[Hypophosphatemic osteomalacia acquired after renal transplantation: a a cause of severe osteoporosis].
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| Abstract |
Renal osteodystrophy improves after renal transplantation but, after the procedure, other forms of bone disease emerge. We report a male patient that received a renal allograft four years before, who consulted for low back pain secondary to multiple vertebral compression fractures. The patient had good renal function, a parathormone independent hyperphosphaturia, normal 25-OH cholecalciferol, increased urinary hydroxyproline, decreased osteocalcin, reduced bone density and a bone biopsy revealing osteomalacia. The diagnosis of hypophosphatemic osteomalacia was reached and treatment with phosphates and ergocalciferol was started but, despite this, the patient suffered a new fracture two years later. Two mechanisms can produce hypophosphatemia after a renal transplantation: a parathormone excess due to the previous renal failure, that disappears during the first year after the transplantation or a derangement in renal phosphate transport that can be due to a generalized proximal tubule solute transport derangement (Fanconi syndrome), parathormone hypersensitivity or to an "idiopathic" hyperphosphaturia. Despite a good treatment, bone mass is not recovered and there is a high fracture risk. Mineral metabolism must be closely monitored after a renal allograft and its alterations must be quickly treated.
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| Authors | F González, C Gómez, A Ayala, E Roessler |
| Journal | Revista medica de Chile (Rev Med Chil) Vol. 123 Issue 1 Pg. 85-9 (Jan 1995) ISSN: 0034-9887 [Print] Chile |
| Vernacular Title | Osteomalacia hipofosfémica adquirida post-trasplante renal: una causa de osteoporosis grave. |
| PMID | 7569451 (Publication Type: Case Reports, English Abstract, Journal Article) |
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