LA HIPERFOSFATEMIA Y SU RELACION CON LA MORTALIDAD CARDIOVASCULAR EN LA INSUFICIENCIA RENAL CRONICA

(especial para SIIC © Derechos reservados)
El manejo adecuado de los trastornos del metabolismo mineral es fundamental para lograr el control de la hiperfosfatemia en pacientes en diálisis por insuficiencia renal crónica.
douthat9.jpg Autor:
Walter guillermo Douthat
Columnista Experto de SIIC

Institución:
Hospital Privado-Centro Médico de Córdoba, Universidad Católica de Córdoba


Artículos publicados por Walter guillermo Douthat
Recepción del artículo
3 de Enero, 2006
Aprobación
24 de Marzo, 2006
Primera edición
4 de Mayo, 2006
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
Si bien la supervivencia de la población con insuficiencia renal crónica en tratamiento con diálisis es cada vez mayor, la mortalidad continúa siendo elevada, especialmente relacionada con trastornos cardiovasculares. Diversos estudios demuestran que niveles elevados de fosfato, calcio, producto fosfo-cálcico y PTH desempeñan un papel fundamental en el desarrollo de las calcificaciones cardiovasculares y tienen una relación directa con la mortalidad de la población en diálisis. Cuando el calcio se deposita en la íntima arterial lo hace sobre placas ateroscleróticas inflamadas, como se observa frecuentemente en la aorta, ilíacas, carótidas y coronarias, aunque la lesión vascular más frecuente es la esclerosis de la media arterial conocida como "esclerosis de Mönckeberg", la cual implica una verdadera osificación de la pared vascular. Las normas K/DOQI y EBPG establecieron las pautas para el manejo adecuado de los trastornos del metabolismo mineral. Sin embargo, diversos estudios demostraron que el cumplimiento de dichas metas es muy dificultoso y la hiperfosfatemia presenta una elevada prevalencia entre la población en diálisis. El nefrólogo cumple una tarea fundamental en el control de la hiperfosfatemia a través del conocimiento de la fisiopatogenia de los trastornos del metabolismo mineral y de su esfuerzo por alcanzar las metas propuestas por las normas.

Palabras clave
Calcificaciones cardiovasculares, osteodistrofia renal, hiperfosfatemia, diálisis, hiperparatiroidismo secundario


Artículo completo

(castellano)
Extensión:  +/-7.69 páginas impresas en papel A4
Exclusivo para suscriptores/assinantes

Abstract
Although survival of patients with end stage renal disease (ESRD) under dialysis is increasing mortality remains high due to cardiovascular disease. Elevated levels of phosphate, calcium, Ca x P product and PTHi play a critical role in cardiac calcifications. Moreover a direct relationship has been established between mortality and content of calcium in the heart.
Calcifications in ESRD seem to occur at 2 sites of the vessel wall. Sclerosis that affect the media -named Monckeberg's sclerosis- represents a real ossification of the vessel. The deposit of calcium could also compromise the atherosclerotic plaques affecting the intima of the aorta, carotid, coronaries and iliac arteries. K/DOQI and EBPG guidelines established the appropriate treatment for these abnormalities. Several trials revealed the difficulty to achieve these aims in clinical settings, and hyperphosphatemia continue to have a high prevalence in dialysis population. Nephrology community has a crucial role in the management of hyperphosphatemia through the understanding of the pathogenic mechanisms operating in these alterations. Many efforts should be made to reach the guidelines objectives.

Key words
renal osteodystrophy, hyperphosphatemia,, dialysis,, secondary hyperparathyroidism, cardiovascular calcification


Clasificación en siicsalud
Artículos originales > Expertos de Iberoamérica >
página   www.siicsalud.com/des/expertocompleto.php/

Especialidades
Principal: Nefrología y Medio Interno
Relacionadas: Bioquímica, Cardiología, Cuidados Intensivos, Diagnóstico por Laboratorio, Endocrinología y Metabolismo, Medicina Interna



