| [ Summary ] |
The classical factors contributing to the development of secondary hyperparathyroidism (II HPT) are (i) hyperphosphatemia or phosphate loadingļ¼(ii) hypocalcemia or calcium deficiency, and (iii) low serum levels of 25-hydroxyvitamin D or 1,25-dihydroxyvitamin D. In pre-dialysis patients, for example, II HPT is usually severe in patients with interstitial nephritis, due to low serum calcitriol levels and resultant hypocalcemia. Much attention is now being paid to factors contributing to II HPT other than mineral disturbances, such as the stimulated renin angiotensin aldosterone system, congestive heart failure, and obesity, where high PTH levels, per se, may lead to their pathophysiolog. In dialysis patients of long duration, longterm mineral disturbance promotes the proliferation of parathyroid chief cells, resulting in nodular hyperplasia, which is resistant to active vitamin D therapy and to the optimal control of serum mineral levels. Diffuse hyperplasia regresses after successful renal transplantation but this is not the case in nodular hyperplasia, which is associated with persistent hyperparathyroidism in renal transplant recipients. |