Skip to main content

Homocysteinemia as a Biomarker in Kidney Disease

  • Living reference work entry
  • First Online:
Biomarkers in Kidney Disease

Abstract

Homocysteine is an amino acid containing sulfur in the form of the thiol group. Homocysteine is a metabolite of the essential amino acid methionine. First, methionine is converted to S-adenosylmethionine, which is then converted to S-adenosylhomocysteine, wherein transmethylation processes take place. Homocysteine finally emerges from S-adenosylhomocysteine. It then enters either the transsulfuration pathway when converted to cystathionine or the remethylation pathway when converted back into methionine in the presence of the 5-methyltetrahydrofolate reductase, cystathionine β-synthase, and methionine synthase and with the participation of vitamin B12 and folic acid. Therefore, the decreased activities of these enzymes, as well as the deficit of the vitamin B12 and folic acid, are frequent causes of hyperhomocysteinemia. In addition, chronic kidney disease and the use of certain drugs are also very important factors that cause hyperhomocysteinemia.

In the bloodstream, homocysteine is found in one of two forms, the bound and the free form, which together makes up the total homocysteine. The most suitable sample for determining the circulating levels of total homocysteine is plasma. Enzymatic and immunochemical methods are most commonly used in routine clinical practice. Reference values of the total homocysteine vary among different countries and even among different laboratories as a result of the use of different methods for determining the levels of total homocysteine but also the different lifestyles of the residence.

The plasma total homocysteine level is positively correlated with the serum creatinine values, and it is in a high inverse correlation with the glomerular filtration rate, so it could be used as a marker of renal hypofunction. In addition, the kidneys possess enzymes involved in metabolic pathways. That is why chronic kidney disease is one of the most common causes of hyperhomocysteinemia. The level of homocysteine in patients with chronic kidney disease can be elevated even in the initial stages. Hyperhomocysteinemia is present in most patients with glomerular filtration rate <60 ml/min/1.73 m2, with the highest values in patients on chronic dialysis treatment. Hyperhomocysteinemia occurs in 50–60 % of patients with transplanted kidneys. On the other hand, hyperhomocysteinemia is an important factor that contributes to the structural damage of the kidney, both glomerular and tubular, along with damage to the interstitial tissue. Therefore, when there are hyperhomocysteinemia and absence of the deficiency of the vitamin B12 and folic acid, it is necessary to examine the renal function.

Homocysteine is a vascular toxin, and it is one of the risk factors for the development of coronary heart disease, cerebrovascular disease, and peripheral artery disease. Also, it has a role in the development of venous thrombosis. Therefore, in patients with chronic kidney disease, the plasma concentration of homocysteine is a significant determinant of the risk of morbidity and mortality from cardiovascular disease. The measurement of homocysteine in patients with renal dysfunction is necessary for making decisions about therapeutic treatment, especially if the patient has not yet had signs of development of cardiovascular disease.

In addition, it is assumed that homocysteine has a role in the pathogenesis of other pathological conditions, such as neurodegenerative diseases, dementia, cognitive disorders, osteoporosis, epigenetic changes, hypertension, as well as the stimulation of an immune response.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Institutional subscriptions

Abbreviations

5-MTHF:

Methyltetrahydrofolate

5-MTHFR:

Methyltetrahydrofolate reductase

ADMA:

Asymmetric dimethylarginine

apo A-I:

Apolipoprotein A-I

ATP:

Adenosine triphosphate

bHcy:

Bound homocysteine

BHL:

Bleomycin hydrolase

BHMT:

Betaine-homocysteine methyltransferase

CBS:

Cystathionine β-synthase

CKD:

Chronic kidney disease

CMIS:

Chronic malnutrition-inflammation state

CSE:

Cystathionine γ-lyase

CVD:

Cardiovascular disease

DM:

Diabetes mellitus

DN:

Diabetic nephropathy

DNA:

Deoxyribonucleic acid

eNOS:

Endothelial nitric oxide synthase

ESRD:

End-stage renal disease

fHcy:

Free homocysteine

GFR:

Glomerular filtration rate

H2S:

Hydrogen sulfide

Hcy:

Homocysteine

HDL:

High-density lipoprotein

HHcy:

Hyperhomocysteinemia

HTL:

Homocysteine thiolactone

IL:

Interleukin

Km:

Michaelis constant

LDL:

Low-density lipoprotein

MAT:

