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      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

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      Studies of bone morphology, bone densitometry and laboratory data in patients on maintenance hemodialysis treatment.

      Nephron. Physiology
      Adolescent, Adult, Aged, Alkaline Phosphatase, blood, Bone and Bones, analysis, pathology, Cell Count, Densitometry, Female, Humans, Male, Middle Aged, Minerals, Osteoclasts, Parathyroid Hormone, Phosphates, Renal Dialysis, adverse effects, Renal Osteodystrophy

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          Abstract

          Bone morphological parameters of renal osteodystrophy such as abundance of osteoid surface, osteoid seam width index, calcification fronts, osteoclast activity and trabecular bone volume were studied in 71 patients on maintenance hemodialysis and compared with bone densitometry, laboratory and clinical data. Increased osteoclast activity (hyperparathyroidism) was by far the most common bone morphological finding. Patients with chronic pyelonephritis or polycystic kidney disease had more than double the amount of osteoid than patients with chronic glomerulonephritis. The trabecular bone volume seemed to be increased in most patients in contrast to the cortical bone volume which was decreased, judged from bone densitometry and previously from X-ray. Despite that patients with polycystic kidney disease were older, their trabecular volume was larger than in patients with glomerulonephritis. The bone mineral content evaluated by bone densitometry was low in most patients, and more associated with bone morphological signs of osteomalacia than with secondary hyperparathyroidism. Serum phosphate (S-PO4) and serum parathyroid hormone (S-PTH) seemed to discriminate better between osteomalacia and secondary hyperparathyroidism than serum alkaline phosphatase (S-Alk. phosph.), which was elevated in both groups. Patients who had been bilaterally nephrectomized were no more abnormal than other patients, and they had lower S-Alk. phosph. The abundance of osteoclasts was found to be a predictor of future development of clinical secondary hyperparathyroidism.

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