Intravenous calcitriol is known to directly suppress PTH secretion and release. We evaluated the effect of four months of treatment with low-dose intravenous calcitriol on PTH levels in 83 hemodialysis patients. The criteria for including patients in the study were a serum PTH levels at least four times the normal limit, a serum total calcium less than 10 mg/dl and good control of the serum phosphorus level. All patients underwent standard bicarbonate or acetate dialysis; dialysate calcium level was maintained at the usual 3.5 mEq/liter concentration. Initial calcitriol dose was 0.87 +/- 0.02 (SEM) micrograms (0.015 micrograms/kg body wt) thrice weekly at the end of dialysis, and it was reduced in case of hypercalcemia or elevated calcium-phosphate product. Seven out of 83 patients dropped out during treatment. Among the 76 patients who completed the study, 58 (76%) showed a highly significant decrease of intact PTH levels (average reduction 48%) and of alkaline phosphatase levels after four months of therapy. Total serum calcium increased slightly but significantly in the responder group but remained unchanged in the non-responders. No significant changes in ionized calcium levels could be detected, even in responders. Treatment was well tolerated by patients, but 60% of them had transient episodes of hyperphosphatemia. Mean serum phosphate was 4.95 mg/dl at the beginning of the study. It increased significantly after four months of treatment in patients who showed a decrease of PTH levels, although it remained within acceptable limits, below 5.5 mg/dl. Twenty-eight of 76 patients (37%) reduced the dose of calcitriol because their calcium-phosphate products exceeded 60.(ABSTRACT TRUNCATED AT 250 WORDS)

Forty-four elements (Al, Sb, As, Ba, Be, B, Br, Cd, Ce, Co, Cr, Cs, Cu, Eu, Ga, Au, Hf, In, Ir, Fe, La, Lu, Mn, Hg, Mo, Nd, Ni, Pb, Rb, Sm, Sc, Se, Ag, Sr, Ta, Tb, Tl, Th, Sn, W, U, V, Zn, Zr) have been determined in the dialysate for hemodialysis (HD) and fluids for hemofiltration (HF) and continuous ambulatory peritoneal dialysis (CAPD). Multiple determinations have been performed for each dialysis fluid. Several trace elements (TE) showed remarkably elevated average levels; moreover, different bathes of the same commercial product may present a wide variability in TE concentration. The data point out the pivotal role of dialysis fluids in contributing to TE imbalance in dialysis patients and allow the assessment of the potential element exposure of patients on regular dialytic treatment. Patients on HD treatment would be exposed on a weekly basis to milligrams of Al, B, Ba, Br, Cu, Fe, Ni, Pb, Rb, Sr and Zn; on HF, the highest exposures are due to Al, B, Br, Fe, Pb and Zn; on CAPD to B, Br, Fe and Zn. The weekly exposure for several TE appears to be 50- to 12,000-fold higher than the corresponding values on the amount absorbed via the diet (HD: Au, Ba, Be, Ce, Ga, La, Sc, Ta, Th, V, Zr; HF: Be, Ce, Ta, Th, V, Zr; CAPD: Au, Be, Ce, Ga, V, Zr). Although the actual contamination could be markedly influenced by other factors, such as the chemical form of the element or its ability to bind carriers, our data on TE exposure from dialysis fluids can give an insight for further studies on TE imbalances in dialyzed patients.

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Substitution of calcium carbonate for aluminum hydroxide in patients on dialysis: effects on acidosis, parathyroid function, and calcemia. We studied the effects of substituting CaCO₃ for aluminum-containing gels on metabolic acidosis and on the response of the parathyroid glands in 11 patients treated with chronic hemodialysis. The 8 men and 3 women were clinically stable, were known to be compliant, and had no clinical evidence of aluminum overload; they were not receiving vitamin D supplements; and they had been on dialysis for an average of 65.6 months (range: 13–188 months). After 3 weeks of CaCO₃ administration plasma phosphate concentration remained well controlled, and plasma calcium concentration increased from 9.2 ± 0.2 (2.3 ± 0.1 mmol/l) to 10.1 ± 0.2 mg/dl (2.5 ± 0.1 mmol/l). Predialysis plasma bicarbonate concentration increased from 19.7 ± 0.6 to 21.9 ± 0.6 mmol/l. Plasma aluminum concentration decreased from 78.7 ± 12.5 to 48.5 ± 3.9 μg/l. Plasma PTH level increased from 2.0 ± 0.7 to 3.3 ± 0.8 ng/ml despite the concurrent increase in plasma calcium levels. All values returned to control levels following discontinuation of CaCO₃ and resumption of aluminum gels. We conclude: (1) In addition to controlling hyperphosphatemia and increasing plasma calcium concentration, CaCO₃ ameliorates metabolic acidosis. (2) Avoidance of oral aluminum intake is followed by prompt lowering of plasma aluminum levels. (3) PTH levels paradoxically increase despite the increment in plasma calcium concentration. The hypercalcemia seen with CaCO₃ administration may be due, in part, to transient parathyroid hypersecretion that develops when aluminum administration is discontinued.

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