Journal Information
Vol. 32. Issue. 6.November 2012
Pages 701-866
Vol. 32. Issue. 6.November 2012
Pages 701-866
Full text access
Acidosis metabólica y avance de la enfermedad renal crónica: incidencia, patogénesis y opciones terapéuticas
Metabolic acidosis and progression of chronic kidney disease: incidence, pathogenesis, and therapeutic options
Visits
35356
WPAHS Division of Nephrology and Hypertension. Allegheny General Hospital, WPAHS, Temple University School of Medicinea, wpahs division of nephrology and hypertension Allegheny general hospital, wpahs, temple university school of medicineb, Luis M. Ortegac, luis M Ortegad, Swati Arorad
a Allegheny General Hospital, Pittsburgh, Pennsylvania, USA,
b nephrology and hypertension, allegheny general hospital, pittsburgh, pennsylvania, USA,
c Nephrology and Hypertension, Allegheny General Hospital. WPAHS, Temple University School of Medicine, Pittsburgh, Pennsylvania, USA,
d nephrology and hypertension, Allegheny general hosptial.WPAHS,Temple University School of Medicine, Pittsburgh, Pennsylvania, USA,
This item has received
Article information

Hay una prevalencia importante de la acidosis metabólica en los pacientes que padecen enfermedad renal crónica, presentándose en niveles tempranos de pérdida de filtrado glomerular. La patogénesis se basa en la falta de síntesis de bicarbonato sérico con la acumulación de ácidos de naturaleza orgánica e inorgánica, ocasionando daño tubulointersticial a través de la retención de amoniaco y el depósito de complemento, aunque esta última hipótesis se ha cuestionado en el pasado. El uso empírico de bicarbonato oral representa una opción terapéutica interesante que ha sido utilizada en estudios clínicos recientes. La disponibilidad de bicarbonato de sodio oral en sus diversas formas representa una opción barata y simple de utilizar para decelerar la progresión de la enfermedad renal, sin mencionar las mejoras en el catabolismo proteico, la osteodistrofia renal y la mortalidad.

Palabras clave:
Amoniaco
Palabras clave:
Bicarbonato sódico
Palabras clave:
ERC
Palabras clave:
Acidosis metabólica
Palabras clave:
Mortalidad

In the chronic kidney disease population metabolic acidosis is prevalent presenting already in the early stages of renal dysfunction. The pathogenesis associates the lack of bicarbonate production with the accumulation of organic/inorganic acids and the development of tubulointerstitial damage through ammonium retention and complement deposition. The empiric use of oral sodium bicarbonate represents an interesting therapeutic option that has been documented in a few clinical trials in human subjects. The availability of oral sodium, in its diverse forms, represents an inexpensive and simple way of treating an entity that could hasten the progression of kidney disease, as well as protein catabolism, bone disease and mortality.

