Complement C3a

CPT: 86160
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  • acylation stimulation factor
  • Complement C3a des-Arginine

Special Instructions

Futhan preservative must be added to samples immediately after collection. Collection kits containing this preservative are available as Labcorp No. 78946.

Expected Turnaround Time

4 - 7 days

Related Documents

For more information, please view the literature below.

Lupus Comprehensive Testing Brochure

Specimen Requirements


Plasma (EDTA) with Futhan, frozen


1 mL

Minimum Volume

0.5 mL (Note: This volume does not allow for repeat testing.)


Lavender-top (EDTA) tube


Collect EDTA whole blood sample into a chilled lavender-top tube. Immediately add Futhan preservative as directed in the Futhan collection kit (Labcorp No. 78946). Recap lavender tube and invert several times to mix well. Centrifuge the whole blood specimen to separate the plasma. Transfer the plasma into the plastic screw-cap tube that is included in the collection kit. The specimen must be submitted in this transfer tube, which is labeled with the words "Futhan Added." Freeze immediately and maintain frozen until tested. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.

Storage Instructions


Stability Requirements



Room temperature

24 hours


6 hours


14 days

Freeze/thaw cycles

Stable x1

Patient Preparation

No radioactive isotopes administered within 48 hours prior to venipuncture.

Causes for Rejection

Any tube other than a tube labeled with the "Futhan Added" sticker will be rejected; nonfrozen specimen received; non-EDTA plasma sample received

Test Details


This test is used for the measurement of complement C3a and C3a-desArg levels in serum.


This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.

Results should not be used as a diagnostic procedure without confirmation of the diagnosis by another medically established diagnostic product or procedure.

Elevation of C3a levels is not predictive of any specific disease.

Normal human pregnancy is associated with evidence of complement activation, with an increase in concentrations of C3a.1

Complement activation split products are present only in trace amounts in normal plasma in vivo.2 It is crucial that samples be collected and stored properly in order to avoid in vitro activation.2 Blood must be drawn directly into tubes containing EDTA at a final concentration of at least 10 mM with the addition of nafamostat mesilate (Futhan, FUT-1750) to further reduce in vitro complement activation.3


Radioimmunoassay (RIA); this assay measures both C3a and C3a-desArg in an equimolar manner

Reference Interval

69.2–273.6 ng/mL

Additional Information

The complement system is an ancient and highly conserved effector mechanism of the innate immune system with important functions in immune defense.4-9 The main outcomes of complement system action are lytic killing of microbes, the rapid clearance of pathogens and dead or dying cells and immune complexes, and the release of pro-inflammatory anaphylatoxins. Activation and amplification of complement leads to destruction of pathogens or abnormal host cells through opsonization – a process by which complement ligands coat surfaces, targeting them for phagocytosis – or by lysis induced upon formation of the membrane attack complex (MAC), also referred to as the terminal complement complex (TCC). The ability to differentiate between self and non-self (or damaged/altered self) is a hallmark feature of the complement system. As a general paradigm, this is accomplished through complement recognition of components unique to microbial entities, often consisting of specific carbohydrate structures that are not found on host surfaces that are referred to as pathogen-associated molecular patterns (PAMPs).10,11 Similarly, activated complement proteins are also able to recognize abnormal glycosylation patterns on the surface of dead or dying host cells (termed damage-associated molecular patterns, or DAMPs) and immune complexes, activating complement mechanisms that lead to their clearance. Complement activation also works to link innate and adaptive immune reactions by mediating T cell and B cell responses. The complement pathway is tightly regulated to avoid uncontrolled activation.12,13

C3, the central component of the complement system, is present in the blood in concentrations of more than 1 mg/mL, which makes it one of the most represented proteins in circulation.14,15 Native C3 is biologically inactive, but its activation fragments have a multitude of biological functions. Complement activation can occur through three separate mechanisms: the classical pathway, the lectin pathway and the alternate pathway, each of which is activated by different molecules.16 In the first pathway to be discovered, the classical pathway, C3 is activated by antigen-antibody complexes that bind complement C1q.7-9 The lectin pathway is initiated by pathogen-associated molecular patterns (PAMPs), small molecular motifs, that are characteristic of microbial pathogens and are not present on mammalian tissues. These include mannose-binding lectin (MBL) and numerous other carbohydrate structures. The alternate pathway is continuously activated at a low level as a result of spontaneous C3 hydrolysis allowing for activation on surfaces that lack proper complement regulation, typically non-host surfaces.12,14,17

