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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.

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.

In this pilot study, sequential ultrasonic scanning was used to assess (a) whether furosemide injection normally causes an enlargement of kidney size, and (b) whether this effect is blunted in renovascular hypertensives to such a degree as to bear potential diagnostic value. Furosemide caused similar degrees of maximal area enlargement in both kidneys of 10 healthy subjects (16.1 +/- 3.9%) and 10 essential hypertensives (14.8 +/- 4.2%) whereas in 11 renovascular patients maximal distension of the affected kidneys was significantly blunted (9.4 +/- 3.7%) in comparison with that of contralateral kidneys (19.6 +/- 7.7%). In the 6 hypertensives with one small kidney not due to renal artery stenosis, maximal enlargement of the affected kidneys averaged 22.8 +/- 5.1%, and that of contralateral kidneys 15.8 +/- 4.2%. In 8 out of the 11 patients with renovascular hypertension the difference in response between the paired kidneys had values outside the ranges of patients with both the other forms of arterial hypertension. The data suggest that the furosemide test may be of value in the screening for renovascular hypertension.

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.

The long-term course of the parasympathetic neuropathy in patients with chronic renal failure maintained on haemodialysis was investigated. Well-established tests of parasympathetic function (deep breathing test, atropine test) were performed in 45 patients who had been dialysed for periods ranging from 1 to 12 years and in 34 normal subjects. The responses to these tests were clearly compromised in dialysis patients but there was no relationship between duration of haemodialysis treatment and results of parasympathetic tests. In the 13 patients who were re-evaluated after an interval of 4 years there was no evidence of progression of the parasympathetic neuropathy. The results suggest that chronic haemodialysis treatment halts parasympathetic damage in patients with chronic renal failure.

To determine the prevalence of hyperchloraemia (plasma chloride concentration of 107 mmol/l or above) in chronic renal failure (CRF), we retrospectively analysed the acid-base and electrolyte status of 102 Italian and 53 English patients with impaired renal function. Hyperchloraemia was a frequent finding at all stages of CRF with a prevalence ranging from 30 to 50%. It was common both in tubulointerstitial nephropathies (45%) and chronic glomerulonephritis (39%). Hyperchloraemic patients were more acidotic than the normochloraemic.

The hemodynamic mechanism of the hypotensive effect of propranolol was studied by quantitative radiocardiography in 8 patients with dialysis-resistant hypertension. Propranolol treatment brought about a decrease in mean arterial pressure and peripheral vascular resistances. The cardiac index was slightly reduced only in the early stage of the treatment. No significant difference was found between patients on treatments lasting longer than 3 months and patients with dialysis-controlled hypertension. The results show that propranolol can be used safely as the sole antihypertensive agent in patients with dialysis-resistant hypertension.

A 54-year-old man on regular haemodialysis developed severe amiodarone-induced hypothyroidism after an unusually short latency period. The iodide accumulation and/or the derangement in thyroid function associated with chronic renal failure may predispose uraemic patients to this serious side effect of amiodarone. Although the pharmacokinetics of amiodarone are not altered by renal failure, caution is advised in prescribing this drug to uraemic patients.