Cardiorenal Medicine最新文献

Introduction: Renal artery stenosis (RAS) is associated with poor outcome in patients with ischemic heart disease. In this study, we investigated the development of coronary collateral in RAS patients and possible association of RAS with a 5-year outcome after chronic total occlusion-percutaneous coronary intervention (CTO PCI).

Methods: Consecutive 58 patients with CTO PCI were enrolled prospectively, including 21 RAS patients (15 unilateral RAS and 6 bilateral RAS) and 37 non-RAS patients. RAS was diagnosed by renal duplex. Coronary collaterals were appraised by CC classification and Rentrop classification.

Results: Development of left anterior descending artery coronary collateral by Rentrop classification was significantly worse in RAS patients than non-RAS patients. Kaplan-Meier curve of survival was significantly worse in RAS patients than non-RAS patients (p = 0.027). By univariate COX proportional hazard regression analysis, collateral development by CC classification was a significant predictor for 5-year survival. When age, RAS, and collateral development by CC classification were included in multivariate COX proportional hazard regression analysis, only age (hazard ratio: 1.349; 95% confidential interval: 1.058-1.720; p = 0.016) and RAS (hazard ratio: 6.680; 95% confidential interval: 1.322-33.747; p = 0.022) were significant predictors for 5-year survival.

Discussion/conclusion: We concluded that survival in RAS patients after CTO PCI is significantly worse than non-RAS patients, and RAS is a significant predictor for survival after CTO PCI. It seems that injured collateral development might partly explain increased all cause death in RAS patients.

Introduction: The dose-response relationship between serum magnesium (sMg) and atrial fibrillation (AF) and the contribution of dysmagnesemia to AF among hemodialysis patients remain unknown. Hence, we examined the dose-response correlation between sMg and AF and estimated the extent of the contribution of dysmagnesemia to AF in this population.

Methods: This was a nationwide cross-sectional study on the Japanese Society for Dialysis Therapy registry, also known as Japanese Renal Data Registry (JRDR), encompassing a nationwide population of dialysis centers, as of the end of 2019. Eligible participants were adult patients undergoing hemodialysis three times per week. The main exposure was sMg, categorized into seven categories (≤1.5, >1.5-≤2, >2-≤2.5, >2.5-≤3, >3-≤3.5, >3.5-≤4, and ≥4.0 mg/dL). The outcome was AF reported by dialysis facilities. The independent contribution to AF was assessed via logistic regression to generate population-attributable fractions, assuming a causal relationship between sMg and AF.

Results: Total 165,926 patients from 2,549 facilities were investigated. AF prevalence was 7.9%. Compared with the reference (>2.5-≤3 mg/dL), lower sMg was associated with increased AF (adjusted odds ratios (ORs) (95% confidence interval, CI) of 1.49 (1.19-1.85), 1.24 (1.17-1.32), and 1.11 (1.06-1.16) for sMg of ≤1.5, >1.5-≤2.0, and >2.0-≤2.5 mg/dL categories, respectively). Elevated sMg was associated with fewer AF (adjusted OR 0.87 [95% CI, 0.79-0.96] for sMg of >3.0-≤3.5 mg/dL). The adjusted population-attributable fraction of lower sMg and higher and lower sMg for AF was 7.4% and 6.9%, respectively. An association did indeed exist between lower sMg and AF, with the lowest percentages of AF at sMg levels above the reference range for the general population.

Conclusion: Dysmagnesemia may be an important contributor to AF among adult hemodialysis patients. Further, longitudinal studies are warranted to determine whether sMg correction reduces the AF incidence.

Introduction: The presence of acute kidney injury (AKI) was shown to increase the risk of mortality following acute myocardial infarction; however, data regarding the prognostic impact of early AKI in patients with concomitant cardiogenic shock (CS) is limited. The study investigates predictors and the prognostic impact of AKI in patients with CS.

