The Role of Oxidative Stress as a Mechanism in the Pathogenesis of Acute Heart Failure in Acute Kidney Injury.

Despite a large amount of research on synchronous and mutually induced kidney and heart damage, the basis of the disease is still not fully clarified. Healthy mitochondria are essential for normal kidney and heart function. Mitochondrial dysfunction occurs when the clearance or process of generation and fragmentation of mitochondria is disturbed. The kidney is the second organ after the heart in terms of the number of mitochondria. Kidney tubules are rich in mitochondria due to the high energy requirements for absorption of large amounts of ultrafiltrate and dissolved substances. The place of action of oxidative stress is the influence on the balance in the production and breakdown of the mitochondrial reactive oxygen species. A more precise determination of the place and role of key factors that play a role in the onset of the disease is necessary for understanding the nature of the onset of the disease and the creation of therapy in the future. This underscores the urgent need for further research. The narrative review integrates results found in previously performed studies that have evaluated oxidative stress participation in cardiorenal syndrome type 3.

Associations of C-reactive protein-albumin-lymphocyte (CALLY) index with cardiorenal syndrome: Insights from a population-based study.

Background: Cardiorenal syndrome (CRS) is a complex condition characterized by the interplay of immune imbalance and inflammation. The C-reactive protein-Albumin-lymphocyte (CALLY) CALLY index serves as a new immune-nutritional scoring system, but its predictive value for CRS remains to be established. Methods: In this study, we analyzed data from 27,978 participants in National Health and Nutrition Examination Survey (NHANES) from 1999 to 2010. The CALLY index was calculated as the ratio of albumin to lymphocyte, divided by C-reactive protein (CRP) multiplied by 104. CRS was defined by the coexistence of cardiovascular disease and chronic kidney disease (eGFR <60 mL/min/1.73 m2). Multivariate weighted logistic regression models were employed to determine the odds ratio and 95 % confidence interval for the association between the CALLY index and CRS. Receiver operating characteristic (ROC) curves and restricted cubic spline (RCS) curves were used to assess the predictive efficacy and nonlinear relationship, respectively. Results: The prevalence of CRS in the study population was 1.22 %. Our findings revealed a significant inverse relationship between the CALLY index and CRS risk, with lower CALLY index values being associated with a higher likelihood of CRS (OR = 0.95, 95 % CI = 0.94-0.96, P < 0.001). Participants in higher quartiles of the CALLY index showed a progressively reduced risk of CRS (P for trend <0.001). Moreover, the CALLY index demonstrated superior predictive performance compared to other inflammatory indicators, such as systemic immune-inflammation index (SII), neutrophil/high-density lipoprotein ratio (NHR), lymphocyte/high-density lipoprotein ratio (LHR), monocyte/high-density lipoprotein ratio (MHR), and platelet/high-density lipoprotein ratio (PHR) (AUC = 0.672, 95 % CI = 0.643-0.701). Conclusions: This study underscores the significant negative correlation between the CALLY index and the risk of cardiorenal syndrome. The CALLY index emerges as a robust and independent predictor of CRS, outperforming traditional inflammatory markers. This finding highlights the potential utility of the CALLY index as a clinical tool for identifying individuals at risk for CRS.

Cardiorenal syndrome: evolving concepts and pediatric knowledge gaps.

Cardiorenal syndrome (CRS) refers to concomitant dysfunction of both the heart and kidneys. The pathology in CRS is bidirectional. Many individuals with kidney disease will develop cardiovascular complications. Conversely, rates of acute kidney injury and chronic kidney disease are high in cardiac patients. While our understanding of CRS has greatly increased over the past 15 years, most research has occurred in adult populations. Improving cardiorenal outcomes in children and adolescents requires increased collaboration and research that spans organ systems. The purpose of this review is to discuss key features of CRS and help bring to light future opportunities for pediatric-specific research.

Implantable Cardioverter Defibrillator and Resynchronization Therapy in Patients With Overt Chronic Kidney Disease: JACC State-of-the-Art Review.