Methionine adenosyltransferase

MCP-1:

Monocyte chemoattractant protein-1

Met:

Methionine

MIP-2:

Macrophage inflammatory protein-2

MMP:

Matrix metalloproteinase

MS:

Methionine synthase

NAC:

N-acetylcysteine

NF-κB:

Nuclear factor kappa-light-chain-enhancer of activated B cells

NO:

Nitric oxide

NS:

Syndroma nephroticum

oxLDL:

Oxidized low-density lipoprotein

PON1:

Paraoxonase-1

ROS:

Reactive oxygen species

SAH:

S-adenosylhomocysteine

SAM:

S-adenosylmethionine

TAFI:

Thrombin activatable fibrinolysis inhibitor

TGF-β1:

Transforming growth factor β1

tHcy:

Total homocysteine

t-PA:

Tissue plasminogen activator

tRNA:

Transfer ribonucleic acid

VSMC:

Vascular smooth muscle cells

References

  • Bergmark C, Mansoor MA, Svardal A, et al. Redox status of plasma homocysteine and related aminothiols in smoking and non smoking young adults. Clin Chem. 1997;43:1997–9.

    CAS  PubMed  Google Scholar 

  • Čabarkapa V. Examination of relationship between homocysteinemia and functional status of kidneys in patients with chronic renal failure. Master thesis. Medical Faculty, University of Novi Sad, 2007. (In Serbian).

    Google Scholar 

  • Čabarkapa V. Relationship of specific biomarkers and progression of chronic renal insufficiency in patients with diabetic nephropathy. Ph.D. thesis. Medical Faculty, University of Novi Sad, 2007. (In Serbian).

    Google Scholar 

  • Čabarkapa V, Stošić Z, Žeravica R, et al. The importance of homocysteinemia measurement in chronic renal failure. Med Pregl. 2007;60 Suppl 2:81–3.

    PubMed  Google Scholar 

  • Čabarkapa V, Djeric M, Stošić Z, et al. Determining relationship between homocysteinemia and biomarkers of inflammation, oxidative stress and functional kidney status in patients with diabetic nephropathy. J Med Biochem. 2012;32:131–9.

    Google Scholar 

  • Chambers JC, Ueland PM, Wright M, et al. Investigation of relationship between reduced, oxidized, and protein-bound homocysteine and vascular endothelial function in healthy human subjects. Circ Res. 2001;89:187–92.

    Article  CAS  PubMed  Google Scholar 

  • Cheng X. Updating relationship between hyperhomocysteinemia lowering therapy and cardiovascular disease. Cardiovasc Ther. 2013;31:19–26.

    Article  CAS  Google Scholar 

  • Chwatko G, Jakubowski H. The determination of homocysteine/thiolactone in human plasma. Anal Biochem. 2005;337:271–7.

    Article  CAS  PubMed  Google Scholar 

  • De Koning L, Hu FB. Homocysteine lowering in end-stage renal disease: is there any cardiovascular benefit? Circulation. 2010;121:1379–81.

    Article  PubMed  Google Scholar 

  • Dhonukshe-Rutten R, de Vries J, de Bree A, et al. Dietary intake and status of folate and vitamin B12 and their association with homocysteine and cardiovascular disease in European population. Eur J Clin Nutr. 2009;63:18–30.

    Article  CAS  PubMed  Google Scholar 

  • Di Minno M, Tremoli E, Coppola A, et al. Homocysteine and arterial thrombosis: challenge and opportunity. Thromb Haemost. 2010;103:942–61.

    Article  PubMed  Google Scholar 

  • Doronzo G, Russo I, Del Mese P, et al. Role of NMDA receptor in homocysteine-induced activation of mitogen-activated kinase and phosphatidyl inositol 3-kinase pathways in cultured human vascular muscle cells. Thromb Res. 2010;125:23–32.

    Article  Google Scholar 

  • Durand P, Prost M, Loreau N, et al. Impaired homocysteine metabolism and atherothrombotic disease. Lab Invest. 2001;81:645–72.

    Article  CAS  PubMed  Google Scholar 

  • Einollahi B, Lessan-Pezeshki M, Kalantar E, et al. Hyperhomocysteinemia after kidney transplantation. Transplant Proc. 2011;43:685–587.

