Osteologie 2008; 17(03): 125-134
DOI: 10.1055/s-0037-1619858
Renale Osteopathie
Schattauer GmbH

Das Syndrom der renalen Osteopathie

Pathogenese, Klinik, Diagnostik und TherapieThe syndrom of renal osteopathypathogenesis, clinic, diagnostic and therapy
P.M. Jehle
1   Ev. Krankenhaus der Paul-Gerhardt-Stiftung, Lutherstadt Wittenberg, Klinik für Innere Medizin und KfH-Nierenzentrum (Chefarzt bzw. leitender Arzt: Prof. Dr. Peter M. Jehle)
› Author Affiliations
Further Information

Publication History

Publication Date:
28 December 2017 (online)

Zusammenfassung

Das Syndrom der renalen Osteopathie ist komplex und führt zu einer erheblichen Zunahme der Morbidität und Mortalität dieser Patienten. Primär sollte der Entstehung eines sekundären Hyperparathyreoidismus (sHPT) präventiv begegnet werden. Hier gilt es, frühzeitig und dauerhaft einen Vitamin-D-Mangel auszugleichen und dann bei Einschränkung der GFR unter 60 ml/min zusätzlich mit niedrigen Dosen aktiver Vitamin-D-Metabolite die fehlende renale Aktivierung von Calcitriol zu ersetzen. In diesem Stadium der Niereninsuffizienz sollte die Hyperphosphatämie bereits behandelt werden. Die Vitamin-D-Therapie hat aufgrund ihrer pleiotropen und wahrscheinlich antiatherogenen Effekte auch einen Stellenwert in der Langzeittherapie. Neue Medikamente wie das Kalzimimetikum Cinacalcet, das aktive Vitamin-D-Analogon Paricalcitol und die kalziumfreien Phosphatbinder Sevelamer und Lanthanumkarbonat haben die Therapie der renalen Osteopathie entscheidend verbessert und tragen dazu bei, dass bei mehr Patienten die in den Leitlinien empfohlenen Referenzwerte für PTH, Serumkalzium und Phosphat erreicht werden können. Dadurch wird die Notwendigkeit der Parathyroidektomie, die bei Patienten mit autonomem HPT immer noch indiziert ist, in den nächsten Jahren noch weiter zurückgehen.

Summary

Renal osteopathy isa complex syndrome which leads to a considerable increase in morbidity and mortality of patients with chronic kidney disease (CKD). Prevention of secondary hyperparathyroidism (sHPT) should be considered in all CKD patients. Vitamin D deficiency should be corrected. With declining renal function (GFR below 60 ml/min) active vitamin D metabolites should additionally be applied. Hyperphosphatemia should also be corrected. Vitamin D therapy exerts pleiotropic effects and antiatherogenic effects and should be therefore considered as a longterm therapy. Therapy of renal osteopathy had considerably improved by new drugs such as the calcimimetic cinacalcet, the active vitamin D analogue paricalcitol and the calcium-free phosphate binders sevelamer and lanthanum with more patients achieving the recommended target values of PTH, serum calcium and phosphate. The frequency of parathyroidectomy which is still indicated in autonomous HPT will decline in the future years.

