**7. References**


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Lafage et al. (Lafage et al., 1992) used a very low protein diet (0.3 g/kg/d) supplemented with amino acids and ketoanalogues and with only 1 g of calcium carbonate and 1,000 IU of vitamin D2 in 17 patients with advanced renal failure. They have shown not only a beneficial effect related to the control of hyperphosphatemia on the biologic and histologic parameters of hyperparathyroidism but also a correction of acidosis, which resulted in the disappearance of the osteomalacic component. Thus, dietary control often considered to be of minor importance, is actually one of the major keys to success in the management of

The work described in this publication was supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology in Japan

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**18** 

*Austria* 

**Management of Secondary** 

Emanuel Zitt1,2 and Ulrich Neyer2

**Hyperparathyroidism in Hemodialysis Patients** 

Secondary hyperparathyroidism (sHPT) represents the adaptive and very often finally maladaptive response of the organism to control the disturbed homeostasis of calcium, phosphorus and vitamin D metabolism caused by declining renal function. Dysregulation of calcium and phosphorus homeostasis leads to elevated levels of the phosphatonin fibroblast growth factor 23 (FGF23), decreased renal phosphorus excretion, increased serum phosphorus, and diminished synthesis of calcitriol (1,25(OH)2D3), the active form of vitamin D. These alterations result in increased secretion and synthesis of parathyroid hormone

Evidence is available that these disturbances in mineral metabolism lead to vascular (Goodman et al., 2000; Raggi et al., 2002) and valvular (Ribeiro et al., 1998) calcifications and are directly linked to an increased risk of cardiovascular morbidity and mortality as well as excess all-cause mortality (Covic et al., 2009). In accordance to a recent systematic review, the risk of cardiovascular and all-cause mortality is greatest with elevated serum phosphorus followed by increased serum calcium and PTH (Covic et al., 2009). Apart from extra-skeletal side effects, sHPT also leads to profound alterations in bone metabolism which become obvious in the different forms of renal osteodystrophy (Malluche & Faugere, 1990; Moe et al., 2006). This clinical syndrome encompassing mineral, bone and cardiovascular abnormalities has been termed CKD-related Mineral and Bone Disorder (CKD-MBD) (Moe et al., 2006). Furthermore, sHPT is thought to play a role in various other complications of end-stage renal disease as bone pain, bone fractures, muscle dysfunction, sexual dysfunction, disturbed hematopoiesis, immune dysfunction, pruritus and calcific uremic arteriolopathy (calciphylaxis) (Rodriguez & Lorenzo, 2009). An overview of the

In an attempt to improve clinical care, the National Kidney Foundation's Kidney Disease Outcomes Quality Initiative (NKF-K/DOQITM [KDOQI]) has recommended target ranges for serum intact PTH, serum phosphorus and total corrected serum calcium (KDOQI, 2003). More recently, the Kidney Disease Improving Global Outcomes (KDIGO) guidelines for diagnosis, evaluation, prevention and treatment of CKD-MBD have been published (KDIGO, 2009) and endorsed by the US KDOQI (Uhlig et al., 2010) and European Renal Best Practice (Goldsmith et al., 2010) groups. These latter guidelines have tried to provide evidence-based recommendations, but due to the very limited availability of high quality

(PTH) and parathyroid cell hyperplasia (Cunningham et al., 2011).

current understanding of the pathogenesis of sHPT is given in Figure 1.

**1. Introduction** 

*1Department of Nephrology and Dialysis, Academic Teaching Hospital Feldkirch, 2Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch,* 

