Chronic Cardiorenal Syndrome Research Articles

The Art of Ultrafiltration, from Pump to Peritoneum.

Heart failure remains a significant public health burden given its prevalence, morbidity, mortality as well its untoward financial consequences. The assessment of congestion and its treatment are integral in heart failure pathophysiology and outcomes. Renal venous congestion and its suboptimal response to diuretic-based and novel pharmacological therapeutic regimens have thus positioned ultrafiltration as a promising therapeutic option for patients with acute decompensated heart failure. As a corollary, peritoneal dialysis has had success establishing itself as a relevant therapeutic option for chronic cardiorenal syndrome in patients with heart failure. Herein, we will discuss the pathophysiologic basis of ultrafiltration and peritoneal dialysis in heart failure with a review of the relevant clinical trials on safety and efficacy profiles in these patient populations.

71-Year-Old Man With a New Heart Murmur

71-Year-Old Man With a New Heart Murmur

Relationships between biomarkers of hypoxia and inflammation in elderly patients with chronic cardiorenal syndrome

Background and Aims : Multibiomarker models are promising for assessing the prognosis in chronic heart failure (CHF). The aim of this study was to investigate relationships between biomarkers of hypoxia and inflammation in elderly patients with chronic cardiorenal syndrome (ССS).

Cardiorenal Syndrome: An Updated Classification Based on Clinical Hallmarks.

Cardiorenal syndrome (CRS) is defined as progressive, combined cardiac and renal dysfunction. In this mini review, a historical note on CRS is presented, the pathomechanisms and clinical hallmarks of both chronic heart failure and chronic kidney disease are discussed, and an updated classification of CRS is proposed. The current consensus classification relies on the assumed etiology and the course of the disease, i.e., acute or chronic CRS. Five types are described: type-I CRS presenting as acute cardiac failure leading to acute renal failure; type-II CRS presenting as chronic cardiac failure leading to chronic renal failure; type-III CRS presenting as acute kidney injury aggravating heart failure; type-IV CRS presenting as chronic kidney failure aggravating heart failure; and type-V CRS presenting as concurrent, chronic cardiac and renal failure. For an updated classification, information on the presence or absence of valvular heart disease and on the presence of hyper- or hypovolemia is added. Thus, CRS is specified as “acute” (type-I, type-III or type-V CRS) or “chronic” (type-II, type-IV or type-V) CRS, as “valvular” or “nonvalvular” CRS, and as “hyper-” or “hypovolemia-associated” CRS if euvolemia is absent. To enable the use of this updated classification, validation studies are mandated.

Comorbidity and quality of life in older patients with chronic cardiorenal syndrome and obstructive sleep apnea

Abstract Funding Acknowledgements Type of funding sources: None. Comorbidity increases with age, including the presence of cardiovascular disease, chronic kidney disease (CKD) and obstructive sleep apnea (OSA). OSA is considered as a risk factor for the progression of CKD. The aim of this study was to investigate сomorbidity and quality of life in older patients with chronic cardiorenal syndrome and obstructive sleep apnea. Materials and methods 80 older patients with stable cardiovascular disease and CKD (43 males, mean age was 67.6 ± 6.1 years) were studied. CKD was diagnosed and classified according to the KDIGO guidelines (2012). OSA was observed according to Clinical Guidelines for Obstructive Sleep Apnea and Insomnia (U.S., 2020). Berlin Questionnaire and Epworth Sleepiness Scale, cardiorespiratory monitoring for screening and diagnosis of OSA were used. Charlson comorbidity index (CCI) was estimated. The patients" quality of life (EQ-5D-5L), the presence of anxiety and depression (Hospital Anxiety and Depression Scale), psychological defense mechanisms were assessed. Results Chronic kidney disease was observed in 48 (60%) patientswith stable cardiovascular disease. OSA was first diagnosed in 31 (64.5%) older patients with CKD. Рatients with CKD had a high comorbidity independently of OSA: CCI was 8 (7; 8) points in patients with OSAS and 7 (7; 8) points in patients without OSAS (p = 0.51). There was a direct relationship between CKD and the severity of daytime sleepiness (r = 0.30, p = 0.02), as well as complaints about the quality of sleep (r = 0.31, p = 0.01) in patients with CKD. Severity of anxiety and depressive reactions, disturbance of habitual activity, increased pain and discomfort, decrease QOL index (EQ-5D-5L) in the presence of disturbed sleep quality and daytime sleepiness were observed. With a Older patients with CKD and decrease in the quality of sleep less commonly used mature mechanisms of psychological defense, such as «рrojection» (r = -0.39, p = 0.04) and «rationalization» (r = -0.41, p = 0.03). There was association between the severity of sleep disorders and the tension of the primitive mechanism of psychological defense «regression» (r = 0.41, p = 0.008), which contributes to the impairment of adaptation in older patients with CKD. Conclusion Older patients with CKD and OSA have a high comorbidity, including cardiovascular comorbidity. There were no differences in the structure of comorbidity in older patients with chronic cardiorenal syndrome, depending on the presence of OSA. Sleep impairment, daytime sleepiness were associated with the severity of anxiety and depression, a decrease in the quality of life, and maladjustment.

