood Draw ◽  
Amino Acid Peptide ◽  
Transcatheter Aortic Valve ◽  
Prolonged Hospital ◽  
Stage 1

Abstract Background Acute kidney injury (AKI) is one of the most prevalent (10–30%) complications after transcatheter aortic valve implantation (TAVI). Furthermore, AKI is accompanied by increased mortality, a higher incidence of dialysis and blood transfusion, and a prolonged hospital stay. Although measurement of serum creatinine is the gold standard in diagnosing AKI, changes in serum creatinine may lag behind compromised renal function. Arginine vasopressin (AVP), or antidiuretic hormone, is a nine-amino acid peptide member of the hypothalamo-neurohypophysial axis. Copeptin is the C-terminal moiety of the AVP precursor pre-proAVP that is secreted into the circulation. Recently, copeptin has been suggested to play a role in chronic kidney injury. We evaluated the value of copeptin in the prediction of AKI in patients undergoing TAVI. Methods All patients with severe aortic valve stenosis undergoing TAVI between May 2011 and May 2016 were included in our study. AKI was defined by the VARC-2 definition. Patients with no AKI and stage 1 AKI were compared with patients with stage 2 or 3 AKI. Routine laboratory parameters, including creatinine, were measured immediately after blood draw. Additionally, venous blood samples were collected on admission and after 24, 48, and 72 hours, processed immediately, and stored at −80°C until assay. The copeptin concentration in serum was measured by a sandwich immunoluminometric assay. Results Copeptin levels were available in 642 patients who were treated by TAVI in our centre from 2012–2016. AKI was detected in 113 patients (17.6%), including 61 patients with stage 1 (9.5%), 29 with stage 2 (4.5%), and 23 with stage 3 (3.6%). There were no differences among these patients in baseline measurements, but serum copeptin increased in all patients with AKI 24 h post-procedure according to the AKI stage: no AKI 34.5 (18.0–59.3 pmol/L), AKI stage 1: 68.7 (34.6–130.1 pmol/L); AKI stage 2: 96.0 (48.1–185.1 pmol/L); AKI stage 3: 154.9 (79.5–280.7 pmol/L); ANOVA p<0.001 (Fig. 1). Copeptin showed an earlier and sharper increase than creatinine (Fig. 1), with a negative predictive value of 0.97 to rule out AKI after 24 h. Conclusion AKI subsequent to TAVI is a common and harmful complication that occurred in almost every 5th patient (17.6%) in our cohort. AVP is secreted in response to hypotension, which commonly occurs during TAVI. In our cohort of TAVI patients, those who developed AKI after TAVI showed a rapid increase in copeptin that was earlier than that of creatinine. In light of these observations, copeptin could be a new parameter for detecting early renal dysfunction. Figure 1 Funding Acknowledgement Type of funding source: None

scholarly journals Preservation of renal endothelial integrity and reduction of renal edema by aprotinin does not preserve renal perfusion and function following experimental cardiopulmonary bypass

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Nicole A. M. Dekker ◽  
Anoek L. I. van Leeuwen ◽  
Matijs van Meurs ◽  
Jill Moser ◽  
Jeannette E. Pankras ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Renal Injury ◽  
Weight Ratio ◽  
Kidney Injury ◽  
Dry Weight ◽  
Renal Perfusion ◽  
Plasma Creatinine ◽  
Microcirculatory Perfusion ◽  
Neutrophil Influx ◽  
Endothelial Integrity