    Google Scholar 

  • Elshorbagy A, Oulhaj A, Konstatinova S, et al. Plasma creatinine as a determinant of plasma total homocysteine concentrations in the hordaland homocysteine study: use of statistical modeling to determine reference limits. Clin Biochem. 2007;40:1209–18.

    Article  CAS  PubMed  Google Scholar 

  • Ferretti G, Bacchetti T, Marotti E, et al. Effect of homocysteinylation on human high-density lipoproteins: a correlation with paraoxonase activity. Metabolism. 2003;52:146–51.

    Article  CAS  PubMed  Google Scholar 

  • Finkelstein J. Metabolic regulatory properties of S-adenosylmethionine and S-adenosylhomocysteine. Clin Chem Lab Med. 2007;45:1694–9.

    Article  CAS  PubMed  Google Scholar 

  • Finkelstein J, Martin J. Homocysteine. Int J Biochem Cell Biol. 2000;32:385–9.

    Article  CAS  PubMed  Google Scholar 

  • Finocchiaro P, Zoccali C. Hyperhomocysteinemia and progression of renal disease. G Ital Nefrol. 2005;22:590–6.

    CAS  PubMed  Google Scholar 

  • Fischer PA, Dominguez GN, Cunibreti LA, et al. Hyperhomocysteinemia induces renal hemodynamic dysfunction: is nitric oxide involved? J Am Soc Nephrol. 2003;14:653–60.

    Article  PubMed  Google Scholar 

  • Francis M, Eggers P, Hostetter T, et al. Association between serum homocysteine and markers of impaired kidney function in adults in US. Kidney Int. 2004;66:303–12.

    Article  CAS  PubMed  Google Scholar 

  • Garibotto G, Valli A, Anderstam B, et al. The kidney is a major site of S-adenosylhomocysteine disposal in humans. Kidney Int. 2009;76:293–6.

    Article  CAS  PubMed  Google Scholar 

  • Garibotto G, Sofia A, Saffioti S, et al. Amino acid and protein metabolism in the human kidney in patients with chronic kidney disease. Clin Nutr. 2010;29:424–33.

    Article  CAS  PubMed  Google Scholar 

  • Golbahar J, Rezaian G, Bararpour H. Distribution of plasma homocysteine concentrations in the healthy Iranians. Clin Biochem. 2004;37:149–51.

    Article  CAS  PubMed  Google Scholar 

  • Grubben MJ, Boers GH, Blom HJ, et al. Unfiltrated coffee increases plasma homocysteine concentrations in healthy volunteers: a randomized trial. Am J Clin Nutr. 2000;71:480–4.

    CAS  PubMed  Google Scholar 

  • Guthikonda S, Haynes WG. Homocysteine: role and implication in atheroscleorsis. Curr Atheroscler Rep. 2006;8:100–6.

    Article  CAS  PubMed  Google Scholar 

  • Heinz J, Kropf S, Luley C, et al. Homocysteine as a risk factor for cardiovascular disease in patients treated by dialysis: a meta-analysis. Am J Kidney Dis. 2009;54:478–89.

    Article  CAS  PubMed  Google Scholar 

  • Herrmann M, Schmidt JP, Umanskaya N, et al. The role of hyperhomocysteinemia as well as folate, vitamin B6 and B12 deficiencies in osteoporosis- a systematic review. Clin Chem Lab Med. 2007;45:1621–32.

    CAS  PubMed  Google Scholar 

  • Hirsch S, Pia De La Maza M, et al. Hyperhomocysteinemia and endothelial function in young subjects- effects of vitamin supplementation. Clin Cardiol. 2002;25:495–501.

    Article  PubMed  Google Scholar 

  • Iacobazzi V, Infantino V, Castenga A, et al. Hyperhomocysteinemia: related genetic diseases and congenital defects, abnormal DNA methylation and newborn screening issues. Mol Genet Metab. 2014. doi:10.1016/j.ymgme.2014.07.016. Accessed 10 Nov 2014.

    PubMed  Google Scholar 

  • Ingrosso D, Perna A. Epigenetics in hyperhomocysteinemic states. A special focus on uremia. Biochim Biophys Acta. 2009;1790:892–9.

    Article  CAS  PubMed  Google Scholar 

  • Jacobsen D, Catanescu O, DiBello P, et al. Molecular targeting by homocysteine: a mechanism for vascular pathogenesis. Clin Chem Lab Med. 2005;43:1076–83.