Awareness and cognitive status of older patients with chronic cardiorenal syndrome in terms of patient-centered approach

Abstract Funding Acknowledgements Type of funding sources: None. A patient-centered approach is the basis for older patients with cardiovascular comorbidity. Collaborative decision making is especially important for older patients with chronic kidney disease (СKD). The aim of the study was to study the possibilities and difficulties of a patient-centered approach in older patients with chronic cardiorenal syndrome. Material and methods. 214 older patients with stable cardiovascular disease (106 males, mean age was 69.5 ± 7.6 years) were studied. CKD was diagnosed and classified according to the KDIGO guidelines (2012). Charlson comorbidity index (CCI) was estimated. Cognitive status was assessed using the Mini-Mental State Examination (MMSE) and the Clinical Dementia Rating scale (CDR). Assessment of socio-demographic characteristics and awareness of patients was determined by questionnaires and interviews. Follow-up period was 12 months. Results. CKD was observed in 144 (67.3%) patients with stable cardiovascular disease. A third of older patients with CKD (48; 33.3%) were informed about impaired renal function (n = 144), and only 23 (16%) older patients with CKD, along with observation by a therapist, consulted a nephrologist . Only half of older patients with cardiovascular pathology, regardless of the presence of CKD, know their cholesterol level and their cardiovascular risk. In 70 (48.6%) older patients with stable cardiovascular pathology and CKD, pre-dementia cognitive impairment was observed, in 28 (19.4%) - mild dementia. A third of older patients with cardiovascular pathology and CKD (47; 32.6%) still have questions about their health. 112 (77.8%) patients would like to be able to remotely communicate with medical personnel in case of health issues. At the same time, only 37 (25.7%) patients with CKD are ready to attend full-time schools for patients. Conclusion. Cognitive impairments and low awareness of older patients with chronic cardiorenal syndrome complicate the implementation of a patient-centered approach.

Evaluation of the level of natriuretic peptides in the diagnosis and characterization of chronic kidney disease and cardiorenal syndrome in children

BACKGROUND. Natriuretic peptides have cardio- and renoprotective effects, inhibiting inflammatory and proliferative processes. The role of natriuretic peptides in the early diagnosis and characterization of chronic kidney disease (CKD) and cardiovascular complications as the disease development and progresses has not been studied.TNEAIM: to study the level of natriuretic peptides in children depending on the stage of CKD development and to assess the significance of this indicator.PATIENTS AND METHODS. The study involved 93 children with congenital diseases of the urinary system at the age from 3 to 18 years. Three groups were identified: group I - 54 patients with CKD stage I , group II - 29 patients with CKD stage II; Group III - 10 children with CKD stages IV-V (patients with CKD stages IV and V were combined due to their small amount). Control group - 10 clinically healthy children of the corresponding age. The N-terminal propeptide of natriuretic hormone (NT-proBNP) was determined in the blood by the enzyme-linked immunosorbent assay.RESULTS. An increase in the level of NT-proBNP by 28.7% takes place already in the early stages of CKD. With the progression of CKD, an increase in the level of NT-proBNP was noted from 57.4 % in children in the group of patients with stage I CKD to 80 % in children in group III patients. The maximum concentrations of NT-proBNP, many times higher than those in CKD stages I and II, were observed in children with CKD stages IV-V. The degree of increase in the level of NT-proBNP correlated with the severity of CKD.CONCLUSION. In the diagnosis and characterization of CKD and cardiorenal syndrome in children, the determination of the level of natriuretic peptides is of great importance. A high level of natriuretic peptides characterizes the presence of cardiorenal relationships and can be used as an additional criterion for assessing the severity of CKD, including at the early stages of its development.