All complement activation pathways converge at the point of C3 cleavage, which results in generation of bioactive fragments including C3b and C3a.18 C3b is an efficient opsonin that marks foreign structures for phagocytosis; C3b also forms a membrane complex with other complement proteins to activate complement C5, yielding C5a and C5b. Like the C3a generated in the proximal portion of the cascade, C5a serves as an anaphylatoxin, a substance released into surrounding fluids and tissues to recruit/activate inflammatory cells. C5b triggers assembly of the membrane attack complex (MAC), also referred to as the terminal complement complex (TCC), a pore-forming structure made up of C5, C6, C7, C8 and multiple C9 molecules. The MAC forms a channel once inserted into the lipid bilayer, leading to lysis of cells or infecting organisms.

C3a is the only bioactive fluid phase fragment generated by C3 cleavage.14 C3a is referred to as anaphylatoxins because it causes smooth muscle contraction, vasodilation, histamine release from mast cells and enhanced vascular permeability.5-7,19,20 C3a is a potent chemoattractant that recruits several types of phagocytes to the site of inflammation and triggers the production of reactive oxygen species in macrophages, eosinophils and neutrophils. C3a exerts bactericidal activity by binding to their membranes and inducing cell lysis.21 C3a can act on neutrophils to prevent their mobilization from the bone marrow to the circulation after ischemia-reperfusion injury.22 C3a supports tissue regeneration after liver injury by stimulating cell proliferation, and it contributes to hematopoietic stem cell retention in the bone marrow, homing and engraftment.23-25 In the brain, the C3a has an important role in the recovery after the acute phase of ischemic injury, modulating neurogenesis and axonal and synaptic plasticity.26

Measurement of plasma C3a levels has been used in the assessment of the extent of complement activation in a variety of clinical conditions.27-29 Excessive complement activation can contribute to the pathogenesis of many acute and chronic inflammatory diseases. C3 has been implicated in several autoimmune19,30 and inflammatory diseases, including acute kidney inflammation,31 neurotrauma, anti-phospholipid thrombosis,32 asthma and allogeneic transplantation.19,33

In susceptible individuals, allergen exposure triggers the activation of complement, leading to the aberrant generation of the C3a anaphylatoxin.20,34-36 C3a has been shown to be important for the development of Th2 responses by driving ILC2-mediated inflammation in response to allergen.37 C3a binds to receptors on mast cells to trigger the release of histamine and chemokines.9,38 Nakano and coworkers found that plasma C3a concentrations were significantly higher in patients seeking emergency treatment for severe asthma exacerbations than in control subjects with stable asthma.39 They found that C3a concentrations were highest among patients who failed to improve with treatment with inhaled bronchodilators and intravenous corticosteroids.39 They also observed that levels of plasma C3a in admitted asthmatic patients decreased significantly within a week after admission.39

Clinical consequences of an overactivated and dysregulated complement system include not only immune complex and autoimmune disorders, such as systemic lupus erythematosus,12,27,40 various forms of nephropathy, like atypical hemolytic uremic syndrome,27,41 and C3 glomerulopathy,27,42,43 ophthalmic disorders, like age-related macular degeneration,44 but also organ failure subsequent to ischemia reperfusion injury.45 Paroxysmal nocturnal hemoglobinuria is an acquired clonal hematopoietic stem cell disorder in which uncontrolled complement activity leads to systemic complications, principally through intravascular hemolysis and thrombosis.27,46 C3a have been reported to be significantly higher in rheumatoid arthritis subjects compared to control subjects.47 Plasma levels of complement C3a measured daily during the first week after onset of symptoms of acute pancreatitis represent highly specific and sensitive parameters for the prediction of severe acute pancreatitis.48,49

Preclinical studies into the mechanism of hepatic regeneration have demonstrated an essential role for C3a in priming the hepatocyte proliferative response after injury or resection.50 C3a has also been implicated in the regeneration of bone, cardiac muscle and skeletal muscle, as well as stem cell engraftment.51-53