Abstract Background Acute kidney injury is a severe complication following cardiopulmonary bypass (CPB) and is associated with capillary leakage and microcirculatory perfusion disturbances. CPB-induced thrombin release results in capillary hyperpermeability via activation of protease-activated receptor 1 (PAR1). We investigated whether aprotinin, which is thought to prevent thrombin from activating PAR1, preserves renal endothelial structure, reduces renal edema and preserves renal perfusion and reduces renal injury following CPB. Methods Rats were subjected to CPB after treatment with 33.000 KIU/kg aprotinin (n = 15) or PBS (n = 15) as control. A secondary dose of 33.000 KIU/kg aprotinin was given 60 min after initiation of CPB. Cremaster and renal microcirculatory perfusion were assessed using intravital microscopy and contrast echography before CPB and 10 and 60 min after weaning from CPB. Renal edema was determined by wet/dry weight ratio and renal endothelial structure by electron microscopy. Renal PAR1 gene and protein expression and markers of renal injury were determined. Results CPB reduced cremaster microcirculatory perfusion by 2.5-fold (15 (10–16) to 6 (2–10) perfused microvessels, p < 0.0001) and renal perfusion by 1.6-fold (202 (67–599) to 129 (31–292) au/sec, p = 0.03) in control animals. Both did not restore 60 min post-CPB. This was paralleled by increased plasma creatinine (p < 0.01), neutrophil gelatinase-associated lipocalin (NGAL; p = 0.003) and kidney injury molecule-1 (KIM-1; p < 0.01). Aprotinin treatment preserved cremaster microcirculatory perfusion following CPB (12 (7–15) vs. 6 (2–10) perfused microvessels, p = 0.002), but not renal perfusion (96 (35–313) vs. 129 (31–292) au/s, p > 0.9) compared to untreated rats. Aprotinin treatment reduced endothelial gap formation (0.5 ± 0.5 vs. 3.1 ± 1.4 gaps, p < 0.0001), kidney wet/dry weight ratio (4.6 ± 0.2 vs. 4.4 ± 0.2, p = 0.046), and fluid requirements (3.9 ± 3.3 vs. 7.5 ± 3.0 ml, p = 0.006) compared to untreated rats. In addition, aprotinin treatment reduced tubulointerstitial neutrophil influx by 1.7-fold compared to untreated rats (30.7 ± 22.1 vs. 53.2 ± 17.2 neutrophil influx/section, p = 0.009). No differences were observed in renal PAR1 expression and plasma creatinine, NGAL or KIM-1 between groups. Conclusions Aprotinin did not improve renal perfusion nor reduce renal injury during the first hour following experimental CPB despite preservation of renal endothelial integrity and reduction of renal edema.

scholarly journals Restrictive versus Liberal Fluid Therapy for Post-Cesarean Acute Kidney Injury in Severe Preeclampsia: a Pilot Randomized Clinical Trial

Clinics ◽  
2020 ◽  
Vol 75 ◽  
Author(s):  
Wallace Andrino da Silva ◽  
Carlo Victor A. Varela ◽  
Aline Macedo Pinheiro ◽  
Paula Castro Scherer ◽  
Rossana P.V. Francisco ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Acute Kidney Injury ◽  
Randomized Clinical Trial ◽  
Fluid Therapy ◽  
Kidney Injury ◽  
Severe Preeclampsia

scholarly journals Impact of Cardiac Function Improvement on Cardiac Surgery Associated Acute Kidney Injury for Patients with Preoperative Renal Dysfunction

2020 ◽  
Author(s):  
Jiarui Xu ◽  
Xin Chen ◽  
Jing Lin ◽  
Yang Li ◽  
Bo Shen ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Cardiac Surgery ◽  
Cardiac Function ◽  
Renal Dysfunction ◽  
Significant Risk ◽  
Kidney Injury ◽  
Normal Function ◽  
Function Group ◽  
Postoperative Aki

