The Complement Profile in Acute Glomerulonephritis Systemic Lupus erythematosus and Hypocomplementemic Chronic Glomerulonephritis

Gewürz, Henry; Pickering, R. J.; Mergenhagen, S. E.; Good, Robert A.

doi:10.1159/000230149

Cited by 129 publications

(46 citation statements)

References 17 publications

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“…liferative nephritis with low C3 levels, the levels of C1, C4, and C2 are, for the most part, normal, whereas in other hypocomplementemic nephritides the levels of these components are usually low. The normal C4 levels observed in the present study as well as measurements of the first three reacting components by other workers, summarized elsewhere (32), agree with the observations of Gewurz et al (31). Thus, in membrano-proliferative nephritis, it would appear that the immune complex and the first three reacting components of complement are bypassed and that some factor, most logically C3NeF, is acting directly on C3 to produce the hypocomplementemia.…”

Section: Discussionsupporting

confidence: 93%

“…Although the lack of exact inverse relationship between C3 and C3NeF levels in the present data precludes final conclusions, data from other sources (31,32) indicates that C3NeF or a similar factor reacting directly with C3 must be responsible for the hypocomplementemia and the low C3 levels in patients with membrano-proliferative nephritis. Gewurz, Pickering, Mergenhagen, and Good (31) have shown that in patients with membrano-pro.…”

Section: Discussioncontrasting

confidence: 73%

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Continuing C3 breakdown after bilateral nephrectomy in patients with membrano-proliferative glomerulonephritis

Vallota¹,

Forristal²,

Spitzer³

et al. 1971

J. Clin. Invest.

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A B S T R A C T Serum levels of complement components and of C3 nephritic factor (C3NeF) were measured serially in two patients with membrano-proliferative glomerulonephritis who were subjected to bilateral nephrectomy and maintained by peritoneal dialysis for 2 wk before renal transplantation. In both patients, low levels of C3 and high levels of preformed alpha 2D, a C3 breakdown product, were present before nephrectomy and remained essentially unchanged during the anephric period. With transplantation, C3 levels rose towards normal and alpha 2D disappeared from the serum. The serum of both patients contained detectable amounts of C3NeF, a factor which has been shown to react with a cofactor found in normal serum to form an enzyme, designated C3 lytic nephritic factor (C3LyNeF), which will cleave C3 to form the breakdown products, plA and alpha 2D. The level of C3NeF was high in one patient before nephrectomy, increased somewhat during the anephric period, and fell after transplantation. In the other patient, the C3NeF level was initially lower, remained relatively constant during the anephric period, and was not significantly affected by transplantation. In both patients, levels of C4 and C5 were either normal or elevated over the period of the study and bore no relationship to the C3 level. The following conclusions can be drawn from the data. The high levels of alpha 2D during the anephric period and the disappearance of this protein as C3 levels approach normal at the time of transplantation indicate that the low C3 levels were largely the result of C3 breakdown rather than diminished synthesis. The presence of C3NeF in detectable amounts in both patients suggest that C3LyNeF, formed by the reaction of C3NeF and cofactor, was responsible for the low Dr. Vallota is a Fellow of the National Kidney Foundation.

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Section: Discussionsupporting

confidence: 93%

Section: Discussioncontrasting

confidence: 73%

Continuing C3 breakdown after bilateral nephrectomy in patients with membrano-proliferative glomerulonephritis

Vallota¹,

Forristal²,

Spitzer³

et al. 1971

J. Clin. Invest.

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“…Increased levels of complement components and hemolytic activity are frequently found in inflammatory disorders, and striking decreases have been reported in diseases such as systemic lupus erythmatosus (SLE)' acute glomerulonephritis, membranoproliferative glomerulonephritis (MPGN), liver disease, and congenital deficiency of complement components (1)(2)(3).…”

Section: Introductionmentioning

confidence: 99%

Complement breakdown products in plasma from patients with systemic lupus erythematosus and patients with membranoproliferative or other glomerulonephritis.

