Myocardial stunning occurs during intermittent haemodialysis for acute kidney injury.
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ABSTRACT:
SUBMITTER: Mahmoud H
PROVIDER: S-EPMC5487536 | biostudies-literature | 2017 Jun
REPOSITORIES: biostudies-literature
Publications
Myocardial stunning occurs during intermittent haemodialysis for acute kidney injury.
Mahmoud Huda H Forni Lui G LG McIntyre Christopher W CW Selby Nicholas M NM
Intensive care medicine 20170328 6
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Project description:The largest study on cyclophosphamide pharmacokinetics in dialysis patients comprises of 6 subjects. In the 2 decades since these data were obtained, dialyser membranes, treatment intensities, and treatment duration have changed considerably making new pharmacokinetic studies desirable. We aimed to readdress the pharmacokinetics of cyclophosphamide in a 74-year-old critically ill male suffering from ANCA-associated vasculitis. Due to an acute-on-chronic kidney injury, he underwent intermittent (IHD) and prolonged intermittent kidney replacement therapy (PIKRT). IHD was started 7 h after end of a cyclophosphamide infusion with a blood/dialysate flow of 300 mL/min for 255 min, followed by PIKRT with a blood/dialysate flow of 140 mL/min for 540 min, both using a 1.3 m2 polysulphone high-flux dialyser (F60S, Fresenius Medical Care). Peak concentration of cyclophosphamide was 20.2 mg/L. Using IHD and PIKRT serum concentration of cyclophosphamide decreased to 1.2 mg/L after IHD and to <0.1 mg/L after PIKRT with dialyser-clearances of 153.0 mL/min and 84.9 mL/min, respectively. Total recovery of cyclophosphamide, calculated from the collected dialysate, was 57.5 mg (7.7% of administered dose) for IHD and was 8.3 mg (1.1% of administered dose) for PIKRT. By using IHD with a high-flux dialyser cyclophosphamide could be eliminated. Remaining cyclophosphamide should be eliminated by PIKRT. Hence, even in the absence of renal function a dose >50% of the recommended for patient with normal renal function may be applied, as complete elimination of the parent drug by modern dialysis is feasible.
| S-EPMC10359690 | biostudies-literature
Project description:BackgroundCardiovascular risk is elevated in end-stage renal disease. Left ventricular (LV) dysfunction is linked to repetitive transient ischaemia occurring during haemodialysis (HD). Cardiomyocyte ischaemia results in 'cardiac stunning', evidenced by regional wall motion abnormalities (RWMAs). Ischaemic RWMA have been documented during HD resulting in maladaptive cardiac remodelling and increased risk of heart failure. Intra-dialytic exercise is well tolerated and can improve quality of life and functional capacity. It may also attenuate HD-induced cardiac stunning.MethodsThis exploratory study aimed to assess the effect of intra-dialytic cycle ergometry on cardiac stunning. Twenty exercise-naïve participants on maintenance HD (mean ± SD, 59 ± 11 years) underwent resting echocardiography and maximal cardiopulmonary exercise testing. Subsequently, cardiac stunning was assessed with myocardial strain-derived RWMAs at four time points during (i) standard HD and (ii) HD with 30 min of sub-maximal intra-dialytic cycle ergometry at a workload equivalent to 90% oxygen uptake at the anaerobic threshold (VO2AT). Central haemodynamics and cardiac troponin I were also assessed.ResultsCompared with HD alone, HD with intra-dialytic exercise significantly reduced RWMAs after 2.5 h of HD (total 110 ± 4, mean 7 ± 4 segments versus total 77 ± 3, mean 5 ± 3, respectively; P = 0.008). Global cardiac function, intra-dialytic haemodynamics and LV volumetric parameters were not significantly altered with exercise.ConclusionsIntra-dialytic exercise reduced cardiac stunning. Thirty minutes of sub-maximal exercise at 90% VO2AT was sufficient to elicit acute cardio-protection. These data potentially demonstrate a novel therapeutic effect of intra-dialytic exercise.
