Bone loss in long-term renal transplantation: Histopathology and densitometry analysis

Cueto-Manzano, Alfonso M.; Konel, Shaikh; Hutchison, Alastair J.; Crowley, Vivion; France, Michael; Freemont, Anthony J.; Adams, Judith E.; Mawer, Barbara; Gokal, Ram

doi:10.1046/j.1523-1755.1999.00445.x

Cited by 127 publications

(88 citation statements)

References 31 publications

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“…These lesions were more severe in patients with less time after transplantation but approached normal values in patients who were Ͼ10 yr after transplantation. Similar results were shown by CuetoManzano et al (21) in the majority of patients. More recently, Monier-Faugere et al (18) in a study of posttransplantation patients after 4 to 6 yr showed bone alterations that were characterized by low bone turnover, decreased bone formation, and prolonged mineralization, whereas increased erosion surface was observed in fewer than 25% of the patients.…”

Section: Alterations Of Bone Remodeling After Transplantationsupporting

confidence: 91%

“…Whereas Velasquez-Forero et al (19) showed mainly alterations that were consistent with adynamic bone disease and increased deposition of iron in the mineralization front, other studies have shown decreased bone formation and prolonged mineralization lag time in the presence of persisting bone resorption (4,20,21). Our studies in patients with normal renal function, after a mean of 7.5 yr after renal transplantation, showed mainly a mixed histologic pattern that was characterized by an increase in bone resorption, whereas bone formation rate was low and mineralization lag time prolonged (4).…”

Section: Alterations Of Bone Remodeling After Transplantationmentioning

confidence: 97%

“…Studies in animals and humans have shown that cyclosporine causes high bone turnover (28 -30). In the rat, cyclosporine causes bone loss that is associated with increased bone resorption and formation (28); however, other studies have failed to demonstrate an effect of the drug on mineral and bone metabolism in renal transplant recipients (4,21,22). It should be considered, however, that the role of cyclosporine in transplant patients has been difficult to evaluate because its effects on bone turnover may be masked by glucocorticoids.…”

Section: Pathogenesis Of Posttransplantation Bone Diseasementioning

confidence: 99%

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Bone Disease after Renal Transplantation

Weisinger¹,

Carlini²,

Rojas³

et al. 2006

Clinical Journal of the American Society of Nephrology

121

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It has been well established that a rapid decrease in bone mineral density (BMD) occurs in the first 6 to 12 mo after a successful renal transplantation and persists, albeit at a lower rate, for many years. This rapid BMD loss significantly increases the fracture risk of these patients to levels that are even higher than those of patients who have chronic kidney disease stage 5 and are on dialysis. The presence of low BMD in renal transplant patients as a predictor of risk fracture is controversial. Indeed, as has been suggested also for patients with postmenopausal osteoporosis, there is not a compelling correlation between the decline in BMD and skeletal fractures. However, bone disease after renal transplantation probably represents a unique bone disorder that must encompass underlying renal osteodystrophy. In fact, this syndrome results from multiple factors that include pretransplantation bone status, use of glucocorticoids and other immunosuppressive drugs, hypophosphatemia, and alterations of the calcium-vitamin D axis. Recent studies have demonstrated decreased osteoblast number, reduced bone formation rate, delayed mineralization, and increased osteoblast and osteocyte apoptosis. Bisphosphonates and vitamin D metabolites may be valuable in preventing or diminishing early bone loss. However, clinicians should be careful with the use of bisphosphonates and oversuppression of bone, especially in patients with low bone turnover. New prospective, controlled trials are required to confirm the real efficacy of these drugs, particularly in long-term renal transplant patients.Clin J Am Soc Nephrol 1: 1300 -1313, 2006. doi: 10.2215/CJN.01510506 K idney, heart, lung, and liver transplantation have become fairly common and successful. As the number of transplants has grown, new challenges have arisen in the management of long-term complications of transplantation. Posttransplantation bone disease represents one such important complication, because it is observed in a substantial proportion of patients. As a consequence, bone mass loss and bone fractures are common in these patients and cause substantial morbidity.In patients with chronic kidney disease (CKD), renal osteodystrophy that begins during the early stages of the disease usually worsens during dialysis and may persist after transplantation, although in many patients, improvement in these bone lesions are observed. In addition to preexisting bone lesions, not only factors that hamper recovery but also new factors could affect bone structure after transplantation. These include the potential deleterious effects on bone of the different immunosuppressive agents, the impaired renal function that frequently is observed in renal transplant patients, and several others factors that are particular to each patient, such as postmenopausal status, presence of diabetes, gender, and time after transplantation. Changes in Bone Mineral DensityBone mineral density (BMD) as assessed by dual x-ray absorptiometry has been used as a noninvasive method to assess bone mass loss...

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Section: Alterations Of Bone Remodeling After Transplantationsupporting

confidence: 91%

Section: Alterations Of Bone Remodeling After Transplantationmentioning

confidence: 97%

Section: Pathogenesis Of Posttransplantation Bone Diseasementioning

confidence: 99%

See 1 more Smart Citation

Bone Disease after Renal Transplantation

Weisinger¹,

Carlini²,

Rojas³

et al. 2006

Clinical Journal of the American Society of Nephrology

121

View full text Add to dashboard Cite

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“…Few studies have described the histology of the bone changes occurring after RT (3)(4)(5)(6). Most investigators have employed bone densitometry in the evaluation of post-transplant bone disease, but it is well known that bone biopsy provides the only reliable information about bone remodeling.…”

Section: Discussionmentioning

confidence: 99%

“…However, these studies were not able to determine the various patterns of renal osteodystrophy (high or low bone turnover) because they were based on BMD findings. Currently, renal osteodystrophy is differentiated solely by means of a bone biopsy and histomorphometric analysis (2) and few prospective studies have evaluated this parameter (3)(4)(5)(6). For example, mild to moderate hyperparathyroidism is spontaneously reversed during the first 1 or 2 years after a successful RT (3).…”

Section: Introductionmentioning

confidence: 99%

Improvement of adynamic bone disease after renal transplantation

Abdallah

Jorgetti

Pereira

et al. 2006

Braz J Med Biol Res

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Low bone remodeling and relatively low serum parathyroid hormone (PTH) levels characterize adynamic bone disease (ABD). The impact of renal transplantation (RT) on the course of ABD is unknown. We studied prospectively 13 patients with biopsy-proven ABD after RT. Bone histomorphometry and bone mineral density (BMD) measurements were performed in the 1st and 12th months after RT. Serum PTH, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and osteocalcin were measured regularly throughout the study. Serum PTH levels were slightly elevated at transplantation, normalized at the end of the third month and remained stable thereafter. Bone biopsies performed in the first month after RT revealed low bone turnover in all patients, with positive bone aluminum staining in 5. In the 12th month, second biopsies were performed on 12 patients. Bone histomorphometric dynamic parameters improved in 9 and were completely normalized in 6, whereas no bone mineralization was detected in 3 of these 12 patients. At 12 months post-RT, no bone aluminum was detected in any patient. We also found a decrease in lumbar BMD and an increase in femoral BMD. Patients suffering from ABD, even those with a reduction in PTH levels, may present partial or complete recovery of bone turnover after successful renal transplantation. However, it is not possible to positively identify the mechanisms responsible for the improvement. Identifying these mechanisms should lead to a better understanding of the physiopathology of ABD and to the development of more effective treatments.

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