 
  • Literatur

  • 1 Brandenburg V, Fassbender WJ, Karges W, Jehle PM. Frakturrisiko bei Dialysepatienten – Welche Therapieoptionen gibt es?. Osteologie forum 2007; 13: 1-10.
  • 2 Brandenburg VM, Floege J. Adynamic bone disease – bone and beyond. NDT Plus 2008; 03: 135-147.
  • 3 Brown EM, Gamba G, Riccardi D. et al. Cloning and characterization of an extracellular Ca(2+)sensing receptor from bovine parathyroid. Nature 1993; 366 6455 575-580.
  • 4 Cunningham J, Danese M, Olson K. et al. Effects of the calcimimetic cinacalcet HCl on cardiovascular disease, fracture, and health-related quality of life in secondary hyperparathyroidism. Kidney Int 2005; 68 (04) 1793-1800.
  • 5 D’Haese PC, Spasovski GB, Sikole A. et al. A multicenter study on the effects of lanthanum carbonate (Fosrenol TM) and calcium carbonate on renal bone disease in dialysis patients. Kidney Int 2003; 63: S73-S78.
  • 6 Fiedler R, Deuber HJ, Langer T. et al. Effects of reduced dialysate calcium on calcium-phosphorus product and bone metabolism in hemodialysis patients. Nephron Clin Pract 2004; 96 (01) c3-c9.
  • 7 Ghazali A, Fardellone P, Pruna A. et al. Is low plasma 25-(OH)vitamin D a major risk factor for hyperparathyroidism and Looser’s zones independent of calcitriol?. Kidney Int 1999; 55 (06) 2169-2177.
  • 8 Goodman WG, Hladik GA, Turner SA. et al. The Calcimimetic agent AMG 073 lowers plasma parathyroid hormone levels in hemodialysis patients with secondary hyperparathyroidism. J Am Soc Nephrol 2002; 13 (04) 1017-1024.
  • 9 Hampl H, Steinmüller T, Fröhling P. et al. Longterm results of total parathyroidectomy without autotransplantation in patients with and without renal failure. Miner Electrolyte Metab 1999; 25 (03) 161-170.
  • 10 Hamdy NA, Kanis JA, Beneton MN. et al. Effect of alfacalcidol on natural course of renal bone disease in mild to moderate renal failure. BMJ 1995; 310 6976 358-363.
  • 11 Holick MF. Vitamin D deficiency. N Engl J Med 2007; 357 (03) 266-281.
  • 12 Jehle PM, Jehle DR, Mohan S, Keller F. Renal osteodystrophy: new insights in pathophysiology and treatment modalities with special emphasis on the insulin-like growth factor system. Nephron 1998; 79 (03) 249-264.
  • 13 Jehle PM, Rehm K, Jentzsch M. Ernährung bei Niereninsuffizienz: Spagat zwischen Nephroprotektion und Vermeidung einer Malnutrition. Der Nephrologe 2008; 03 (02) 108-117.
  • 14 Kates DM, Sherrard DJ, Andress DL. Evidence that serum phosphate is independently associated with serum PTH in patients with chronic renal failure. Am J Kidney Dis 1997; 30 (06) 809-813.
  • 15 Ketteler M, Bongartz P, Westenfeld R. et al. Association of low fetuin-A (AHSG) concentrations in serum with cardiovascular mortality in patients on dialysis: a cross-sectional study. Lancet 2003; 361 9360 827-833.
  • 16 Ketteler M, Westenfeld R, Schlieper G, Brandenburg V. Pathogenesis of vascular calcification in dialysis patients. Clin Exp Nephrol 2005; 09 (04) 265-270.
  • 17 Lehmann G, Ott U, Stein G. et al. Renal osteodystrophy after successful renal transplantation: a histomorphometric analysis in 57 patients. Transplant Proc 2007; 39 (10) 3153-3158.
  • 18 London GM, Marty C, Marchais SJ. et al. Arterial calcifications and bone histomorphometry in end-stage renal disease. J Am Soc Nephrol 2004; 15 (07) 1943-1951.
  • 19 Lorenz K, Ukkat J, Sekulla C. et al. Total parathyroidectomy without autotransplantation for renal hyperparathyroidism: experience with a qPTH-controlled protocol. World J Surg 2006; 30 (05) 743-751.
  • 20 Lucas RC. On a form of late rickets associated with albuminuria, rickets of adolscents. Lancet 1883; 01: 993-994.
  • 21 MacCallum WG. Tumor of the parathyroid gland. John Hopkins Hosp Bull 1905; 16: 87-89.
  • 22 Martinez I, Saracho R, Montenegro J, Llach F. The importance of dietary calcium and phosphorous in the secondary hyperparathyroidism of patients with early renal failure. Am J Kidney Dis 1997; 29 (04) 496-502.
  • 23 National Kidney Foundation. K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis 2003; 42 (4 Suppl 3): S1-S201.
  • 24 Qunibi WY, Hootkins RE, McDowell LL. et al. Treatment of hyperphosphatemia in hemodialysis patients: The Calcium Acetate Renagel Evaluation (CARE Study). Kidney Int 2004; 65 (05) 1914-1926.
  • 25 Qunibi W, Moustafa M, Muenz LR. et al. CARE-2 Investigators. A 1-year randomized trial of calcium acetate versus sevelamer on progression of coronary artery calcification in hemodialysis patients with comparable lipid control: the Calcium Acetate Renagel Evaluation-2 (CARE-2) study. Am J Kidney Dis 2008; 51 (06) 952-965 Epub 2008 Apr 18.
  • 26 Shoji T, Shinohara K, Kimoto E. et al. Lower risk for cardiovascular mortality in oral 1alpha-hydroxy vitamin D3 users in a haemodialysis population. Nephrol Dial Transplant 2004; 19 (01) 179-184.
  • 27 Slatopolsky E, Finch J, Clay P. et al. A novel mechanism for skeletal resistance in uremia. Kidney Int 2000; 58 (02) 753-761.
  • 28 Spasovski GB, Sikole A, Gelev S. et al. Evolution of bone and plasma concentration of lanthanum in dialysis patients before, during 1 year of treatment with lanthanum carbonate and after 2 years of follow-up. Nephrol Dial Transplant 2006; 21 (08) 2217-2224 Epub 2006 Apr 4.
  • 29 Stracke S, Jehle PM, Sturm D. et al. Clinical course after total parathyroidectomy without autotransplantation in patients with end-stage renal failure. Am J Kidney Dis 1999; 33 (02) 304-311.
  • 30 Taal MW, Roe S, Masud T. et al. Total hip bone mass predicts survival in chronic hemodialysis patients. Kidney Int 2003; 63 (03) 1116-1120.
  • 31 Teng M, Wolf M, Lowrie E. et al. Survival of patients undergoing hemodialysis with paricalcitol or calcitriol therapy. N Engl J Med 2003; 349 (05) 446-456.
  • 32 Tominaga Y, Takagi H. Molecular genetics of hyperparathyroid disease. Curr Opin Nephrol Hypertens 1996; 05 (04) 336-341.
  • 33 Virchow R. Kalk-Metastasen. Arch Pathol Anat Physiol 1877; 08: 103-107.
  • 34 White KE, Jonsson KB, Carn G, Hampson G. et al. The autosomal dominant hypophosphatemic rickets (ADHR) gene is a secreted polypeptide overexpressed by tumors that cause phosphate wasting. J Clin Endocrinol Metab 2001; 86 (02) 497-500.
  • 35 Wu-Wong JR, Nakane M, Ma J. et al. Effects of Vitamin D analogs on gene expression profiling in human coronary artery smooth muscle cells. Atherosclerosis 2006; 186 (01) 20-28 Epub 2005 Aug 10.