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The case of a 67-year-old man who has had psoriasis with multiple joints involvement for 30 years and renal failure for 1 year is described. He was admitted because of uremic symptoms and exacerbation of psoriasis. Hypocalcemia and low serum active 1.25(OH)2D3 were also observed. Hemodialysis, oral 1.25(OH)2D3 and CaCO3 supplement were employed. Interestingly, the psoriasis strikingly improved. The relationships among psoriasis, renal failure, 1.25(OH)2D3, serum calcium level and dialysis are discussed.

Metabolic acidosis has been shown to alter vitamin D metabolism. There is also evidence that calcium may modulate 1,25(OH)2D3 by a parathyroid hormone (PTH)-independent mechanism. To investigate the effect of rapid correction of chronic metabolic acidosis on serum 1,25(OH)2D3 levels by free calcium clamp in chronic renal failure, 20 patients with mild to moderate metabolic acidosis (mean pH 7.31 +/- 0.04) and secondary hyperparathyroidism (mean intact PTH 156.47 +/- 84.20 ng/l) were enrolled in this study. None had yet received any dialysis therapy. Metabolic acidosis was corrected by continuous bicarbonate infusion for 3-4 h until plasma pH was around 7.4, while plasma ionized calcium was held at the preinfusion level by calcium solution infusion during the entire procedure. The plasma pH, bicarbonate, total CO2, sodium, and serum total calcium levels were significantly increased while serum concentrations of alkaline phosphatase and albumin were significantly decreased after bicarbonate infusion. The plasma ionized calcium, potassium, serum magnesium, inorganic phosphorus, and 25(OH)D levels showed no significant change before and after bicarbonate infusion. The serum 1,25(OH)2D3 levels were significantly increased (38.66 +/- 11.77 vs. 47.04 +/- 16.56 pmol/l, p < 0.05) after correction of metabolic acidosis. These results demonstrate that rapid correction of metabolic acidosis raises serum 1,25(OH)2D3 levels in vitamin D-deficient chronic renal failure patients, and may underline the importance of maintaining normal acid-base homeostasis in the presence of secondary hyperparathyroidism in chronic renal failure.

1. Secondary hyperparathyroidism in chronic renal failure may contribute to abnormalities of lipid metabolism and glucose tolerance. Amelioration of secondary hyperparathyroidism has been reported to mitigate the hyperlipidaemia and improve glucose tolerance experimentally. 2. The effect of the partial suppression of hyperparathyroidism by intravenous calcitriol on lipid levels and glucose tolerance was studied in 15 haemodialysis patients with secondary hyperparathyroidism. All received intravenous calcitriol 1 microgram at the end of haemodialysis thrice weekly for eight weeks. Oral glucose tolerance test and plasma lipid profiles including triglyceride, total cholesterol, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), apoprotein A-I and apoprotein B were determined simultaneously before and after eight weeks of therapy. 3. Before calcitriol treatment, uraemic patients with secondary hyperparathyroidism displayed a significant higher triglyceride and a significant lower HDL-C and apoprotein A-I as well as marked glucose intolerance with an increment of the area below the glucose curve when compared with healthy control subjects. 4. After eight weeks of calcitriol treatment, there was a significant decrement in serum intact parathyroid hormone (476.45 +/- 48.33 versus 191.37 +/- 30.17 ng/l, P < 0.001) and plasma triglyceride (2.24 +/- 0.34 versus 1.80 +/- 0.29 mmol/l, P < 0.05) as well as a significant increment of plasma apoprotein A-I (38.13 +/- 2.14 versus 44.19 +/- 2.18 mumol/l, P < 0.05), whereas there was no significant change in serum total cholesterol, LDL-C, HDL-C, and apoprotein B.(ABSTRACT TRUNCATED AT 250 WORDS)

Background: To investigate the effect of the reversal of hyperparathyroidism on platelet intracellular free calcium ([Ca2+]i) by pharmacological parathyroidectomy with intravenous calcitriol in uremic patients with secondary hyperparathyroidism (2 degrees HPT)., Methods: Serum concentrations of intact parathyroid hormone (I-PTH) were measured by two-site immunometric assay, and platelet [Ca2+]i was assessed using the fluorescent indicator fura-2. Fifteen hemodialysis patients with 2 degrees HPT and serum I-PTH 4 times greater than the normal upper limits, were selected for treatment with intravenous calcitriol 1 microgram thrice weekly for one month., Results: An increase of serum I-PTH (449.17 +/- 52.35 vs 32.52 +/- 1.95 pg/ml) and elevated platelet [Ca2+]i (139.49 +/- 8.78 vs 74.70 +/- 6.48 nM/L) was observed in uremic patients with 2 degrees HPT. Serum I-PTH levels were significantly correlated with platelet [Ca2+]i in uremic patients with 2 degrees HPT (r = 0.736, p = 0.002). The serum I-PTH levels decreased from 449.17 +/- 52.35 to 221.27 +/- 35.66 pg/ml (p < 0.001) and platelet [Ca2+]i fell from 139.49 +/- 8.78 to 97.86 +/- 7.25 nM/L (p < 0.001) after treatment. Fall in platelet [Ca2+]i was related to concomitant reduction in PTH levels (r = 0.572, p = 0.026)., Conclusions: It was concluded that an increase in cytosolic calcium in uremia may be at least in part induced by PTH. Besides, intravenous calcitriol can provide an effective way to suppress elevated serum I-PTH and attenuate platelet free calcium in uremia with 2 degrees HPT.

