La Osteodistrofia Renal y la Paratohormona supresora de la remodelación ósea

Abstract

Hyperparatiroidism plays a central role in renal osteodystrophy (ROD) in patients with chronic renal failure (CRF). The first plasmatic paratohormone (PTH) determinations back in 1960 were based in radioinmunoanalysis (RIA), using one antibody against the carboxiterminal or middle region of the hormone. In 1987, an inmunometric method (IMA) based on two antibodies, denominated or sandwich assay was introduced, and it is used until today in clinical treatment, guideliness, and investigation of ROD. In the late 1990s, authors detected two inmunoreactive peaks using the traditional method; one of them moved with intact PTH 1-84 and the second peak migrated with the fraction 7-84, which suggested that an important inactive segment was included in the IMA quantifications, increasing the real value of PTH, therefore, exposing the patient to high doses of active vitamin D. This method allowed the separation of a biologically active fraction (CAP-PTH) from a bone-metabolism suppressor fraction (CIP-PTH), maybe associated to the lack of correlation between bone histomorphometry and intact PTH 1-84. The increase of the adynamic form of ROD and the presence of vascular calcifications in uremic adults have been related to high dosis of vitamin D, along with calcium and phosphorus therapies, that were orientated by plasmatic PTH levels until nowadays. The current treatment of ROD must be re-evaluated according to new knowledge, and future laboratory research will allow a better control of this CRF complication.