Tendon disease and adjacent bone erosion in dialysis patients

Abstract

Six out of 169 patients on maintenance haemodialysis showed spontaneous tendon rupture. In all six, bone erosion had previously been observed at the site of tendon insertion. In a further 13 patients whose tendons had never ruptured, marked bone erosions at the sites of tendon insertions were also observed. Both groups of patients, with tendon rupture and with bone erosion only, showed significantly greater blood alkaline phosphatase and parathyroid hormone levels than all the others. Moreover, osseous radiological findings of hyperparathyroidism were more marked in all these 19 patients than in the others. Bone erosion at the site of tendon insertion may be a true and specific sign of tendon disease in patients with uraemia. Our series shows that it bears a close relationship to hyperparathyroidism, and suggests that tendon disease is a specific sign of severe secondary hyperparathyroidism in patients with uraemia.

Acute calcific tendinitis of the pectoralis major insertion associated with cortical bone erosion

“…Similar cases were reported by Chadwick [4]. In haemodialysis patients, tendon rupture and bone erosion at the insertion site was found in 6 of 169 cases [13]. The pathomechanism in this particular condition might be linked to severe secondary hyperparathyroidism, but also structural disorders of collagen due to chronic acidosis have been shown [14].…”

Quadriceps tendon rupture in maintenance haemodialysis patients: Results of surgical treatment and analysis of risk factors

“…It was suggested that tendon rupture might be secondary to sub-tendon bone reabsorption, which weakens the tendon insertion [29,30]. Some authors have pointed out that the association of long term haemodialysis and the occurrence of spontaneous tendon ruptures may involve progressive deposition of b2-amyloid [23,31].…”

Role of secondary hyperparathyroidism in spontaneous rupture of the quadriceps tendon complicating chronic renal failure

“…In this last situation, the frequency of this complication, although difficult to determine, is thought to be lower than 3.5% [2]. Previous reports have pointed out a relation between the duration of haemodialysis and the occurrence of spontaneous tendon ruptures, suggesting that tendinous weakness resulted in these patients, from malnutrition, 2 -amyloidosis [3] or accumulation of uraemic toxins [4], all classical complications of long-term chronic haemodialysis.…”

“…High PTH levels result in high bone turnover, which in turn is responsible for subtendinous bone resorption at the sites of insertion. The occurrence of repeated minor avulsion fractures of the weakened bone cortex at the tendon insertion site precedes the final total tendon rupture, which then occurs after a minor trauma (spontaneous rupture) [2].…”