| S-EPMC8087145 | biostudies-literature
Project description:AimIntradialytic hypotension often complicates haemodialysis for patients with acute kidney injury (AKI) and may impact renal recovery. Sodium modelling is sometimes used as prophylaxis against intradialytic hypotension in the chronic haemodialysis population, but there is little evidence for its use among critically ill patients with AKI.MethodsA retrospective cohort with AKI requiring intermittent haemodialysis in the intensive care unit from 2001 to 2008 was used to study the association of prophylactic sodium modelling and multiple outcomes. Outcomes included a composite of in-hospital death or dialysis dependence at hospital discharge, as well as intradialytic hypotension, ultrafiltration goal achievement and net ultrafiltration volume. Associations were estimated using logistic regression, mixed linear models and generalized estimating equations adjusting for demographic and clinical characteristics.ResultsOne hundred and ninety-one individuals who underwent 892 sessions were identified; sodium modelling was prescribed in 27.1% of the sessions. In adjusted analyses, sodium modelling was not significantly associated with intradialytic hypotension (P = 0.67) or with the ultrafiltration goal achievement (P = 0.06). Sodium modelling during the first dialysis session was numerically associated with lower risk for the composite of in-hospital death or dialysis dependence: adjusted odds ratio (95% confidence interval) 0.39 (0.15-1.02; P = 0.06); however, this association did not reach statistical significance.ConclusionWe did not observe statistically significant associations between sodium modelling and improved outcomes among AKI patients receiving intermittent dialysis in the intensive care unit. However, suggestive findings warrant further study.
| S-EPMC4875881 | biostudies-literature
Project description:Mitochondrial malfunction leads to the remodeling of myocardial energy metabolism during myocardial ischemia (MI). However, the alterations to the mitochondrial proteome profile during this period has not yet been clarified. An acute MI model was established by high position ligation of the left anterior descending artery in 8-week-old C57BL/6N mice. After 15 min of ligation, the animals were euthanized, and their hearts were collected. The myocardial ultrastructure was observed using transmission electron microscopy (TEM). The cardiac mitochondrial proteome profile was analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) and bioinformatics analyses. TEM showed that the outer membrane of the mitochondria was dissolved, and the inner membrane (cristae) was corrupted and broken down extensively in the MI group. The mitochondrial membrane potential was decreased. More than 1,700 mitochondrial proteins were identified by LC-MS/MS analysis, and 119 were differentially expressed. Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes functional enrichment analysis showed that endopeptidase activity regulation, the mitochondrial inner membrane, oxidative phosphorylation, the hypoxia-inducible factor-1 signaling pathway, the pentose phosphate pathway and the peroxisome proliferator-activated receptor signaling pathway were involved in the pathophysiological process in the early stage of acute MI. Extensive and substantial changes in the mitochondrial proteins as well as mitochondrial microstructural damage occur in the early stages of acute MI. In the present study, the series of proteins crucially involved in the pathways of mitochondrial dysfunction and metabolism were identified. Further studies are needed to clarify the roles of these proteins in myocardial metabolism remodeling during acute MI injury.
| S-EPMC8688935 | biostudies-literature
Project description:The incidence of premature myocardial infarction (PMI) has been rising and acute kidney injury (AKI) occurring in PMI patients severely impacts prognosis. This study aimed to develop and validate a prediction model for AKI specific to PMI patients. The MIMIC-Ⅲ-CV and MIMIC-Ⅳ databases were utilized for model derivation of PMI patients. Single-center data served for external validation. There were 571 and 182 AKI patients in the training set (n = 937) and external validation set (n = 292) cohorts, respectively. Finally, a 7-variable model consisting of: Sequential Organ Failure Assessment (SOFA) score, coronary artery bypass grafting (CABG), ICU stay time, loop diuretics, estimated glomerular filtration rate (eGFR) HCO3- and Albumin was developed, achieving an AUC of 0.85 (95% CI: 0.83-0.88) in the training set. External validation also confirmed model robustness. This model may assist clinicians in the early identification of patients at elevated risk for PMI. Further validation is warranted before clinical application.
| S-EPMC10882170 | biostudies-literature
Project description:Pregnancy-related acute kidney injury (AKI) is a public health problem and remains an important cause of maternal and fetal morbidity and mortality. The incidence of pregnancy-related AKI has increased in developed countries due to increase in maternal age and higher detection rates. Pregnancy in women with kidney transplants is associated with higher adverse outcomes like preeclampsia, preterm births, and allograft dysfunction, but limited data exists on causes and outcomes of pregnancy-related AKI in the kidney transplant population. Diagnosis of AKI during pregnancy remains challenging in kidney transplant recipients due to lack of diagnostic criteria. Management of pregnancy-related AKI in the kidney transplant population requires a multidisciplinary team consisting of transplant nephrologists, high-risk obstetricians, and neonatologists. In this review, we discuss pregnancy-related AKI in women with kidney transplants, etiologies, pregnancy outcomes, and management strategies.