Comprar este artículo
Extensión: 7.69 páginas impresas en papel A4

file05.gif (1491 bytes) Artículos seleccionados para su compra



Enviar correspondencia a:
Walter Gui Douthat, Hospital Privado Centro Médico de Córdoba, Universidad Católica de Córdoba, 5016, Naciones Unidas 346, Bº Parque Vélez Sarsfield, Córdoba, Argentina
Patrocinio y reconocimiento:
A los Dres. Alles, Peñalba y Tirado por el trabajo conjunto en estudios de osteodistrofia renal. A todos los nefrólogos participantes de la encuesta multicéntrica Argentina sobre osteodistrofia renal.
Bibliografía del artículo
1. US Renal Data System: USDRS 2003 Annual Data Report: Atlas of End-Stage Renal Disease in the United State, Bathesda; MD, National Institute of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 2003.
2. Szcech L, Lazar I. Projecting the United State ESRD population: Issues regarding treatment of patients with ESRD. Kidney Int 66 (Suppl 90): S3-S7, 2004.
3. Foley R, Parfrey P, Sarnak M. Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis 32 (Suppl 3):112-119, 1998.
4. Ounibi W, Nolan D, Ayus J. Cardiovascular calcification in patients with end-stage renal disease: A century-old phenomenon. Kidney Int 62 (Suppl 82):S73-S80, 2002.
5. Rostand G, Tilman D. Parathyroid hormone, vitamin D, and cardiovascular disease in chronic renal failure. Kidney Int 56:383-392, 1999.
6. Wong N, Abrahamson D, et al. Detection of coronary artery calcium by ultrafast computed tomography and its relation to clinical evidence of coronary artery disease. Am J Cardiol 73:223-227, 1994.
7. Goodman W, Goldin J, Kuizon B, et al. Coronary-artery calcification in young adults with end-stage renal disease who are undergoing dialysis. N Engl J Med 342:1478-1483, 2000.
8. Sakata N, Noma A, Yamamoto Y, et al. Modifications of elastin by pentosidine is associated with the calcification of aortic media in patients with end-stage renal disease. Nephrol Dial Transplant 18:1601-1609, 2003.
9. Bostrom K, Watson K, Horn S, et al. Bone morphogenetic protein expression in human atherosclerotic lesions. J Clin Invest 91:1800-1809, 1993.
10. McCullough P, Soman S. Cardiovascular calcification in patients with chronic renal failure: Are we on target with this risk factor? Kidney Iny 66 (Suppl 90):S18-S24, 2004.
11. Goldsmith D, Ritz E, Covic A. Vascular calcification: A stiff challenge for the nephrologist. Does preventing bone disease cause arterial disease? Kidney Int 66:1315-1333, 2004.
12. Braun J, Oldendorf M, Moshage W, et al. Electronic beam computed tomography in the evaluation of cardiac calcification in chronic dialysis patients. Am J Kidney Dis 27:394-401, 1996.
13. Joki N, Hase H, Nakamura R, Yamaguchi T. Onset of coronary artery disease prior to initiation of hemodialysis in patients with end-stage renal disease. Nephrol Dial Transplant 12:718-723, 1997.
14. Wright R, Reeder G, Herzog C, et al. Acute myocardial infarction and renal dysfunction: A high risk combination. Ann Intern Med 137:563-570, 2002.
15. London G, Panner B, Marchais S, Guerin A. Calcification of the aortic valve in dialyzed patients. J Am Soc Nephrol 11:778-783, 2000.
16. Delmez J, Slatopolsky E: Hyperphosphatemia: Its consequences and treatment in patients with chronic renal disease. Am J Kidney Dis 19:303-317, 1992.
17. Block G, Hulbert-Shearon T, Levin N, Port F: Association of serum phosphorous and calcium x phosphorous product with mortality risk in chronic hemodialysis patients: A national study. Am J Kidney Dis 31:607-17, 1998.
18. Block G, Port F: Re-evaluation of risks associated with hyperphosphatemia and hyperparathyroidism in dialysis patients: Recommendations for a change in management. Am J Kidney Dis 35:1226-1237, 2000.
19. Slatopolsky E, Brown A, Dusso A. Role of phosphorous in the pathogenesis of secondary hyperparathyroidism. Am J Kidney Dis 37 (Suppl 2):54-57, 2001.
20. Dusso A, Pavlopoulos T, Naumovich L, et al. p21 (WAF1) and transforming growth factor-alpha mediate dietary phosphate regulation of parathyroid cell growth. Kidney Int 59:855-865, 2001.
21. Ganesh S, Stack A, Levin N, et al. Association of elevated serum PO4, Ca x PO4 product, and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients. J Am Soc Nephrol 12:2131-2138, 2001.
22. Lopez-Hilker D, Dusso A, Rapp N, et al. Phosphorus restriction reverses hyperparathyroidism in uremia independent of changes in calcium and calcitriol. Am J Physiol 259:432-437, 1990.
23. Slatopolsky E, Finch J, Denda M, et al. Phosphorus restriction prevents parathyroid glang growth. High phosphorus directly stimulates PTH secretion in vitro. J Clin Invest 97:2534-2540, 1996.
