Albuminuria and Renal Pathology in Right Heart Failure: Congestive Kidney?
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ABSTRACT:
SUBMITTER: Terashita M
PROVIDER: S-EPMC8897300 | biostudies-literature | 2022 Mar
REPOSITORIES: biostudies-literature
Publications
Albuminuria and Renal Pathology in Right Heart Failure: Congestive Kidney?
Terashita Maho M Taki Yasuhiro Y Sumi Hirofumi H Sugaya Takeshi T Koike Junki J Kamijo-Ikemori Atsuko A Shibagaki Yugo Y Tominaga Naoto N
Kidney international reports 20220112 3
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Project description:Congestive heart failure was done by artificial myocardial infarction. After extracting total RNA from control and infarcted ventricles with Triazol, messenger RNA was isolated with Qiagen mRNA isolation kit. About 1.5ug poly A+ RNA was taken for probe preparation. Probe was labeled with Alexa Fluor 546 and 657. Labeled probes were hybridized with Qiagen rat unigene oligo library. After 2 low and 1 high stringency washes Prolong Antifade was added to the slides to prevent bleaching effect. The data ratio was normalized using a location and intensity dependent Lowess formula. Keywords: other
2003-09-08 | GSE632 | GEO
Project description:Canine tachycardia-induced cardiomyopathy caused by several weeks of rapid ventricular pacing is a well-established animal model of congestive heart failure. However, little is known about the underlying changes in gene expression that occur in the canine myocardium after the induction of heart failure. This project aims to compare expression profiles in left ventricular free wall samples from control dogs and dogs with pacing-induced heart failure on the custom MuscleChip. Keywords: other
2003-07-16 | GSE472 | GEO
Project description:Congestive heart failure was done by artificial myocardial infarction. After extracting total RNA from control and infarcted ventricles with Triazol, messenger RNA was isolated with Qiagen mRNA isolation kit. About 1.5ug poly A+ RNA was taken for probe preparation. Probe was labeled with Alexa Fluor 546 and 657. Labeled probes were hybridized with Qiagen rat unigene oligo library. After 2 low and 1 high stringency washes Prolong Antifade was added to the slides to prevent bleaching effect. The data ratio was normalized using a location and intensity dependent Lowess formula.
2010-06-05 | E-GEOD-632 | biostudies-arrayexpress
Project description: Not available
| S-EPMC5864775 | biostudies-literature
Project description:We investigated 180 consecutive patients with congestive heart failure (CHF), of whom 83 had type 2 diabetes (T2DM) and 97 did not have diabetes as well as 223 controls without CHF, of whom 39 had T2DM and 184 did not have diabetes. Data was recorded by standardized interviews and by standardized examination protocols at our institution and were extracted from medical records. Here, we analyzed data on gender differences. Further, we examined the effect of CHF and T2DM on moderate albuminuria, i.e. on an albumin-creatinine ratio (ACR) of 30-300 mg/g. Table 1 shows baseline characteristics of our patients stratified by gender. Table 2 gives ACRs and prevalence rates of albuminuria separately for men and women. In logistic regression analyses adjusting for age, sex, body mass index, LDL cholesterol, history of smoking, history of hypertension, use of statins, ACE inhibitors/angiotensin II receptor blockers, aldosterone antagonists and other antihypertensive medication CHF and T2DM predicted the prevalence of albuminuria in a mutually independent manner in men (OR 4.93 [95% CI 1.76-13.85]; p = 0.002 and OR 2.38 [1.11-5.11]; p = 0.027, respectively), as well as in women (OR 5.66 [95% CI 1.76-18.20]; p = 0.004 and OR 3.53 [1.38-9.08]; p = 0.009, respectively). There was no significant interaction between gender and CHF or T2DM regarding the presence of albuminuria (p = 0.933 and 0.533, respectively), indicating that the association of CHF and T2DM with albuminuria did not differ significantly between men and women. In multivariate analysis of covariance, CHF and T2DM proved to be independent predictors of ACR in women after adjustment for age, sex, body mass index, LDL cholesterol, history of smoking, history of hypertension, use of statins, ACE inhibitors/angiotensin II receptor blockers, aldosterone antagonists and other antihypertensive medication (F = 5.38; p = 0.022 and F = 4.95; p = 0.028, respectively); for men the corresponding F-values were 2.70; p = 0.102 and 3.12; p = 0.079, respectively. There was no significant interaction between gender and CHF or T2DM regarding ACR (p = 0.464 and 0.202, respectively), indicating that the association of CHF and T2DM with the ACR did not differ significantly between men and women. Regarding moderate albuminuria, both CHF and T2DM predicted moderate albuminuria adjusted in a mutually independent manner after the adjustments described above, with ORs of 4.75 [95% CI 2.16-10.45]; p< 0.001 and OR 2.08 [1.13-3.83]; p=0.018, respectively. The data set presented here could be reused with similar patient cohorts for pooled analysis.