Abstract Background: We aim to investigate whether the postoperative cardiac function improve or not would affect the risk of cardiac surgery associated acute kidney injury (AKI) for patients with preoperative renal dysfunction. Method: Data from patients underwent cardiac surgery from April 2012 to February 2016 were collected. Renal dysfunction was defined as preoperative SCr >1.2 mg/dL (females) or >1.5 mg/dL (males). Patients were grouped as normal renal function group, renal dysfunction with chronic kidney disease (CKD group), and non CKD group. △LVEF=postoperative LVEF - preoperative LVEF. Cardiac function improved was defined as △LVEF ≥10. Patients were further divided into non CKD & cardiac function improved (non CKD+), non CKD & cardiac function not improved (non CKD-), CKD & cardiac function improved (CKD+) and CKD & cardiac function not improved (CKD-) subgroups.Results: A total of 8,661 patients were allocated as normal renal function (n=7,903), non CKD(n = 662) and CKD (n = 136) groups. Both non CKD and CKD groups had higher AKI incidence than normal function group (39.5% vs 30.0%, P < 0.001; 61.8% vs 30.0%, P<0.001), and non CKD+ group had the similar AKI incidence with normal function group (30.9% vs 30.0%, P=0.729). Multivariate logistic regression analysis revealed that non CKD-, CKD+ and CKD- were significant risk factors, whereas non CKD+ was not a significant risk factor for postoperative AKI. The SCr at discharge in non CKD+ subgroup was significantly lower than its preoperative SCr (1.4 ± 0.8 vs 1.7 ± 0.9 mg/dL, P = 0.020).Conclusions: For renal dysfunction patients with no CKD, the risk of postoperative AKI did not exist if the cardiac function improved after surgery. For CKD patients, the risk of postoperative AKI increase regardless whether the cardiac function improved or not.

scholarly journals Perioperative evaluation of kidney function for patients with complicated forms of coronary artery disease

2020 ◽  
pp. 52-58
Author(s):  
O. Gogayeva ◽  
V. Lazoryshynets ◽  
A. Rudenko ◽  
L. Dzakhoieva ◽  
O. Yuvchyk
Keyword(s):  
Coronary Artery Disease ◽  
Acute Kidney Injury ◽  
Coronary Artery ◽  
Kidney Function ◽  
Postoperative Period ◽  
Kidney Injury ◽  
Perioperative Period ◽  
Early Postoperative Period ◽  
Chronic Obstructive ◽  
Artery Disease

The study aimed to analyze kidney function for patients with complicated forms of coronary artery disease (CAD) in the perioperative period. Methods. It was a retrospective analysis of 110 high-risk patients with complicated forms of CAD, who were operated on and discharged from the National M. Amosov Institute for the period from 2009 till 2019 years. Kidney function was evaluated by glomerular filtration rate (GFR), calculated online with СKD-EPI formula. Results. Among the included patients there were 86 (78.1%) patients with metabolic syndrome, 81 (73.59%) patients with disorders of glucose metabolism, 82 (74.5%) subjects with chronic obstructive pulmonary disease and 38 (34.5%) patients had chronic kidney disease (CKD) 3-5 stage. Preoperative risk stratification with EuroScore II scale was 9.4%. All operations performed in cardiopulmonary bypass; Custodial cardioplegia was used in 53 (48.1%) patients. The average perfusion time was 111 minutes, average cross-clamping time was 73.9 minutes. Acute kidney injury in the early postoperative period had 9 (8.1%) patients. Conclusions. At the admittance 38 (34.5%) patients with complicated forms of CAD had CKD 3-5 st. Analysis of the GFR dynamic in the early postoperative period shown a decrease in GFR in 71.05% of patients. Transient acute kidney injury with 50% sCr growth had 9 (8.1%) patients but didn’t require hemodialysis.

scholarly journals Attenuation of Circulating Trimethylamine N-Oxide Prevents the Progression of Cardiac and Renal Dysfunction in a Rat Model of Chronic Cardiorenal Syndrome

2021 ◽  
Vol 12 ◽  
Author(s):  
Deling Zou ◽  
Yanyu Li ◽  
Guangping Sun
Keyword(s):  
Gene Expression ◽  
Renal Dysfunction ◽  
Treatment Options ◽  
Elevated Serum ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Current Treatment ◽  
Sprague Dawley ◽  
Kidney Injury Molecule 1 ◽  
And Control