Perrin¹,

Lambert²,

Miescher³

1975

J. Clin. Invest.

255

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A B S T R A C T A dynamic estimation of the involvement of the complement system in various diseases was obtained by the direct quantitation of breakdown products of C3 and of properdin factor B. The methods used were based, first, on the separation of native and fragmented molecules according to their molecular size through a precipitation with polyethylene glycol and, secondly, on an immunochemical quantitation, using specific antisera for the major antigens of C3 and factor B. The sensitivity and the specificity of these methods were demonstrated by activation of complement in vitro with generation of C3 and factor B fragments.A clinical investigation was carried out in 41 patients with systemic lupus erythematosus (SLE), 31 with membranoproliferative glomerulonephritis (MPGN), 26 with other types of glomerulonephritis, and 6 with severe alcoholic cirrhosis of the liver. The following observations were made: (a) an elevated plasma level of C3d fragment of C3 was found in 68% of SLE patients, in 87% of MPGN patients, in 62% of patients with other hypocomplementemic nephritis, and in 15% of those with normocomplementemic nephritis, but in only 33% of patients with liver cirrhosis and very low levels of C3; (b) a significant difference was observed between the levels of C3 obtained with either anti-"native" C3 or anti-C3c sera for immunochemical quantitation, in patients with SLE or MPGN, indicating the presence of "altered" or fragmented C3 in plasma; (c) an elevated plasma level of Ba fragment of properdin factor B was found in 46% of SLE patients, in 67% of MPGN patients, in 50% of patients with otherThis work was presented in part at the European Complement Workshop, Heidelberg, May 1974.Dr. Lambert's address is: Centre de Transfusion, HopitalCantonal, 1211 Geneva 4, Switzerland. Received for publication 9 December 1974 and in revised form 18 March 1975. hypocomplementemic nephritis, and in 9% of patients with normocomplementemic nephritis, while the level of properdin factor B was only slightly decreased in these diseases; (d) in SLE and MPGN there was an inverse correlation between the levels of C3d and Ba and the level of C3 in plasma. The level of these fragments was directly correlated with the clinical manifestations of SLE; (e) some patients with a normal C3 level exhibited an elevated plasma concentration of C3 and factor B fragments, suggesting the coexistence of an increased synthesis with a hypercatabolism of complement components.

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“…The complement (C) component profile has been useful in studies of various diseases (1)(2)(3). Hemolytic assays based on the reaction of serum dilutions with erythrocyte, antibody and complement (C) component intermediates were utilized at first.…”

mentioning

confidence: 99%

Serum levels of C1q, C1r and C1s in normal and pathologic sera

Bracco

Manni

1974

Arthritis & Rheumatism

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C1q, C1r and C1s protein concentrations were simultaneously assayed in sera of patients with systemic lupus erythematosus (SLE), rheumatoid arthritis, autoimmune hemolytic anemia, and viral hemorrhagic fever as well as in healthy adult control subjects. Correlation coefficients between the three subunits of C1 were calculated and the sequential evolution of C1q, C1r, and C1s levels was studied in patients with SLE. In the majority of cases there was a good correlation between C1q, C1r, and C1s; subunit levels increased or decreased in a coordinated fashion. A marked discrepancy between C1q, C1r, and C1s serum concentration was observed in 3 instances. Low C1q coexisted with extremely high C1r and C1s values. It appears that C1r and C1s are closely linked while C1q may vary in a more independent way.

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The Complement Profile in Acute Glomerulonephritis Systemic Lupus erythematosus and Hypocomplementemic Chronic Glomerulonephritis

Cited by 129 publications

References 17 publications

Continuing C3 breakdown after bilateral nephrectomy in patients with membrano-proliferative glomerulonephritis

Continuing C3 breakdown after bilateral nephrectomy in patients with membrano-proliferative glomerulonephritis

Complement breakdown products in plasma from patients with systemic lupus erythematosus and patients with membranoproliferative or other glomerulonephritis.

Serum levels of C1q, C1r and C1s in normal and pathologic sera

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