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Association between Inflammatory Markers, Left Ventricular Systo – Diastolic Dysfunction and Right Heart Involvement in CKD Patients
No full textBackground: Chronic kidney disease (CKD) is characterized by an increased mortality
and morbidity due to cardiovascular involvement. Both left ventricular systolic and
diastolic function are affected since CKD early stages. Pathophysiology of heart failure in
CKD patients involves left ventricular hyperthophy, dilated cardiomiopathy, arrythmias
and cardiac fi brosis together with widespread infl ammatory status accountable for early
atheroembolic disease.
Methods: We have enrolled 146 patients (96 males and 50 females aged 68 ± 9 years
with mean dialytic age of 18 ± 0.4 months) on hemodialysis treatment and 120 patients (
72 males and 48 females aged 57 ± 8 years) on stage III – V CKD. They underwent trans
– thoracic ecocardiography and screened for infl ammatory markers (CRP, IL-6, TNF-).
Results: Hemodialysis patients showed signifi cant correlations between IL – 6, CRP
and TNF- blood levels and systo - diastolic dysfunction parameters such as E/E’ ratio.
Therefore, they also showed strong and signifi cant correlation between IL-6, CRP levels
and right ventricular dysfunction indexes, such as TAPSE (tricuspid annulus plane systolic
excursion) and systolic pulmonary artery pressure (PAPs). On the other hand, CKD patients
showed no correlations between infl ammatory asset and right heart dysfunction.
Conclusions: Our data confi rm close correlation between systolic dysfunction and
infl ammatory markers in CKD and hemodialysis patients. Therefore, our fi ndings underline
close relationships between infl ammatory markers and right heart dysfunction parameters
in hemodialysis patients such as TAPSE and PAPs refl ecting right heart involvement in
the development of cardio – renal syndrome
FGF-23 but Not Klotho Predicts the Presence of Aortic Valve Calcifi cations in Moderate Chronic Kidney Disease
No full textBackground: Cardiovascular calcifi cation (CVC) is a frequent complication in chronic
kidney disease (CKD) patients. Abnormalities in vitamin D receptor (VDR) activation and
hyperphosphoremia are all supposed to contribute to CVC. Fibroblast Growth Factor 23
(FGF-23) is a phosphaturic glycoprotein, linked to phosphate and vitamin D metabolism
as well as poor outcome in CKD. We investigated association between FGF-23 and cardiac
valvular calcifi cation in moderate CKD.
Methods: In this cross-sectional study, 100 (60 men; mean age of 51 ± 4.6 years) CKD
stage IIIB-IV patients were enrolled and underwent laboratory (25-OH Vitamin D, Klotho,
FGF-23, CRP, serum calcium and phosphorus, iPTH, phosphaturia) and echocardiography
testing to assess mineral metabolism such as mitral and aortic valve calcifi cation.Parametric
and non-parametric tests were used. Finally, Receiving Operating Curve (ROC) was used
to test the model performance.
Results: Overall mean serum calcium (9,2±0,4 mg/dl), phosphorus (4,3±0,2 mg/dl)
25OH vitamin D (34,8±13,5 ng/ml) and iPTH (59,11±8,6 pg/ml) were within the reference
ranges. Serum FGF-23 and Klotho mean values were 10,4±1,7 pg/ml and 887,8±110,3
pg/ml, respectively. Phosphaturia was 1,043±258 g/day. At univariable and multivariable
adjusted analyses, aortic but not mitral valve calcifi cation was associated with FGF-23
levels. Notably, Klotho, iPTH, 25OH Vitamin D, serum phosphorous, phosphaturia and
CRP were not associated with either valvular calcifi cation.