Chronic heart failure (HF) frequently causes progressive decline in kidney function, known as cardiorenal syndrome-2 (CRS2). Current treatment options for CRS2 remain unacceptably limited. Trimethylamine-N-oxide (TMAO), a metabolite of gut microbiota, has recently been implicated in the pathogenesis of both HF and chronic kidney disease. Here we examined whether circulating TMAO is elevated in CRS2 and if so, whether attenuation of circulating TMAO would ameliorate the progression of CRS2. Sprague-Dawley rats underwent surgery for myocardial infarction (MI) or sham (week 0) followed by subtotal (5/6) nephrectomy (STNx) or sham at week 4 to induce CRS2 or control. At week 6, MI + STNx rats and control rats received vehicle or 1.0% 3,3-Dimethyl-1-butanol (DMB, a TMAO inhibitor) treatment for 8 weeks. Compared with control rats, MI + STNx rats exhibited elevated serum TMAO at week 6, which was increased further at week 14 but was attenuated by DMB treatment. MI + STNx rats showed cardiac dysfunction as assessed by echocardiography and renal dysfunction as evidenced by increased serum creatinine and urinary kidney injury molecule-1 and decreased creatinine clearance at week 6. The cardiac and renal dysfunction in MI + STNx rats was exacerbated at week 14 but was prevented by DMB treatment. Molecular and histological studies revealed myocyte hypertrophy and increases in interstitial myocardial fibrosis and gene expression of pro-hypertrophic and pro-fibrotic markers in both heart and kidney at week 14, which were accompanied by elevated gene expression of proinflammatory cytokines. The changes in molecular and histological parameters observed in MI + STNx rats were significantly reduced by DMB treatment. These findings suggest that rats with CRS2 have elevated circulating TMAO, which is associated with the exacerbation of cardiac and renal dysfunction. Attenuation of circulating TMAO can ameliorate cardiac and renal injury and prevents the progression of CRS2.

scholarly journals Sepsis Associated Acute Kidney Injury

2021 ◽  
Author(s):  
Titik Setyawati ◽  
Ricky Aditya ◽  
Tinni Trihartini Maskoen
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Fluid Therapy ◽  
Urine Volume ◽  
Kidney Injury ◽  
Rapid Identification ◽  
Hospital Death ◽  
Cell Arrest ◽  
Sepsis And Septic Shock ◽  
Clinical Conditions

AKI is a syndrome consisting of several clinical conditions, due to sudden kidney dysfunction. Sepsis and septic shock are the causes of AKI and are known as Sepsis-Associated AKI (SA-AKI) and accounted for more than 50% of cases of AKI in the ICU, with poor prognosis. Acute Kidney Injury (AKI) is characterized by a sudden decline in kidney function for several hours/day, which results in the accumulation of creatinine, urea and other waste products. The most recent definition was formulated in the Kidney Disease consensus: Improving Global Outcome (KDIGO), published in 2012, where the AKI was established if the patient’s current clinical manifestation met several criteria: an increase in serum creatinine levels ≥0.3 mg/dL (26.5 μmol/L) within 48 hours, an increase in serum creatinine for at least 1.5 times the baseline value within the previous 7 days; or urine volume ≤ 0.5 ml/kg body weight for 6 hours. The AKI pathophysiology includes ischemic vasodilation, endothelial leakage, necrosis in nephrons and microtrombus in capillaries. The management of sepsis associated with AKI consisted of fluid therapy, vasopressors, antibiotics and nephrotoxic substances, Renal Replacement Therapy (RRT) and diuretics. In the analysis of the BEST Kidney trial subgroup, the likelihood of hospital death was 50% higher in AKI sepsis compared to non-sepsis AKI. Understanding of sepsis and endotoxins that can cause SA-AKI is not yet fully known. Some evidence suggests that renal microcirculation hypoperfusion, lack of energy for cells, mitochondrial dysfunction, endothelial injury and cycle cell arrest can cause SA-AKI. Rapid identification of SA-AKI events, antibiotics and appropriate fluid therapy are crucial in the management of SA-AKI.

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