Secondary hyperparathyroidism in patients with chronic kidney disease: Diagnosis, pharmacological and surgical treatment

Secondary hyperparathyroidism (SHPT) is a secondary adaptive response to maintain calcium homeostasis and caused by any condition associated with chronically reduced serum calcium (Ca) levels, and low serum Ca levels lead to compensatory overactivity of the parathyroid gland. It is a common complication of chronic kidney disease (CKD) and is part of the CKD-mineral bone disorder (CKD-MBD). SHPT is associated with increased risk of morbidity and mortality; thus, SHPT control is recommended. SHPT develops in patients with CKD due to a variety of mechanisms including increased phosphorus and fibroblast growth factor 23 (FGF23), and decreased calcium and 1.25 dihydroxyvitamin D levels. Patients present with various bone disorders, cardiovascular disease, and certain patterns of biochemical abnormalities. The diagnosis of patients with SHPT require a combination of clinical investigation and laboratory findings. Many patients with this disease are asymptomatic and only have abnormalities detectable by laboratory and radiologic studies. Laboratory tests may reveal hypocalcemia, normocalcemia or hypercalcemia and hyperphosphatemia. In addition, patients wirh SHPT have extremely elevated parathyroid hormone (PTH) levels, elevated or normal alkaline phosphatase (ALP) levels and decereased vitamin D (vit D) levels. Patients also can become symptomatic. Untreated SHPT leads to progressive bone disease, osteitis fibrosa cystic, and soft tissue calcifications. Patients may experience intractable bone pain, fractures, pruritis, soft tissue or vascular calcifications, calciphylaxis, erythropoietin resistant anemia, and mental status changes. Medical treatment consists of controlling hyperphosphatemia, vit D analogs and Ca administration, and calcimimetic agents. The majority of patients with SHPT can be managed by medical treatment. Despite improvements in medical therapy, it does not always provide control of the SHPT. Some patients require surgical treatment. The surgical indications include PTH levels >500-800 pg/ml associated with hypercalcemia and/or hyperphosphatemia despite medical therapy. Other indications include calciphylaxis, fractures, bone pain or pruritis. Pre-operative imaging is only occasionally helpful except in re-operative parathyroidectomy (PTX). Operative approaches include subtotal PTX, total PTX (TPTX) with or without autotransplantation, and possible thymectomy. Each approach has its own proponents, advantages and disadvantages which are discussed. Hypocalcemia is the most common postoperative complication requiring aggressive calcium administration. Benefits of surgical treatment may include improved survival, bone mineral density and alleviation of symptoms.

Kronik böbrek hastalýklý hastalarda sekonder hiperparatiroidizm: Taný, medikal ve cerrahi tedavi

Sekonder hiperparatiroidizm (SHPT) serum kalsiyum (Ca) düzeylerinin kronik düþüþü ile ilgili herhangi bir durum tarafýndan neden olunan ve Ca dengesini sürdürmek için sekonder adaptif cevaptýr. Düþük serum Ca düzeyleri paratiroid bezlerinin kompansatuar aþýrý aktivitesine yol açar. SHPT kronik böbrek hastalýðýnýn sýk bir komplikasyonudur ve kronik böbrek hastalýðýnýn mineral kemik bozukluklarýnýn bir parçasýdýr. SHPT artan mobidite ve mortalite riski ile iliþkilidir, bu nedenle SHPT’nin kontrolü önerilir. SHPT kronik böbrek hastalýklý hastalarda artan fosdor ve fibroblast büyüme faktörü 23 (FGF23), düþen Ca ve 1.25 dihidroksivitamin D3 düzeylerini içeren deðiþik mekanizmalaradan dolayý geliþir. Hastalarda deðiþiþik kemik bozukluklarý, kardiyovasküler hastalýk ve belirli biyokimyasal anormallikler vardýr. SHPT’li hastalarýn tanýsýnda klinik inceleme ve laboratuvar bulgularýnýn kombinasyonu gerekir. Birçok hasta asemptomatiktir ve sadece laboratuvar ve radyolojik çalýþmalarla saptanabilen anormalliklere sahiptir. Laboratuvar testleri, hipokalsemi, normokalsemi veya hiperkalsemi ve hiperfosfatemi gösterebilir. Ek olarak SHPT’li hastalar, aþýrý paratiroid hormon düzeyleri (PTH), artmýþ veya normal alkalin fosfataz (ALP) seviyeleri ve azalmýþ vitamin D (vit D) düzeylerine sahiptir. Hastalar semptomatik hale gelebilir. Tedavi edilmeyen SHPT, ilerleyici kemik hastalýðý, osteitis fibroza sistika ve yumuþak doku kalsifikasyonlarýna yol açar. Hastalar; dirençli kemik aðrýsý, kýrýklar, kaþýntý, yumuþak doku veya vasküler kalsifikasyonlar, kalsifilaksi, eritropoietine dirençli anemi ve zihinsel durum deðiþiklikleri yaþayabilir. Medikal tedavi hiperfosfateminin kontrolü, vit D analoglarý, Ca uygulamasý ve kalsimimetik ajanlarý içerir. SHPT’li hastalarýn çoðunluðu týbbi tedavi ile tedavi edilebilir. Medikal tedavideki geliþmelere raðmen, medikal tedavi ile SHPT’nin kontrolü her zaman saðlanamaz. Bazý hastalarda cerrahi tedavi gerekir. Cerrahi endikasyonlar medikal tedaviye raðmen hiperkalsemi ve / veya hiperfosfatemi ile iliþkili 500-800 pg/ml’den yüksek PTH düzeylerini içerir. Diðer endikasyonlar kalsifiklaksi, kýrýklar, kemik aðrýsý veya kaþýntýdýr. Preoperatif görüntüleme reoperatif paratiroidektomi (PTX) haricinde nadiren yardýmcýdýr. Operatif yaklaþýmlar, subtotal PTX, ototransplantasyonlu veya ototransplantasyonsuz total PTX (TPTX) ve olasý timektomiyi içerir. Her yaklaþýmýn önerileri, avantajlarý ve dezavantajlarý tartýþýlmýþtýr. Hipokalsemi, agresif Ca uygulamasý gerektiren en yaygýn postoperatif komplikasyondur. Cerrahi tedavinin faydalarý, sað kalým artýþý, kemik mineral yoðunluðu artýþý ve semptomlarýn hafifletilmesini içerebilir.