The relationship between arteriovenous fistula blood flow rate and pulmonary artery pressure in hemodialysis patients

Acartürk, Gürsel; Albayrak, Ramazan; Melek, Mehmet; Yüksel, Şeref; Uslan, Mustafa İhsan; Atli, Hüseyin; Çölbay, Mehmet; Ünlü, Mehmet; Fidan, Fatma; Aşcı, Zerrin; Cander, Soner; Karaman, Ozcan; Açar, Murat

doi:10.1007/s11255-007-9269-8

Cited by 38 publications

(48 citation statements)

References 18 publications

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“…13,18,26,27 We could not show any significant difference with respect to CaXiP product and iPTH on comparing the patients with and without PHT ( Table 5). Total cholesterol levels were not found to be different in two different groups of dialysis patients; hence, we could not relate hyperlipidemia with PHT.…”

Section: Discussionmentioning

confidence: 82%

“…However in literature, there are results contradicting ours such that they could not show any relationship between hemoglobin levels and sPAP. 12,18 HbA1c levels were also significantly lower in diabetic patients without PHT than the ones with PHT. This finding supported our previous finding of the higher sPAP levels in diabetic patients which probably got worsened with bad control of blood glucose shown by high HbA1c levels.…”

Section: Discussionmentioning

confidence: 86%

“…[12][13][14][15][16][17][18][19][20] On comparing the patients with and without PHT, levels of hemoglobin (p ¼ 0.01), HbA1c in diabetics (p ¼ 0.03), and serum albumin (p ¼ 0.003) were found to be significantly higher in patients with PHT, while CaXiP product, iPTH, and total cholesterol levels were not found to be significantly different between the two groups of patients (Table 5). We believe that anemia, which can be a factor in the development of LVH and increased cardiac output, may help in the pathogenesis of PHT.…”

Section: Discussionmentioning

confidence: 99%

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Pulmonary Hypertension in Dialysis Patients

Oygar

Zekican

2012

Renal Failure

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Cardiovascular complications are encountered frequently in end-stage renal disease (ESRD) patients. The study was designed as a prospective cohort study and a total of 105 dialysis patients, 77 hemodialysis and 28 peritoneal dialysis patients, were investigated. All patients had undergone M-Mode Doppler echocardiography every 6 months by which their systolic pulmonary arterial pressures (sPAPs) and left ventricular mass indices (LVMIs) were recorded. Thirty-nine (37.1%) patients had pulmonary hypertension (PHT), that is, a mean sPAP of more than 35 mmHg. The frequency of PHT was higher in peritoneal dialysis patients but the difference was insignificant (p ¼ 0.08). However, the frequency of left ventricular hypertrophy (LVH) was found to be significantly higher in peritoneal dialysis patients than in hemodialysis patients (p ¼ 0.001). When patients with and without PHT were compared, the duration of dialysis (p ¼ 0.02), hemoglobin (p ¼ 0.01), HbA1c (p ¼ 0.03), and serum albumin levels (p ¼ 0.003) were found to be significantly higher in patients with PHT than those without PHT. In conclusion, although nonsignificant, we found a higher prevalence of PHT in peritoneal dialysis patients when compared with hemodialysis patients. This might be due to the significantly higher prevalence of LVH, hence hypervolemia, in peritoneal dialysis patients. The prevention and treatment of PHT in dialysis patients is very important for the improvement of survival in these patients. Hence, the increased prevalence of PHT in ESRD patients necessitates understanding the multiple and interacting factors, such as LVH, serum albumin and hemoglobin levels, and control of diabetes, that might contribute to this pathology in these patients.

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Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

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Pulmonary Hypertension in Dialysis Patients

Oygar

Zekican

2012

Renal Failure

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“…7 Nevertheless, in a recent study by Acarturk et al, there was no direct relationship between blood flow rate of arteriovenous fistula and PAP. 35 The reduction of PAP in transplant recipients seems to be independent of the functional status of the arteriovenous fistula even though in the ones without a functioning fistula the cardiac output was significantly reduced, thereby indicating that non-hemodynamic and mainly uremia related-but still unknown-factors may be associated with the development of PH in this group of patients.…”

Section: Etiologic Factors For Ph-pathophysiology Of Phmentioning

confidence: 84%

Pulmonary Hypertension in Dialysis Patients

et al. 2013

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Pulmonary hypertension in end-stage renal disease patients is associated with significantly increased morbidity and mortality. The prevalence of pulmonary hypertension in dialysis patients is relatively high and varies in different studies from 17% to 49.53% depending on the mode of dialysis and other selection factors, such as the presence of other cardiovascular comorbidities. The etiopathogenic mechanisms that have been studied in relatively small studies mainly include arteriovenous fistula-induced increased cardiac output, which cannot be accomodated by, the spacious under normal conditions pulmonary circulation. Additionally, pulmonary vessels show signs of endothelial dysfunction, dysregulation of vascular tone due to an imbalance in vasoactive substances, and local as well as systemic inflammation. It is also believed that microbubbles escaping from the dialysis circuit can trigger vasoconstriction and vascular sclerosis. The non-specific therapeutic options that proved to be beneficial in pulmonary artery pressure reduction are endothelin inhibitors, phosphodiesterase inhibitor sildenafil, and vasodilatory prostaglandins in various forms. The specific modes of treatment are renal transplantation, size reduction or closure of high-flow arteriovenous fistulas, and transfer from hemodialysis to peritoneal dialysis-a modality that is associated with a lesser prevalence of pulmonary hypertension.

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“…The first published study (Acarturk et al, 2008) used mean PAP calculated from the right ventricular outflow tract acceleration time according to the Mahan's equation (mPAP in mmHg =79 -0.45 x acceleration time in ms); AVF blood flow rate was estimated by Doppler sonography. Thirty-two patients were included, 24 with a radial and 8 with a brachial AVF created 32±34 months before evaluation.…”

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confidence: 99%