Methods: Consecutive patients with CS from 2019 to 2021 were included at one institution. Laboratory values were retrieved from day of disease onset (day 1) and days 2, 3, 4, and 8 thereafter. Predictors for AKI (defined as an increase of plasma creatinine >50% within 48 h referring to pre-admission or baseline creatinine on day 1 and/or the need for continuous veno-venous hemodiafiltration [CVVHDF]) and the prognostic impact of early AKI with regard to 30-day all-cause mortality were assessed. Statistical analyses included t test, Spearman's correlation, C-statistics, Kaplan-Meier, and Cox proportional regression analyses.

Results: A total of 219 CS patients were included with an incidence of early CS-related AKI of 52%. With an area under the curve of up to 0.689 (p = 0.001), creatine discriminated 30-day mortality in CS. Increasing lactate levels (OR = 1.194; 95% CI: 1.083-1.316; p = 0.001; per increase of 1 mmol/L) was associated with the occurrence of AKI. The presence of AKI was associated with an increased risk of 30-day all-cause mortality (63% vs. 36%; HR = 2.138; 95% CI: 1.441-3.171; p = 0.001), even after multivariable adjustment (HR = 1.861; 95% CI: 1.207-2.869; p = 0.005). Finally, highest risk of all-cause mortality was observed in patients with AKI requiring CVVHDF (75% vs. 44%; log rank p = 0.001; HR = 2.211; 95% CI: 1.315-3.718; p = 0.003).

Conclusion: Early AKI affects more than half of patients with CS and is independently associated with 30-day all-cause mortality in CS, with highest risk of death among patients with AKI requiring CVVHDF.

Background: The vascular endothelium serves as a semi-selective permeable barrier as a conduit for transport of fluid, solutes, and various cell populations between the vessel lumen and tissues. The endothelium thus has a dynamic role in the regulation of coagulation, immune system, lipid and electrolyte transport, as well as neurohumoral influences on vascular tone and end-organ injury to tissues such as the heart and kidney.

Summary: Within this framework, pharmacologic strategies for heart and kidney diseases including blood pressure, glycemic control, and lipid reduction provide significant risk reduction, yet certain populations are at risk for substantial residual risk for disease progression and treatment resistance and often have unwanted off-target effects leaving the need for adjunct, alternative targeted therapies. Recent advances in techniques in sequencing and spatial transcriptomics have paved the way for the development of new therapies for targeting heart and kidney disease that include various gene, cell, and nano-based therapies. Cell-specific endothelium-specific targeting of viral vectors will enable their use for the treatment of heart and kidney diseases with gene therapy that can avoid unwanted off-target effects, improve treatment resistance, and reduce residual risk for disease progression.

Key messages: The vascular endothelium is an important therapeutic target for chronic kidney and cardiovascular diseases. Developing endothelial-specific gene therapies can benefit patients who develop resistance to current treatments.

Background: The maladaptive neurohormonal activation, an integral mechanism in the pathophysiology of heart failure (HF) and cardiorenal syndrome, has a profound impact on renal sodium handling. Congestion is the primary reason for hospitalization of patients with HF and the main target of therapy. As sodium is the main determinant of extracellular volume, the goal is to enhance urinary sodium excretion in order to address excess fluid. The interventions to increase natriuresis have conventionally focused on distal nephron as the primary segment that counterbalances the effects of loop diuretics.

Summary: Recent developments in the field of cardiorenal medicine have resulted in a shift of attention to renal proximal tubules (e.g., emerging evidence on proximal tubular dysfunction beyond handling of sodium). Herein, we discuss the three main mechanisms of sodium transport in the proximal tubules with emphasis on their intrinsic links to one another as well as to more distal transporters of sodium. Then, we provide an overview of the findings of the most recent clinical studies that have tried to enhance the conventional decongestive strategies through simultaneous blockade of these mechanisms.

Key message: Interventions aiming at renal proximal tubules have the potential to significantly improve our ability to decongest patients with acute HF.

Introduction: Limited data have addressed frailty's role in cardiorenal risk among older adult patients with chronic kidney disease (CKD). We investigated whether frailty could predict major renal and cardiovascular events, healthcare utilization, and mortality in these patients.