Heart failure and chronic kidney disease are common and clinically important conditions that regularly coexist. Electrophysiologic changes of advanced heart failure often result in abnormal conduction, causing dyssynchronous contraction, and development of ventricular arrhythmias, which can lead to sudden cardiac arrest. In the last 2 decades, implantable cardioverter-defibrillator and cardiac resynchronization therapy devices have been developed to address these complications. However, when the coexisting chronic kidney disease is advanced, the associated pathophysiologic cardiovascular changes can alter the efficacy and safety of those interventions and complicate the management. This review explores the impact of comorbid advanced heart failure and advanced chronic kidney disease on the efficacy and safety of implantable cardioverter-defibrillator and cardiac resynchronization therapy, the currently available evidence, and potential future directions.

Galectin-3 and Soluble CD146 Identify Cardiorenal Injuries in Severe Burn Patients: A Biomarker-Based Approach.

INTRODUCTION: Acute kidney injury (AKI) and myocardial injury (MI) are severe conditions in patients with severe burn injury, and combination of both is even worst and is called the cardiorenal syndrome (CRS). Identifying a distinct cardiorenal phenotype could significantly enhance the management of these patients. Galectin-3 (Gal3) and soluble CD146 (sCD146) are biomarkers for renal and cardiac injuries. This study aims to assess the occurrence and reliability of these biomarkers in recognizing CRS in individuals who have been severely burn. METHODS: This study is a single-center prospective proof-of-concept study involving patients with severe burn injuries. Plasma samples for Gal3 and sCD146 measurements were collected daily during the initial 7 days following admission. CRS was defined after 24 h of admission by the association of AKI stage 1 or more (KDIGO definition) and MI defined on high sensitive troponin (hsTnT) (variation >20% baseline value or absolute value >40 ng/mL). RESULTS: Forty patients met the inclusion criteria and were included in this study. Thirty-eight patients had CRS. The pooled values of Gal3 or combination of Gal3 and sCD146 values following 7 days after admission were associated with CRS with an odds ratio (OR) of 1.145 (95% CI: 1.081-1.211), p < 0.001, and 1.147 (95% CI: 1.085-1.212), p < 0.001, respectively. Gal3 values at admission (D0) had a predictive performance for CRS with an AUC of 0.78 (95% CI: 0.63-0.93), and this performance improved when using the combination of Gal3 and sCD146 values at admission (D0), with an AUC of 0.81 (95% CI: 0.66-0.96). Gal3 levels during the first 7 days were associated with patients experiencing AKI and no MI, with an OR of 1.129 (95% CI: 1.065-1.195), p < 0.001, and MI without AKI with an OR of 1.095 (95% CI: 1.037-1.167), p < 0.001. sCD146 alone was not associated with AKI without MI or MI without AKI and was poorly associated with CRS. CONCLUSION: In severely burned patients, CRS is a frequent and severe condition. Gal3 values during the first 7 days following admission were associated with CRS. The use of sCD146 with Gal3 improved prediction performance for CRS identification. The use of such biomarkers to identify CRS is important and needs to be confirmed in other studies.

Central Venous Pressure and Impaired Renal Function in Children and Young Adults With Cardiovascular Disease.

Background: Traditionally, low cardiac output has been considered the primary hemodynamic driver of renal function and injury. Adult data suggest that central venous pressure (CVP) is a more important factor. Objectives: The authors hypothesized that in children with cardiovascular disease, higher CVP predicts lower estimated glomerular filtration rate (eGFR) and worsening renal function (WRF). Methods: We performed a single-center cohort study of patients aged 3 months to 21 years with biventricular circulation undergoing cardiac catheterization. Pearson's correlation and linear and Cox regression analyses were performed to determine associations with eGFR at the time of catheterization and WFR within 180 days after catheterization. Results: 312 patients had median age 7.9 years (IQR: 2.3 to 14.5 years), median eGFR 97 mL/min/1.73 m2 (IQR: 81-118 mL/min/1.73 m2), median CVP 7 mm Hg (IQR: 5-9 mm Hg), and median cardiac index 3.7 mL/min/m2 (IQR: 2.9-4.6 mL/min/m2). Nearly half (48%) were transplant recipients. In multivariable analysis, CVP was independently associated with eGFR (ß = -2.65; 95% CI: -4.02, -1.28; P < 0.001), as was being a transplant recipient (ß = -10.20; 95% CI: -17.74, -2.65; P = 0.008), while cardiac index was not. Fifty-one patients (16%) developed WRF. In a proportional hazards model adjusting for cardiac index, only higher CVP (HR: 1.10; 95% CI: 1.04-1.17; P = 0.002) and greater contrast volume by weight (HR: 1.05; 95% CI: 1.01-1.10; P = 0.021) predicted WRF. CVP ≥7 mm Hg likewise predicted WRF (HR: 2.57; 95% CI: 1.29-5.12; P = 0.007). Conclusions: Among children with a spectrum of cardiovascular disease, higher CVP is associated with lower eGFR and development of WRF, independent of cardiac index.

