Pulmonary Hypertension and Erythropoietin

Buemi, Michele; Senatore, Massimino; Gallo, Giovanna; Crascì, Eleonora; Campo, Sebastiano; Sturiale, Alessio; Coppolino, Giuseppe; Bolignano, Davide; Frisina, N

doi:10.1159/000104443

Cited by 36 publications

(30 citation statements)

References 52 publications

(37 reference statements)

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“…22,23 In a study of 124 adults with sickle cell disease, no relationship between erythropoietin and pulmonary hypertension was detected. 24 We, however, observed that serum erythropoietin concentration is associated with higher tricuspid regurgitation velocity in sickle cell disease patients even after adjustment for the degree of hemolysis and other significant covariates, providing evidence for the concept that erythropoietin may be related to the development of pulmonary hypertension.…”

Section: Discussionmentioning

confidence: 99%

Relationship of erythropoietin, fetal hemoglobin, and hydroxyurea treatment to tricuspid regurgitation velocity in children with sickle cell disease

Gordeuk

Campbell

Rana

et al. 2009

Blood

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Hydroxyurea and higher hemoglobin F improve the clinical course and survival in sickle cell disease, but their roles in protecting from pulmonary hypertension are not clear. We studied 399 children and adolescents with sickle cell disease at steady state; 38% were being treated with hydroxyurea. Patients on hydroxyurea had higher hemoglobin concentration and lower values for a hemolytic component derived from 4 markers of hemolysis (P ≤ .002) but no difference in tricuspid regurgitation velocity compared with those not receiving hydroxyurea; they also had higher hemoglobin F (P < .001) and erythropoietin (P = .012) levels. Hemoglobin F correlated positively with erythropoietin even after adjustment for hemoglobin concentration (P < .001). Greater hemoglobin F and erythropoietin each independently predicted higher regurgitation velocity in addition to the hemolytic component (P ≤ .023). In conclusion, increase in hemoglobin F in sickle cell disease may be associated with relatively lower tissue oxygen delivery as reflected in higher erythropoietin concentration. Greater levels of erythropoietin or hemoglobin F were independently associated with higher tricuspid regurgitation velocity after adjustment for degree of hemolysis, suggesting an independent relationship of hypoxia with higher systolic pulmonary artery pressure. The hemolysis-lowering and hemoglobin F–augmenting effects of hydroxyurea may exert countervailing influences on pulmonary blood pressure in sickle cell disease.

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Section: Discussionmentioning

confidence: 99%

Relationship of erythropoietin, fetal hemoglobin, and hydroxyurea treatment to tricuspid regurgitation velocity in children with sickle cell disease

Gordeuk

Campbell

Rana

et al. 2009

Blood

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“…The prevalence of PH ranges from 9-39% in predialysis patients with stage-5 CKD (Yigla et al, 2003;Buemi et al, 2007;Havlucu et al, 2007;Abdelwhab and Elshinnawy, 2008;Issa et al, 2008), 18.8-68.8% in hemodialysis patients, and 0-42% in individuals on peritoneal dialysis therapy (Kumbar et al, 2007;Bozbas et al, 2009;Unal et al, 2009;Casas-Aparicio et al, 2010;Kiykim et al, 2010;Fabbian et al, 2011;Agarwal, 2012;Etemadi et al, 2012). In our study, 37 of 128 (28.91%) CKD patients from China, who accepted no dialysis or renal transplantation, had Doppler-derived PASP ≥ 35 mmHg.…”

Section: Discussionmentioning

confidence: 55%

“…Varied cutoffs of PH have been adopted in studies, ranging from 25 to ≥45 mmHg (Yigla et al, 2009;Kiykim et al, 2010), which result in different conclusions about PH prevalence. Here, we adopted the PH diagnostic criteria as a PASP ≥ 35 mmHg (Buemi et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

“…PH in patients with CKD may be induced and/or aggravated by left ventricular (LV) disorders as well as the presence of risk factors typical to CKD, including volume overload, an arteriovenous fistula (Abdelwhab and Elshinnawy, 2008), sleep-disordered breathing (Sakaguchi et al, 2011), exposure to dialysis membranes (Kiykim et al, 2010), endothelial dysfunction (Zoccali, 2007), vascular calcification and stiffening, and severe anemia (Buemi et al, 2007). Preventing PH in this population is crucial, as even kidney transplantation may not reverse the high mortality associated with PH.…”

Section: Introductionmentioning

confidence: 99%

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Pulmonary hypertension in patients with stage 1-3 chronic kidney disease

Yang

Bao

2014

Genet. Mol. Res.

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ABSTRACT. Pulmonary hypertension (PH) secondary to chronic kidney disease (CKD) is common, but in stages 1-3 CKD patients, it remains unclear. We sought to evaluate the prevalence of PH and elucidate the possible pathogenesis in Chinese patients with early stage kidney disease. Doppler-estimated pulmonary systolic artery pressure (PASP) was measured in 101 CKD patients with glomerular filtration rate (GFR) ≥60 mL/min/1.73 m 2 and 27 CKD patients with GFR < 60 mL/min/1.73 m 2 . Echocardiographic parameters, plasma brain natriuretic peptide (BNP), and baseline characteristics of patients were recorded. PH was defined as a PASP ≥ 35 mmHg. PH prevalence was 23.76% (24/101) in GFR ≥ 60 mL/min/1.73 m 2 group and 48.15% (13/27) in GFR < 60 mL/min/1.73 m 2 group, P < 0.05. Mean lnBNP was 4.93 ± 1.60 pg/mL in 37 cases with PH and 2.89 ± 1.29 pg/mL in those without, P < 0.01. Left atrial diameter (LA) showed deviation between patients with (43.94 ± 5.81 mm) and without PH (37.76 ± 7.48 mm), P < 0.01. GFR declined significantly in PH group (44.10 ± 22.90 mL/ min/1.73 m 2 ) compared to non-PH group (75.59 ± 31.62 mL/min/1.73 m 2 ), P < 0.01. lnBNP, LA and GFR were independent determinants (r = 0.651, 0.595, -0.488, P < 0.01) of PASP. PH is prevalent among stage 1-3 CKD patients in China. Doppler-estimated PASP is strongly associated with lnBNP, enlarged LA and GFR. Monitoring PASP, plasma BNP and evaluation renal function may help to detect and

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“…Uremia (leading to pulmonary arterial vasoconstriction), the presence of an AVF, low bioavailability of nitric oxide (17), an elevated endothelin level (18,19), vascular calcification, hypervolemia, exposure to dialysis membranes, endothelial dysfunction, and anemia (20,21) are the reported pathogenetic mechanisms for the development of PHT in patients with CKD. Patients with an AVF had a high incidence of PHT due to increased cardiac output and it has been reported that the incidence of PHT in stage 5 CKD patients with an AVF was 40-50% (12,22).…”

Section: Discussionmentioning

confidence: 99%