Methods: We conducted a prospective cohort enrolling patients aged ≥75 years with a stable estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2. The frailty phenotype consists of shrinking, low activity, exhaustion, weakness, and slowness, scored 0 to 5. The primary composite renal outcome was a ≥25% decrease in eGFR concurrent with CKD stage progression or dialysis initiation. Secondary outcomes included major adverse cardiovascular events (MACE), emergency room (ER) visits, all-cause mortality, and hospitalization. Using multivariate Cox models with/without competing risk analyses, we explored frailty's impact on these outcomes.

Results: Among 203 older CKD patients (mean age: 81.6 ± 5.0 years, female: 40.9%, diabetes: 33.0%, body mass index: 24.9 ± 3.7 kg/m2), 67.9% were frail. Over 3.47 years, 38.9% faced composite renal outcomes; 13.3%, MACE; 15.3%, mortality; and more than half utilized healthcare. Every one-point frailty elevated renal outcome risk by 28.0% (HR: 1.28, 95% confidence interval [CI]: 1.03-1.59) and significantly increased secondary outcomes (MACE [HR: 1.43, 95% CI: 0.99-2.08], hospitalization [HR: 1.24, 95% CI: 1.06-1.46], unexpected ER visit [HR: 1.20, 95% CI: 1.03-1.39], and mortality [HR: 1.51, 95% CI: 1.06-2.16]). Results were consistent across subgroups and competing risk analysis.

Conclusion: In CKD patients aged ≥75 years, frailty was associated with progressive kidney disease, increased mortality, and healthcare utilization.

Introduction: Cardiorenal syndrome encompasses a range of disorders involving both the heart and kidneys, wherein dysfunction in one organ may induce dysfunction in the other, either acutely or chronically.

Methods: This study conducted a literature search on cardiorenal syndrome from January 1, 2003, to September 8, 2023. Meanwhile, a quantitative analysis of the developmental trajectory, research hotspots and evolutionary trends in the field of cardiorenal syndrome through bibliometric analysis and knowledge mapping was carried out.

Results: The annual publication trend analysis revealed a consistent annual increase in cardiorenal syndrome literature over the last 20 years. The IL6, REN, and INS genes were identified as the current research hotspots.

Conclusion: The field of cardiorenal syndrome exhibits promising potential to grow and is emerging as a prominent research area. Future endeavours should prioritise a comprehensive understanding of the field and foster multi-centre co-operation among different countries and regions.

Introduction: Studies exploring the relationship between peripheral arterial disease (PAD), critical limb ischemia (CLI), and chronic kidney disease (CKD) and its effect on in-hospital outcomes are limited. We aimed to analyze the outcomes of patients with CKD and PAD who are admitted for CLI.

Methods: We utilized the National Inpatient Sample (NIS) to capture hospitalizations for CLI from 2012 to 2020 and then identified cases with concomitant CKD. The primary outcome was mortality, and secondary outcomes were cerebrovascular accident, major bleeding, vasopressor requirement, percutaneous coronary intervention, cardiac arrest, acute respiratory failure, transfusion, length of stay, and total hospital charges. Multivariable logistic regression was performed to adjust for covariates.

Results: A total of 441,245 patients with CLI were identified, of which 122,370 (27.7%) reported concomitant CKD. Patients with CKD had higher in-patient mortality (odds ratio [OR] 1.68, 95% confidence interval [CI], 1.17-1.68, p < 0.001), vascular complications (OR 1.31, 95% CI, 1.17-1.48, p < 0.001), acute kidney injury requiring hemodialysis (OR 3.17, 95% CI, 2.64-3.80, p < 0.001), and major bleeding (OR 1.12, 95% CI, 1.05-1.19, p < 0.001). Patients with CKD underwent minimally invasive endovascular therapy (31.08% vs. 36.73%, p < 0.0001) and invasive procedures (14.73% vs. 23.55%, p < 0.0001) less often. PAD-CLI with CKD was associated with major (20.54% vs. 16.17%, OR 1.04; p < 0.0001) and minor (26.87% vs. 19.53%, OR 1.2, p < 0.0001) amputations more often.

Conclusion: Patients admitted for PAD-CLI with concomitant CKD have significantly higher in-hospital mortality as compared to patients without CKD. Moreover, patients with CKD and PAD-CLI are less likely to receive revascularization and more likely to undergo amputation.