Metabolic acidosis induces a combination of inhibited osteoblastic and stimulated osteoclastic activity. To determine the role of alkali therapy in osteoblast function in chronic renal failure, serum bone isoenzyme of alkaline phosphatase (BAP) and osteocalcin were assessed before and after bicarbonate infusion. Eighteen patients with mild to moderate metabolic acidosis, none of whom had received dialysis therapy, were enrolled in this study. Metabolic acidosis was corrected by continuous bicarbonate infusion while plasma ionized calcium was monitored at 5 min intervals and held at the preinfusion level by calcium solution infusion during the entire procedure. The end-point of the study was reached when the plasma bicarbonate was approximately 24 mmol/l or pH was approximately 7.4 and plasma ionized calcium was clamped at the preinfusion level with only a 0.01 mmol/l fluctuation. The plasma pH (7.31 +/- 0.04 vs. 7.40 +/- 0.03, P < 0.001), bicarbonate (18.46 +/- 2.49 vs. 23.66 +/- 2.72 mmol/l, P < 0.001), serum total calcium, and osteocalcin (15.61 +/- 6.45 vs. 18.79 +/- 6.71 mg/l, P < 0.05) levels were significantly increased, whereas serum concentrations of alkaline phosphatase and albumin levels were significantly decreased after bicarbonate infusion. The serum BAP (1.85 +/- 1.29 vs. 1.79 +/- 1.18 mukat/l, P = 0.252), and inorganic phosphorus levels showed no significant differences before and after bicarbonate infusion. These results demonstrate that rapid correction of metabolic acidosis improves osteoblast function and may underline the importance of maintaining normal acid-base homeostasis in chronic renal failure.

Disturbance in the vitamin D/parathyroid hormone (PTH) axis may be important in the pathogenesis of glucose intolerance and insulin resistance in uraemia. To investigate possible relationships between hyperparathyroidism, intracellular free calcium ([Ca2+]i), and glucose tolerance in chronic renal failure, we measured serum intact PTH (I-PTH) by two-site immunometric assay, platelet [Ca2+]i using the fluorescent indicator fura-2, and plasma glucose and insulin after 14 h overnight fast and at 30, 60 and 120 min following a 75 g oral glucose load, in 18 chronic haemodialysis patients with elevated serum I-PTH. Calcitriol (1 microgram) was administered parenterally at the end of each dialysis session for four weeks. This significantly decreased serum I-PTH (p < 0.001) and platelet [Ca2+]i (p < 0.01). Uraemic patients initially showed marked glucose intolerance, with increased area below the glucose curve compared to healthy controls, but after 4 weeks of calcitriol treatment, this effect was significantly decreased, and there was a significant rise in the area under the insulin curve after glucose load. The insulinogenic index also increased significantly after calcitriol treatment. These data suggest that calcitriol treatment of haemodialysis patient with secondary hyperparathyroidism is associated with increased insulin secretion in response to glucose challenge, and that this change is linked to the decrease in intracellular free calcium.

To clarify the role of serum vitamin D and bone remodeling markers in postmenopausal diabetic azotemics, we designed a study involving 3 different postmenopausal patient groups. Group I consisted of 20 diabetic women with renal insufficiency who were not yet on dialysis therapy. Group II consisted of 15 age-matched nondiabetic women with comparable degrees of renal insufficiency. Group III consisted of 20 age-matched women with normal renal function. We investigated the overnight fasting serum 25 (OH) vit-D, 1,25(OH)2 vit-D3, osteocalcin (OC), bone isoenzyme of alkaline phosphatase (ALK-PB) and intact parathyroid hormone (I-PTH) levels in these cases. The serum I-PTH and OC levels were statistically significantly higher, whereas 1,25(OH)2vit-D3 were significantly lower in Group I and Group II patients than in Group III patients. We found no significant correlation between elevation of I-PTH and reduced 1,25(OH)2 vit-D3 levels in Group I and Group II patients. I-PTH levels correlated positively with OC in Group I and Group II patients. There was no significant difference in serum 25(OH) vit-D among these 3 groups of patients. We conclude that (1) serum OC level may serve as a good parameter in evaluating secondary hyperparathyroidism in postmenopausal azotemics with or without diabetes, (2) even in the presence of menopause, renal failure per se is the main factor in determining serum 1,25(OH)2 vit-D3 levels in diabetic azotemics.