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Correction of metabolic acidosis in hemodialysis: consequences on serum leptin and mineral metabolism

  • Nephrology - Original Paper
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Abstract

Purpose

Hyperleptinemia and metabolic acidosis (MA) are frequently observed in patients on hemodialysis (HD). While the role of leptin in patients on HD is not completely understood, HD only partially corrects MA. Both leptin and acidosis have effect on bone disease. The goal of the present study was to evaluate the effects of MA correction on chronic kidney disease–mineral and bone disorder laboratory parameters and leptin levels.

Methods

Forty-eight patients on HD, aged 43 ± 19 years, were prospectively studied. Individual adjustments in the bicarbonate dialysate concentration were made to maintain pre-dialysis concentration ≥22 mEq/l. Blood gas analysis was done monthly for 4 months (M1–M4).

Results

From M0 to M4, serum albumin increased (from 3.5 ± 0.3 to 4.0 ± 0.3 g/l, p < 0.0001) while β2 microglobulin decreased (from 27.6 ± 8.3 to 25.8 ± 6.8 µg/ml, p = 0.025). Serum leptin decreased in all but three patients, as well as leptin/adiponectin ratio (p < 0.0001). There was a decrease in ionized serum calcium (from 5.0 ± 0.5 to 4.7 ± 0.5 mg/dl, p = 0.002) and an increase in parathyroid hormone (PTH) [from 191 (85, 459) to 446 pg/ml (212, 983), p < 0.0001] and in serum phosphate (from 5.4 ± 1.4 to 5.8 ± 1.1 mg/dl, p = 0.048).

Conclusion

MA correction in HD patients can decrease leptin, an atherogenic marker. The impact of such treatment extends to uremic bone disease, as decrease in serum calcium and increase in PTH. However, this could be an undesirable effect because it may aggravate a secondary hyperparathyroidism. Whether the reduction in leptin levels has impact on outcomes in patients on hemodialysis deserves further investigation.

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References

  1. Kopple JD, Kalantar-Zadeh K, Mehrotra R (2005) Risks of chronic metabolic acidosis in patients with chronic kidney disease. Kidney Int 67(Suppl):S21–S27

    Article  Google Scholar 

  2. Kovacic V, Roguljic L, Kovacic V (2003) Metabolic acidosis of chronically hemodialyzed patients. Am J Nephrol 23:158–164

    Article  CAS  PubMed  Google Scholar 

  3. Mehrotra R, Kopple JD, Wolfson M (2003) Metabolic acidosis in maintenance dialysis patients: clinical considerations. Kidney Int 63(Suppl):S13–S25

    Article  Google Scholar 

  4. Kraut JA, Kurtz I (2005) Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am J Kidney Dis 45:978–993

    Article  CAS  PubMed  Google Scholar 

  5. Reaich D, Channon SM, Scrimgeour CM, Daley SE, Wilkinson R et al (1993) Correction of acidosis in humans with CRF decreases protein degradation and amino acid oxidation. Am J Physiol 265:E230–E235

    CAS  PubMed  Google Scholar 

  6. Castaneda-Sceppa C, Sarnak MJ, Wang X, Greene T, Madero M et al (2007) Role of adipose tissue in determining muscle mass in patients with chronic kidney disease. J Ren Nutr 17:314–322

    Article  PubMed Central  PubMed  Google Scholar 

  7. Aguilera A, Bajo MA, Rebollo F, Diez JJ, Diaz C et al (2002) Leptin as a marker of nutrition and cardiovascular risk in peritoneal dialysis patients. Adv Perit Dial 18:212–217

    CAS  PubMed  Google Scholar 

  8. Mora Palma FJ, Ellis HA, Cook DB, Dewar JH, Ward MK et al (1983) Osteomalacia in patients with chronic renal failure before dialysis or transplantation. Q J Med 52:332–348

    CAS  PubMed  Google Scholar 

  9. Burton RF (1992) The roles of intracellular buffers and bone mineral in the regulation of acid-base balance in mammals. Comp Biochem Physiol Comp Physiol 102:425–432

    Article  CAS  PubMed  Google Scholar 

  10. Green J, Kleeman CR (1991) The role of bone in the regulation of systemic acid-base balance. Contrib Nephrol 91:61–76