Conclusions: Our data suggests that FGF-23 but not Klotho is strongly and
independently associated with aortic valvular calcifi cation. Future studies should test
whether therapeutic strategies aimed at lowering FGF23 (diet, phosphate binders,
calcimimetics) can affect calcifi cation progression and cardiovascular damage
FIBROBLAST GROWTH FACTOR-23 AND PARATHYROID HORMONE PREDICT THE EXTENT OF AORTIC VALVE CALCIFICATIONS IN PATIENTS WITH CHRONIC KIDNEY DISEASE NOT ON DIALYSIS
No full textINTRODUCTION AND AIMS: Cardiac valve calcification (CVC) are commonly present in patients on dialysis and dependent on deranged mineral metabolism. Few data are available in patients with chronic kidney disease not on dialysis (CKD-ND patients).
In this study association between CVC and levels of PTH, phosphorus, calcium, 25-OH vitamin D, FGF-23, Klotho, C-Reactive protein was contemporaneously evaluated in CKD-ND patients.
METHODS: This is a multicenter study performed in consecutive patients referring to five Nephrology Clinics. Inclusion criteria were: age>18 years, CKD stage 3-4, presence of aortic or mitral valve calcification. Clinical examination, routine biochemistry measurements, extent of mitral (MVC) and aortic valve calcification (AVC) by echocardiography were performed.
RESULTS: One hundred patients met inclusion criteria and underwent final evaluation. AVC was found in n.100 patients; MVC was found in n.96 patients. In univariate analysis, no association was found between MVC and e-GFR, serum phosphorus , PTH, FGF-23, Klotho, 25-OH vitamin D, 24/h phosphaturia, CRP. AVC was positively associated with PTH (r2 = 0.212; p=0.034), FGF-23 (r2 = 0.272; p=0.006), and negatively with Klotho (r2 = - 0.208; p=0.038). In multivariable analysis FGF-23 and PTH were significantly associated with AVC score.
CONCLUSIONS: FGF-23 and PTH were associated to AVC extent of CKD-ND patients. No association was found with other variables of interest. These data indicate that FGF-23 and PTH play a direct action on AVC calcification; the role of FGF-23 and PTH was independent from markers of mineral metabolism and inflammation. These data may come into the still open debate on the usefulness of FGF-23 assay in routine clinical care of CKD-ND as part of cardiovascular risk stratification.
Session: Poster Session: Chronic Kidney Disease. Bone diseas
Chronic kidney disease and cardiovascular complications
No full textAbstract Cardiovascular diseases such as coronary artery
disease, congestive heart failure, arrhythmias and sudden
cardiac death represent main causes of morbidity and
mortality in patients with chronic kidney disease (CKD).
Pathogenesis includes close linkage between heart and
kidneys and involves traditional and non-traditional cardiovascular
risk factors. According to a well-established
classification of cardiorenal syndrome, cardiovascular
involvement in CKD is known as ‘‘type-4 cardiorenal
syndrome’’ (chronic renocardiac). The following review
makes an overview about epidemiology, pathophysiology,
diagnosis and treatment of cardiovascular complications in
CKD patients
[Management of color-Doppler imaging in dialysis patients]
No full text: In recent decades, the survival of dialysis patients has gradually increased thanks to the evolution of dialysis techniques and the availability of new drug therapies. These elements have led to an increased incidence of a series of dialysis-related diseases that might compromise the role of dialysis rehabilitation: vascular disease, skeletal muscle disease, infectious disease, cystic kidney disease and cancer. The nephrologist is therefore in charge of a patient group with complex characteristics including the presence of indwelling vascular and/or peritoneal catheters, conditions secondary to chronic renal failure (hyperparathyroidism, anemia, amyloid disease, etc.) and superimposed disorders due to old age (cardiac and respiratory failure, cancer, type 2 diabetes mellitus, etc.). Early clinical and organizational management of such patients is essential in a modern and ''economic'' vision of nephrology. The direct provision of ultrasound services by the nephrologist responds to these requirements. A minimum level of expertise in diagnostic ultrasonography of the urinary tract and dialysis access should be part of the nephrologist's cultural heritage, acquired through theoretical and practical training programs validated by scientific societies, especially for those who choose to specialize in these procedures and become experts in imaging or interventional ultrasonography