The Need to Identify Novel Markers for Early Renal Injury in Cardiorenal Syndrome.

The term "Cardiorenal Syndrome" (CRS) refers to the complex interplay between heart and kidney dysfunction. First described by Robert Bright in 1836, CRS was brought to its modern view by Ronco et al. in 2008, who defined it as one organ's primary dysfunction leading to secondary dysfunction in the other, a view that led to the distinction of five different types depending on the organ of primary dysfunction and the temporal pattern (acute vs. chronic). Their pathophysiology is intricate, involving various hemodynamic, neurohormonal, and inflammatory processes that result in damage to both organs. While traditional biomarkers have been utilized for diagnosing and prognosticating CRS, they are inadequate for the early detection of acute renal damage. Hence, there is a pressing need to discover new biomarkers to enhance clinical outcomes and treatment approaches.

CA125 outperforms NT-proBNP in the prediction of maximum aerobic capacity in heart failure with preserved ejection fraction and kidney dysfunction.

Background: Heart failure with preserved ejection fraction (HFpEF) often coexists with chronic kidney disease (CKD). Exercise intolerance is a major determinant of quality of life and morbidity in both scenarios. We aimed to evaluate the associations between N-terminal pro-B-type natriuretic peptide (NT-proBNP) and carbohydrate antigen 125 (CA125) with maximal aerobic capacity (peak VO2) in ambulatory HFpEF and whether these associations were influenced by kidney function. Methods: This single-centre study prospectively enrolled 133 patients with HFpEF who performed maximal cardiopulmonary exercise testing. Patients were stratified across estimated glomerular filtration rate (eGFR) categories (<60 ml/min/1.73 m2 versus ≥60 ml/min/1.73 m2). Results: The mean age of the sample was 73.2 ± 10.5 years and 56.4% were female. The median of peak VO2 was 11.0 ml/kg/min (interquartile range 9.0-13.0). A total of 67 (50.4%) patients had an eGFR <60 ml/min/1.73 m2. Those patients had higher levels of NT-proBNP and lower peak VO2, without differences in CA125. In the whole sample, NT-proBNP and CA125 were inversely correlated with peak VO2 (r = -0.43, P < .001 and r = -0.22, P = .010, respectively). After multivariate analysis, we found a differential association between NT-proBNP and peak VO2 across eGFR strata (P for interaction = .045). In patients with an eGFR ≥60 ml/min/1.73 m2, higher NT-proBNP identified patients with poorer maximal functional capacity. In individuals with eGFR <60 ml/min/1.73 m2, NT-proBNP was not significantly associated with peak VO2 [ß = 0.02 (95% confidence interval -0.19-0.23), P = .834]. Higher CA125 was linear and significantly associated with worse functional capacity without evidence of heterogeneity across eGFR strata (P for interaction = .620). Conclusions: In patients with stable HFpEF, NT-proBNP was not associated with maximal functional capacity when CKD was present. CA125 emerged as a useful biomarker for estimating effort intolerance in HFpEF irrespective of the presence of CKD.

Prognostic effect of a vasopressin V2 receptor antagonist in acute congestive heart failure patients with hypoperfusion, the wet-cold pattern.

