Reply from the authors

Abstract

We welcome the letter from Dr. Ureña Torres as it offers us an opportunity to clarify and emphasize several aspects of our measurements of the different bone alkaline phosphatase (BALP) isoforms in patients with chronic renal failure (CRF)1.Magnusson P. Sharp C.A. Magnusson M. et al.Effect of chronic renal failure on bone turnover and bone alkaline phosphatase isoforms.Kidney Int. 2001; 60: 257-265https://doi.org/10.1046/j.1523-1755.2001.00794.xAbstract Full Text Full Text PDF PubMed Scopus (73) Google Scholar. In reply to his queries regarding questions 1 and 2, total ALP was significantly increased; however, the majority of the patients had activities within the reference interval for healthy adults. We agree with the suggestion that the increase of BALP isoform B2 in CRF patients may be clinically useful. None of the patients in this study had any biochemical or clinical evidence of hepatic disorder. To answer the third question, we used the previously reported reference intervals for all three BALP immunoassay kits (Alkphase-B, Tandem-R Ostase and Tandem-MP Ostase) and refer him to Figure 21.Magnusson P. Sharp C.A. Magnusson M. et al.Effect of chronic renal failure on bone turnover and bone alkaline phosphatase isoforms.Kidney Int. 2001; 60: 257-265https://doi.org/10.1046/j.1523-1755.2001.00794.xAbstract Full Text Full Text PDF PubMed Scopus (73) Google Scholar. To respond to his fourth question, discordant findings between different studies are not uncommon, which probably reflects the heterogeneity of bone disorders in CRF patients. We did, however, find a significant correlation between the novel BALP isoform B1x and PTH, which might contribute to the positive correlations previously reported2.Ureña P. Hruby M. Ferreira A. et al.Plasma total versus bone alkaline phosphatase as markers of bone turnover in hemodialysis patients.J Am Soc Nephrol. 1996; 7: 506-512PubMed Google Scholar. We suggested that B1x should be further evaluated as a marker of adynamic bone disease. This will indeed require a classification of patients by bone histomorphometry, which was not obtained in this study. Although adynamic bone disease is usually associated with relatively low parathyroid hormone (PTH) levels, PTH may fail to discriminate between adynamic and moderate hyperparathyroid states and even high PTH levels may occur3.Monier-Faugere M-C. Malluche H.H. Calcitriol pulse therapy in patients with end-stage renal failure.Curr Opin Nephrol Hypertens. 1994; 3: 615-619Crossref PubMed Scopus (11) Google Scholar. Another important point, discussed in our paper1.Magnusson P. Sharp C.A. Magnusson M. et al.Effect of chronic renal failure on bone turnover and bone alkaline phosphatase isoforms.Kidney Int. 2001; 60: 257-265https://doi.org/10.1046/j.1523-1755.2001.00794.xAbstract Full Text Full Text PDF PubMed Scopus (73) Google Scholar, is that PTH was analyzed using a commercial assay originally reported to detect only the intact (1-84 PTH) circulating molecule. However, it has recently been demonstrated that a fragment (most likely the 7-84 PTH) interferes with this assay4.Slatopolsky E. Finch J. Clay P. et al.A novel mechanism for skeletal resistance in uremia.Kidney Int. 2000; 58: 753-761https://doi.org/10.1046/j.1523-1755.2000.00222.xAbstract Full Text PDF PubMed Scopus (361) Google Scholar. Thus, the PTH values reported in our study (and other studies) might well be higher than the true circulating levels of intact 1-84 PTH. Bone mineral density was not assessed and we prefer not to speculate as to whether these patients were osteopenic or osteoporotic.