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To assess whether parathyroidectomy (PTx) affects blood pressure (BP) in hemodialysis (HD) patients, we studied 11 uremics on HD treatment for 8.2 +/- 0.9 years who underwent successful PTx. As the control group, we selected 11 HD patients not submitted to PTx, matched with the study group for sex, age, years on HD, dialysis procedure and BP values. In the controls, BP and body weight did not change during the 2 years of observation. In the patients, BP remained stable in the year before PTx. PTx caused a progressive reduction in BP in 7 of the 11 patients. The fall was significant from the 3rd quarter onward (mean BP values before PTx: 139/82 mm Hg, 1 year after PTx: 122/75 mm Hg). The magnitude of the hypotensive effect of PTx was related to the pre-PTx systolic BP value (r = -0.70, p = 0.016). PTx also caused a significant progressive increase in body weight (1.56 +/- 0.57 kg 1 year after PTx). In conclusion, PTx causes BP fall in HD patients regardless of whether their preintervention values are normal or increased. The BP reduction occurs in concomitance with a consistent increase in body weight. BP variations are clinically relevant and may be related to the post-PTx calcium efflux from the vessel wall.

35 dialysis patients underwent anti-HBV vaccination. We classified patients in responders or non-responders using an anti-HBs titer of 50 UI/l as the discriminating serum level and tried to assess whether the antibody response bears any relationship with the nutritional status. 26 patients (74%) reached the target atb titer, which was maintained during follow-up (average 360 UI/l). The weak response in the other 9, with values never exceeding 20 UI/l, was short-lived. Anthropometric and impedenziometric parameters were higher in responders than in nonresponders, but the difference did not reach statistical significance. We conclude that the atb titer which discriminates uremics in responders or not must be greater than 50 UI/l and that the nutritional status may interfere with the seroconversion rate, but this conclusion needs to be validated in a wider population.

To assess the effect of long-term propranolol therapy on uremic osteodystrophy, we evaluated retrospectively the biochemical, X-ray, and bone histological changes in 9 dialysed hypertensives who had been on propranolol treatment for periods ranging from 1 to 8 years. The control group included 9 well-matched dialysed uremics never treated with beta-blockers. The two groups did not differ in serum ionized calcium or iPTH levels. The incidence of bone resorption evaluated on X-ray findings and on bone biopsy specimens was of a comparable degree in the two groups. Our data show that propranolol even if started early in the course of renal failure, is of no benefit in preventing uremic bone disease.

To assess whether parathyroid hormone (PTH) has any effect on bone aluminium (A1) accumulation, we evaluated the relationship between bone quantitative histomorphometry and bone A1 content in 25 dialysis patients with clinical features of secondary hyperparathyroidism. By means of bone biopsy, patients were classified as showing predominant hyperparathyroidism in 17 cases and mixed lesions in 8. The A1 burden was low, judging from the dialysate A1 and the oral A1 assumption. Bone A1 content and serum A1 levels were higher than normal in both groups, particularly so in the patients with predominant hyperparathyroidism. Significant positive correlations were found between bone indexes of hyperparathyroidism and bone A1 content. Moreover, bone and serum A1 concentrations were directly related. Aluminium staining appeared faintly positive only in a minority of bone samples, and was mainly localized at the neutral bone surfaces. We conclude that in dialysis osteodystrophies with features of secondary hyperparathyroidism and in a clinical setting characterized by low-grade A1 burden, PTH may favour A1 accumulation into the bone.

Urine alkalinization favours the formation of calcium phosphate (CaP) and struvite stones. In this retrospective study we analyze the effect of chronic urinary acidification on phosphatic stone recurrence. Twenty-four patients with CaP-struvite recurrent stones and persistently high urinary pH were divided in two groups: group A, 11 patients who failed to lower the urinary pH below 5.5 during a standard acid load test: group B, 13 patients with preserved acidification power. Ammonium sulfate 2-3 g/day was given for 4.7 and 6.5 years to groups A and B, respectively. A persistent reduction in urinary pH, relative saturation for CaP and stone formation rate was observed in both groups. The treatment did not cause systemic acidosis as long as renal function remained normal. Urinary daily excretion of Ca and P as well as their renal tubular handling did not change with time. Results suggest acidifying agents might be useful in preventing recurrence of CaP-struvite stones even in the presence of a mild acidification defect and encourage undertaking properly controlled prospective trials.