What is the pathophysiology of kidney transplantation-related osteoporosis?

Updated: Jul 02, 2020
  • Author: Carmel M Fratianni, MD, FACE; Chief Editor: George T Griffing, MD  more...
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Nearly all cross-sectional studies of renal transplant recipients demonstrate that BMD is below normal levels. [42] A fracture prevalence of 5-11% has previously been reported in cross-sectional studies, which is similar to or greater than rates observed in women with postmenopausal osteoporosis. [43, 44] Hyperparathyroidism preceding renal transplantation accelerates trabecular bone loss at the spine in the early transplant period. [45]

Most patients with end-stage renal disease (ESRD) are hypogonadal and have some degree of renal osteodystrophy. (For a comprehensive discussion of renal osteodystrophy, which is beyond the scope of this chapter, please see Goodman et al, 2003. [46] ) Most patients with ESRD have been exposed to drugs that negatively affect bone metabolism. In one large series of 250 such patients, risk factors for low bone mass included secondary amenorrhea, prior failed renal transplantation, chronic metabolic acidosis, and chronic heparin and aluminum exposure. Having had a prior failed renal transplant is probably associated with increased immunosuppressant exposure to prevent rejection and to hyperphosphatemia associated with osteomalacia and osteoporosis. [47]

In recent years, continuous use of aluminum-containing phosphate binders has largely been abandoned; therefore, aluminum toxicity is not presently a significant problem in transplant-related bone disease. [48, 49] However, adynamic bone disease has become increasingly prevalent in the chronic kidney disease population, evident in 27% of transiliac bone biopsy specimens [50] and up to 50% of renal transplant patients prior to bisphosphonate treatment for osteoporosis. [51]

After successful renal transplantation, secondary hyperparathyroidism usually resolves gradually, with normalized vitamin D metabolism and creatinine clearance (CrCl). PTH levels frequently normalize or improve by 1 month posttransplant because of immediate improvement in phosphate retention. Cortical bone density improves secondarily, with significantly better z scores at the distal radius occurring by 6 months after renal transplantation. However, in approximately a third of cases, persistent hyperparathyroidism and hypercalcemia are noted. [52]

In cases of refractory hyperparathyroidism in which surgery is indicated, parathyroidectomy has been associated with a marked improvement in BMD.

With successful renal transplantation, improvement also occurs in aluminum bone disease and dialysis-associated amyloidosis. [53]

Overall, the transplant-related bone disease in kidney recipients does not appear to be as severe as in other solid organ transplant recipients, with the possible exception of kidney recipients with type 1 diabetes. [54] This is perhaps because kidney transplant recipients are younger on average than other organ recipients at the time of transplantation and they may have had better recognition and management of pretransplant bone disease. Kidney transplant recipients may receive lower doses of immunosuppression overall. Rejection may also be more easily detected in renal recipients and, therefore, treated earlier than in other solid organ transplant recipients, resulting in lower total doses of immunosuppression.

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