| S-EPMC8762350 | biostudies-literature
Project description:BackgroundPreoperative kidney dysfunction is a risk factor for right heart failure (RHF) after implantation of a left ventricular assist device (LVAD). However, characteristic kidney function trajectories before and after post-LVAD RHF are uncertain, so we investigated this.Methods and resultsWe identified individuals who received primary continuous-flow LVAD implantation from July 1, 2014 to December 31, 2017 in the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) data set. Incident RHF was ascertained using the INTERMACS definition at 1 and 3 months and classified as transient or persistent. Kidney function trajectories before and after RHF onset, and relationships of baseline kidney function with RHF risk at the different time points, were assessed. We identified 8076 LVAD recipients who met inclusion criteria. Incident RHF was present at 1 month in 26.4%. There were 4850 individuals with follow-up at 3 months, with incident RHF in 4.2%. Kidney function trajectories differed from pre-LVAD implantation to 1-month follow-up by RHF category, with those developing persistent RHF having no improvement in baseline kidney function. For trajectories before the 3-month RHF ascertainment time, the shape was similar for those with and without RHF, with lower estimated glomerular filtration rate levels among those who developed RHF. Baseline estimated glomerular filtration rate levels below the normal range were associated with higher risk of RHF at 1 and 3 months.ConclusionsIn LVAD recipients, preimplantation kidney function and subsequent kidney function trajectories differed substantially by RHF at 1 and 3 months postimplantation, even after adjustment for several confounders. This may demonstrate bidirectional associations between kidney function and right ventricular function in LVAD recipients.
| S-EPMC10944080 | biostudies-literature
Project description:This study investigated histopathological changes and apoptotic factors that may be involved in the renal damage caused by congestive heart failure in a rat model of infrarenal aortocaval fistula (ACF).Heart failure was induced using a modified approach of ACF in male Wistar rats. Sham-operated controls and ACF rats were characterized by their morphometric and hemodynamic parameters and investigated for their histopathological, ultrastructural, and apoptotic factor changes in the kidney.ACF-induced heart failure is associated with histopathological signs of congestion and glomerular and tubular atrophy, as well as nuclear and cellular degeneration in the kidney. In parallel, overexpression of proapoptotic Bax protein, release of cytochrome C from the outer mitochondrial membrane into cell cytoplasm, and nuclear transfer of activated caspase 3 indicate apoptotic events. This was confirmed by electron microscopic findings of apoptotic signs in the kidney such as swollen mitochondria and degenerated nuclei in renal tubular cells.This study provides morphological evidence of renal injury during heart failure which may be due to caspase-mediated apoptosis via overexpression of proapoptotic Bax protein, subsequent mitochondrial cytochrome C release, and final nuclear transfer of activated caspase 3, supporting the notion of a cardiorenal syndrome.
| S-EPMC5555028 | biostudies-other
Project description: Not available
| S-EPMC10787441 | biostudies-literature
Project description:BackgroundIn patients with refractory heart failure (HF) peritoneal dialysis (PD) is associated with improved functional status and decrease in hospitalization. However, previous studies did not focus on right ventricular dysfunction as an important pathophysiologic component of cardiorenal syndrome.MethodsIn a prospective cohort study PD was started in 40 patients with refractory right HF (with/without left HF). Refractoriness to conservative therapy was defined as persistent right heart congestion/ascites with intensified diuretic treatment and/or ≥2 hospitalizations within 6 months because of cardiac decompensation despite optimal medical treatment, and/or acute renal failure during intensified conservative treatment of cardiac decompensations.ResultsPatient survival was 55.0% at 1 year, 35.0% at 2 years and 27.5% at 3 years. The number of hospitalization days declined after initiation of PD for both cardiac [13 (IQR 1-53) days before vs. 1 (IQR 0-12) days after start of PD, p<0.001] and unplanned reasons [12 (IQR 3-44) days before vs. 1 (IQR 0-33) days after start of PD, p = 0.007]. Using a combined endpoint including survival time of ≥1 year and either improvement in quality of life or decline in hospitalizations we found that patients with extended ascites, higher systolic pulmonary artery pressure, more marked impairment of right ventricular function and tricuspid valve insufficiency, higher residual renal function as well as those who could perform PD without assistance have benefited most from this therapy.ConclusionsPatients with more pronounced backward failure, less marked residual renal functional impairment and those not depending on assistance for therapy are likely to profit most from PD.
| S-EPMC6242305 | biostudies-literature
Project description:Congestive heart failure is a major cause of morbidity and mortality with increasing social and economic costs. There have been no new high impact therapeutic agents for this devastating disease for more than a decade. However, many pivotal regulators of cardiac function have been identified using cardiac-directed transgene expression and gene deletion in preclinical studies. Some of these increase function of the failing heart. Altering the expression of these pivotal regulators using gene transfer is now either being tested in clinical gene transfer trials, or soon will be. In this review, we summarize recent progress in cardiac gene transfer for clinical congestive heart failure.
| S-EPMC3602385 | biostudies-literature