Fibroblast growth factor 23 and parathyroid hormone predict extent of aortic valve calcifications in patients with mild to moderate chronic kidney disease
No full textCardiac valve calcifications are present in dialysis patients and regarded as dependent on a deranged mineral metabolism. Few data are available for patients with chronic kidney disease (CKD) not on dialysis. This study evaluates the potential association between the extent of cardiac valve calcification and levels of intact parathyroid hormone (i-PTH), phosphorus, calcium, 25-OH vitamin D, fibroblast growth factor 23 (FGF-23), Klotho and C-reactive protein (CRP) simultaneously measured in patients with mild to moderate CKD
A new CHA2DS2VASC score integrated with estimated glomerular filtration rate, left ventricular hypertrophy, and pulse pressure is highly effective in predicting adverse cardiovascular outcome in chronic kidney disease
No full textChronic hyperkalemia in non-dialysis CKD: controversial issues in nephrology practice
No full textChronic hyperkalemia is a major complication of chronic kidney disease (CKD) that occurs frequently, heralds poor prognosis, and necessitates careful management by the nephrologist. Current strategies aimed at prevention and treatment of hyperkalemia are still suboptimal, as evidenced by the relatively high prevalence of hyperkalemia in patients under stable nephrology care, and even in the ideal setting of randomized trials where best treatment and monitoring are mandatory. The aim of this review was to identify and discuss a range of unresolved issues related to the management of chronic hyperkalemia in non-dialysis CKD. The following topics of clinical interest were addressed: diagnosis, relationship with main comorbidities of CKD, therapy with inhibitors of the renin–angiotensin–aldosterone system, efficacy of current dietary and pharmacological treatment, and the potential role of the new generation of potassium binders. Opinion-based answers are provided for each of these controversial issues
Finerenone: Questions and Answers—The Four Fundamental Arguments on the New-Born Promising Non-Steroidal Mineralocorticoid Receptor Antagonist
Full text linkChronic kidney disease (CKD) is one of the most common complications of diabetes mellitus and an independent risk factor for cardiovascular disease. Despite guideline-directed therapy of CKD in patients with type 2 diabetes, the risk of renal failure and cardiovascular events still remains high, and diabetes remains the leading cause of end-stage kidney disease in affected patients. To date, current medications for CKD and type 2 diabetes mellitus have not reset residual risk in patients due to a high grade of inflammation and fibrosis contributing to kidney and heart disease. This question-and-answer-based review will discuss the pharmacological and clinical differences between finerenone and other mineralocorticoid receptor antagonists and then move on to the main evidence in the cardiovascular and renal fields, closing, finally, on the potential role of therapeutic combination with sodium-glucose cotransporter 2 inhibitors (SGLT2is)
Left Ventricular Hypertrophy in Chronic Kidney Disease Patients: From Pathophysiology to Treatment
No full textCardiovascular diseases represent the main causes of morbidity and mortality in patients with
chronic kidney disease (CKD). According to a well-established classification, cardiovascular
involvement in CKD can be set in the context of cardiorenal syndrome type 4. Left ventricular
hypertrophy (LVH) represents a key feature to provide an accurate picture of systolic-diastolic
left heart involvement in CKD patients. Cardiovascular involvement is present in about 80%
of prevalent hemodialysis patients, and it is evident in CKD patients since stage IIIb–IV renal
disease (according to the K/DOQI CKD classification). According to the definition of cardiorenal
syndrome type 4, kidney disease is detected before the development of heart failure, although
timing of the diagnosis is not always possible. The evaluation of LVH is a bit heterogeneous,
and few standard imaging methods can provide the accuracy of either CT- or
MRI-derived left ventricular mass. Key principles in the treatment of LVH in CKD patients are
mainly based on anemia and blood pressure control, together with the management of secondary
hyperparathyroidism and sudden cardiac death prevention. This review is mainly focused
on the clinical aspects of CKD-related LVH to provide practical guidelines both for cardiologists
and nephrologists in the daily clinical approach to CKD patients
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