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

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.

Chronic Secondary Cardiorenal Syndrome: The Sixth Innovative Subtype.

Heart failure, as the leading cause of cardiovascular death, has seen an increased prevalence nowadays, along with renal insufficiency. It's estimated that 25–63% of heart failure patients have the comorbidity of renal insufficiency, an independent risk factor of various cardiovascular events and predictors of poor prognosis (1). A therapeutic principle of heart failure emphasizing decongestive treatment is limited by the demand for sufficient perfusion in terms of renal insufficiency therapy, making the treatment of both concomitant diseases more complicated and contradictory, with mild balance; hence, the great interest in cardiorenal interactions has broadened among researchers and clinicians, and the concept of cardiorenal syndrome (CRS) was first proposed in 2004. CRS, defined as a pathophysiological process of adverse interaction between the heart and kidneys, encompasses a spectrum of diseases involving acute or chronic dysfunction in one organ that induces decompensated dysfunction in the other, and eventually they evolve into an interrelated and vicious cycle of declining function in both organs. CRS was first categorized into five subtypes in 2008 based on sequential organ involvement and the course of progression over time (i.e., acute or chronic), including acute cardiorenal syndrome, chronic cardiorenal syndrome, and acute renocardiac syndrome, chronic renocardiac syndrome, secondary cardiorenal syndrome, of which a brief definition, etiology, and pathophysiology are given in Table 1 (2). With the consideration that the previous secondary CRS subtype has a shortcoming in that it is not as symmetrical as the first four subtypes, as well as the huge difference of pathophysiological changes, the treatment principles of the two organs, and of gradually increasing in-depth knowledge of fibrosis pathogenesis over the past few years, it's become quite necessary to propose a new CRS classification. And that's why we now first propose the sixth innovative CRS subtype on the basis of the concept of “chronic co-impairment” of the heart and kidneys, further classifying traditional secondary CRS as acute secondary CRS and chronic secondary CRS, thus making the novel six kinds of CRS categories paired and matched correspondingly. The most common precipitant of acute secondary CRS is biotoxin damage and a cytokine storm generated by acute sepsis, and the primary treatment principles are cause-related treatment as aggressive anti-infective therapy, as well as symptomatic treatment of cardiac and renal dysfunction. However, the novel type 6 CRS (chronic secondary CRS) is actually more prevalent in clinical practice, and its pathophysiological and clinical characteristics as well as diagnosis and treatment principles vary dramatically from other subtypes of CRS, which will be described in detail in the following article. Table 1 New classification of CRS based on disease acuity and sequential organ involvement.

Use of cystatin C to estimate glomerular filtration rate

Glomerular filtration rate (GFR) is routinely estimated using endogenous biomarkers due to the complexity of direct measurement methods. Cystatin C is a protease inhibitor produced in all nucleated cells. It is freely filtered and then catabolized by renal tubular cells. Therefore, plasma concentration of cystatin C depends primarily on GFR. Serum cystatin C is less affected by muscle mass, diet, race, gender and age than creatinine. In the general population, equations to estimate GFR based on cystatin C do not have a better performance than those based on creatinine. However, formulas that combine creatinine and cystatin C are more accurate and precise. Estimation of GFR based on cystatin C could be useful in populations in which creatinine value may be biased, such as people with extremely low or high muscle mass, cirrhosis and chronic cardiorenal syndrome. Due to its higher cost in comparison to creatinine, we recommend measuring cystatin C on these clinical situations and when a more accurate estimation of GFR is required.

Association between lipoprotein (a) level and chronic cardio-renal syndrome in elderly patients