PURPOSE: This study investigated whether the oral vasopressin V2 receptor antagonist tolvaptan has beneficial effects on mortality in real-world congestive heart failure (CHF) patients with hypoperfusion (i.e. the wet-cold pattern), from the viewpoint of cardiorenal syndrome. METHODS: Data on 5511 consecutive CHF patients were extracted from the Tokyo CCU Network data registry. Congestion and hypoperfusion were defined by Nohria-Stevenson clinical profiles at the time of hospitalization. Propensity scores for tolvaptan use were calculated for each patient and used to assemble two matched cohorts of patients receiving tolvaptan or not in the CHF with and without hypoperfusion groups. RESULTS: Of the entire study cohort, 1073 patients (19%) had CHF with hypoperfusion (i.e. the wet-cold pattern). In-hospital mortality was significantly higher for CHF patients with than without hypoperfusion (log-rank, P < 0.001). The rate of tolvaptan use did not differ significantly between CHF patients with and without hypoperfusion (15% vs. 14%, respectively; P = 0.7848). In the propensity-matched CHF with hypoperfusion cohort, there was a significant association between the use of tolvaptan and a reduction in in-hospital mortality (log-rank, P = 0.0052). Conversely, in the matched CHF without hypoperfusion cohort, tolvaptan use was not associated with in-hospital mortality (log-rank, P = 0.4417). CONCLUSION: There was a significant association between the use of tolvaptan and a reduction in in-hospital mortality in CHF patients with, but not without, hypoperfusion. These findings hint at possible individualized therapies for patients with CHF.

A Systematic Review of Uremic Toxin Concentrations and Cardiovascular Risk Markers in Pediatric Chronic Kidney Disease.

Chronic kidney disease (CKD) can lead to cardiac dysfunction in a condition known as cardiorenal syndrome (CRS). It is postulated that the accumulation of uremic toxins in the bloodstream, as a consequence of declining kidney function, may contribute to these adverse cardiac effects. While CRS in adults has been extensively studied, there is a significant knowledge gap with pediatric patients. Uremic toxin levels in children remain inadequately characterized and quantified compared to adults. This review aims to systematically evaluate the association between uremic toxin concentrations and cardiac changes in pediatric CRS and to examine the impact of different dialysis modalities, specifically hemodialysis and peritoneal dialysis, on uremic toxin clearance and cardiovascular parameters. To address this, we conducted a systematic literature search of PubMed, following PRISMA guidelines. We used the terms "uremic toxins" and "cardiorenal syndrome" with variations in syntax to search for studies discussing the relationship between uremic toxin levels in CKD, the subsequent impact on cardiac parameters, and the emergence of cardiac dysfunction. Full-text articles written in English, conducted on humans aged from birth to 18 years, and published until December 2021 were included. A comprehensive literature search yielded six studies, and their risk of bias was assessed using JBI Critical Appraisal Checklists. Our systematic review is registered on PROSPERO, number CRD42023460072. This synthesis intends to provide an understanding of the role of uremic toxins in pediatric CRS. The findings reveal that pediatric patients with end-stage CKD on dialysis exhibit elevated uremic toxin levels, which are significantly associated with cardiovascular disease parameters. Additionally, the severity of CKD correlated with higher uremic toxin levels. No conclusive evidence was found to support the superiority of either hemodialysis or peritoneal dialysis in terms of uremic toxin clearance or cardiovascular outcomes. More pediatric-specific standardized and longitudinal studies are needed to develop targeted treatments and improve clinical outcomes and the quality of life for affected children.

SGLT2 inhibitor downregulated oxidative stress via activating AMPK pathway for cardiorenal (CR) protection in CR syndrome rodent fed with high protein diet.