Keywords:
Ammonium
Keywords:
Sodium bicarbonate
Keywords:
CKD
Keywords:
Metabolic acidosis
Keywords:
Mortality
Full text is only aviable in PDF
Bibliografía
[1]
Kraut JA, Kurtz I. Metabolic acidosis of CKD; diagnosis,clinical characteristics and treatment. Am J Kidney Dis 2005;45:978-93. [Pubmed]
[2]
Coresh J, Selvin E, Stevens LA, Manzi J, Kusek JW, Eggers P, et al. Prevalence of chronic kidney disease in the United States. JAMA 2007;298(17):2038-47. [Pubmed]
[3]
Kraut JA, Madias NE. Consequences and therapy of the metabolic acidosis of chronic kidney disease. Pediatr Nephrol 2011;26:19-28. [Pubmed]
[4]
Di Iorio B, Aucella F, Conte G, Cupisti A, Santoro D. A prospective, multicenter, randomized, controlled study: The correction of metabolic acidosis with use of bicarbonate in chronic renal insufficiency (UBI0 study). J Nephrol 2012;25:437-40. [Pubmed]
[5]
Kraut JA, Kurtz I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am J Kidney Dis 2005;45:978-93. [Pubmed]
[6]
Coresh J, Astor BC, Greene T, Eknoyan G, Levey AS. Prevalence of chronic kidney disease and decreased kidney function in the adult US population: Third National Health and Nutrition Examination Survey. Am J Kidney Dis 2003;41:1-12. [Pubmed]
[7]
Frassetto L, Sebastian A. Age and systemic acid-base equilibrium: Analysis of published data. J Gerontol 1996;51:B91-B99.
[8]
Hakim RM, Lazarus JM. Biochemical parameters in chronic renal failure. Am J Kidney Dis 1988;11:238-47. [Pubmed]
[9]
Relman AS. Renal acidosis and renal excretion of acid in health and disease. Adv Intern Med 1964;12:295-347. [Pubmed]
[10]
Caravaca F, Arrobas M, Pizarro JL, Esparrago JF. Metabolic acidosis in advanced renal failure:differences between diabetic and nondiabetic patients. Am J Kidney Dis 1999;5:892-8.
[11]
Widmer B, Gehardt RE, Harrington JT, Cohen JJ. Serum electrolytes and acid base composition. The influence of graded degrees of chronic renal failure. Arch Int Med 1979;139:1099-102.
[12]
Eustace JA, Astor B, Muntner PM, Ikizler A, Coresh J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int 2004;65:1031-40. [Pubmed]
[13]
Shah SN, Abramowitz M, Hosletter TH, Melamed ML. Serum bicarbonate levels and the progression of kidney disease:a cohort study. Am J Kidney Dis 2009;54:270-7. [Pubmed]
[14]
Kovesdy CP, Anderson JE, Kalantar-Zadeh K. Association of serum bicarbonate levels with mortality in patients with non-dialysis-dependent CKD. Nephrol Dial Transplant 2009;24:1232-7. [Pubmed]
[15]
Raphael KL, Wei G, Baird BC, Greene T, Beddhu S. Higher serum bicarbonate levels within the normal range are associated with better survival and renal outcomes in African Americans. Kidney Int 2011;79:356-62. [Pubmed]
[16]
Dass PD, Kurtz I. Renal ammonia and bicarbonate production in chronic renal failure. Miner Electrolyte Metab 1990;16:308-14. [Pubmed]
[17]
Kraut JA, Madias NE. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol 2007;2:162-74. [Pubmed]
[18]
Sabatini S, Kutzman NA. Enzyme activity in obstructive uropathy: Basis for salt wastage and the acidification defect. Kidney Int 1990;37:79-84. [Pubmed]
[19]
Maclean AJ, Hayslett JP, Klein-Robbenhaar T, Myketey N. Adaptative change in ammonia excretion in renal insufficiency. Kidney Int 1980;17:595-606. [Pubmed]
[20]
Tizianello A, Ferrari GD, Garibotto G, Gurreri G, Robaudo C. Renal metabolism of amino acids in subjects with normal renal function and in patients with chronic renal insufficiency. J Clin Invest 1980;65:1162-73. [Pubmed]
[21]
Lameire N, Matthys E. Influence of progressive salt restriction on urinary bicarbonate wasting in uremic acidosis. Am J Kidney Dis 1986;8:151-8. [Pubmed]
[22]
Battle DC. Segmental characterization of defects in collecting tubule acidification. Kidney Int 1986;30:546-54. [Pubmed]
[23]
Klahr S, Morrissey J. Progression of chronic renal disease. Am J Kidney Dis 2003;41:S3-S7(Suppl 1). [Pubmed]
[24]
Gadola L, Noboa O, Marquez MN, Rodriguez MJ, Nin N, Boggia J, et al. Calcium citrate ameliorates the progression of chronic renal injury. Kidney Int 2004;65:1224-30. [Pubmed]
[25]