C3a has been used as a marker of neurodegenerative disease.54 C3a elevated in plasma one to 14 days after stroke and correlated with prognosis.55-57 C3a elevated in serum immediately after traumatic brain injury and remains chronically elevated.58 C3a levels have been shown to correlate with disease severity in patients with COVID-1959 and in patients with septic shock.60

In cancer, C3a can have pro-tumor effects impacting immune system activation at the tumor site and favoring tumor progression. C3a binding to its receptor maintains an immunosuppressive environment in sarcoma and promotes tumor progression by skewing the phenotype of tumor-associated macrophages61 while in lung cancer, C3a signaling acts on CD4+ T cells and induces an inhibitory phenotype.62 In pancreatic ductal adenocarcinoma, C3a activates the extracellular-regulated kinase pathway, inducing an epithelial-to-mesenchymal transition.63,64

In plasma, C3a is quickly converted by carboxypeptidase N into C3a-desArg by cleavage of the C-terminal arginine.65-67 C3a-desArg does not bind to the human C3a receptor.68 A number of studies have shown that there is a positive relationship between C3a-desArg levels, adipose tissue and risk factors for cardiovascular disease, metabolic syndrome and diabetes.69,70 C3a-desArg, also known as acylation stimulation factor, has been purported to play a role in transporting fatty acids to adipocytes and triacylglycerol synthesis.71 It has been suggested that production of C3a (and C5a) in adipose tissue triggers a cytokine and chemokine response in proportion to the amount of adipose tissue present and induces inflammation and mediate metabolic effects such as insulin resistance. These observations support the concept that complement activation may be an important participant in lipid metabolism and in obesity, contributing to the metabolic syndrome and to the low-grade inflammation associated with obesity.


