PubMed · 3550983
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M H Jouvin, M Kazatchkine. [Complement system].. https://doi.org/10.1016/s0248-8663(87)80106-6
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If a single component is lowered, it is reasonable to question whether the patient has a genetically-controlled defect. Studies of family members may be required. If split products, complexes, or neoantigens are present, it is likely that there is ongoing complement activation. If most of the components of a pathway are lowered, a reasonable supposition is that complement is being activated. We then turn to a consideration of the factors that may activate complement. When hypocomplementemia is associated with a decrease in titer of several components, it is often possible to determine whether the classic or alternative pathway is the major pathway being activated; this, in turn, may suggest certain diagnoses and rule out other diagnoses. The nature of the circulating complexes or split products may provide the same information. Thus, a consideration of the pathophysiology of the complement system and of the factors that activate complement provides an approach to an understanding of the function of complement and the role of complement causing a damage in a clinical setting.
The activation of human polymorphonuclear leukocytes (PMN) by particulate Tamm-Horsfall glycoprotein (THG) represents an interaction hitherto unrecognized. The potential pathophysiological effect of this phenomenon within the interstitium of the kidney is highlighted by the activation of the respiratory burst, as well as by comprehensive PMN degranulation. Products of the interaction are expressed in terms of phagocytosis, luminol-dependent chemiluminescence, granule marker enzyme release and arachidonic acid metabolism. Significant quantities of the primary, secondary and tertiary granule markers, myeloperoxidase, vitamin B12 binding protein and N-acetyl-beta-D-glucosaminidase, respectively, were secreted in a dose and time-dependent manner. Phagocytosis of the glycoprotein was accompanied by the generation of significant quantities of leukotriene B4. Furthermore, the ability of such a particulate ligand to activate the alternative pathway of complement clearly represents a capacity to augment the inflammatory response. Should the interaction of THG with PMN take place within the interstitium of the kidney, augmented by the deposition of complement proteins on the surface of insoluble aggregates, the resulting inflammatory response may lead to marked tissue damage and eventually result in interstitial fibrosis.
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