Original investigation
Prevalence and risk factors for osteopenia in dialysis patients

https://doi.org/10.1016/S0272-6386(96)90461-8Get rights and content

Abstract

Dialysis patients are at risk for low bone mineral density (BMD) consequent of hyperparathyroidism, 1,25-dihydroxyvitamin D deficiency, previous immunosuppression, chronic acidosis, secondary amenorrhea, and chronic heparin and aluminum exposure. We wanted to determine the prevalence and distribution of osteopenia and the influence of risk factors for osteopenia in dialysis patients. Dual energy x-ray absorptiometry was used to record BMD at the lumbar spine (LS), hip, and nondominant forearm. Results were expressed as Z-scores (standard deviations from the mean of a healthy age- and gender-matched reference population). Osteopenia was defined as a Z-score worse than −2. In the 250 dialysis patients studied, the prevalence of osteopenia at the LS, femoral neck (FN) and ultradistal radius (UD) was 8%, 13% and 20%, respectively. The median Z-scores at these sites were all significantly different from the healthy reference population median of 0 and were 0.29 (P = 0.008), −0.67 (P < 0.001), and −1.01 (P < 0.001), respectively. Previous transplantation was associated with as much as a one Z-score lower BMD at the FN (P = 0.0069) and UD (P = 0.0011) and a marginally significant reduction at the LS (P = 0.0777). Previous parathyroidectomy was associated with a markedly higher LS BMD (P = 0.0001) and a higher BMD at the FN (P = 0.0017) but not the UD (P = 0.3691). A history of secondary amenorrhea was associated with a lower FN BMD (P = 0.0047) but not a significantly lower BMD at the LS (P = 0.0978) or UD (P = 0.2327). In hemodialysis patients without a history of transplantation, parathyroidectomy, or secondary amenorrhea, there was no correlation between Z-score at any site and duration of dialysis. Thus, osteopenia in dialysis patients occurs in both axial and appendicular sites and sites of compact and cancellous bone. It is more common with previous transplantation and secondary amenorrhea, whereas a history of parathyroidectomy is associated with increased BMD. No relationship was found between BMD and duration of hemodialysis, which suggests that important changes in BMD occur during the predialysis stage of chronic renal failure.

References (35)

  • MV Devita et al.

    Assessment of renal osteodystrophy in hemodialysis patients

    Medicine

    (1992)
  • A Sanchez Casajus

    Utility of bone densimetry in haemodilaysis

    Nephrol Dial Transplant

    (1992)
  • C Gabay et al.

    Bone mineral density in patients with end-stage renal failure

    Am J Nephrol

    (1993)
  • S Huraib et al.

    Pattern of renal osteodystrophy in haemodialysis patients in Saudi Arabia

    Nephrol Dial Transplant

    (1993)
  • AJ Hutchison et al.

    Histological, radiological, and biochemical features of the adynamic bone lesion in continuous ambulatory peritoneal dialysis patients

    Am J Nephrol

    (1994)
  • HW Wahner et al.

    Instruments and measurement techniques

  • FF Horber et al.

    Changes in bone mass early after kidney transplantation

    J Bone Miner Res

    (1994)
  • Cited by (143)

    • Osteoporosis in organ transplant patients

      2020, Marcus and Feldman’s Osteoporosis
    • Bone-Vascular Axis in Chronic Kidney Disease

      2019, Advances in Chronic Kidney Disease
    • Bone mineral density, bone turnover markers, and incident fractures in de novo kidney transplant recipients

      2019, Kidney International
      Citation Excerpt :

      We assessed aBMD by DXA in a large cohort of renal transplant candidates at the time of transplantation and observed that median Z-scores (expressing the SD relative to age- and gender-matched control subjects) were below zero across all skeletal sites examined. This confirms CKD as a state of low aBMD.21–23 Applying WHO criteria, osteopenia and osteoporosis at the FN region was present in 55.0% and 22.1% of the study population, respectively.

    View all citing articles on Scopus

    Supported by The Wenkart Foundation.

    View full text