    CAS  PubMed  Google Scholar 

  11. Bushinsky DA (1995) Stimulated osteoclastic and suppressed osteoblastic activity in metabolic but not respiratory acidosis. Am J Physiol 268:C80–C88

    CAS  PubMed  Google Scholar 

  12. Krieger NS, Sessler NE, Bushinsky DA (1992) Acidosis inhibits osteoblastic and stimulates osteoclastic activity in vitro. Am J Physiol 262:F442–F448

    CAS  PubMed  Google Scholar 

  13. Reseland JE, Syversen U, Bakke I, Qvigstad G, Eide LG et al (2001) Leptin is expressed in and secreted from primary cultures of human osteoblasts and promotes bone mineralization. J Bone Miner Res 16:1426–1433

    Article  CAS  PubMed  Google Scholar 

  14. Margetic S, Gazzola C, Pegg GG, Hill RA (2002) Leptin: a review of its peripheral actions and interactions. Int J Obes Relat Metab Disord 26:1407–1433

    Article  CAS  PubMed  Google Scholar 

  15. Daugirdas JT (1989) The post: pre dialysis plasma urea nitrogen ratio to estimate K.t/V and NPCR: validation. Int J Artif Organs 12:420–427

    CAS  PubMed  Google Scholar 

  16. Kim HJ, Han SW (2007) Metabolic acidosis in maintenance hemodialysis patients: clinical impact and intervention. Electrolyte Blood Press 5:42–46

    Article  CAS  PubMed Central  PubMed  Google Scholar 

  17. Movilli E, Gaggia P, Camerini C, Brunori G, Vizzardi V et al (2005) Effect of oral sodium bicarbonate supplementation on interdialytic weight gain, plasma sodium concentrations and predialysis blood pressure in hemodialysis patients. Blood Purif 23:379–383

    Article  CAS  PubMed  Google Scholar 

  18. Brady JP, Hasbargen JA (2000) A review of the effects of correction of acidosis on nutrition in dialysis patients. Semin Dial 13:252–255

    Article  CAS  PubMed  Google Scholar 

  19. Avesani CM, Draibe SA, Kamimura MA, Dalboni MA, Colugnati FA et al (2004) Decreased resting energy expenditure in non-dialysed chronic kidney disease patients. Nephrol Dial Transplant 19:3091–3097

    Article  PubMed  Google Scholar 

  20. Bossola M, Tazza L, Giungi S, Luciani G (2006) Anorexia in hemodialysis patients: an update. Kidney Int 70:417–422

    CAS  PubMed  Google Scholar 

  21. Bergstrom J (1995) Nutrition and mortality in hemodialysis. J Am Soc Nephrol 6:1329–1341

    CAS  PubMed  Google Scholar 

  22. Nasri H (2006) Serum leptin concentration and left ventricular hypertrophy and function in maintenance hemodialysis patients. Minerva Urol Nefrol 58:189–193

    CAS  PubMed  Google Scholar 

  23. Wallace AM, McMahon AD, Packard CJ, Kelly A, Shepherd J et al (2001) Plasma leptin and the risk of cardiovascular disease in the west of Scotland coronary prevention study (WOSCOPS). Circulation 104:3052–3056

    Article  CAS  PubMed  Google Scholar 

  24. Kokot F, Chudek J, Adamczak M, Wiecek A (2001) Interrelationship between plasma leptin concentration and severity of metabolic acidosis in haemodialysed patients with chronical renal failure. Exp Clin Endocrinol Diabetes 109:370–373

    Article  CAS  PubMed  Google Scholar 

  25. Fluck CE, Kuhlmann BV, Mullis PE (1999) Insulin increases serum leptin concentrations in children and adolescents with newly diagnosed type I diabetes mellitus with and without ketoacidosis. Diabetologia 42:1067–1070

    Article  CAS  PubMed  Google Scholar 

  26. Hathout EH, Sharkey J, Racine M, Ahn D, Mace JW et al (1999) Changes in plasma leptin during the treatment of diabetic ketoacidosis. J Clin Endocrinol Metab 84:4545–4548