Objective: To explore the relationship between lipoprotein(a) [Lp(a)] and chronic cardio-renal syndrome (CRS) in elderly patients. Methods: Chronic heart failure (CHF) patients age ≥ 65 years old, who hospitalized in the department of Cardiology of Hebei General Hospital from December 2017 to October 2019, were included in this study. According to the estimate glomerular filtration rate (eGFR) level, patients were divided into CRS group (eGFR<60 ml·min-1·1.73 m-2) and CHF group (eGFR ≥60 ml·min-1·1.73 m-2). The blood index and basic disease information were collected and compared. Left ventricular ejection fraction (LVEF) were measured by echocardiography. The correlation between clinical indicators and cardio-renal function (LVEF and eGFR) was assessed. The multivariate logistic regression analysis was used to evaluate the related risk factors of CRS in elderly patients; subgroup logistic regression analysis was performed according to the basic disease of patients to assess the relationship between Lp(a) and CRS. Results: A total of 172 elderly patients (85 males (49.4%), aged 79 (71, 84) years) were finally enrolled. Among them, 88 cases (51.2%) were in CRS group and 84 cases (48.8%) were in CHF group. Age (80 (74, 84) years old vs. 74 (70, 82) years old) and LP (a) levels (222.0 (112.0, 445.3) mg/L vs. 155.0 (97.0, 348.7) mg/L) were significantly higher in the CRS group than in the CHF group (P<0.05). Lp(a) levels were negatively correlated with LVEF (r=-0.155, P=0.043) and eGFR (r=-0.220, P=0.004) in total cohort. In the subgroup analysis of patients with 2 high-incidence basic diseases (coronary heart disease and hypertension), Lp(a) was negatively correlated with LVEF (r=-0.250, P=0.007) in the coronary heart disease group, and negatively correlated with eGFR (r=-0.233, P=0.013) in the hypertension group. Multivariate logistic regression analysis showed that age (OR = 1.069, 95%CI: 1.017-1.124, P= 0.009) and Lp(a) (OR = 3.719, 95%CI: 1.339-10.326, P = 0.012) were independent correlates of CRS. The results of logistic regression analysis showed that Lp(a) was an independent correlative factor of CRS in the subgroups of coronary heart disease (OR=3.207, 95%CI: 1.129-9.108, P=0.029) and hypertension (OR=3.054, 95%CI: 1.086-8.587, P=0.034). Conclusion: Serum Lp(a) level is independently related with CRS in elderly patients.

Biomarkers of hypoxia in patients with chronic cardiorenal syndrome

Background and Aims: Modern guidelines discuss in detail the treatment of patients with chronic heart failure (CHF), however hypoxia biomarkers depending on kidney dysfunction have not been insufficiently studied. The aim of this study was to investigate hypoxia biomarkers including serum hypoxia-1-induced factor (HIF-1) and erythropoietin in patients with chronic heart failure, depending on the presence of chronic kidney disease (CKD).

Reduced Albuminuria and Potassemia Indicate Early Renal Repair Processes after Resynchronization Therapy in Cardiorenal Syndrome Type 2.

Background Patients with chronic cardiorenal syndrome type 2 (T2-CRS) who qualify for resynchronization therapy (CRT) are exposed perioperatively to potentially nephrotoxic factors including contrast agents and blood loss. Methods The objective of this prospective interventional study was to assess the effects of CRT on renal function in patients with T2-CRS within the first 48 hours following implantation. Initially, 76 patients (15% female; aged 69 ± 9.56 years) with heart failure (New York Heart Association classes II–IV), ejection fraction ≤ 35%, and QRS > 130 ms were included in the study. During CRT implantation, a nonionic contrast agent (72.2 ± 44.9 mL) was administered. Prior to and 48 hours following implantation, renal function was evaluated using the following serum biomarkers: creatinine (sCr), estimated glomerular filtration rate (using the Chronic Kidney Disease Epidemiology Collaboration equation [eGFRCKD-EPI]), and the electrolyte and urine biomarkers albumin (uAlb), albumin/creatinine ratio (UACR), and neutrophil gelatinase-associated lipocalin (uNGAL). Results Before CRT, patients classified as NYHA class III or IV had higher uNGAL levels in comparison to uNGAL levels after CRT (43.63 ± 60.02 versus 16.63 ± 18.19; p=0.041). After CRT implantation, uAlb, UACR, and potassium levels were reduced (p < 0.05), and uNGAL, sCr, and eGFRCKD-EPI were unchanged. The contrast medium volume did not correlate with the test biomarkers (p > 0.05). Conclusions In patients with T2-CRS, uNGAL is a biomarker of kidney injury that correlates with the NYHA classes. A stable uNGAL value before and after CRT implantation confirms the lack of risk of contrast-induced nephropathy. Reduced albuminuria and blood potassium are biomarkers of improving T2-CRS in the early post-CRT period.

