Renal Osteodystrophy

James N. Suojanen, M.D.

S. James Adelstein, M.D., Ph.D.

April 16, 1985

Case Presentation:

A 58 year-old female with a long history of non-insulin dependent diabetes mellitus, essential hypertension and chronic renal failure presented with a several week long course of progressive bilateral ankle, foot, elbow and rib pain. She had no history of trauma, or of swelling or redness of the affected joints. She has a past history of gout, congestive heart failure, subendocardial myocardial infarction and anemia. Her medications include digoxin, lasix, Aldomet, Colchicine, Allopurinol, Amphagel, Kayexalate and folic acid.

The patient was afebrile and in no acute distress. Her feet, ankles, and elbows had normal ranges of motion with no point tenderness, crepitus, swelling or erythema. Her lower extremities had normal pulses, intact skin and no edema. She had stable mild cardiomegaly and retinopathy. Radiographs of the feet showed osteopenia, but no other signs or hyperparathyroidism fracture.

Chemistries were:

			2/82		5/83		6/84		2/85

Ca++			9.2		-----		9.3		9.1
(9.1-10.9 mg/dl)

PO4			4.9		-----		4.1		4.4
(2.3-4.3 mg/dl)

Alk Phosphatase	98		271		328		633
(16-95 IU/I)

Creatinine		3.6		5.0		5.2		6.9
(< 1.2 mg/dl)


Her physician suspected renal osteodystrophy and obtained a bone scintigram. This demonstrated diffuse uptake throughout the skeleton, particularly the skull, with little renal uptake and minimal bladder activity ("superscan"). Radiographs revealed some resorption of the distal clavicles (arrows) and diffuse granularity of the calvarium with indistinct outer cortex, vascular grooves and sella. These findings are diagnostic of hyperparathyroidism, confirming the impression of renal osteodystrophy. Appropriate therapy was begun.


The etiology of renal osteodystrophy is incompletely understood. However, two mechanisms predominate: secondary hyperparathyroidism and abnormal vitamin D metabolism. The later results mainly from the loss of functioning renal parenchyma and subsequent decreased renal synthesis of active vitamin D. This leads to reduced gastrointestinal absorption of calcium, producing hypocalcemia. Reduced renal function also produces hypocalcemia by favoring phosphate retention. Low serum calcium and high phosphate cause increased parathyroid hormone (PTH) released by the parathyroid glands. Elevated PTH levels are sustained by decreased renal degradation and reduced negative feedback suppression by vitamin D. PTH acts to raise calcium by osteoclast activation, stimulation of intestinal absorption and various renal effects.

The major bony changes which can occur as a result of chronic renal failure are osteitis fibrosa cystica, osteomalacia or rickets, osteosclerosis and osteoporosis. The clinical presentation is influenced by the patient's age at onset of renal failure, the etiology of the renal disease, dietary content (protein, phosphate and calcium) and treatment modalities. The reported predominance of each variety of bony change varies and doesn't correlate well with clinical findings or laboratory data. About 15% of patients with hyperparathyroidism (primary or secondary) have roentgen changes in the calvarium.

Diffuse increased scintigraphic skeletal:renal uptake ratio of bone agent can occur in any disease process in which there is increased bone turnover. Uptake may be heterogeneous or homogeneous, depending upon the predominate pathophysiologic mechanism. Increased turnover can result from local processes such as widespread metastases, fibrous dysplasia, Paget's disease, or myeloproliferative disorders. Examples of the later are myelofibrosis, mastocytosis, leukemia, lymphoma, aplastic anemia and Waldenstrom's macroglobulinemia. Increased bone turnover also occurs with endocrine/metabolic abnormalities such as hyperparathyroidism, hypervitaminosis D, rickets, or combinations of these as seen in renal failure. Differentiation is based on clinical data and radiographs in many cases.


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4) Resnick D, Niwayama G. Diagnosis of bone and joint disease. Philadelphia: W.B. Saunders Company, 12981; 1702-1842.


J. Anthony Parker, MD PhD,