Increase of Calcitriol during Treatment with Protein-Reduced Diet in Patients with Renal Failure

Wilske, Jan; Attman, Per‐Ola

doi:10.1159/000187857

Cited by 6 publications

(3 citation statements)

References 8 publications

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“…Data from the literature demonstrate that only in the early stages of renal failure calcitriol serum levels can be increased by dietary phosphorus restriction. Instead, when the residual renal function is very poor, as in our patients studied, calcitriol serum levels cannot be modulated by dietary management [16, 17]. …”

Section: Discussionmentioning

confidence: 99%

Secondary Hyperparathyroidism in Severe Chronic Renal Failure Is Corrected by Very-Low Dietary Phosphate Intake and Calcium Carbonate Supplementation

Barsotti

Cupisti

Morelli

et al. 1998

Nephron

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The main purpose of our study was to verify the effect of a very-low-protein, low-phosphorus diet, supplemented with essential amino acids and keto analogues and with calcium carbonate, on circulating levels of intact parathyroid hormone (i-PTH) in severe chronic renal failure patients with secondary hyperparathyroidism, not treated with any vitamin D preparation. To this aim, we shifted 21 chronic uremics (12 males, 9 females; age 56 ± 13 years) with serum creatinine >6.5 mg/dl and i-PTH >150 pg/ml, from a standard low-protein diet (0.6 g/kg/day approximately) to a very-low-protein (0.3 g/kg/day), very-low-phosphorus (5 mg/kg/day) diet supplemented with a mixture of essential amino acids and calcium keto analogues (Ketodiet), calcium carbonate (2–4 g/day), iron, and vitamin B₁₂ preparations. The energy supply of both diets was 30–35 kcal/kg/day. Exclusion criteria were a poor compliance with dietary or supplement prescriptions or signs of autonomic hyperparathyroidism. After 4 ± 2 months of Ketodiet, the i-PTH serum levels decreased by 49% as a mean (from 441 ± 233 to 225 ± 161 pg/ml, p < 0.001); serum phosphorus and alkaline phosphatase decreased, whereas serum calcium increased. The great reduction of serum and urinary urea demonstrated a good compliance with Ketodiet, and no sign of protein malnutrition was observed. These findings confirm that even in severe chronic uremic patients dietary phosphorus restriction and calcium carbonate supplementation lower i-PTH serum levels. This is one of the goals of the dietary treatment that can be safely achieved, provided good compliance both with the dietary prescriptions and with adequate energy and supplement intakes.

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Section: Discussionmentioning

confidence: 99%

Secondary Hyperparathyroidism in Severe Chronic Renal Failure Is Corrected by Very-Low Dietary Phosphate Intake and Calcium Carbonate Supplementation

Barsotti

Cupisti

Morelli

et al. 1998

Nephron

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“…In compliant patients this could lead to the cure of osteitis fibrosa and osteomalacia within 1 year (85), and after 5 years (86) this treatment could even lead in a few cases to ABD. It is interesting to note that this approach was efficient despite the lack of increase of plasma calcitriol levels in contrast to what had been observed in less advanced renal failure (87–90). The future availability of noncalcemic nonaluminic phosphate binders will make the necessity of such protein restriction more seldom, and the challenge will be to assess in native vitamin D replete predialysis patients the cost effectiveness of 2 alternative treatments: 1α(OH)D 3 derivatives versus CaCO 3 both in association if necessary with nonaluminic noncalcemic phosphate binders.…”

Section: Treatment Of Renal Osteodystrophymentioning

confidence: 89%

Renal Osteodystrophy in Dialysis Patients: Diagnosis and Treatment

et al. 1998

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This article reviews the clinical, biological, radiological, and pathological procedures and their respective indications for the practical diagnosis of the following various histological patterns of renal osteodystrophy: osteitis fibrosa due to parathyroid hormone (PTH) hypersecretion: osteomalacia or rickets due to native vitamin D deficiency and/or aluminum overload; and adynamic bone disease (ABD) due to aluminum overload and/or PTH secretion oversuppression. Our advice regarding bone biopsy is to restrict it to patients with symptoms and hypercalcemia, especially those who have been previously exposed to aluminum. In other cases, we propose relying merely on the determination of the plasma concentrations of calcium, protide, phosphate, bicarbonate, intact PTH, aluminum, 25(OH)D3, and alkaline phosphatase (total and bony if hepatic disease is associated) to choose the appropriate treatment. Because of the danger of the desferrioxamine treatment necessary to chelate and remove aluminum, the suspicion of aluminic bone disease (osteomalacia or ABD) will always be confirmed by a bone biopsy. In the case of nonaluminic osteomalacia, correction of the vitamin D deficiency by native vitamin D or 25(OH)D3, and of the calcium deficiency and acidosis by alkaline salts of calcium and if necessary sodium bicarbonate are sufficient to cure the disease. In the case of nonaluminic ABD, the stimulation of PTH secretion by the discontinuation of 1alpha hydroxylated vitamin D and the induction of a negative calcium balance during dialysis by decreasing the calcium concentration in the dialysate will allow an increase of the CaCO3 dose to correct for hyperphosphatemia without inducing hypercalcemia. For hyperparathyroidism, i.e., plasma intact PTH levels greater than two- or four-fold the upper limit of normal levels (according to the absence or presence of previous aluminum exposure), the treatment will consist in increasing the CaCO3 dose to correct for hyperphosphatemia together with a decrease of the calcium concentration in the dialysate if the dose of CaCO3 is so high that it induces hypercalcemia. When the hyperphosphatemia has been corrected and there is still a low or normal corrected plasma calcium level, 1alpha(OH)D3 in an oral bolus 2 or 3 times a week should be given at the minimal dose of 1 microg. When the PTH level stays above 400 pg while hypercalcemia occurs and hyperphosphatemia persists, surgical subtotal parathyroidectomy is recommended or the injection of calcitriol into the big nodular hyperplastic parathyroid glands under sonography control in high surgical risk patients. Special recommendations are given for children.