Introduction: A comprehensive assessment of congestion, including circulating biomarkers, is recommended in patients with acute heart failure. The circulating biomarkers natriuretic peptides (NPs) and carbohydrate antigen-125 (CA125) could be useful for congestion assessment in ambulatory chronic heart failure (CHF), but there is only limited information about their applicability in this context. Therefore, this study aimed to examine the association of plasma CA125 and NP levels with clinical and ultrasound congestion parameters in CHF.

Methods: This is a cross-sectional substudy of the Cardioren Spanish Registry, which enrolled 1,107 patients with CHF from 13 tertiary hospitals in Spain between October 2021 and February 2022. Through ambulatory visits, we performed a comprehensive assessment of congestion-related parameters, including clinical variables (orthopnea, peripheral edema, and jugular engorgement, represented by the composite congestion score [CCS]), echocardiography variables (lung B-lines and inferior vena cava [IVC] diameter), and circulating biomarkers (CA125 and NPs). The association of the NP and CA125 levels with the clinical and echocardiographic congestion parameters was examined by multiple linear and logistic regression analyses.

Results: This substudy included 802 patients for whom all the biomarker parameters were available {median age, 74 (interquartile range [IQR], 63-81) years; 65% male}. The proportion of patients with left ventricular ejection fraction ≥50% and estimated glomerular filtration rate <60 was 34% and 58%, respectively. The median CCS was 0 (IQR: 0-1), with 45% of the sample exhibiting a median CCS of ≥1. The jugular engorgement, peripheral edema, and orthopnea rates were 32%, 21%, and 21%, respectively. A total of 35% of patients who underwent ultrasound examination showed lung B-lines, and the median IVC diameter was 16 mm. The median CA125 and NTproBNP levels were 14 U/mL (IQR: 9-28) and 1,382 pg/mL (IQR: 563-3,219), respectively. Multivariate analysis showed that higher CA125 levels were independently associated with higher odds of peripheral edema (p = 0.023) and lung B-lines (p < 0.001). Further, NTproBNP was positively associated with jugular engorgement (p < 0.001), orthopnea (p = 0.034), and enlarged IVC diameter (p = 0.031).

Conclusions: Clinical signs of congestion are frequent in CHF. In the ambulatory setting, NTproBNP was associated with parameters linked to intravascular congestion such as orthopnea, jugular engorgement, and IVC diameter, whereas CA125 was associated with extravascular volume overload parameters (peripheral edema and lung B-lines).

Introduction: Diabetes mellitus is the most common cause of end-stage kidney disease (ESKD) in Singapore. ESKD patients have high disease burden and are at increased risk of recurrent hospitalizations, including fluid overload. This study aimed to characterize the risk factors associated with readmissions for fluid overload that will identify high-risk hospitalizations for interventions to reduce readmissions.

Methods: Retrospective cohort study of all hospitalizations for fluid overload in adults with diabetes and ESKD on dialysis in SingHealth hospitals between 2018 and 2021. Fluid overload was defined by discharge codes for fluid overload, heart failure, pulmonary edema, and generalized edema. Multivariable Cox regression analysis using the Prentice, Williams and Peterson Total Time model was performed for the outcomes of readmissions for fluid overload within 30 days and 90 days of discharge.

Results: Among 3,234 hospitalizations for fluid overload, readmission for fluid overload within 30 days and 90 days occurred in 585 (18.1%) and 967 (29.9%) hospitalizations, respectively. Ischemic heart disease, peripheral vascular disease, and lower hemoglobin level were independently associated with readmissions for fluid overload within 30 and 90 days. Additionally, heart failure, hemodialysis (compared to peritoneal dialysis), and lack of statin at discharge were associated with increased 90-day readmission risk.

Conclusion: Modifiable (hemoglobin level, statin use) and non-modifiable factors (ischemic heart disease, peripheral vascular disease, and heart failure) influenced the risk of readmission for fluid overload. These results may guide risk stratification and inform targeted interventions to reduce avoidable, unplanned readmissions for recurrent fluid overload among individuals with diabetes and ESKD.