EXCESS PTH IN CRF INDUCES PULMONARY CALCIFICATION, PULMONARY-HYPERTENSION AND RIGHT-VENTRICULAR HYPERTROPHY

Calcification of the lungs occurs in chronic renal failure (CRF) and may adversely affect both pulmonary and right ventricular function. The present study examined the role of excess parathyroid hormone (PTH) in the genesis of pulmonary calcifications in dogs with experimental CRF and evaluated calcium content of lungs, diffusing lung capacity (DCO), mean pulmonary artery pressure (MPAP), right ventricular pressure (RVP), and right ventricular hypertrophy (RVH) in six normal, six with CRF, and six thyroparathyroidectomized (CRF-PTX) dogs. CRF-PTX animals were maintained normocalcemic and euthyroid. The degree and duration of CRF were not different between the two groups with CRF. The mean value of the serum PTH in CRF dogs was 166 +/- 42 mu lEq/ml, but was undetectable in CRF-PTX animals. Thallium scan provided evidence consistent with RVH in CRF dogs but not in CRF-PTX animals. Calcium content of lungs was markedly elevated in CRF dogs (7656 +/- 1657 mg/kg dry wt) but modestly increased in CRF-PTX (1057 +/- 117 mg/kg dry wt) as compared to normal (673 +/- 34 mg/kg dry wt). RVP and MPAP were significantly (P < 0.01) higher and DCO significantly lower in CRF dogs than in normal or CRF-PTX animals. These parameters were not different in the latter two group of dogs. In three additional dogs with CRF of one year duration which were followed for an additional year after parathyroidectomy, these abnormalities were corrected. The data demonstrate that: (1) pulmonary calcification of CRF is, at least partly, due to the secondary hyperparathyroidism; (2) this pulmonary calcification impairs lung function and exerts adverse effects on the right ventricle; and (3) prevention of the secondary hyperparathyroidism of CRF by PTX prevented and/or reversed these derangements.