After reading this article, the reader will be able to:
1. Briefly describe the pathology associated with development of osteitis fibrosa.
2. Identify clinical criteria supporting the diagnosis of osteitis fibrosa.
3. Summarize the implications of medical and surgical management of osteitis fibrosa.
This offering for 2.3 contact hours is being provided by the American Nephrology Nurses' Association (ANNA), which is accredited as a provider and approver of continuing education in nursing by the American Nurses' Credentialing Center-Commission on Accreditation (ANCC-COA). This educational activity is approved by most states and specialty organizations that recognize the ANCC-COA accreditation process. ANNA is an approved provider of continuing education in nursing by the California Board of Registered Nursing, BRN Provider No. 00910; the Florida Board of Nursing, BRN Provider No. 27F0441; the Alabama Board of Nursing, BRN Provider No. P0324; and the Kansas State Board of Nursing, Provider No. LT0148-0738. This offering is accepted for RN and LPN relicensure in Kansas.
To receive continuing education credit, you must read the information in this article, complete and return the answer form on page 30 and appropriate fee to the ANNA National Office. Please refer to the answer form for the appropriate fee and address of the National Office.
The treatment of hyperparathyroid bone disease, otherwise known as osteitis fibrosa, requires an interdisciplinary approach to achieve an optimal clinical outcome. Dietary modification, medication compliance, and patient education are all essential components of medical therapy. This article will discuss the biochemical, radiographic, pathological, and clinical findings associated with osteitis fibrosa. A detailed discussion of medical and surgical management is given, emphasizing treatment choices based upon specific clinical presentations.
Pathophysiology of osteitis fibrosa begins prior to the development of end stage renal disease (ESRD). When renal function deteriorates to a glomerular filtration rate of less than 50%, the kidneys are no longer able to fully excrete the daily phosphorus load. In addition, there is a decreased capacity to produce 1alpha hydroxylase, an enzyme required for the production of the active metabolite of Vitamin D (Malluche & Monier-Faugere, 1991). The activated form of vitamin D (1,25 dihydroxycholecalciferol) enhances the absorption of calcium from the gut. In the absence of 1-alpha hydroxylase, decreased calcium absorption from the gut contributes to the development of hypocalcemia. Hypocalcemia directly stimulates parathyroid hormone (PTH) secretion. Hyperphosphatemia contributes to enhanced PTH secretion primarily by physiologically inhibiting 1-alpha hydroxylase activity (see Figure 1). Over time, there is also a characteristic increase in the calcium concentration required to suppress PTH secretion (shift in the calcium "set point"). The net result of these changes is that the parathyroid glands become hypertrophied and hypersecretory (Slatopolsky, Finch, Ritter, & Brown, 1995).
[Figure 1 ILLUSTRATION OMITTED]
Excessive parathyroid hormone secretion stimulates an increase in the number of osteoclasts (bone-resorbing cells) and osteoblasts (bone-forming cells), which creates a high turnover state in bone. This high turnover state is associated with increased bone remodeling and is characterized by the deposition of irregularly mineralized bone, "osteoid woven." This bone is weaker than normal bone and more susceptible to stress fractures (Malluche, Hartmut, & Monier-Faugere, 1990).
Renal osteodystrophy encompasses a broad spectrum of metabolic bone diseases associated with renal failure. Bone biopsy is considered the "gold standard" for classification of osteopathies associated with ESRD (Malluche et al., 1990); however, bone biopsy is not routinely performed, and when it is an accurate interpretation requires extensive experience and expertise (D'haese, Couttenye, & Broe, 1994). A correct diagnosis can often be made through an indepth examination of clinical, laboratory, and radiographic findings.
Osteitis fibrosa is one of the common forms of renal osteodystrophy. Other osteopathies associated with progressive kidney disease include beta-2-microglobulin amyloid osteoarthropathy, osteomalacia, and adynamic osteopathy (Torres, Lorenzo, Hernandez, & Rodriguez, 1995). One or a combination of these bone diseases may be present, making diagnosis difficult.
The clinician must also keep in mind that osteoporosis occurs frequently in the aging dialysis population. One study described increased severity of bone mineral loss in subjects with combined osteoporosis and osteitis fibrosa (Bianchi et al., 1992). Dialysis patients (more females than males) are subject to a hypogonaldal state. This predisposes women to premature menopause and osteoporosis even though they may continue to menstruate. Exercise, estrogen replacement, and calcium supplements are frequently prescribed for nondialysis patients with osteoporosis; further investigation is required to establish benefit in renal failure.
Renal bone disease is due to alterations in mineral metabolism that occur in association with progressive impairment of renal function. When the glomerular filtration rate declines to less than 50% of normal levels, bone histology shows characteristic changes consistent with renal osteodystrophy (Malluche et al., 1990). Early recognition and treatment prior to the initiation of dialysis therapy has been shown to slow the progression of osteitis fibrosa (Lindberg, 1993). Prevention of hyperphosphatemia in the patient with chronic …