Metabolic bone diseases in kidney transplant recipients

Abstract

Metabolic bone disease after kidney transplantation has a complex pathophysiology and heterogeneous histology. Pre-existing renal osteodystrophy may not resolve completely, but continue or evolve into a different osteodystrophy. Rapid bone loss immediately after transplant can persist, at a lower rate, for years to come. These greatly increase the risk of bone fracture and vertebral collapse. Each patient may have multiple risk factors of bone loss, such as steroids usage, hypogonadism, persistent hyperparathyroidism (HPT), poor allograft function, metabolic acidosis, hypophosphatemia, vitamin D deficiency, aging, immobility and chronic disease. Clinical management requires a comprehensive approach to address the underlying and ongoing disease processes. Successful prevention of bone loss has been shown with vitamin D, bisphosphonates, calcitonin as well as treatment of hypogonadism and HPT. Novel approach to restore the normal bone remodeling and improve the bone quality may be needed in order to effectively decrease bone fracture rate in kidney transplant recipients.

Management of Bone Disease in Kidney Transplant Recipients

“…Persistent hyperparathyroidism and elevated phosphotonin fibroblast growth factor 23 (FGF23) are the main causes of hyperphosphaturia. Other possible causes include steroid therapy, reduced intestinal phosphorus absorption, reduced proximal tubular Na/Pi cotransporter expression or increased tubular sensitivity to PTH (Heaf et al, 2003;Levi, 2001;Zhang et al, 2008). Serum FGF23 level was found to be the best predictor of serum phosphate nadir after kidney transplant.…”

“…About 5% of kidney transplant recipients, with a reported range of 1 to 20%, undergo a surgical parathyroidectomy. The indications for surgery vary among the transplant centers, but the two major indications for parathyroidectomy in renal transplant patients are severe symptomatic hypercalcemia (> 11.5 mg/dl), usually occurring in the early post transplant period, and persistent hypercalcemia more than 1 year after transplant (Kandil et al,2010;Zhang et al, 2008). BMD usually increases after surgical correction of HPT (Eknoyan 2003;Heaf et al, 2003;Jeffery et al, 2003;Levi, 2001).…”

“…The prevention and treatment of adynamic bone disease is avoidance of over suppression of PTH secretion (Eknoyan et al, 2003). Historically, excessive aluminum accumulation was a major cause of adynamic bone disease in ESRD patients before the strict water purification and the avoidance of aluminum-containing phosphate binders were adopted (Zhang et al, 2008).…”

“…Treatments are targeted toward the underlying causes and include Ca and vitamin D supplementations. The treatment of osteomalacia from aluminum toxicity is desferoxamine administration or kidney transplantation (Malluche et al, 1984;Zhang et al, 2008).…”

Kidney transplantation and bone disease: risk factors of development and diagnostics

“…Кроме того, в посттрансплан DOI: 10.15825/1995-1191-2017-1-111-121 трАНСПлАНтАЦиЯ ПОчКи и КОСтНАЯ БОлеЗНь: ФАКтОрЫ риСКА рАЗВитиЯ, диАГНОСтиКА тационном периоде появляются новые причины, участвующие в развитии костной болезни. Интерес специалистов многих стран к данной проблеме ве лик, об этом свидетельствуют публикации послед них лет [1][2][3][4][5][6].…”