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[Hyperparathyroidism secondary to renal insufficiency. Physiopathology, clinicoradiological aspects and treatment].
Ann Endocrinol (Paris). 1994; 55(5):147-58.AE

Abstract

Stimulation of PTH secretion and synthesis in chronic renal failure involves direct and indirect factors. The indirect ones are those contributing to a decrease of plasma ionized calcium concentration which stimulates the release of PTH (1) primarily the negative calcium balance due to the iatrogenic reduction of dietary calcium intake associated with an inadequate synthesis of calcitriol, this latter being explained by a reduction in the nephronic mass, the phosphate retention, the acidosis and the retention of uremic toxins (2) more accessorily, the physicochemical dysequilibrium induced by the late occurring hyperphosphatemia. The factors acting directly on the parathyroid gland stimulating synthesis of prepro PTH at its transcription level: not only hypocalcitriolemia but also hypocalcemia and hyperphosphatemia. The clinicoradiological manifestations appear late, mostly only after the patient has been put on dialysis. The most precocious sign is the subperiosteal resorption assessed on the hand X-rays. Therefore diagnosis of hyperparathyroidism relies mainly on the measurement of plasma concentration of intact PTH. In dialysis patients the optimal range corresponding to the best bone histology is between 1 an 3 times the upper limit of normal. No such data exist for predialysis patients. Medical treatment of hyperparathyroidism should primarily be preventive, probably in predialysis lipin patient as soon as plasma intact PTH is greater than the normal upper limit. This treatment is based primarily on the prevention of phosphate retention, of negative calcium balance and acidosis by the use of oral alkaline salts of calcium given with the meals in association with appropriate dietary protein and phosphate restriction. Native vitamin D depletion should also be prevented but use of 1 alpha OH vitamin D3 metabolites in controversial: it is reasonable to administer them only when plasma intent PTH is above 3-7 the normal upper limit and when plasma phosphate is below 1.2 in predialysis patients below 1.5 mmol/l in dialysis patients and plasma calcium remains below 2.3 mmol/l in spite of CaCO3 administration. This situation is encountered in less than 50% of the dialysis patients and rarely in predialysis patients. In dialysis patients the calcium concentration in the dialysate should be chosen in relation to the dose of oral calcium and the use of 1 alpha OH vitamin D3. The superiority of the intermittent (oral or intravenous) over the daily oral administration is not yet clinically proven. The surgical parathyroidectomy is indicated when hypercalcemia and/or hyperphosphatemia occur under medical treatment, whereas the intact PTH levels remain very high (> 500 pg/ml).(

ABSTRACT

TRUNCATED AT 400 WORDS)

Authors+Show Affiliations

Service de Néphrologie-Médecine Interne, Réanimation et Transplantation, CHU d'Amiens, Hôpital Sud, Amiens.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

fre

PubMed ID

7857079

Citation

Ben Hamida, F, et al. "[Hyperparathyroidism Secondary to Renal Insufficiency. Physiopathology, Clinicoradiological Aspects and Treatment]." Annales D'endocrinologie, vol. 55, no. 5, 1994, pp. 147-58.
Ben Hamida F, Ghazali A, Boudzernidj M, et al. [Hyperparathyroidism secondary to renal insufficiency. Physiopathology, clinicoradiological aspects and treatment]. Ann Endocrinol (Paris). 1994;55(5):147-58.
Ben Hamida, F., Ghazali, A., Boudzernidj, M., Amar, M., Morinière, P., Westeel, P., & Fournier, A. (1994). [Hyperparathyroidism secondary to renal insufficiency. Physiopathology, clinicoradiological aspects and treatment]. Annales D'endocrinologie, 55(5), 147-58.
Ben Hamida F, et al. [Hyperparathyroidism Secondary to Renal Insufficiency. Physiopathology, Clinicoradiological Aspects and Treatment]. Ann Endocrinol (Paris). 1994;55(5):147-58. PubMed PMID: 7857079.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Hyperparathyroidism secondary to renal insufficiency. Physiopathology, clinicoradiological aspects and treatment]. AU - Ben Hamida,F, AU - Ghazali,A, AU - Boudzernidj,M, AU - Amar,M, AU - Morinière,P, AU - Westeel,P, AU - Fournier,A, PY - 1994/1/1/pubmed PY - 1994/1/1/medline PY - 1994/1/1/entrez SP - 147 EP - 58 JF - Annales d'endocrinologie JO - Ann. Endocrinol. (Paris) VL - 55 IS - 5 N2 - Stimulation of PTH secretion and synthesis in chronic renal failure involves direct and indirect factors. The indirect ones are those contributing to a decrease of plasma ionized calcium concentration which stimulates the release of PTH (1) primarily the negative calcium balance due to the iatrogenic reduction of dietary calcium intake associated with an inadequate synthesis of calcitriol, this latter being explained by a reduction in the nephronic mass, the phosphate retention, the acidosis and the retention of uremic toxins (2) more accessorily, the physicochemical dysequilibrium induced by the late occurring hyperphosphatemia. The factors acting directly on the parathyroid gland stimulating synthesis of prepro PTH at its transcription level: not only hypocalcitriolemia but also hypocalcemia and hyperphosphatemia. The clinicoradiological manifestations appear late, mostly only after the patient has been put on dialysis. The most precocious sign is the subperiosteal resorption assessed on the hand X-rays. Therefore diagnosis of hyperparathyroidism relies mainly on the measurement of plasma concentration of intact PTH. In dialysis patients the optimal range corresponding to the best bone histology is between 1 an 3 times the upper limit of normal. No such data exist for predialysis patients. Medical treatment of hyperparathyroidism should primarily be preventive, probably in predialysis lipin patient as soon as plasma intact PTH is greater than the normal upper limit. This treatment is based primarily on the prevention of phosphate retention, of negative calcium balance and acidosis by the use of oral alkaline salts of calcium given with the meals in association with appropriate dietary protein and phosphate restriction. Native vitamin D depletion should also be prevented but use of 1 alpha OH vitamin D3 metabolites in controversial: it is reasonable to administer them only when plasma intent PTH is above 3-7 the normal upper limit and when plasma phosphate is below 1.2 in predialysis patients below 1.5 mmol/l in dialysis patients and plasma calcium remains below 2.3 mmol/l in spite of CaCO3 administration. This situation is encountered in less than 50% of the dialysis patients and rarely in predialysis patients. In dialysis patients the calcium concentration in the dialysate should be chosen in relation to the dose of oral calcium and the use of 1 alpha OH vitamin D3. The superiority of the intermittent (oral or intravenous) over the daily oral administration is not yet clinically proven. The surgical parathyroidectomy is indicated when hypercalcemia and/or hyperphosphatemia occur under medical treatment, whereas the intact PTH levels remain very high (> 500 pg/ml).(ABSTRACT TRUNCATED AT 400 WORDS) SN - 0003-4266 UR - https://www.unboundmedicine.com/medline/citation/7857079/[Hyperparathyroidism_secondary_to_renal_insufficiency__Physiopathology_clinicoradiological_aspects_and_treatment]_ L2 - https://medlineplus.gov/kidneyfailure.html DB - PRIME DP - Unbound Medicine ER -