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“…It should be stressed that if both CaCOi and calcitriol have beneficial effects by correcting the negative calcium balance and the tendency to hypocal cemia, only CaCOy has a beneficial effect on the phos phate retention which is, on the other hand, aggravated by calcitriol. This correction of the phosphate restriction explains why the endogenous synthesis of calcitriol may be increased by CaCO.i and dietary phosphate restriction, at least when the glomerular filtration rate remains >20 ml/min [81,82], The argument that calcitriol re placement is mandatory to increase plasma calcitriol lev els above normal is doubtful, since downregulation of the parathyroid receptors for calcitriol is questionable, a few studies being in favor -a human study [83] and three ani mal studies [84,86] -whereas one recent animal study [87], challenging the methods of previous studies, is against this concept. The recent immunohistological study in uremic patients performed by Fukuda et al .…”

Section: Use O F 10(0 11) 0 } Derivatives In Hyperparathyroidism Prementioning

confidence: 99%

1-Alpha-Hydroxyvitamin D<sub>3 </sub>Derivatives in the Treatment of Renal Bone Diseases: Justification and Optimal Modalities of Administration

Fournier

Morinière

Oprisiu

et al. 1995

Nephron

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The use of 1 α-hydroxyvitamin D3 [ 1 α(OH)D3] derivatives in a uremic patient is justified only in the treatment of hyperparathyroidism (i.e. when plasma intact parathyroid hormone -PTH – levels are above five or three times the upper limit of normal according to whether the patient is on continuous ambulatory peritoneal dialysis or on hemodialysis and between 0.5-1.5, 1-2 and 2-3 times the upper limit of normal for a creatinine clearance of, respectively, 30, between 30 and 10, or below 10 ml/min/1.73m²). The following prerequisites have however to be satisfied: (1) a good vitamin D3 repletion should be secured by plasma 25(OH)D levels of 20-30 ng/ml (if necessary by administration of native vitamin D or 25(OH)D3), and (2) phosphate retention (which is aggravated by the increased phosphate intestinal absorption induced by the 1α(OH)D derivatives) and the consequent possible hyperphosphatemia should be prevented or corrected by the oral administration of alkaline salts of calcium given before the meals as phosphate binders without inducing hypercalcemia. These prerequisites explain the narrow therapeutical margin of lα(OH)D₃ derivatives in uremic patients before dialysis (more so in the adult than in the child) and the possible broadening of this margin in the patients on dialysis by the use of low dialysate calcium concentrations (1.25-1.00 mmol/l) in order to prevent hypercalcemia by inducing a negative perdialytic calcium balance. Once hyperphosphatemia is prevented by oral calcium, 1α(OH)D₃ derivatives have the advantage to suppress the transcription of the prepro PTH gene by a mechanism independent of an increase in plasma calcium. Controlled randomized trials have not confirmed the claimed advantage in efficacy and safety of the parenteral versus the oral route nor of the intermittent versus the daily mode of their administration. The advantages of using the so called ‘nonhy-percalcemic hyperphosphatemic’ vitamin D3 derivatives in combination with oral calcium over 1α(OH)D3 derivatives in the treatment of uremic hyperparathyroidism are still waiting for clinical demonstration. Vitamin D derivatives have no place in the treatment of aluminic bone diseases which necessitate long term deferoxamine treatment and prevention of aluminum exposure by the dialysate and the phosphate binders. They are not indicated in the treatment of’idiopathic’ adynamic bone disease which is due to uremia per se combined with an excessive PTH suppression for the degree of renal failure. This low bone turnover pattern is associated with an increased risk of hypercalcemia and hyperphosphatemia and necessitates only a stimulation of PTH secretion by inducing a negative calcium balance with a lower dialysate calcium concentration or simply by discontinuing the oral calcium supplement in the uremic patient not yet dialyzed. In rare cases this pattern is due to a granulomatosis and is corrected by prednisone.

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Increase of Calcitriol during Treatment with Protein-Reduced Diet in Patients with Renal Failure

Cited by 6 publications

References 8 publications

Secondary Hyperparathyroidism in Severe Chronic Renal Failure Is Corrected by Very-Low Dietary Phosphate Intake and Calcium Carbonate Supplementation

Secondary Hyperparathyroidism in Severe Chronic Renal Failure Is Corrected by Very-Low Dietary Phosphate Intake and Calcium Carbonate Supplementation

Renal Osteodystrophy in Dialysis Patients: Diagnosis and Treatment

1-Alpha-Hydroxyvitamin D<sub>3 </sub>Derivatives in the Treatment of Renal Bone Diseases: Justification and Optimal Modalities of Administration

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