Hypocomplementemia of Membranoproliferative Nephritis DEPENDENCE OF THE NEPHRITIC FACTOR REACTION ON PROPERDIN FACTOR B

Ruley, Edward J.; Forristal, Judith; Davis, Neil C.; Andres, Cynthia; West, Clark D.

doi:10.1172/jci107254

Cited by 56 publications

(15 citation statements)

References 27 publications

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“…The loss of the native (B) antigen of C3 was used in the past to detect C3 activation in serum [15]. This procedure has not found widespread popularity.…”

Section: Measurement Of C3 Activation By the Detection Of C3 Neoantigensmentioning

confidence: 99%

Measurement of Complement Activation in Clinical Practice

Whaley

1989

Complement Inflamm

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Many new tests which measure complement activation are now available, although it is unclear which tests or group of tests are appropriate for monitoring complement activation in clinical samples. Carefully planned prospective studies are required to resolve this issue, and to identify which groups of patients in which the monitoring of complement activation improves the quality of their medical management.

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“…The loss of the native (B) antigen of C3 was used in the past to detect C3 activation in serum [15]. This procedure has not found widespread popularity.…”

Section: Measurement Of C3 Activation By the Detection Of C3 Neoantigensmentioning

confidence: 99%

Measurement of Complement Activation in Clinical Practice

Whaley

1989

Complement Inflamm

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“…It is known that, in vitro, the interaction be tween C3 Nef and normal human serum results in C3 cleavage requiring factors B and D, but neither early complement components of the classical pathway [35,36], nor properdin [37], In fact, properdin levels in these patients are always normal [15].…”

Section: Complement Abnormalitiesmentioning

confidence: 99%

Dense Deposits Disease

Droz¹,

Zanetti²,

Nôël³

et al. 1977

Nephron

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“…A recent study [19] of the C3NeF reaction, stimulated by the obser vations of the alternate pathways, has shown that the C3 proactivator is the effector of C3 breakdown in that system also. Adequate levels of C3 proactivator were found to be necessary if C3 breakdown was to occur in vitro in reaction mixtures containing C3NeF.…”

Section: The Hypocomplementemiamentioning

confidence: 99%

“…With diminished synthesis as the sole cause of the low C3 levels, it is difficult to explain the presence of circulating a-2D and the low levels of C5 and other terminal components in the hypocomplementemic patients. Studies of the kinetics of the nephritic factor reaction have, however, thrown some light on these seeming paradoxical observations [19,23]. The rate of C3 breakdown in this system appears markedly substrate dependent.…”

Section: The Hypocomplementemiamentioning

confidence: 99%

Membranoproliferative Hypocomplementemic Glomerulonephritis

West¹

1973

Nephron

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The diagnosis of membranoproliferative glomerulonephritis is made by its distinctive glomerular morphology. Early there may be an acute glomerulonephritis and late, a lobular glomerulonephritis. Hypocomplementemia often accompanies the disease in children. Onset is usually in childhood as a nephrotic or acute nephritic syndrome or a chance proteinuria. Origin is unknown and onset may be insidious. The disease is typically long standing with, terminally, rapid deterioration. Children may have a long interval of ‘silent’ nephritis. Activation of C3 by an alternate pathway involving a nephritic factor and the C3 proactivator produces the hypocomplementemia but has not been demonstrated to produce the nephritis. No treatment is consistently successful. The disease can recur in a renal transplant.

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Hypocomplementemia of Membranoproliferative Nephritis DEPENDENCE OF THE NEPHRITIC FACTOR REACTION ON PROPERDIN FACTOR B

Cited by 56 publications

References 27 publications

Measurement of Complement Activation in Clinical Practice

Measurement of Complement Activation in Clinical Practice

Dense Deposits Disease

Membranoproliferative Hypocomplementemic Glomerulonephritis

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