Biomaterial Database

[Immunopathological study in membranoproliferative glomerulonephritis]. 1976

F Mota, and L Lecona, and V Zúñiga, and G Gordillo

In 39 renal percutaneous biopsies, practiced to 31 patients with membranoproliferative glomerulonephritis (GMP) with subendothelial deposits (DSE), a study with immunofluorescence technique and light microscopy was carried out. In all cases, heavy granular deposits of C3 were detected in the loops of the glomerular capillaries and in a variable proportion of cases, deposits of IgM, IgA, C3PA (factor B) and C1q of similar aspect and localizacion were found. These findings suggest immunologic pathogenesis. In the absence of C1q, no cases with factor B were found; thus, it is possible to assert that the activation of the complement system takes place exclusively through an alternate pathway, as was previously accepted. On the other hand, it was found that the presence of C1q was correlated with a faster evolution to chronic renal failure and with the presence of a higher percentage of glomeruli with extracapillary proliferation (crescents). Thus, it is concluded that activation of C1q in patients with MPG and SED, may play a role in formation of crescent and consequently, it is a sign of poor prognosis.

UI	MeSH Term	Description	Entries
D007136	Immunoglobulins	Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.	Globulins, Immune,Immune Globulin,Immune Globulins,Immunoglobulin,Globulin, Immune
D007668	Kidney	Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.	Kidneys
D007676	Kidney Failure, Chronic	The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.	ESRD,End-Stage Renal Disease,Renal Disease, End-Stage,Renal Failure, Chronic,Renal Failure, End-Stage,Chronic Kidney Failure,End-Stage Kidney Disease,Chronic Renal Failure,Disease, End-Stage Kidney,Disease, End-Stage Renal,End Stage Kidney Disease,End Stage Renal Disease,End-Stage Renal Failure,Kidney Disease, End-Stage,Renal Disease, End Stage,Renal Failure, End Stage
D002648	Child	A person 6 to 12 years of age. An individual 2 to 5 years old is CHILD, PRESCHOOL.	Children
D002675	Child, Preschool	A child between the ages of 2 and 5.	Children, Preschool,Preschool Child,Preschool Children
D003172	Complement C1	The first complement component to act in the activation of CLASSICAL COMPLEMENT PATHWAY. It is a calcium-dependent trimolecular complex made up of three subcomponents: COMPLEMENT C1Q; COMPLEMENT C1R; and COMPLEMENT C1S at 1:2:2 ratios. When the intact C1 binds to at least two antibodies (involving C1q), C1r and C1s are sequentially activated, leading to subsequent steps in the cascade of COMPLEMENT ACTIVATION.	C1 Complement,Complement 1,Complement Component 1,C1, Complement,Complement, C1,Component 1, Complement
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
D003937	Diagnosis, Differential	Determination of which one of two or more diseases or conditions a patient is suffering from by systematically comparing and contrasting results of diagnostic measures.	Diagnoses, Differential,Differential Diagnoses,Differential Diagnosis
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

Related Publications

F Mota, and L Lecona, and V Zúñiga, and G Gordillo

Membranoproliferative glomerulonephritis: a clinicopathologic study.

July 1973, Beitrage zur Pathologie,

F Mota, and L Lecona, and V Zúñiga, and G Gordillo

[Membranoproliferative glomerulonephritis].

January 2010, Nihon Jinzo Gakkai shi,

F Mota, and L Lecona, and V Zúñiga, and G Gordillo

[Membranoproliferative glomerulonephritis].

September 1989, Tidsskrift for den Norske laegeforening : tidsskrift for praktisk medicin, ny raekke,

F Mota, and L Lecona, and V Zúñiga, and G Gordillo

Membranoproliferative glomerulonephritis.

January 2001, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association,

F Mota, and L Lecona, and V Zúñiga, and G Gordillo

[Membranoproliferative glomerulonephritis].

September 1977, Deutsche medizinische Wochenschrift (1946),

F Mota, and L Lecona, and V Zúñiga, and G Gordillo

Membranoproliferative glomerulonephritis.

January 2000, Journal of insurance medicine (New York, N.Y.),

F Mota, and L Lecona, and V Zúñiga, and G Gordillo

Membranoproliferative glomerulonephritis.

December 1971, Archives of disease in childhood,

F Mota, and L Lecona, and V Zúñiga, and G Gordillo

[Membranoproliferative glomerulonephritis].

May 2005, Nihon rinsho. Japanese journal of clinical medicine,