    Article  CAS  PubMed  Google Scholar 

  • Jakubowski H. Protein homocysteinylation: possible mechanism underlying pathological consequences of elevated homocysteine levels. FASEB J. 1999;13:2277–83.

    CAS  PubMed  Google Scholar 

  • Jakubowski H. The molecular basis of homocysteine thiolactone-mediated vascular disease. Clin Chem Lab Med. 2007;45:1704–16.

    Article  CAS  PubMed  Google Scholar 

  • Jamison RI, Hartigan P, Kaufman JS, et al. Effect of homocysteine lowering on mortality and vascular disease in advanced chronic kidney disease and end-stage renal disease: a randomized controlled trial. J Am Med Assoc. 2007;298:1163–70.

    Article  CAS  Google Scholar 

  • Jardine M, Kang A, Zoungas S, et al. The effect of folic acid based homocysteine lowering on cardiovascular events in people with kidney disease: systematic review and meta-analysis. BMJ. 2012;344:e3533. doi:10.1136/bmj.e3533. Accessed 21 Oct 2014.

    Article  PubMed Central  PubMed  Google Scholar 

  • Kalantar-Zadeh K, Block G, Humpheys MH, et al. A low, rather than a high, total plasma homocysteine is an indicator of poor outcome in hemodialysis patients. J Am Soc Nephrol. 2004;15:442–53.

    Article  CAS  PubMed  Google Scholar 

  • Karolczak K, Olas B. Mechanism of action of homocysteine and its thiolactone in hemostasis system. Physiol Res. 2009;58:623–33.

    CAS  PubMed  Google Scholar 

  • Kulkarni A, Mehendale S, Pisal H, et al. Association of omega-3 fatty acids and homocysteine concentrations in pre-eclampsia. Clin Nutr. 2011;30:60–4.

    Article  CAS  PubMed  Google Scholar 

  • Mann JF, Sheridan P, McQueen MJ, et al. Homocysteine lowering with folic acid and B vitamins in people with chronic kidney disease-results of the renal hope-2 study. Nephrol Dial Transplant. 2008;23:645–53.

    Article  CAS  PubMed  Google Scholar 

  • Mao S, Xiang W, Huang S, et al. Association between homocysteine status and the risk of nephropathy in type 2 diabetes mellitus. Clin Chim Acta. 2014;431:206–10.

    Article  CAS  PubMed  Google Scholar 

  • Marcus J, Sarnak MJ, Menon V. Homocysteine lowering and cardiovascular disease risk: lost in translation. Can J Cardiol. 2007;23:707–10.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  • McLean R, Karasik D, Selhub J, et al. Association of a common polymorphism in methylenetetrahydrofolate reductase (MTHFR) gene with bone phenotypes depends on plasma folate status. J Bone Miner Res. 2004;19:410–8.

    Article  CAS  PubMed  Google Scholar 

  • Medina MA, Urdiales JL, Amores-Sanchez MI. Roles of homocysteine in cell metabolism. Eur J Biochem. 2001;268:3871–82.

    Article  CAS  PubMed  Google Scholar 

  • Mtiraoui N, Ezzidi I, Chaieb M, et al. MTHFR C677T and A1298C gene polymorphisms and hyperhomocysteinemia as risk factor of diabetic nephropathy in type 2 diabetes patients. Diabetes Res Clin Pract. 2007;75:99–106.

    Article  CAS  PubMed  Google Scholar 

  • Nakao A, Suzuki H, Ueno H, et al. Discovery of S-adenosyl-l-homocysteine hydrolase inhibitors based on non-adenosine analogs. Bioorg Med Chem Lett. 2014;24:4336–40.

    Article  CAS  PubMed  Google Scholar 

  • Nekrassova O, Lawrence N, Compton R. Analytical determination of homocysteine: a review. Talanta. 2003;60:1085–95.

    Article  CAS  PubMed  Google Scholar 

  • Nurk E, Tell GS, Nygard O, et al. Plasma total homocysteine is influenced by prandial status in humans: the Hordaland homocysteine study. J Nutr. 2001;131:1214–6.

    CAS  PubMed  Google Scholar 

  • Pan Y, Guo LL, Cai LL, et al. Homocysteine-lowering therapy does not lead to reduction in cardiovascular outcomes in chronic kidney disease patients: a meta-analysis of randomised, controlled trials. Br J Nutr. 2012;16:1–8.

