The appearance of nonfamilial rickets in adults is most frequently due to generalized gastrointestinal malabsorption. Recent studies suggest that rickets secondary to a specific gastrointestinal malabsorption of vitamin D and of calcium is now more common in adults and especially in elderly individuals, possibly because of concomitant dietary deficiencies, inadequate exposure to sunlight, and previous gastric surgery.1 Other conditions which commonly cause rickets are chronic renal glomerular insufficiency and renal tubular disorders such as renal tubular acidosis and the Fanconi syndrome.2 On rare occasions, rickets may complicate hypoparathyroidism, hyperthyroidism, ureterosigmoidostomy, the prolonged ingestion of magnesiumaluminum gel antacids, and hypophosphatasia.2,3Primary hypophosphatemic rickets (phosphate diabetes) unrelated to the conditions enumerated above may be either familial or sporadic.2 The familial variety is transmitted by sex-linked or autosomal inheritance and usually begins in infancy or childhood, whereas the sporadic variety may occur at any age. The biochemical characteristics of the two varieties of hypophosphatemic rickets are similar, and defective renal tubu¬ lar reabsorption of phosphorus can be demonstrated uniformly. Controversy exists as to whether the renal wast¬ age of phosphorus is the basic bio¬ chemical defect or whether the phosphaturia is a manifestation of secondary hyperparathyroidism. Al¬ ternately, the primary defect may be in the activation of vitamin D or in the ability of the gastrointestinal tract to absorb calcium and phos¬ phorus.2·4·5 Case reports of sporadic primary hypophosphatemic rickets in the United States during the past 20 years do not include any patients with the onset of the condition after the age of 60 years.68 This patient summary is presented to demonstrate that sporadic hypophosphatemic rick¬ ets can occur in elderly patients. Patient SummaryA 77-year-old black woman was hospital¬ ized in February 1967 because of bilateral hip and thigh pain of two years' duration. With the onset of the pain in 1965, the pa¬ tient began to use a cane and, ultimately, crutches. Diabetes mellitus and mild hy¬ pertension had been present for several years and the patient took 40 units of ¡so¬ pitane insulin suspension (NPH insulin) daily. A fracture of the ankle 25 years pre¬ viously had healed uneventfully. No symp¬ toms referable to the gastrointestinal and renal systems were present. The patient denied the recent intake of antacids and antibiotics and had no idiosyncrasies of ac¬ tivity or diet which would have caused an abnormally low exposure to sunlight or an inadequate intake of vitamin D. A dietary history taken by a research dietician indi¬ cated the patient had a daily minimum in¬ take of 600 mg calcium, 1,000 mg phos¬ phorus, and 300 USP units of vitamin D. There was no family history of rickets or other skeletal diseases. Findings of a phys¬ ical examination were normal except for a bood pressure of 220/110 mm Hg and ten¬ derness of both hips and the r...