1. Richani K, Soto E, Romero R, et al. Normal pregnancy is characterized by systemic activation of the complement system. J Matern Fetal Neonatal Med. 2005 Apr;17(4):239-245.16147832
2. Mollnes TE, Garred P, Bergseth G. Effect of time, temperature and anticoagulants on in vitro complement activation: Consequences for collection and preservation of samples to be examined for complement activation. Clin ExpImmunol. 1988 Sep;73(3):484-488.2463123
3. Pfeifer PH, Kawahara MS, Hugli TE. Possible mechanism for in vitro complement activation in blood and plasma samples: Futhan/EDTA controls in vitro complement activation. Clin Chem. 1999 Aug;45(8 Pt 1):1190-1199.10430784
4. Haas PJ, van Strijp J. Anaphylatoxins: Their role in bacterial infection and inflammation. Immunol Res. 2007;37(3):161-175.17873401
5. Klos A, Tenner AJ, Johswich KO, Ager RR, Reis ES, Köhl J. The role of the anaphylatoxins in health and disease. Mol Immunol. 2009 Sep;46(14):2753-2766.19477527
6. Hawlisch H, Wills-Karp M, Karp CL, Köhl J. The anaphylatoxins bridge innate and adaptive immune responses in allergic asthma. Mol Immunol. 2004 Jun;41(2-3):123-131.15159057
7. Gasque P. Complement: A unique innate immune sensor for danger signals. Mol Immunol. 2004 Nov;41(11):1089-1098.15476920
8. Peng Q, Li K, Sacks SH, Zhou W. The role of anaphylatoxins C3a and C5a in regulating innate and adaptive immune responses. Inflamm Allergy Drug Targets. 2009 Jul;8(3):236-246.19601884
9. Wills-Karp M. Complement activation pathways: A bridge between innate and adaptive immune responses in asthma. Proc Am Thorac Soc. 2007 Jul;4(3):247-251.17607007
10. Merle NS, Church SE, Fremeaux-Bacchi V, Roumenina LT. Complement System Part I - Molecular Mechanisms of Activation and Regulation. Front Immunol. 2015 Jun 2;6:262.26082779
11. Merle NS, Noe R, Halbwachs-Mecarelli L, Fremeaux-Bacchi V, Roumenina L. Complement System Part II: Role in Immunity. Front Immunol. 2015 May 26;6:257.26074922
12. Ricklin D, Barratt-Due A, Mollnes TE. Complement in clinical medicine: Clinical trials, case reports and therapy monitoring. Mol Immunol. 2017 Sep;89:10-21.28576323
13. Ekdahl KN, Persson B, Mohlin C, Sandholm K, Skattum L, Nilsson B. Interpretation of Serological Complement Biomarkers in Disease. Front Immunol. 2018 Oct 24;9:2237.30405598
14. Ricklin D, Reis ES, Mastellos DC, Gros P, Lambris JD. Complement component C3 - The "Swiss Army Knife" of innate immunity and host defense. Immunol Rev. 2016 Nov;274(1):33-58.27782325
15. Zarantonello A, Revel M, Grunenwald A, Roumenina LT. C3-dependent effector functions of complement. Immunol Rev. 2023 Jan;313(1):120-138.36271889
16. Varela JC, Tomlinson S. Complement: an overview for the clinician. Hematol Oncol Clin North Am. 2015 Jun;29(3):409-427.26043382
17. Hajishengallis G, Reis ES, Mastellos DC, Ricklin D, Lambris JD. Novel mechanisms and functions of complement. Nat Immunol. 2017 Nov 16;18(12):1288-1298.29144501
18. Xie CB, Jane-Wit D, Pober JS. Complement Membrane Attack Complex: New Roles, Mechanisms of Action, and Therapeutic Targets. Am J Pathol. 2020 Jun;190(6):1138-1150.32194049
19. Verschoor A, Karsten CM, Broadley SP, Laumonnier Y, Köhl J . Old dogs-new tricks: immunoregulatory properties of C3 and C5 cleavage fragments. Immunol Rev. 2016 Nov;274(1):112-126.27782330
20. Schanzenbacher J, Köhl J, Karsten CM. Anaphylatoxins spark the flame in early autoimmunity. Front Immunol. 2022 Jul 25;13:958392.35958588
21. Nordahl EA, Rydengård V, Nyberg P, et al. Activation of the complement system generates antibacterial peptides. Proc Natl Acad Sci USA. 2004 Nov 30;101(48):16879-16884.15550543
22. Wu MCL, Brennan FH, Lynch JPL, et al. The receptor for complement component C3a mediates protection from intestinal ischemia-reperfusion injuries by inhibiting neutrophil mobilization. Proc Natl Acad Sci USA. 2013 Jun 4;110(23):9439-9444.23696668
23. Ratajczak J, Reca R, Kucia M, et al. Mobilization studies in mice deficient in either C3 or C3a receptor (C3aR) reveal a novel role for complement in retention of hematopoietic stem/progenitor cells in bone marrow. Blood. 2004 Mar 15;103(6):2071-2078.14604969