This study tested the hypothesis that empagliflozin (EMPA) therapy effectively protected renal and heart functions via downregulating reactive oxygen species (ROS) and activating AMPK signaling in cardiorenal syndrome (CRS) (induced by doxorubicin-5/6 nephrectomy) rats. In vitro result showed that underwent p-Cresol treatment, the H9C2/NRK-52E cell viabilities, were significantly suppressed, whereas cellular levels of ROS and early/late apoptosis of these cells were significantly increased that were significantly reversed by EMPA treatment (all p < 0.001). The protein levels of the cell-stress/oxidative signaling (p-PI3K/p-Akt/p-mTOR/NOXs/p-DRP1) were significantly activated, whereas the mitochondrial biogenesis signaling (p-AMPK/SIRT-1/TFAM/PGC-1α) was significantly repressed in these two cell lines treated by p-Cresol and all of these were significantly reversed by EMPA treatment (all p < 0.001). Male-adult-SD rats were categorized into groups 1 [sham-operated control (SC)]/2 [SC + high protein diet (HPD) since day 1 after CKD induction]/3 (CRS + HPD)/4 (CRS + HPD+EMPA/20 mg/kg/day) and heart/kidney were harvested by day 60. By day 63, the renal function parameters (creatinine/BUN/proteinuria)/renal artery restrictive index/cellular levels of ROS/inflammation were significantly increased in group 3 than in groups 1/2, whereas heart function exhibited an opposite pattern of ROS among the groups, and all of these parameters were significantly reversed by EMPA treatment (all p < 0.0001). The protein levels of inflammation/ oxidative-stress/cell-stress signalings were highest in group 2, lowest in group 1 and significantly lower in group 4 than in group 2, whereas the AMPK-mitochondrial biogenesis displayed an opposite manner of oxidative-stress among the groups (all p < 0.0001). EMPA treatment effectively protected the heart/kidney against CRS damage via suppressing ROS signaling and upregulating AMPK-mediated mitochondrial biogenesis.

A new animal model of cardiorenal syndrome could be established by inducing heart failure through coronary artery ligation in spontaneously hypertensive rats.

In rats with unilateral nephrectomy and cardiac dysfunction, renal function deteriorates at an accelerated rate, as evidenced by increased proteinuria. Whether myocardial infarct-induced heart failure (HF) exacerbates renal injury in hypertensive rats with mild renal injury has not been reported. Rats underwent either coronary ligation or sham surgery. Thirty spontaneously hypertensive rats (SHRs) aged 8 weeks were randomly divided into two groups. Group 1 was the sham group, in which the rats underwent thoracotomy without ligation of the coronary artery. Group 2 underwent coronary artery ligation. The rats in group 2 underwent coronary artery ligation on week 0. The experiment lasted 12 weeks. Urine was collected in metabolic cages over a 24-h period. Urine was collected from the rats 2 days before the end of the experiment, and the ratio of urinary protein to urinary creatinine was measured in the clinical laboratory. All rats were examined by echocardiogram one day before the end of the experiment. On the last day of the experiment, blood was collected and sent to the laboratory for analysis. Hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining were performed on heart and kidney sections. The ejection fraction in group 2 was lower than that in group 1 (P < 0.001). The urinary albumin to creatinine ratio in group 2 was greater than that in group 1 (P < 0.001). The urea and creatinine levels in group 1 were significantly lower than those in group 2 (P < 0.01). The levels of brain natriuretic peptide (BNP), neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C were greater in the second group than in the first group (P < 0.05). The interleukin-1ß (IL-1ß) and interleukin-6 (IL-6) levels in group 2 were significantly greater than those in group 1 (P < 0.001). The malondialdehyde (MDA) levels in Group 2 were greater than those in Group 1 (P < 0.01). The glutathione peroxidase (GSH-Px) levels in Group 2 were lower than those in Group 1 (P < 0.05). The level of angiotensin II (AT-II) in group 1 was lower than that in group 2 (P < 0.001). Cardiac dysfunction secondary to myocardial infarction could induce cardiorenal interactions in SHRs. It could be interpreted by the activation of oxidative stress, changes in inflammation and alteration of renin-angiotensin-aldosterone system.

Biomarkers in cardiorenal syndrome, a potential use in precision medicine.

Cardiorenal syndrome refers to the interrelated dysfunction of the heart or kidney resulting in a cascade of feedback mechanisms, hemodynamic, neurohormonal, and immunological and/or biochemical feedback pathways causing damage in the other organ. Cardiorenal syndrome is categorized into five clinical subtypes depending on the perceived primary precipitant of organ injury and is associated with high morbidity and mortality. Therefore, the development of tools for the earliest identification of cardiorenal syndrome in hospitalized patients is of extremely high significance to ameliorate the prognosis and outcome of these patients. There is increasing interest in identifying molecules serving as biomarkers, reflecting hemodynamic changes, heart and kidney damage and/or dysfunction and oxidative stress-induced cell damage or changes in the extracellular matrix of both the heart and kidneys. Biomarkers provide important insights into the pathophysiology of cardiorenal syndrome and are invaluable tools to predict the decrease in renal function during cardiac dysfunction and vice versa. Based on the pathophysiological mechanisms of cardiorenal syndrome, we reviewed and evaluated the available literature on serum and urinary biomarkers as predictors of kidney and/or heart injury. In addition, heart- and kidney-specific biomarkers were also evaluated based on their reference to kidney and cardiac (dys)function respectively, and whether they would provide any prediction and prognostication of cardiorenal syndrome. In this article, we discuss the current knowledge on the pathophysiology of different types of cardiorenal syndrome, examine the clinical utility of candidate biomarkers in the early diagnosis of cardiorenal syndrome, and guide treatment by evaluating the respective roles of the involved pathophysiological pathways.