    Google Scholar 

  • Perez F, Ilie J, Zhou X, et al. Pathomolecular effects of homocysteine on the aging process: a new theory of aging. Med Hypotheses. 2007;69:149–60.

    Article  CAS  PubMed  Google Scholar 

  • Perła-Kajàn J, Twardowski T, Jakubowski H. Mechanisms of homocysteine toxicity in humans. Amino Acids. 2007;32:561–72.

    Article  PubMed  Google Scholar 

  • Perna A, Acanfora F, Luciano MG, et al. Plasma protein homocysteinylation in uremia. Clin Chem Lab Med. 2007;45:1678–82.

    Article  CAS  PubMed  Google Scholar 

  • Rafii M, Elango R, House J, et al. Measurement of homocysteine and related metabolites in human plasma and urine by liquid chromatography electrospray tandem mass spectrometry. J Chromatogr B. 2009;877:3282–91.

    Article  CAS  Google Scholar 

  • Ramakrishnan S, Sulochana KN, Lakshmi S, et al. Biochemistry of homocysteine in health and diseases. Ind J Biochem Biophys. 2006;43:275–83.

    CAS  Google Scholar 

  • Rasmussen K, Møller J. Total homocysteine determination in clinical practice. Ann Clin Biochem. 2000;37:627–48.

    Article  CAS  PubMed  Google Scholar 

  • Refsum H, Smith D, Ueland P, et al. Facts and recommendations about total homocysteine determinations: an expert opinion. Clin Chem. 2004;50:3–32.

    Article  CAS  PubMed  Google Scholar 

  • Sarwar AB, Sarwar A, Rosen B, et al. Measuring subclinical atherosclerosis: is homocysteine relevant? Clin Chem Lab Med. 2007;45:1667–77.

    Article  CAS  PubMed  Google Scholar 

  • Scholze A, Rinder C, Beige J, et al. Acetylcysteine reduces plasma homocysteine concentration and improves pulse pressure and endothelial function in patients with end-stage renal failure. Circulation. 2004;109:369–74.

    Article  CAS  PubMed  Google Scholar 

  • Sen U, Basu P, Abe OA, et al. Hydrogen sulfide ameliorates hyperhomocysteinemia-associated chronic renal failure. Am J Physiol Ren Physiol. 2009;297:410–9.

    Article  Google Scholar 

  • Sen U, Munjal C, Qipshidze N, et al. Hydrogen sulfide regulates homocysteine-mediated glomerulosclerosis. Am J Nephrol. 2010;31:442–55.

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  • Sen U, Pushpakumar S, Amin M, et al. Homocysteine in renovascular complications: hydrogen sulfide is a molecular and plausible anaerobic ATP generator. Nitric Oxide. 2014. doi:10.1016/i.niox.2014.06.006. Accessed 5 Nov 2014.

    PubMed Central  PubMed  Google Scholar 

  • Sengoegle G, Kletzmayr J, Papagiannopoulos M, et al. TGF-B1 impairs homocysteine metabolism in human renal cells: possible implications for transplantation. Transplant Int. 2003;16:843–8.

    Article  Google Scholar 

  • Stanger O, Herrmann W, Pietrzik K, et al. DACH-LIGA homocysteine (German, Austrian and Swiss Homocysteine Society): consensus paper on the rational clinical use of homocysteine, folic acid and B-vitamins in cardiovascular and thrombotic disease: guidelines and recommendations. Clin Chem Lab Med. 2003;41:1392–403.

    CAS  PubMed  Google Scholar 

  • Stanislawska-Sachadyn A, Woodside J, Brown K, et al. Evidence for sex differences in the determinants of homocysteine concentrations. Mol Genet Metabol. 2008;93:355–62.

    Article  CAS  Google Scholar 

  • Stehouwer C, van Guldener C. Does homocysteine cause hypertension? Clin Chem Lab Med. 2003;41:1408–11.

    Article  CAS  PubMed  Google Scholar 

  • Stenvinkel P, Karimi M, Johansson S, et al. Impact of inflammation on epigenetic DNA methylation-a novel risk factor for cardiovascular disease? J Intern Med. 2007;261:488–99.

    Article  CAS  PubMed  Google Scholar 

  • Suszynska-Zajczyk J, Sikora M, Jakubowski H. Paraoxonase 1 deficiency and hyperhomocysteinemia alter the expression of mouse kidney proteins involved in renal disease. Mol Genet Metab. 2014. doi:10.1016/j.ymgme.2014.07.011. Accessed 7 Nov 2014.