| S-EPMC9285565 | biostudies-literature
Project description: Not available
| S-EPMC4320982 | biostudies-literature
Project description:Acute kidney injury (AKI) predicts poor prognosis in patients with acute myocardial infarction (MI) and diabetes mellitus (DM) is an independent risk factor of AKI. Recent clinical studies have shown the beneficial effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors on cardiovascular and renal outcomes in patients with DM. We recently reported that canagliflozin normalized susceptibility of diabetic rats to AKI after acute MI via ?-hydroxybutyrate-mediated suppression of NOX expression. Here we examined whether the same renoprotective effect is shared by empagliflozin. Serum creatinine levels were not changed by MI induced by coronary artery occlusion in LETO, non-diabetic control rats, and OLETF, obese type 2 diabetic rats. However, immunohistochemistry revealed that MI increased renal expression of NGAL and KIM-1, early markers of tubular injury, by 3.2-fold and 2.6-fold, respectively, in OLETF. These increases in injury markers were not observed in LETO. Pretreatment with empagliflozin of OLETF for 2 weeks improved hyperglycemia, increased blood ?-hydroxybutyrate level, and suppressed MI-induced expression of NGAL and KIM-1. Empagliflozin suppressed upregulation of NOX2 and NOX4 in the kidney of OLETF. Taken together with the results of our previous study, it was concluded that treatment with the SGLT2 inhibitor protects the diabetic kidney from MI-induced AKI.
| S-EPMC7190820 | biostudies-literature
Project description:BackgroundGalectin-3, a biomarker of inflammation and fibrosis, can be associated with renal and myocardial damage and dysfunction in patients with acute heart failure (AHF).Methods and resultsWe retrospectively analyzed 790 patients with AHF who were enrolled in the AKINESIS study. During hospitalization, patients with galectin-3 elevation (> 25.9 ng/mL) on admission more commonly had acute kidney injury (assessed by KDIGO criteria), renal tubular damage (peak urine neutrophil gelatinase-associated lipocalin [uNGAL] > 150 ng/dL) and myocardial injury (≥ 20% increase in the peak high-sensitivity cardiac troponin I [hs-cTnI] values compared to admission). They less commonly had ≥ 30% reduction in B-type natriuretic peptide from admission to last measured value. In multivariable linear regression analysis, galectin-3 was negatively associated with estimated glomerular filtration rate and positively associated with uNGAL and hs-cTnI. Higher galectin-3 was associated with renal replacement therapy, inotrope use and mortality during hospitalization. In univariable Cox regression analysis, higher galectin-3 was associated with increased risk for the composite of death or rehospitalization due to HF and death alone at 1 year. After multivariable adjustment, higher galectin-3 levels were associated only with death.ConclusionsIn patients with AHF, higher galectin-3 values were associated with renal dysfunction, renal tubular damage and myocardial injury, and they predicted worse outcomes.
| S-EPMC11427130 | biostudies-literature
Project description:IntroductionIntensive care participants that need dialysis frequently suffer from increased risk of bleeding. Standard intermittent haemodialysis (SHD) includes anticoagulation to avoid clotting of the dialysis system. The aim of this study was to clarify which of four different low-dose anticoagulant modes was preferable in reducing the exposure to i.v. unfractionated heparin (heparin) and maintaining patency of the dialysis circuit.MethodsTwenty-three patients on SHD were included to perform haemodialysis with four modes of low-dose anticoagulation. For comparative analyses, patients served as their own control. Haemodialysis with a single bolus of tinzaparin at the start was compared to haemodialysis initiated without i.v. heparin but priming with (1) heparin in saline (H), (2) heparin and albumin in saline (HA), (3) heparin and albumin in combination with a citrate-containing dialysate (HAC), (4) saline and usinga heparin-coated filters (Evodial®). The priming fluid was discarded before dialysis started. Blood samples were collected at 0, 30 and 180 min during haemodialysis. Smaller bolus doses of heparin (500 Units/dose) were allowed during the modes to avoid interruption by clotting.FindingsThe mean activated partial thromboplastin (APTT) time as well as the doses of anticoagulation administered was highest with SHD and least with HAC and Evodial®. Mode H versus SHD had the highest rate of prematurely interrupted dialyses (33%, p = 0.008). The urea reduction rate was less with Evodial® vs. SHD (p < 0.01). One hypersensitivity reaction occurred with Evodial®. Changes in blood cell concentrations and triglycerides differed between the modes.DiscussionIf intermittent haemodialysis is necessary in patients at risk of bleeding, anticoagulation using HAC and Evodial® appeared most preferable with least administration of heparin, lowest APTT increase and lowest risk for prematurely clotted dialyzers in contrast to the least plausible H mode.
| S-EPMC5808085 | biostudies-literature