Cardiorenal Syndrome and Inflammation: A Forgotten Frontier Resolved by Sorbents?

Cardiorenal syndrome (CRS) describes the maladaptive relationship between heart and kidney dysfunction, with different pathways perpetuating the pathophysiology. Inflammation is one of these mechanisms. It contributes to the final nonhemodynamic pathways of organ dysfunction in the heart-kidney cross-talk. It may be a mediator and amplifier of this pathological communication, playing a vital role in both acute and chronic cardiorenal dysfunction. Current therapeutic strategies are not satisfactory in mitigating the inflammatory pathway in CRS. Hemoadsorption overcomes this limitation, and the soluble mediators of inflammation are potentially amenable to removal by hemoadsorption. This perspective article describes the inflammatory mechanisms in CRS and the rationality of using hemoadsorption in this scenario.

Susceptibility of hepato-splanchnic perfusion to intra-abdominal pressure in peritoneal dialysis patients.

BACKGROUND: The impact of peritoneal filling on hepato-splanchnic perfusion during peritoneal dialysis has not been fully elucidated yet. METHODS: Measurements were done in 20 prevalent peritoneal dialysis patients during a peritoneal equilibration test (PET) with 2L of standard dialysate. Data were obtained in the drained state at baseline (T0), after instillation (T1), and after 2 h of dwell time (T2). Intra-abdominal pressure (IAP) was measured by Durand's approach. The hepatic clearance index (KI) of indocyanine-green (ICG) was determined as an indirect measure of hepato-splanchnic blood flow. Cardiac index (CI), heart rate (HR), and total peripheral resistance index (TPRI) were derived from continuous arterial pulse analysis. Fluid volume overload (VO) was evaluated by multifrequency bioimpedance analysis. Ejection fraction (EF) was obtained from echocardiographic examination. RESULTS: IAP was 5.8 ± 3.5 mmHg at baseline (T0), rose to 9.4 ± 2.8 mmHg after instillation of dialysate (T1), and further to 9.7 ± 2.8 mmHg after 2 h of dwell time (p < 0.001). KI slightly declined from 0.60 ± 0.22 L/min/m2 at T0 to 0.53 ± 0.15 L/min/m2 at T1 (p = 0.075), and returned to 0.59 ± 0.22 L/min/m2 at T2 (p = 0.052). CI, HR, and TPRI did not change significantly. In five patients with an EF < 40% KI was significantly lower at T1 (0.42 ± 0.12 L/min/m2; p = 0.039), and further decreased at T2 (0.40 ± 0.04 L/min/m2; p = 0.016) compared to patients with normal EF (T1: 0.58 ± 0.15 L/min/m2 and T2: 0.67 ± 0.22 L/min/m2). CONCLUSIONS: Overall, hepatic clearance of ICG as a marker of hepato-splanchnic blood flow is not affected by the filling of the peritoneal cavity.

Cutting the Gordian knot of diuretic resistance using continuous ultrafiltration in a Holt-Oram patient with decompensated heart failure and Eisenmenger syndrome: a case report.

