Large tendon rupture is a rare catastrophic occurrence in dialysis patients. Pathogenesis of this has been variably thought to be due to malnutrition, insufficient dialysis, amyloidosis, chronic acidosis, or hyperparathyroidism. We investigated contributory causes and timing of this complication in 44 dialysis patients (42 hemodialysis and two peritoneal dialysis patients). Five cases were our own; the other 39 were reported in the literature during the last two decades. Data were compared with a hospital database of 916 patients. The patients who experienced tendon ruptures had been on dialysis longer (mean duration, 7.6 years v 4.0 years; P = 0.001), were younger (mean age, 39.7 years v 48.4 years; P = 0.0001), had much higher parathyroid hormone levels (1,802 pg/mL v 202 pg/mL; P = 0.0001), had a higher phosphate level (6.8 mg/dL v 5.9 mg/dL; P = 0.001), had a slightly higher calcium level (9.2 mg/dL v 8.8 mg/dL; P = 0.038), and had a higher alkaline phosphatase level (649 IU/L v 109 IU/L; P = 0.0001) than control patients. Patients with tendon ruptures had no evidence of malnutrition (albumin 3.7 g/dL v 3.8 g/dL; P = 0.237) and had the same acidosis (bicarbonate 22.2 mEq/L v 22.0 mEq/L; P = 0.180). The time on dialysis to rupture was inversely related to the patient's age (r = 0.47, P = 0.004). Most patients had evidence of years of poorly controlled hyperparathyroidism with high and increasing levels of parathyroid hormone and alkaline phosphatase. Previous steroid use was also much more common in patients with tendon ruptures, as was radiographic evidence of osteitis fibrosa. The disease led to long hospitalization and prolonged morbidity, with mobility limitations in several patients. Spontaneous large tendon rupture in patients is secondary to hyperparathyroidism; is more common in young patients, particularly if exposed to corticosteroids; leads to long-lasting morbidity; and should be preventable by better supervision and treatment of hyperparathyroidism.