24. Barsotti G, Giannoni A, Morelli E, et al. The decline of renal function slowed by very-low phosphorus intake in chronic renal patients following a low nitrogen diet. Clin Nephrol 21:54-59, 1984.
25. Hsu C, Are we mismanaging calcium and phosphate metabolism in renal failure? Am J kidney Dis 29:641-649, 1997.
26. Muczi I, Hercz G, Uldall R, Ouwendyk M, Francoeur R, Pierratos A. Control of serum phosphate without any phosphate binders in patients treated with nocturnal hemodialysis. Kidney Int 53:1399-1404, 1998.
27. National Kidney Foundation: K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis 42 (Suppl 3):S1-S201, 2003.
28. Emmett M. A comparison of clinically useful phosphorus binders for patients with chronic kidney failure. Kidney Int 66 (Suppl 90):S25-S32, 2004.
29. Douthat W, Acuña G, Fernández Martín JL, Serrano M, González Carcedo A, Canteros A, Menéndez Fraga P, Cannata J. Exposición al aluminio y calidad del baño de diálisis: repercusión sobre los niveles de aluminio sérico. Nefrología 14(6):695-700, 1994.
30. Cannata J, Douthat W, Acuña G, Fernández Martín JL. Aluminum toxicity: the role of prevention. Life Chemistry Reports 11:207-213; 1994.
31. Douthat W, de Arteaga J, Garay G, Canteros A, Cannata J, Massari P. Niveles de aluminio en el agua de centros de diálisis de la provincia de Córdoba, Argentina. Nefrología Latinoamericana 5:11-16, 1998.
32. Douthat W, Acuña Aguerre G, Fernández Martín JL, Mouzo R, Cannata Andía JB. Treatment of aluminium intoxication: a new scheme for desferrioxamine administration. Revista: Nephrol Dial Transplant Vol 9:1132-1135, 1994.
33. Douthat W, Giraudo L, Martinez Colombres C, Aguirre E, Capra R, de Arteaga J, Massari P: Eficacia y tolerancia del acetato vs carbonato de calcio como quelantes del fósforo en pacientes en diálisis. Nefrología Latinoamericana 4:274-279, 1997.
34. Chertow G, Raggi P, Chasan-Taber S, et al. Determinant of progressive vascular calcification in haemodialysis patients: Nephrol Dial Transplant 19:1489-1496, 2004.
35. Winkelmayer W, Levin R, Avorn J. The nephrologist`s role in the management of calcium-phosphorous metabolism in patients with chronic kidney disease. Kidney Int 63:1836-1842, 2003.
36. Young E, Akiba T, Albert J, et al. Magnitude and impact of abnormal mineral metabolism in hemodialysis patients in the dialysis outcomes and practice patterns study (DOPPS). Am J Kidney Dis 44 (Suppl 2):34-38, 2004.
37. Young E, Albert J, Satayathum S, et al. Predictors and consequences of altered mineral metabolism: The dialysis outcomes and practice patterns study. Kidney Int 67:1179-1187, 2005.
38. Kessler M, Canaud B, Pedrini L, et al. The EBPG expert group on haemodialysis. European best practice guidelines for haemodialysis. Nephrol Dial Transplant 17 (Suppl 17):1-111, 2002.
39. Douthat W, Alles A, Marinovich S, Tirado S, Peñalba A. Importancia del Concepto "Fosfatemia Adecuada" como Factor de Riesgo de Hiperfosfatemia. Nefrología 23 (Supl 2):95-99, 2003.
40. Llach F. Hyperphosphatemia in end-stage renal disease patients: Pathophysiological consequences: Kidney Int 56 (Suppl 73):S31-S37, 1999.
41. Kim S, Golstein M, Szabo T, Pierratos A. Resolution of massive uremic calcinosis with daily nocturnal home hemodialysis. Am J Kidney Dis 41:12, 2000.
42. Alfrey A. The role of abnormal phosphorous metabolism in the progression of chronic kidney disease and metastatic calcification. Kidney Int 66 (Suppl 90):S13-S17, 2004.
43. Kutsumata K, Kusano K, Hirata M, et al. Sevelamer hydrochloride prevents ectopic calcification and renal osteodystrophy in chronic renal failure rats. Kidney Int 64:441-450, 2003.
44. Chertow G, Burke S, Raggi P, et al. Sevelamer attenuates the progression of coronary and aortic calcification in hemodialysis patients. Kidney Int 62:245-252, 2002.
45. Giachelli C, Jono S, Shioi A, et al. Vascular calcification and inorganic phosphate. Am J Kidney Dis 38:34-37, 2001.
46. Floege J. When man turns to stone: Extraosseous calcification in uremic patients. Kidney Int 65:2447-2462, 2004.
47. Chen N, O`Neill K, Duan D, Moe S. Phosphorous and uremic serum up-regulate osteopontin expression in vascular smooth muscle cells. Kidney Int 62:1724-1731, 2002.
48. Schafer C, Heiss A, Schwarz A, et al. The serum protein alpha 2-Hereman-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification. J Clin Invest 112:357-366, 2003.

 
 
 
 
 
 
 
 
 
 
 
 
Está expresamente prohibida la redistribución y la redifusión de todo o parte de los contenidos de la Sociedad Iberoamericana de Información Científica (SIIC) S.A. sin previo y expreso consentimiento de SIIC.
ua31618
Home

Copyright siicsalud © 1997-2024 ISSN siicsalud: 1667-9008