The spectrum of bone disease in end-stage renal failure—An evolving disorder

Abstract

We have assessed the bone histology in 259 chronic dialysis patients, all of whom were in the same dialysis program. All patients had bone biopsies with quantitative histomorphometry, intact parathyroid hormone (PTH) measurements, basal and deferoxamine stimulated serum aluminum levels. Results demonstrate the increased incidence of the recently described aplastic bone lesion, particularly in patients treated with peritoneal dialysis (PD). Aluminum-related bone disease is much less common than previously described, perhaps in relation to the declining use of aluminum as a phosphate binder. A different pattern of bone lesions is seen in PD as compared with hemodialysis (HD), with low turnover disorders comprising 66% of the lesions seen in PD and high turnover lesions accounting for 62% of the bone histologic findings in HD. The difference in these patterns may relate to alterations in PTH levels, as mean PTH levels in HD patients were 2-1/2 times the levels found in PD patients (P < 0.0005), while older age, higher prevalence of diabetes and a shorter duration of dialysis may also have contributed to the findings in the PD patients. We suggest that PD, perhaps by maintaining calcium at higher levels, may more effectively suppress the parathyroid gland.

Value of the New Bone Classification System in Pediatric Renal Osteodystrophy

“…Although reports from prior decades demonstrated a prevalence of the mixed lesion of renal osteodystrophy in adult and pediatric dialysis patients (1,14), these lesions were defined primarily by excess osteoid accumulation, which was attributed to aluminum intoxication and/or to the stimulatory effects of PTH on osteoblast matrix secretion. However, in these findings, the mineralization defect was defined as a combination of osteoid accumulation and delayed osteoid maturation-a parameter that would not be expected to be altered by excess PTH alone.…”

“…Traditionally, renal osteodystrophy has been diagnosed by bone histomorphometry and classified according to lesions of bone turnover ranging from high rates of bone formation (mild lesions of secondary hyperparathyroidism and osteitis fibrosa) to low turnover (adynamic bone) (1,2). However, alterations in skeletal mineralization and bone volume also occur in a substantial proportion of pediatric patients with CKD (2,3) and may contribute to the increased fracture rates, boney deformities, poor linear growth, and chronic bone pain that persist despite adequate control of secondary hyperparathyroidism (4).…”

Association between Increased Serum Osteoprotegerin Levels and Improvement in Bone Mineral Density after Parathyroidectomy in Hemodialysis Patients

“…In medically refractory SHPT, the new bone formed is structurally inferior and fragile, with an increased fracture risk. The typical histological form of this condition is called either osteitis fibrosis or mixed osteodystrophy (Malluche and Faugere 1990;Sherrard et al 1993).…”

Impact of Treatment with Calcimimetics on Hyperparathyroidism and Vascular Mineralization

“…S econdary hyperparathyroidism (SHPT) generally develops early in chronic kidney disease (CKD), before dialysis is needed; consequently, most patients who have ESRD and are undergoing dialysis will have elevated parathyroid hormone (PTH) and SHPT of variable severity (1)(2)(3). Cardiovascular disease accounts for almost half of all deaths in patients with ESRD, with risk being particularly elevated in younger individuals (4).…”