The Cardiorenal Syndrome

In patients with chronic cardio renal syndrome chronic heart disease coexists with chronic kidney disease and poses the patients to a specifically high risk for cardiovascular events and mortality. Treatment recommendations in this condition with a high level of evidence are sparse. Mainstay of therapy in cardiorenal syndrome is fluid metabolism control and stabilization of renal and cardiac function, which can basically been achieved by substances modifying the renin-angiotensin-aldosterone-system as well as diuretics. Noteworthy, despite inducing short-term decreases in renal function, inhibition of the RAAS and diuretic medication associate with the long-term improvements of outcome (so-called pseudo-worsening of renal function). The chronic cardiorenal syndrome calls for interdisciplinary care by both nephrologists and cardiologists in order to allow high-end patient care with a maximum of beneficial effect and a minimum of treatment-related side effects.

Dipeptidyl Peptidase 4 Inhibition Ameliorates Chronic Kidney Disease in a Model of Salt-Dependent Hypertension.

Cardiovascular diseases frequently coexist with chronic kidney disease that constitutes a major determinant of outcome in patients with heart failure. Dysfunction of both organs is related to chronic inflammation, endothelial dysfunction, oxidative stress, and fibrosis. Widespread expression of serine protease DPP4 that degrades varieties of substrates suggests its involvement in numerous physiological processes. In this study, we tested the effects of selective DPP4 inhibition on the progression of renal disease in a nondiabetic model of hypertensive heart disease using Dahl salt-sensitive rats. Chronic DPP4 inhibition positively affected renal function with a significant reduction in albuminuria and serum creatinine. DPP4 inhibition attenuated the inflammatory component by reducing the expression of NF-κB, TNFα, IL-1β, IL-6, and MCP-1. Kidney macrophages expressed GLP-1R, and DPP4 inhibition promoted macrophage polarization toward the anti-inflammatory M2 phenotype. Finally, high degrees of NADPH oxidase 4 expression and oxidation of nucleic acids, lipids, and proteins were reduced upon DPP4 inhibition. Our study provides evidence of renoprotection by DPP4 inhibition in a nondiabetic hypertension-induced model of chronic cardiorenal syndrome, indicating that DPP4 pathway remains a valid object to study in the context of chronic multiorgan diseases.

Working Toward an Improved Understanding of Chronic Cardiorenal Syndrome Type 4.

Chronic diseases of the heart and of the kidneys commonly coexist in individuals. Certainly combined and persistent heart and kidney failure can arise from a common pathologic insult, for example, as a consequence of poorly controlled hypertension or of severe diffuse arterial disease. However, strong evidence is emerging to suggest that cross talk exists between the heart and the kidney. Independent processes are set in motion when kidney function is chronically diminished, and these processes can have distinct adverse effects on the heart. The complex chronic heart condition that results from chronic kidney disease (CKD) has been termed cardiorenal syndrome type 4. This review will include an updated description of the cardiac morphology in patients who have CKD, an overview of the most likely CKD-sourced culprits for these cardiac changes, and the potential therapeutic strategies to limit cardiac complications in patients who have CKD.

Left Ventricular Assist Devices and the Kidney.

Left ventricular assist devices (LVADs) are common and implantation carries risk of AKI. LVADs are used as a bridge to heart transplantation or as destination therapy. Patients with refractory heart failure that develop chronic cardiorenal syndrome and CKD often improve after LVAD placement. Nevertheless, reversibility of CKD is hard to predict. After LVAD placement, significant GFR increases may be followed by a late return to near baseline GFR levels, and in some patients, a decline in GFR. In this review, we discuss changes in GFR after LVAD placement, the incidence of AKI and associated mortality after LVAD placement, the management of AKI requiring RRT, and lastly, we review salient features about cardiorenal syndrome learned from the LVAD experience. In light of the growing number of patients using LVADs as a destination therapy, it is important to understand the effect of these devices on the kidney. Additional research and long-term data are required to better understand the relationship between the LVAD and the kidney.

Role of Bile Acid-Regulated Nuclear Receptor FXR and G Protein-Coupled Receptor TGR5 in Regulation of Cardiorenal Syndrome (Cardiovascular Disease and Chronic Kidney Disease).

