Impact of acidosis in the evoluton of the patients cohort in the renal health program of Uruguay
Keywords:
ACIDOSIS, CHRONIC RENAL FAILURE, EVALUATION, CLINICAL EVOLUTIONAbstract
Objective: to evaluate the prevalence of metabolic acidosis in chronic kidney disease and its impact on the evolution of the condition.
Method: we conducted a retrospective study of patients in the Renal Health Program of Uruguay (from October, 2004 through October, 2011) with two control groups six months or longer apart, and at least one bicarbonatemia datum. We analysed: creatininemia, proteinuria, venous bicarbonatemia and alcalinizing treatment. The start of dialysis, transplant and/or death were considered final events. Statistical analysis: t test, chi2, ANOVA, Kaplan-Meier and multivariate analysis using Cox method (meaningful p < 0,05).
Results: we analyzed 921 patients with at least one bicarbonatemia datum (232 patients with two or more data). Creatininemia was greater in the tubulo-interstitial nephritis and in the groups with bicarbonatemia lower than 23 mEq/l (acidosis) or greater than 32 mEq/l, rather than in the intermediate group. Bicarbonatemia was lower in the IV-V stages than in the I-II stages of chronic kidney disease. In stages I-II bicarbonatemia was lower in the presence of proteinuria. Seven point three percent of patients received alkalinizers at the start, and 31% at the end. In the group with acidosis, increase of creatininemia/year (n = 232) was greater and survival (combined) was lower. Bicarbonatemia, creatininemia and proteinuria levels were independently correlated with the combined final event (entering the renal substitution treatment/death).
Conclusions: metabolic acidosis may be observed since initial stages of the chronic kidney disease and it constitutes an independent factor of progression and death. Thus, early detection and correction are advisable.
References
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(33) Wesson DE, Simoni J, Prabhakar S. Endothelin-induced increased nitric oxide mediates augmented distal nephron acidification as a result of dietary protein. J Am Soc Nephrol 2006; 17(2):406-13.
(34) Mahajan A, Simoni J, Sheather SJ, Broglio KR, Rajab MH, Wesson DE. Daily oral sodium bicarbonate preserves glomerular filtration rate by slowing its decline in early hypertensive nephropathy. Kidney Int 2010; 78(3):303-9.
(35) Wesson DE. Endothelin role in kidney acidification. Semin Nephrol 2006; 26(5):393-8.
(36) Turner JM, Bauer C, Abramowitz MK, Melamed ML, Hostetter TH. Treatment of chronic kidney disease. Kidney Int 2012; 81(4):351-62.
(37) Goraya N, Simoni J, Jo C, Wesson DE. Dietary acid reduction with fruits and vegetables or bicarbonate attenuates kidney injury in patients with a moderately reduced glomerular filtration rate due to hypertensive nephropathy. Kidney Int 2012; 81(1):86-93.
(38) Uribarri J, Oh MS. The key to halting progression of CKD might be in the produce market, not in the pharmacy. Kidney Int 2012; 81(1):7-9.
(2) Eustace JA, Astor B, Muntner PM, Ikizler TA, Coresh J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int 2004; 65(3):1031-40.
(3) Kraut JA, Madias NE. Consequences and therapy of the metabolic acidosis of chronic kidney disease. Pediatr Nephrol 2011; 26(1):19-28.
(4) Ling H, Ardjomand P, Samvakas S, Simm A, Busch GL, Lang F, et al. Mesangial cell hypertrophy induced by NH4Cl: role of depressed activities of cathepsins due to elevated lysosomal pH. Kidney Int 1998; 53(6):1706-12.
(5) Throssell D, Harris KP, Bevington A, Furness PN, Howie AJ, Walls J. Renal effects of metabolic acidosis in the normal rat. Nephron 1996; 73(3):450-5.
(6) Farber MO, Szwed JJ, Dowell AR, Strawbridge RA. The acute effects of respiratory and metabolic acidosis on renal function in the dog. Clin Sci Mol Med 1976; 50(3):165-9.
(7) 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(2):667-75.
(8) Nath KA, Hostetter MK, Hostetter TH. Increased ammoniagenesis as a determinant of progressive renal injury. Am J Kidney Dis 1991; 17(6):654-7.
(9) Wesson DE, Simoni J. Increased tissue acid mediates a progressive decline in the glomerular filtration rate of animals with reduced nephron mass. Kidney Int 2009; 75(9):929-35.
(10) 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(11):1128-35.
(11) Gadola L, Noboa O, Rodríguez M, Sierra M, Márquez M, Ravaglio S. Transdiferenciación de células tubulares humanas (HK2) en cultivo en medio ácido. En: Libro de Resúmenes. III Congreso Latinoamericano de IRA. Montevideo: IRA, 2003. p 81.
(12) Gadola L, Noboa O, Márquez MN, Rodriguez MJ, Nin N, Boggia J, et al. Calcium citrate ameliorates the progression of chronic renal injury. Kidney Int 2004; 65(4):1224-30.