24. Reca R, Mastellos D, Majka M, et al. Functional receptor for C3a anaphylatoxin is expressed by normal hematopoietic stem/progenitor cells, and C3a enhances their homing-related responses to SDF-1. Blood. 2003 May 15;101(10):3784-3793.12511407
25. Lee H, Ratajczak MZ. Innate immunity: a key player in the mobilization of hematopoietic stem/progenitor cells. Arch Immunol Ther Exp (Warsz). 2009 Jul-Aug;57(4):269-278.19578812
26. Stokowska A, Pekna M. Complement C3a: shaping the plasticity of the Post-stroke brain. In: Lapchak PA, Zhang JH, eds. Cellular and Molecular Approaches to Regeneration and Repair. Springer series in translational stroke research. Springer International Publishing; 2018:521-541.
27. Prohászka Z, Nilsson B, Frazer-Abel A, Kirschfink M. Complement analysis 2016: Clinical indications, laboratory diagnostics and quality control. Immunobiology. 2016 Nov;221(11):1247-1258.27475991
28. Baines AC, Brodsky RA. Complementopathies. Blood Rev. 2017 Jul;31(4):213-223.28215731
29. Frazer-Abel A, Kirschfink M, Prohászka Z. Expanding Horizons in Complement Analysis and Quality Control. Front Immunol. 2021 Aug 9;12:697313.34434189
30. Jia C, Tan Y, Zhao M. The complement system and autoimmune diseases. Chronic Dis Transl Med. 2022 Apr 6;8(3):184-190.36161202
31. Mizuno M, Blanchin S, Gasque P, Nishikawa K, Matsuo S. High levels of complement C3a receptor in the glomeruli in lupus nephritis. Am J Kidney Dis. 2007 May;49(5):598-606.17472841
32. Oku K, Atsumi T, Bohgaki M, et al. Complement activation in patients with primary antiphospholipid syndrome. Ann Rheum Dis. 2009 Jun;68(6):1030-1035.18625630
33. Coulthard LG, Woodruff TM. Is the complement activation product C3a a proinflammatory molecule? Re-evaluating the evidence and the myth. J Immunol. 2015 Apr 15;194(8):3542-3548.25848071
34. Zhang X, Köhl J. A complex role for complement in allergic asthma. Expert Rev Clin Immunol. 2010 Mar;6(2):269-277.20402389
35. Gour N, Smole U, Yong HM, et al. C3a is required for ILC2 function in allergic airway inflammation. Mucosal Immunol. 2018 Nov;11(6):1653-1662.30104625
36. Schmudde I, Laumonnier Y, Köhl J. Anaphylatoxins coordinate innate and adaptive immune responses in allergic asthma. Semin Immunol. 2013 Feb;25(1):2-11.23694705
37. Laumonnier Y, Wiese AV, Figge J, Karsten C. Regulation and function of anaphylatoxins and their receptors in allergic asthma. Mol Immunol. 2017 Apr;84:51-56.27916272
38. Hugli TE. Structure and function of C3a anaphylatoxin. In: Lambris JD, ed. The Third Component of Complement. Current Topics in Microbiology and Immunology. Springer International Publishing; 1990:181-208.
39. Nakano Y, Morita S, Kawamoto A, Suda T, Chida K, Nakamura H. Elevated complement C3a in plasma from patients with severe acute asthma. J Allergy Clin Immunol. 2003 Sep;112(3):525-530.13679811
40. Weinstein A, Alexander RV, Zack DJ. A Review of Complement Activation in SLE. Curr Rheumatol Rep. 2021 Feb 10;23(3):16.33569681
41. Morigi M, Galbusera M, Gastoldi S, et al. Alternative pathway activation of complement by Shiga toxin promotes exuberant C3a formation that triggers microvascular thrombosis. J Immunol. 2011 Jul 1;187(1):172-180.21642543
42. Kaartinen K, Safa A, Kotha S, Ratti G, Meri S. Complement dysregulation in glomerulonephritis. Semin Immunol. 2019 Oct;45:101331.31711769
43. Wong EKS, Kavanagh D. Diseases of complement dysregulation-an overview. Semin Immunopathol. 2018 Jan;40(1):49-64.29327071
44. Armento A, Ueffing M, Clark SJ. The complement system in age-related macular degeneration. Cell Mol Life Sci. 2021 May;78(10):4487-4505.33751148
45. Farrar CA, Asgari E, Schwaeble WJ, Sacks SH. Which pathways trigger the role of complement in ischaemia/reperfusion injury? Front Immunol. 2012 Nov 19;3:341.23181062
46. Brodsky RA. Paroxysmal nocturnal hemoglobinuria. Blood. 2014 Oct 30;124(18):2804-2811.25237200
47. Bemis EA, Norris JM, Seifert J, et al. Complement and its environmental determinants in the progression of human rheumatoid arthritis. Mol Immunol. 2019 Aug;112:256-265.31207549
48. Bettac L, Denk S, Seufferlein T, Huber-Lang M. Complement in Pancreatic Disease-Perpetrator or Savior? Front Immunol. 2017 Jan 17;8:15.28144242