    Google Scholar 

  • Tan R, Liu Y. Matrix metalloproteinases in kidney homeostasis and diseases. Am J Physiol Ren Physiol. 2012;302:1351–61.

    Article  Google Scholar 

  • Urquhart BL, Freeman DJ, Spence JD, et al. The effect of mesna on plasma total homocysteine concentration in hemodialysis patients. Am J Kidney Dis. 2007;49:109–17.

    Article  CAS  PubMed  Google Scholar 

  • Van Guldener C, Stehouwer C. Homocysteine metabolism in renal disease. Clin Chem Lab Med. 2003;41:1412–7.

    Article  PubMed  Google Scholar 

  • Wada J, Makino H. Inflammation and the pathogenesis of diabetic nephropathy. Clin Sci. 2013;124:139–52.

    Article  CAS  PubMed  Google Scholar 

  • Wald DS, Law M, Morris JK. Homocysteine and cardiovascular disease: evidence on causality from meta-analysis. Br Med J. 2002;325:1202–6.

    Article  Google Scholar 

  • Walker MC, Smith GN, Perkins SL, et al. Changes in homocysteine levels during normal pregnancy. Am J Obstet Gynecol. 1999;180:660–4.

    Article  CAS  PubMed  Google Scholar 

  • Wu CC, Zheng CM, Lin YF, et al. Role of homocysteine in end-stage renal disease. Clin Biochem. 2012;45:1286–94.

    Article  CAS  PubMed  Google Scholar 

  • Zappacosta B, Persichilli S, Iacoviello L, et al. Folate, vitamin B12 and homocysteine status in an Italian blood donor population. Nutr Metab Cardiovasc Dis. 2013;23:473–80.

    Article  CAS  PubMed  Google Scholar 

  • Zimny J, Sikora M, Guranowski A, et al. Protective mechanisms against homocysteine toxicity: the role of bleomycin hydrolase. J Biol Chem. 2006;281:22485–92.

    Article  CAS  PubMed  Google Scholar 

  • Zoccali C, Benedetto FA, Mallamaci F, et al. Inflammation is associated with carotid atherosclerosis in dialysis patients. Creed investigators. Cardiovascular risk extended evaluation in dialysis patients. J Hypertens. 2000;18:1207–13.

    Article  CAS  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Velibor Čabarkapa .

Editor information

Editors and Affiliations

Definitions

Homocysteinylation

The reaction in which the Hcy in the form of homocysteine thiolactone binds to amino groups of amino acids, leading to a dysfunction of the proteins.

Hyperhomocysteinemia

Increasing levels of total homocysteine (tHcy), which implies an increase in the level of the free (fHcy) and bound Hcy (bHcy).

Hypomethylation

Reduction in the volume of the transmethylation reactions in hyperhomocysteinemia (HHcy), due to the inhibition of the methyltransferase by the increased levels of S-adenosylhomocysteine (SAH).

Remethylation

The conversion of Hcy into methionine by the enzyme methionine synthase, the folic acid as a donor of the methyl groups, and of vitamin B12 as a cofactor.

Transmethylation

The reaction of the methyl group transfer from the donor to the acceptor. This reaction takes place during the conversion of methionine into Hcy, and it is dependent on the intermediates S-adenosylmethionine (SAM) and SAH.

Transsulfuration

Reaction to the conversion of Hcy into cystathionine with the participation of vitamin B6. Cystathionine, after being converted into various compounds, is excreted by the kidneys, which are the pathways for eliminating Hcy from the body.

Rights and permissions

Reprints and permissions

Copyright information

© 2015 Springer Science+Business Media Dordrecht

About this entry

Cite this entry

Čabarkapa, V., Đerić, M. (2015). Homocysteinemia as a Biomarker in Kidney Disease. In: Patel, V. (eds) Biomarkers in Kidney Disease. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-7743-9_2-1

Download citation

  • DOI: https://doi.org/10.1007/978-94-007-7743-9_2-1

  • Received:

  • Accepted:

  • Published:

  • Publisher Name: Springer, Dordrecht

  • Online ISBN: 978-94-007-7743-9

  • eBook Packages: Springer Reference Biomedicine and Life SciencesReference Module Biomedical and Life Sciences

Publish with us

Policies and ethics