Long-Term Results of Total Parathyroidectomy without Autotransplantation in Patients with and without Renal Failure

Abstract

The optimal surgical procedure for severe renal secondary hyperparathyroidism (sHPT) is still a point of controversy. Total parathyroidectomy (PTX) without auto-transplantation was abandoned for fear of an adynamic bone condition; however, in the case of autotransplantation recurrent sHPT is frequent and promotes atherosclerosis. We studied 11 hemodialysis patients (age 59±12 years) on dialysis for 18 (12–30) years in whom total PTX was performed due to severe sHPT (group I; intact PTH: 1,240±230 pg/ml), and 5 patients (age 55±10 years) without renal insufficiency who inadvertently received total PTX during thyroid surgery (group II). After total PTX (group I, 26±18 [9–59] months; group II, 252±188 [22^480] months) both groups showed no measurable intact PTH levels. Calcium homeostasis was maintained by oral substitution with calcium (group I, calcium dialysate of 2.0 mmol/l), vitamin D and calcitriol (serum parameters in groups I and II: calcium 2.4 and 2.2 mmol/l; phosphate 1.8 and 1.1 mmol/l; 25(OH)-vitamin D₃ 21 and 34 ng/ml; 1,25(OH)₂-vitamin D₃ 32 and 41 pg/ml, respectively). In group I, after total PTX there was a rapid and sustained improvement in bone pain with markedly enhanced physical activity and endurance. High turnover osteopathy markedly improved as indicated by declining levels of native osteocalcin (90±17 vs. 26±18 ng/ml), bone alkaline phosphatase (74±12 vs. 12±6 ng/ml), and carboxyterminal cross-linked telopeptide of type-I collagen (65±16 vs. 40±21 ng/ml) but increasing levels of carboxyterminal propeptide of type-I procollagen (120±36 vs. 148±41 ng/ml). Recalcification of bone was excellent as demonstrated by X-ray and confirmed by bone histology. Itching extravascular calcific deposits and calcifications of blood vessel and cardiac valves immediately stopped after total PTX. Moreover, 6 sHPT patients suffered from severe atherosclerotic lesions such as thoracic aortic aneurysm (n = 3) or abdominal aortic aneurysm (n = 3) which showed size progression before but not after total PTX when annually controlled by ultrasonography. In group II, even long after total PTX, there was no clinical, radiological, histological or biochemical evidence for low turnover osteopathy. In conclusion, our data indicate that substitution with vitamin D₃ metabolites and calcium can prevent deleterious bone effects of hypoparathyroidism in hemodialysis patients and in patients with normal kidney function and may compensate for the missing PTH action. Over this, a better survival rate is expected as a consequence of the beneficial effect of total PTX on the progression of atherosclerotic lesions. We suggest reconsideration of total PTX without autotransplantation in dialysis patients with severe sHPT who are not eligible for renal transplantation.

Parathyroidectomy after successful kidney transplantation: a single centre study

“…Persistent or transient hypoparathyroidism, a condition feared because of the associated risk of adynamic bone disease, was observed in up to 68.3% of the patients during prolonged follow-up. Hampi et al [22], however, reported that even 20 years after total PTX without autograft a normal bone metabolism could be maintained in haemodialysis patients by adequate substitution with oral calcium and vitamin D despite almost undetectable PTH levels. This observation needs confirmation in the setting of renal transplantation.…”

Long-Term Outcome after Total Parathyroidectomy for the Management of Secondary Hyperparathyroidism

“…Although there is some fear of adynamic bone disease in case of hypoparathyroidism and some resistance to constantly supplementing patients with active vitamin D postoperatively, tPTX without autotransplantation has found more followers during the last 5 years [22,23,24]. The procedure had already been suggested in the late 1980s and 1990s [6, 19,25,26,27,28]. In these centers, tPTX without autotransplantation (and mostly also without routine thymectomy) has been proven a useful and in the short and mid-term an easily manageable operative approach for end-stage renal failure patients with severe sHPT.…”

“…If an aluminum overload of the bone is excluded prior to PTX, the risk for low-turnover osteopathy after PTX is low. In a prospective study with protocol bone biopsies, no adynamic bone disease could be seen after tPTX alone [28]. On the other hand, adynamic bone disease is not exclusively associated with low PTH but also with a variety of other conditions such as aluminum overload, malnutrition, inflammation, osteoporosis and β 2 -microglobulin [38].…”

“…Hypoparathyroidism per se does not cause bone disease, but is due to the concomitant hypocalcemia [41]. Hypocalcemia should therefore be corrected with adequate doses of active vitamin D. It appears that the appropriate treatment with vitamin D can prevent adynamic bone disease in hypoparathyroid patients with and without renal failure [28]. As with declining renal function levels of active vitamin D fall, supplementation of active vitamin D is a therapy that every uremic patient should receive anyway to prevent hyperparathyroidism.…”

Calcium Requirements after Parathyroidectomy in Patients with Refractory Secondary Hyperparathyroidism

“…Despite the expanding medical armamentarium to treat SHPT, PTX remains a valuable treatment option, especially in those patients who are refractory to medical treatment or cannot afford the expensive drugs [3]. Overall, parameters of mineral metabolism change favorably after a successful PTX [4,5,6]. Hypocalcemia, however, remains a frequently encountered complication and its prevention represents a clinical challenge as pronounced hypocalcemia is not without risks.…”