    Article  CAS  PubMed  Google Scholar 

  27. Malyszko J, Malyszko J, Wolczynski S, Mysliwiec M (2006) Adiponectin, leptin and thyroid hormones in patients with chronic renal failure and on renal replacement therapy: are they related? Nephrol Dial Transplant 21:145–152

    Article  CAS  PubMed  Google Scholar 

  28. Ouchi N, Kihara S, Arita Y, Maeda K, Kuriyama H et al (1999) Novel modulator for endothelial adhesion molecules: adipocyte-derived plasma protein adiponectin. Circulation 100:2473–2476

    Article  CAS  PubMed  Google Scholar 

  29. Teta D, Maillard M, Halabi G, Burnier M (2008) The leptin/adiponectin ratio: potential implications for peritoneal dialysis. Kidney Int 73(Suppl):S112–S118

    Article  Google Scholar 

  30. Kraut JA (2000) Disturbances of acid-base balance and bone disease in end-stage renal disease. Semin Dial 13:261–266

    Article  CAS  PubMed  Google Scholar 

  31. Lefebvre A, de Vernejoul MC, Gueris J, Goldfarb B, Graulet AM et al (1989) Optimal correction of acidosis changes progression of dialysis osteodystrophy. Kidney Int 36:1112–1118

    Article  CAS  PubMed  Google Scholar 

  32. Confavreux CB (2011) Bone: from a reservoir of minerals to a regulator of energy metabolism. Kidney Int 79(Suppl):S14–S19

    Article  Google Scholar 

  33. Cornish J, Callon KE, Bava U, Lin C, Naot D et al (2002) Leptin directly regulates bone cell function in vitro and reduces bone fragility in vivo. J Endocrinol 175:405–415

    Article  CAS  PubMed  Google Scholar 

  34. Coen G, Ballanti P, Fischer MS, Balducci A, Calabria S et al (2003) Serum leptin in dialysis renal osteodystrophy. Am J Kidney Dis 42:1036–1042

    Article  CAS  PubMed  Google Scholar 

  35. Kokot F, Chudek J, Karkoszka H, Adamczak M, Wiecek A et al (1999) Does PTH influence leptin concentration in haemodialysed uraemic patients? Nephron 82:372–373

    Article  CAS  PubMed  Google Scholar 

  36. Zoccali C, Panuccio V, Tripepi G, Cutrupi S, Pizzini P et al (2004) Leptin and biochemical markers of bone turnover in dialysis patients. J Nephrol 17:253–260

    CAS  PubMed  Google Scholar 

  37. Merabet E, Dagogo-Jack S, Coyne DW, Klein S, Santiago JV et al (1997) Increased plasma leptin concentration in end-stage renal disease. J Clin Endocrinol Metab 82:847–850

    CAS  PubMed  Google Scholar 

  38. Polymeris A, Doumouchtsis K, Grapsa E (2012) Bone mineral density and bone metabolism in hemodialysis patients. Correlation with PTH, 25OHD3 and leptin. Nefrologia 32:73–78

    CAS  PubMed  Google Scholar 

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Authors and Affiliations

  1. Division of Nephrology, Hospital das Clinicas da FMUSP - Disciplina de Nefrologia, Universidade de São Paulo, Rua Dr. Enéas de Carvalho Aguiar 255, 7º andar, São Paulo, SP, CEP 05403-000, Brazil

    Alessandra M. Bales, Rosa M. A. Moysés, Luciene M. dos Reis, Fabiana G. Graciolli, James Hung, Manuel Carlos Martins Castro & Rosilene M. Elias

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  1. Alessandra M. Bales
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  2. Rosa M. A. Moysés
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  3. Luciene M. dos Reis
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  4. Fabiana G. Graciolli
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  5. James Hung
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  7. Rosilene M. Elias
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Correspondence to Rosilene M. Elias.

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Bales, A.M., Moysés, R.M.A., dos Reis, L.M. et al. Correction of metabolic acidosis in hemodialysis: consequences on serum leptin and mineral metabolism. Int Urol Nephrol 47, 177–182 (2015). https://doi.org/10.1007/s11255-014-0844-5

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  • DOI: https://doi.org/10.1007/s11255-014-0844-5

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