Key result
Serum ADMA levels were significantly elevated in hemodialysis patients with pulmonary hypertension compared to those without (1.32 vs 0.99 µmol/L; p<0.001) and independently related to sPAP.
Why the study?
Are elevated serum ADMA levels associated with pulmonary hypertension in patients undergoing hemodialysis?
Observational (n=94)
Are elevated serum ADMA levels associated with pulmonary hypertension in patients undergoing hemodialysis?
p-value: p=< .001
Elevated serum ADMA levels are independently associated with pulmonary hypertension in patients on hemodialysis, suggesting a role for the nitric oxide pathway in its pathogenesis.
ADMA elevation was associated with pulmonary hypertension in hemodialysis; hypothesis-generating and requires prospective validation before clinical consideration.
BACKGROUND Asymmetrical dimethylarginine (ADMA) is an endogenous nitric oxide (NO) inhibitor. Increased con‐centrations of serum ADMA may also contribute to endothelial dysfunction in patients with pulmonary vascular dis‐ease. Pulmonary hypertension in patients with end‐stage renal disease (ESRD) on hemodialysis is a newly described entity. The pathogenesis of pulmonary hypertension (PH) is considered to be ESRD‐related endothelial dysfunction. The aim of our study was to elucidate the possible relationship between serum ADMA and PH in patients undergo‐ing hemodialysis (HD). METHODS The incidence of PH was prospectively estimated by Doppler echocardiography in 69 patients with ESRD undergoing long‐term HD (2 hrs of completion of HD). Serum ADMA levels were measured using the enzyme‐linked immunosorbent assay (ELISA) method. Pulmonary hypertension was defined as pulmonary artery systolic pressure (sPAP) >35 mmHg as determined by Doppler echocardiography using the modified Bernouli equation. Then, the relationship between ADMA and pulmonary arterial pressure (PAP) was analyzed. RESULTS Pulmonary hypertension was detected in 31.9% of patients receiving HD. Pulmonary artery systolic pressure was significantly higher in patients with PH compared with patients without PH (40.79 ± 12.32 versus 24.81 ± 4.54 mmHg; p < .001), whereas the patients with PH had significantly higher cardiac output (6.41 ± 0.74 versus 5.08 ± 0.61 mL/min/m 2 , p < .001). Serum ADMA levels were significantly elevated in patients with PH compared with those without PH and 25 matched control subjects (1.32 ± 0.15 µmol/L versus 0.99 ± 0.19 µmol/L versus 0.22 ± 0.05 µmol/L; p < .001). Multiple regression analysis showed that sPAP was independently related to ADMA and arteriovenous fistula (AVF) flow ( p < .01). CONCLUSIONS Increased ADMA levels and their positive association with PAP suggest that the NO pathway is involved in the development of pulmonary vascular disease.
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Meng et al. (2010) conducted an observational in End-stage renal disease on hemodialysis (n=94). Serum ADMA levels vs. Patients without pulmonary hypertension and healthy controls was evaluated on Relationship between ADMA and pulmonary arterial pressure (p=< .001). Serum ADMA levels were significantly elevated in hemodialysis patients with pulmonary hypertension compared to those without (1.32 vs 0.99 µmol/L; p<0.001) and independently related to sPAP.
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