It is well known that chronic kidney disease (CKD) is associated with increased risk of cardiovascular disease. In fact, studies have shown that cardiovascular event rates and all-cause mortality increase as a function of CKD as determined by decrease in estimated glomerular filtration rate and presence of microalbuminuria.1,2 In recent years, the term cardiorenal syndrome (CRS) has been proposed to define the relationship between cardiac disease and renal disease. Ronco et al has defined CRS as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other.3–6 CRS Type 1: acute CRS is defined as sudden worsening of cardiac function (acute cardiogenic shock or acutely decompensated heart failure), leading to acute kidney injury. CRS Type 2: chronic CRS is defined as chronic abnormalities in cardiac function (chronic congestive heart failure) causing progressive and potentially permanent CKD. CRS Type 3: acute renocardiac syndrome is defined as sudden worsening of kidney function (acute kidney injury or acute glomerulonephritis) causing acute cardiac disorder (heart failure, arrhythmia, or ischemia). CRS Type 4: chronic renocardiac syndrome is defined as CKD contributing to decreased cardiac function, cardiac hypertrophy, and increased risk of adverse cardiovascular events. CRS Type 5: secondary CRS is defined as systemic condition (obesity, diabetes mellitus, sepsis) causing simultaneous cardiac and renal dysfunction. In this review, I will be discussing mainly the type 5 CRS associated with obesity and diabetes mellitus and models of atherosclerosis and vascular calcification. In addition to discussing renal disease, I will also be discussing vascular disease because vascular dysfunction is a well-characterized complication of renal disease, and vascular dysfunction is also a leading cause of cardiac disease. Our work early on determined an important role for altered renal lipid …

Crosstalk of Various Biomarkers That Might Provide Prompt Identification of Acute or Chronic Cardiorenal Syndromes

Introduction: Pathophysiological interaction between the heart and kidneys represents the basis for clinical entities called cardiorenal syndromes. The purpose of the study was to assess the relations between acute and chronic cardiorenal syndromes and biomarkers [advanced oxidation protein products, brain natriuretic peptide, malondialdehyde, xanthine oxidoreductase (XOD), xanthine oxidase, xanthine dehydrogenase, interleukin 8, cystatin C, plasminogen activator inhibitor-1, high-sensitive troponin T, C-reactive protein and glomerular filtration rate, measured by the Modification of Diet in Renal Disease (MDRD) formula], to hypothesize biomarkers that might provide a prompt identification of acute or chronic cardiorenal syndromes, and to distinguish acute versus chronic types of these syndromes. Methods: A total of 114 participants were enrolled in this study, i.e. 79 patients divided into subgroups of acute and chronic cardiorenal syndromes and 35 volunteers. Results: Nonadjusted odds ratio (OR) showed that there was a significant risk for acute cardiorenal syndrome with increased XOD activity (p = 0.037), elevated cystatin C concentration (p = 0.038) and MDRD (p = 0.028). Multivariable adjusted OR, on the other hand, revealed that only glomerular filtration rate measured by the MDRD formula had a significance for acute cardiorenal syndrome (p = 0.046). Nonadjusted OR showed a significant risk for chronic cardiorenal syndrome only in elderly (p = 0.002). Multivariable adjusted OR exhibited that age was the only risk factor for chronic cardiorenal syndrome (p = 0.012). Conclusion: Cystatin C, glomerular filtration rate measured by the MDRD equation and XOD were independent risk factors for acute cardiorenal syndrome, while age remained an independent risk factor for chronic cardiorenal syndrome. When comparing ORs of evaluated parameters, the highest significance for acute cardiorenal syndrome was plasma concentration of cystatin C.

The Cardio-renal Syndrome (CRS)

The presence of impaired kidney function during heart failure and vice versa is a frequent occurrence. This situation is defined “Cardio-renal Syndrome”.In the Cardio-renal Syndrome (CRS) are included 5 different sub-syndromes defined on the basis of the organ primitively responsible: Acute Cardio-renal Syndrome (Type 1), Chronic Cardio-renal Syndrome (Type 2), Acute Reno-cardiac Syndrome (Type 3), Chronic Renal-cardiac Syndrome (Type 4) and Secondary Cardio-renal Syndrome (Type 5).The physiopathologic mechanisms underlying CRS are still partially obscure, but, a key role seems to be played by the renin-angiotensin-aldosterone axis.Therapeutic strategies involved in CRS treatment include the use of diuretics, ACE inhibitors, Angiotensin Receptor Blockers and β-Blockers, emphasizing the role of a proper use of medication indicated for the treatment of cardiac decompensation.