49. Gloor B, Stahel PF, Müller CA, Schmidt OI, Büchler MW, Uhl W. Predictive value of complement activation fragments C3a and sC5b-9 for development of severe disease in patients with acute pancreatitis. Scand J Gastroenterol. 2003 Oct;38(10):1078-1082.14621284
50. Strey CW, Markiewski M, Mastellos D, et al. The proinflammatory mediators C3a and C5a are essential for liver regeneration. J Exp Med. 2003 Sep 15;198(6):913-923.12975457
51. Phieler J, Garcia-Martin R, Lambris JD, Chavakis T. The role of the complement system in metabolic organs and metabolic diseases. Semin Immunol. 2013 Feb;25(1):47-53.23684628
52. Rutkowski MJ, Sughrue ME, Kane AJ, Mills SA, Fang S, Parsa AT. Complement and the central nervous system: emerging roles in development, protection and regeneration. Immunol Cell Biol. 2010 Nov-Dec;88(8):781-786.20404838
53. Mastellos DC, Deangelis RA, Lambris JD. Complement-triggered pathways orchestrate regenerative responses throughout phylogenesis. Semin Immunol. 2013 Feb;25(1):29-38.23684626
54. Schartz ND, Tenner AJ. The good, the bad, and the opportunities of the complement system in neurodegenerative disease. J Neuroinflammation. 2020 Nov 25;17(1):354.33239010
55. Lee JD, Coulthard LG, Woodruff TM. Complement dysregulation in the central nervous system during development and disease. Semin Immunol. 2019 Oct;45:101340.31708347
56. Széplaki G, Szegedi R, Hirschberg K, et al. Strong complement activation after acute ischemic stroke is associated with unfavorable outcomes. Atherosclerosis. 2009 May;204(1):315-320.18804761
57. Mocco J, Wilson DA, Komotar RJ, et al. Alterations in plasma complement levels after human ischemic stroke. Neurosurgery. 2006;59(1):28-33.16823297
58. Burk AM, Martin M, Flierl MA, et al. Early complementopathy after multiple injuries in humans. Shock. 2012 Apr;37(4):348-354.22258234
59. de Nooijer AH, Grondman I, Janssen NAF, et al. Complement Activation in the Disease Course of Coronavirus Disease 2019 and Its Effects on Clinical Outcomes. J Infect Dis. 2021 Feb 3;223(2):214-224.33038254
60. Charchaflieh J, Wei J, Labaze G, et al. The role of complement system in septic shock. Clin Dev Immunol. 2012;2012:407324.23049598
61. Magrini E, Di Marco S, Mapelli SN, et al. Complement activation promoted by the lectin pathway mediates C3aR-dependent sarcoma progression and immunosuppression. Nat Cancer. 2021 Feb;2(2):218-232.34505065
62. Kwak JW, Laskowski J, Li HY, et al. Complement activation via a C3a receptor pathway alters CD4+ T lymphocytes and mediates lung cancer progression. Cancer Res. 2018 Jan 1;78(1):143-156.29118090
63. Suzuki R, Okubo Y, Takagi T, et al. The complement C3a-C3a receptor Axis regulates epithelial-to-mesenchymal transition by activating the ERK pathway in pancreatic ductal adenocarcinoma. Anticancer Res. 2022 Mar;42(3):1207-1215.35220210
64. Speth C, Bellotti R, Schäfer G, et al. Complement and Fungal Dysbiosis as Prognostic Markers and Potential Targets in PDAC Treatment. Curr Oncol. 2022 Dec 14;29(12):9833-9854.36547187
65. Campbell WD, Lazoura E, Okada N, Okada H. Inactivation of C3a and C5a octapeptides by carboxypeptidase R and carboxypeptidase N. Microbiol Immunol. 2002;46(2):131-134.11939578
66. Matthews KW, Mueller-Ortiz SL, Wetsel RA. Carboxypeptidase N: a pleiotropic regulator of inflammation. Mol Immunol. 2004 Jan;40(11):785-793.14687935
67. Bajic G, Yatime L, Klos A, Andersen GR. Human C3a and C3a desArg anaphylatoxins have conserved structures, in contrast to C5a and C5a desArg. Protein Sci. 2013 Feb;22(2):204-212.23184394
68. Wilken HC, Götze O, Werfel T, Zwirner J. C3a(desArg) does not bind to and signal through the human C3a receptor. Immunol Lett. 1999 Apr 1;67(2):141-145.10232396
69. Nilsson B, Hamad OA, Ahlström H, et al. C3 and C4 are strongly related to adipose tissue variables and cardiovascular risk factors. Eur J Clin Invest. 2014 Jun;44(6):587-596.24754458
70. Barbu A, Hamad OA, Lind L, Ekdahl KN, Nilsson B. The role of complement factor C3 in lipid metabolism. Mol Immunol. 2015 Sep;67(1):101-107.25746915
71. Copenhaver M, Yu CY, Hoffman RP. Complement Components, C3 and C4, and the Metabolic Syndrome. Curr Diabetes Rev. 2019;15(1):44-48.29663892


Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
004220 Complement C3a 4488-3 004221 Complement C3a ng/mL 4488-3

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