(13) Gadola L, Noboa O, Márquez M, Rodríguez MJ, Ferrreiro A, Vallega A, et al. Calcium citrate attenuates tubulointerstitial damage in the rat model of obstructive nephropathy. J Am Soc Nephrol 2001; 12:703A.
(14) Tanner GA, Tanner JA. Dietary citrate treatment of polycystic kidney disease in rats. Nephron Physiol 2003; 93(1):P14-20.
(15) Toblli JE, DeRosa G, Lago N, Angerosa M, Nyberg C, Pagano P. Potassium citrate administration ameliorates tubulointerstitial lesions in rats with uric acid nephropathy. Clin Nephrol 2001; 55(1):59-68.
(16) Noboa O, Gadola L, Márquez M, Nin N, Ferreiro A, Sesser P, et al. Tubular function and tubulointersticial lesion in chronic glomerulopathies. J Am Soc Nephrol 1998; 9:77A.
(17) Shah SN, Abramowitz M, Hostetter TH, Melamed ML. Serum bicarbonate levels and the progression of kidney disease: a cohort study. Am J Kidney Dis 2009; 54(2):270-7.
(18) 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(4):1232-7.
(19) Kovesdy CP, Kalantar-Zadeh K. Oral bicarbonate: renoprotective in CKD? Nat Rev Nephrol 2010; 6(1):15-7.
(20) de Brito-Ashurst I, Varagunam M, Raftery MJ, Yaqoob MM. Bicarbonate supplementation slows progression of CKD and improves nutritional status. J Am Soc Nephrol 2009; 20(9):2075-84.
(21) Menon V, Tighiouart H, Vaughn NS, Beck GJ, Kusek JW, Collins AJ, et al. Serum bicarbonate and long-term outcomes in CKD. Am J Kidney Dis 2010; 56(5):907-14.
(22) Navaneethan SD, Schold JD, Arrigain S, Jolly SE, Wehbe E, Raina R, et al. Serum bicarbonate and mortality in stage 3 and stage 4 chronic kidney disease. Clin J Am Soc Nephrol 2011; 6(10):2395-402.
(23) Chiu YW, Mehrotra R. What should define optimal correction of metabolic acidosis in chronic kidney disease? Semin Dial 2010; 23(4):411-4.
(24) Couser WG, Nangaku M. Mechanism of bicarbonate effect in CKD. Kidney Int 2010; 78(8):817.
(25) 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(3):356-62.
(26) Yaqoob MM. Acidosis and progression of chronic kidney disease. Curr Opin Nephrol Hypertens 2010; 19(5):489-92.
(27) Kraut JA, Madias NE. Consequences and therapy of the metabolic acidosis of chronic kidney disease. Pediatr Nephrol 2011; 26(1):19-28.
(28) Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med 1999; 130(6):461-70.
(29) Schwedt E, Solá L, Ríos P, Mazzuchi N. Guía clínica para identificación, evaluación y manejo del paciente con enfermedad renal crónica en el primer nivel de atención. Montevideo: Fondo Nacional de Recursos, 2006. Disponible en: http://www.nefroprevencion.org.uy/Guias.pdf Consulta: 15 de jun de 2012
(30) Adrogué HE, Adrogué HJ. Acid-base physiology. Respir Care 2001; 46(4):328-41.
(31) 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(2):192-9.
(32) 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(7):617-23.
(33) Wesson DE, Simoni J, Prabhakar S. Endothelin-induced increased nitric oxide mediates augmented distal nephron acidification as a result of dietary protein. J Am Soc Nephrol 2006; 17(2):406-13.
(34) Mahajan A, Simoni J, Sheather SJ, Broglio KR, Rajab MH, Wesson DE. Daily oral sodium bicarbonate preserves glomerular filtration rate by slowing its decline in early hypertensive nephropathy. Kidney Int 2010; 78(3):303-9.
(35) Wesson DE. Endothelin role in kidney acidification. Semin Nephrol 2006; 26(5):393-8.
(36) Turner JM, Bauer C, Abramowitz MK, Melamed ML, Hostetter TH. Treatment of chronic kidney disease. Kidney Int 2012; 81(4):351-62.
(37) Goraya N, Simoni J, Jo C, Wesson DE. Dietary acid reduction with fruits and vegetables or bicarbonate attenuates kidney injury in patients with a moderately reduced glomerular filtration rate due to hypertensive nephropathy. Kidney Int 2012; 81(1):86-93.
(38) Uribarri J, Oh MS. The key to halting progression of CKD might be in the produce market, not in the pharmacy. Kidney Int 2012; 81(1):7-9.
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Published
2013-03-31
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Gadola L, Ríos P, Canzani O, Perg N, Canon A, Daglio M, et al. Impact of acidosis in the evoluton of the patients cohort in the renal health program of Uruguay. Rev. Méd. Urug. [Internet]. 2013 Mar. 31 [cited 2024 Nov. 24];29(1):4-11. Available from: https://revista.rmu.org.uy/index.php/rmu/article/view/293
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