[Measurements of serum C3d in primitive chronic glomerular nephropathies (author's transl)]. 1979

G Lagrue, and A Branellec, and L Intrator, and M Moisy, and A Sobel

Measurement of serum C3 does not provide precise informations concerning an eventual consumption of this complement component during an immunological process. An increased synthetic rate may compensate an accelerated catabolism. The study of breakdown products of C3, such as C3d is a more sensitive approach of the role of complement in some immunological disorders. Therefore C3d was measured in the serum of patients with chronic non systemic glomerular diseases. High values of serum C3d were found in all cases of hypocomplementemic glomerulonephritis. Circulating C3d was also increased to a lower extent, in patients with normocomplementemic nephritis such as minimal change disease, mesangial nephritis with IgA deposits and membraneoproliferative (type I) glomerulonephritis. The data suggested the involvement of complement in a number of glomerulonephritis. Participation of complement in immunological disorders particularly in chronic non systemic glomerulonephritis could require a reevaluation when functional tests are performed in addition to static measurements.

UI MeSH Term Description Entries
D009402 Nephrosis, Lipoid A kidney disease with no or minimal histological glomerular changes on light microscopy and with no immune deposits. It is characterized by lipid accumulation in the epithelial cells of KIDNEY TUBULES and in the URINE. Patients usually show NEPHROTIC SYNDROME indicating the presence of PROTEINURIA with accompanying EDEMA. Glomerulonephritis, Minimal Change,Glomerulopathy, Minimal Change,Nephropathy, Minimal Change,Nephrotic Syndrome, Minimal Change,Idiopathic Minimal Change Nephrotic Syndrome,Minimal Change Disease,Minimal Change Glomerulopathy,Minimal Change Nephrotic Syndrome,Change Diseases, Minimal,Disease, Minimal Change,Diseases, Minimal Change,Glomerulonephritides, Minimal Change,Glomerulopathies, Minimal Change,Lipoid Nephroses,Lipoid Nephrosis,Minimal Change Diseases,Minimal Change Glomerulonephritides,Minimal Change Glomerulonephritis,Minimal Change Nephropathies,Minimal Change Nephropathy,Nephropathies, Minimal Change,Nephroses, Lipoid
D009404 Nephrotic Syndrome A condition characterized by severe PROTEINURIA, greater than 3.5 g/day in an average adult. The substantial loss of protein in the urine results in complications such as HYPOPROTEINEMIA; generalized EDEMA; HYPERTENSION; and HYPERLIPIDEMIAS. Diseases associated with nephrotic syndrome generally cause chronic kidney dysfunction. Childhood Idiopathic Nephrotic Syndrome,Frequently Relapsing Nephrotic Syndrome,Multi-Drug Resistant Nephrotic Syndrome,Pediatric Idiopathic Nephrotic Syndrome,Steroid-Dependent Nephrotic Syndrome,Steroid-Resistant Nephrotic Syndrome,Steroid-Sensitive Nephrotic Syndrome,Multi Drug Resistant Nephrotic Syndrome,Nephrotic Syndrome, Steroid-Dependent,Nephrotic Syndrome, Steroid-Resistant,Nephrotic Syndrome, Steroid-Sensitive,Nephrotic Syndromes,Steroid Dependent Nephrotic Syndrome,Steroid Resistant Nephrotic Syndrome,Steroid Sensitive Nephrotic Syndrome,Steroid-Dependent Nephrotic Syndromes,Steroid-Resistant Nephrotic Syndromes,Steroid-Sensitive Nephrotic Syndromes,Syndrome, Nephrotic,Syndrome, Steroid-Sensitive Nephrotic
D003176 Complement C3 A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase. C3 Complement,C3 Precursor,Complement 3,Complement C3 Precursor,Complement Component 3,Precursor-Complement 3,Pro-C3,Pro-Complement 3,C3 Precursor, Complement,C3, Complement,Complement, C3,Component 3, Complement,Precursor Complement 3,Precursor, C3,Precursor, Complement C3,Pro C3,Pro Complement 3
D005921 Glomerulonephritis Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY. Bright Disease,Kidney Scarring,Glomerulonephritides,Scarring, Kidney
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man

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