Jara A, Felsenfeld AJ, Bover J, Kleeman CR. Chronic metabolic acidosis in azotemic rats on a high phosphate diet halts the progression of renal disease. Kidney Int 2000;58:1023-32. [Pubmed]
[26]
Agroyannis B, Tzanatos H, Kopelias I, Fourtounas K, Koutsikos D. Renal ammoniagenesis and tubulointerstitial injury in hypertension. Nephrol Dial Transplant 1995;10:2372-3. [Pubmed]
[27]
Chodanican MC, Julin C. Angiotensin II stimulates ammoniagensis in canine renal proximal tubular segments. Am J Physiol 1991;260:F16-F27.
[28]
Nath KA, Hostetter MK, Hostetter TH. Pathophysiology of chronic tubulo-interstitial disease in rats. Interactions of dietary acid load, ammonia, and complement component C3. J Clin Invest 1985;76:667-75. [Pubmed]
[29]
Halperin ML, Eithier JH, Kamel KS. Ammonium excretion in chronic metabolic acidosis: Benefits and risks. Am J Kidney Dis 1989;14:267-71. [Pubmed]
[30]
Nath KA, Hostetter MK, Hostetter TH. Increased ammoniagenesis as a determinant of progressive renal injury. Am J Kidney Dis 1991;17:654-7. [Pubmed]
[31]
Wesson DE, Simoni J. Acid retention during kidney failure induces endothelin and aldosterone production which lead to progressive GFR decline, a situation ameliorated by alkali diet. Kidney Int 2010;78:1128-35. [Pubmed]
[32]
Mitch WE. Influence of metabolic acidosis on nutrition. Am J Kidney Dis 1997;29:xlvi-xlviii.
[33]
Tsantoulas DC, McFarlane IG, Portman B, Eddelston ALWF, Williams R. Cell mediated immunity to human Tamm-Horsfall glycoprotein in autoimmune liver disease with renal tubular acidosis. Br Med J 1974;4:491-4. [Pubmed]
[34]
Wallia R, Greenberg A, Piraino B, Mitro R, Puschett JB. Serum electrolyte patterns in end-stage renal disease. Am J Kidney Dis 1986;8:98. [Pubmed]
[35]
Torres VE, Cowley BDJ, Branden MG, Yoshida I, Gattone VH. Long-term ammonium chloride or sodium bicarbonate treatment in two models of polycystic kidney disease. Exp Nephrol 2001;9:171-80. [Pubmed]
[36]
Wesson DE, Nathan T, Rose T, Simone J, Tran RM. Dietary protein induces endothelin-mediated kidney injury through enhanced intrinsic acid production. Kidney Int 2007;71:210-7. [Pubmed]
[37]
Roderick P, Willis NS, Blakeley S, Jones C, Tomson P. Correction of chronic metabolic acidosis for chronic kidney disease patients. Cochrane Data Base Syst Rev(1):2007,CD001890.
[38]
Rustom R, Grime JS, Costigan M, Maltby P, Hughes A, Taylor W, et al. Oral sodium bicarbonate reduces proximal renal tubular peptide catabolism, ammoniogenesis, and tubular damage in renal patients. Ren Fail 1998;20:371-82. [Pubmed]
[39]
Brito-Ashurst ID, Varagunam M, Raftery MJ, Yaqoop MM. Bicarbonate supplementation slows progression of ckd and improves nutritional status. J Am Soc Nephrol 2009;20:2075-84. [Pubmed]
[40]
Phisitkul S, Khanna A, Simoni J, Broglio K, Sheather S, Rajab MH, et al. Amelioration of metabolic acidosis in patients with low GFR reduced kidney endothelin production and kidney injury, and better preserved GFR. Kidney Int 2010;77:617-23. [Pubmed]
[41]
Mahajan A, Simoni J, Sheather SJ, Broglio KR, Rajab MH, Wesson DE, et al. Daily oral sodium bicarbonate preserves glomerular filtration rate by slowing its decline in early hypertensive nephropathy. Kidney Int 2010;78:303-9. [Pubmed]
[42]
Wesson DE, Simoni J, Broglio K, Sheather SJ. Acid retention accompanies reduced GFR in humans and increase plasma levels of aldosterone and endothelin. Am J Physiol Renal Physiol 2011;300:F830-7. [Pubmed]
[43]
Kraut JA. Effect of metabolic acidosis on progression of chronic kidney disease. Am J Physiol Renal Physiol 2011;300:F828-9. [Pubmed]
[44]
Wesson DE, Simoni J. Increased tissue acid mediates progressive GFR decline in animals with reduced nephron mass. Kidney Int 2009;75:929-35. [Pubmed]
[45]
Phisitkul S, Hacker C, Simoni J, Tran RM, Wesson DE. Dietary protein causes a decline in the glomerular filtration rate of the remnant kidney mediated by metabolic acidosis and endothelin receptors. Kidney Int 2008;73:192-9. [Pubmed]
Download PDF
Idiomas
Nefrología (English Edition)
Article options
Tools
es en

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?