Background: Continuous ultrafiltration consists a decongestion method for patients with refractory decompensated heart failure with diuretic resistance as it enables the energetic withdrawal of isotonic fluid under controlled rate according to the patient's vital signs, offering decongestion without exceeding plasma refill rate. Case summary: A 62-year-old male with history of Holt-Oram syndrome with Eisenmenger physiology presented with worsening dyspnoea. Patient initial clinical and laboratory examination, renal vein ultrasound, and echocardiogram were consistent with significant congestion. A combined strategy of intravenous furosemide with early initiation of continuous ultrafiltration at an adjustable rate for 4 days was finally selected. Patient remained haemodynamically stable during the total treatment time and exhibited significant clinical and laboratory improvement. Consecutive renal vein ultrasounds and echocardiograms demonstrated a continuous and steady recession of congestion. During the 4 days of ultrafiltration, total fluid loss was estimated at 42 L. Patient remained asymptomatic without signs of worsened congestion at 1, 3, and 5 months follow-up. Discussion: Our case depicts that continuous ultrafiltration without exceeding plasma refill rate allows an impaired right ventricle to maintain significant preload. This suggests that it might be considered for patients in whom a session of short classic ultrafiltration might have detrimental results regarding cardiac output.

Blood Volume Analysis and Cardiorenal Syndrome: From Bench to Bedside.

BACKGROUND: This review delves into the intricate landscape of cardiorenal syndrome (CRS) and highlights the pivotal role of blood volume analysis (BVA) in improving patient care and outcomes. SUMMARY: BVA offers a direct and highly accurate quantification of intravascular volume, red blood cell volume, and plasma volume, complete with patient-specific norms. This diagnostic tool enhances the precision of diuretic and red cell therapies, significantly elevating the effectiveness of conventional care. KEY MESSAGES: Our objectives encompass a comprehensive understanding of how BVA informs the evaluation and treatment of CRS, including its subtypes, pathophysiology, and clinical significance. We delve into BVA principles, techniques, and measurements, elucidating its diagnostic potential and advantages compared to commonly used surrogate measures. We dissect the clinical relevance of BVA in various CRS scenarios, emphasizing its unique contributions to each subtype. By assessing the tangible impact of BVA on patient outcomes through meticulous analysis of relevant clinical studies, we unveil its potential to enhance health outcomes and optimize resource utilization. Acknowledging the challenges and limitations associated with BVA's clinical implementation, we underscore the importance of multidisciplinary collaboration among cardiologists, nephrologists, and other clinicians. Finally, we identify research gaps and propose future directions for BVA and CRS, contributing to ongoing advancements in this field and patients affected by this complicated clinical syndrome.

Inflammation Links Cardiac Injury and Renal Dysfunction: A Cardiovascular Magnetic Resonance Study.

Background: Inflammation is essential in cardiorenal syndrome, however there is still a lack of evidence proving the interaction between cardiac injury, renal dysfunction and the inflammatory response. This study aimed to illustrate the association between renal dysfunction and cardiac injury with a specific focus on the role of inflammation. Methods: A single-center, retrospective study included patients with heart failure admitted to the cardiovascular department from September 2019 to April 2022. Patients received cardiovascular magnetic resonance (CMR) imaging (T1 mapping and late gadolinium enhancement (LGE)). Demographic, creatinine and native T1 were analyzed using pearson correlation, linear regression and adjusted for confounders. Interaction and subgroup analysis were performed. Results: Finally, 50 validated heart failure (HF) patients (age 58.5 ± 14.8 years; 78.0% men) were included. Cardiac global native T1 for the high estimated glomeruar filtration rate (eGFR) group was 1117.0 ± 56.6 ms, and for the low eGFR group was 1096.5 ± 61.8 ms. Univariate analysis identified global native T1 ( ß = 0.16, 95% confidence interval (CI): 0.04-0.28, p = 0.014) and C-reactive protein (CRP) ( ß = 0.30, 95% CI: 0.15-0.45, p < 0.001) as determinants of creatinine. Multivariable linear regression analysis identified global native T1 ( ß = 0.12, 95% CI: 0.01-0.123, p = 0.040) as a determinant of creatinine while age and diabetes were adjusted. Significant interactions between CRP and global native T1 in relation to creatinine level (p for interaction = 0.005) were identified. Conclusions: Kidney dysfunction was associated with cardiac injury and inflammation, respectively. The interaction between myocardial injury and kidney dysfunction is contingent on the severity of the inflammatory response. Further studies were needed to identify the mechanisms of the inflammatory response in cardiorenal syndrome.