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Research Article Free access | 10.1172/JCI105555

Evidence for In Vivo Breakdown of β1C-Globulin in Hypocomplementemic Glomerulonephritis

Clark D. West, Sara Winter, Judith Forristal, Janice M. McConville, and Neil C. Davis

Children's Hospital Research Foundation, Cincinnati, Ohio

Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio

†

Address requests for reprints to Dr. Clark D. West, The Children's Hospital Research Foundation, Elland Ave. and Bethesda, Cincinnati, Ohio 45229.

*

Submitted for publication July 15, 1966; accepted December 20, 1966.

Supported in part by a grant from United Health Foundations, Inc., and by grants AI-03429 and AI-04472 from the National Institute of Allergy and Infectious Diseases, U. S. Public Health Service.

Presented in part at the annual meeting of the Society for Pediatric Research, Atlantic City, N. J., April 1966.

Find articles by West, C. in: PubMed | Google Scholar

Children's Hospital Research Foundation, Cincinnati, Ohio

Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio

†

Address requests for reprints to Dr. Clark D. West, The Children's Hospital Research Foundation, Elland Ave. and Bethesda, Cincinnati, Ohio 45229.

*

Submitted for publication July 15, 1966; accepted December 20, 1966.

Supported in part by a grant from United Health Foundations, Inc., and by grants AI-03429 and AI-04472 from the National Institute of Allergy and Infectious Diseases, U. S. Public Health Service.

Presented in part at the annual meeting of the Society for Pediatric Research, Atlantic City, N. J., April 1966.

Find articles by Winter, S. in: PubMed | Google Scholar

Children's Hospital Research Foundation, Cincinnati, Ohio

Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio

†

Address requests for reprints to Dr. Clark D. West, The Children's Hospital Research Foundation, Elland Ave. and Bethesda, Cincinnati, Ohio 45229.

*

Submitted for publication July 15, 1966; accepted December 20, 1966.

Supported in part by a grant from United Health Foundations, Inc., and by grants AI-03429 and AI-04472 from the National Institute of Allergy and Infectious Diseases, U. S. Public Health Service.

Presented in part at the annual meeting of the Society for Pediatric Research, Atlantic City, N. J., April 1966.

Find articles by Forristal, J. in: PubMed | Google Scholar

Children's Hospital Research Foundation, Cincinnati, Ohio

Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio

†

Address requests for reprints to Dr. Clark D. West, The Children's Hospital Research Foundation, Elland Ave. and Bethesda, Cincinnati, Ohio 45229.

*

Submitted for publication July 15, 1966; accepted December 20, 1966.

Supported in part by a grant from United Health Foundations, Inc., and by grants AI-03429 and AI-04472 from the National Institute of Allergy and Infectious Diseases, U. S. Public Health Service.

Presented in part at the annual meeting of the Society for Pediatric Research, Atlantic City, N. J., April 1966.

Find articles by McConville, J. in: PubMed | Google Scholar

Children's Hospital Research Foundation, Cincinnati, Ohio

Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio

†

Address requests for reprints to Dr. Clark D. West, The Children's Hospital Research Foundation, Elland Ave. and Bethesda, Cincinnati, Ohio 45229.

*

Submitted for publication July 15, 1966; accepted December 20, 1966.

Supported in part by a grant from United Health Foundations, Inc., and by grants AI-03429 and AI-04472 from the National Institute of Allergy and Infectious Diseases, U. S. Public Health Service.

Presented in part at the annual meeting of the Society for Pediatric Research, Atlantic City, N. J., April 1966.

Find articles by Davis, N. in: PubMed | Google Scholar

Published April 1, 1967 - More info

Published in Volume 46, Issue 4 on April 1, 1967
J Clin Invest. 1967;46(4):539–548. https://doi.org/10.1172/JCI105555.
© 1967 The American Society for Clinical Investigation
Published April 1, 1967 - Version history
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Abstract

Evidence has been obtained for the presence in vivo of alpha2D-globulin, a breakdown product of serum β1C-globulin, in patients with acute and persistent hypocomplementemic glomerulonephritis. The protein has been identified by immunoelectrophoretic analysis, and the amounts present have been determined by direct measurement of specific antigenic determinants present on alpha2D. β1A-Globulin, another breakdown product of β1C-globulin, may also be present in vivo in severely hypocomplementemic patients, but its levels are much lower than those of alpha2D-globulin.

Alpha2D-globulin has been identified by immunoelectrophoretic analysis of fresh EDTA plasma from patients with hypocomplementemic nephritis as an arc in the alpha2 region that shows a reaction of identity with the arc representing alpha2D-globulin produced by aged normal serum. β1A-Globulin was not seen in these patterns.

Measurement of specific antigenic determinants has been carried out in both fresh EDTA plasma and aged serum. In the fresh plasma, the concentration of D antigen, found on both β1C- and alpha2D-globulins, has been related to that of B antigen, found only on β1C and taken as a measure of the concentration of this protein. In the hypocomplementemic patients, the concentration of D antigen, in comparison to that of B, was greater than in the normal subjects. Similarly, in aged serum, the level of alpha2D was greater than would be expected from the amount of β1C that had been broken down in vitro, measured by the concentration of β1A.

Calculations indicated that the in vivo alpha2D level in severely hypocomplementemic patients ranged from 7.5 to 18% of that which would be found in a pool of aged normal serum in which β1C is completely broken down. The levels tended to be lower in less severely hypocomplementemic patients, and none could be detected in normal plasma.

Only small quantities of A and D antigens are detectable in the urine of patients with hypocomplementemic nephritis. The rate of excretion is about equal to that of the normal subject.

The study indicates that the low serum levels of β1C-globulin that may be present over long periods in patients with persistent hypocomplementemic glomerulonephritis can be ascribed, in part, to in vivo breakdown of this protein as a result of reaction with immune complexes. The contribution of β1C deposition on immune complexes and of diminished synthesis to the depressed serum levels cannot be assessed by the present study.

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