[Membranoproliferative glomerulonephritis with semilunar forms and massive deposits of IgA associated with HBsAg]. 1990

J E Toblli, and A M Chirife, and A M Budani, and A Marcuzzi, and M C Digioia, and H Collado
Servicio de Nefrología, Hospital Alemán, Buenos Aires, Argentina.

The association of HBV infection and glomerular damage was first reported by Combes et al in 1971, in a patient with nephrotic syndrome due to membranous glomerulopathy and chronic hepatitis B. Since, then, other glomerular diseases have been reported such as a) minimal changes nephropathy, b) IgA nephropathy, c) membranous-proliferative glomerulonephritis (MPGN), d) membranous, e) mesangial proliferative and f) lupus nephritis. All of them are associated with chronic hepatic disease and some of the following antigens: 1) HBsAg; 2) HBeAg; 3) HBcAg. These disorders are very frequent in Southeast Asia. Vertical transmission from mothers to fetuses may be important in maintaining the high carrier rate, and possibly plays a role in the development of glomerular damage. On the other hand, MPGN associated with HBsAg has rarely been reported and always with a favorable benign course. The present report describes interesting findings in a renal biopsy from a HBsAg and HBeAg carrier, who developed renal failure requiring hemodialysis. A 21 year old Korean man was admitted to the Hospital for nephrotic syndrome, microhematuria hypertension and renal failure. He had no previous history of blood transfusion, intravenous drug addiction, jaundice or liver disease. His father was HBsAg carrier with hepatic cirrhosis. An ultrasound examination showed normal renal size. Renal biopsy was performed and the patient received hemodialysis treatment. The specimen was processed for light microscopy, immunofluorescent studies and peroxidase-antiperoxidase technique. Frozen sections were studied by direct immunofluorescence for the identification of IgG, IgA, C1q, C3, fibrinogen and albumin. Paraffin sections stained by immunoperoxidase technique for HBsAg, using polyclonal monospecific rabbit anti-Human antisera (Dakopatts, Copenhagen).(ABSTRACT TRUNCATED AT 250 WORDS)

UI MeSH Term Description Entries
D007070 Immunoglobulin A Represents 15-20% of the human serum immunoglobulins, mostly as the 4-chain polymer in humans or dimer in other mammals. Secretory IgA (IMMUNOGLOBULIN A, SECRETORY) is the main immunoglobulin in secretions. IgA,IgA Antibody,IgA1,IgA2,Antibody, IgA
D008297 Male Males
D005922 Glomerulonephritis, IGA A chronic form of glomerulonephritis characterized by deposits of predominantly IMMUNOGLOBULIN A in the mesangial area (GLOMERULAR MESANGIUM). Deposits of COMPLEMENT C3 and IMMUNOGLOBULIN G are also often found. Clinical features may progress from asymptomatic HEMATURIA to END-STAGE KIDNEY DISEASE. Berger Disease,Immunoglobulin A Nephropathy,Nephropathy, IGA,Berger's Disease,IGA Glomerulonephritis,IGA Nephropathy,Iga Nephropathy 1,Nephritis, IGA Type,Bergers Disease,Glomerulonephritides, IGA,IGA Type Nephritis,Nephropathy 1, Iga,Nephropathy, Immunoglobulin A
D006509 Hepatitis B INFLAMMATION of the LIVER in humans caused by a member of the ORTHOHEPADNAVIRUS genus, HEPATITIS B VIRUS. It is primarily transmitted by parenteral exposure, such as transfusion of contaminated blood or blood products, but can also be transmitted via sexual or intimate personal contact. Hepatitis B Virus Infection
D006514 Hepatitis B Surface Antigens Those hepatitis B antigens found on the surface of the Dane particle and on the 20 nm spherical and tubular particles. Several subspecificities of the surface antigen are known. These were formerly called the Australia antigen. Australia Antigen,HBsAg,Hepatitis B Surface Antigen,Antigen, Australia
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000328 Adult A person having attained full growth or maturity. Adults are of 19 through 44 years of age. For a person between 19 and 24 years of age, YOUNG ADULT is available. Adults
D015432 Glomerulonephritis, Membranoproliferative Chronic glomerulonephritis characterized histologically by proliferation of MESANGIAL CELLS, increase in the MESANGIAL EXTRACELLULAR MATRIX, and a thickening of the glomerular capillary walls. This may appear as a primary disorder or secondary to other diseases including infections and autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Various subtypes are classified by their abnormal ultrastructures and immune deposits. Hypocomplementemia is a characteristic feature of all types of MPGN. C3G Complement 3 Glomerulopathy,Complement 3 Glomerulopathies,Complement 3 Glomerulopathy,Glomerulonephritis, Mesangiocapillary,MPGN Membranoproliferative Glomerulonephritis,Membranoproliferative Glomerulonephritis,Mesangiocapillary Glomerulonephritis,DDD MPGNII,Dense Deposit Disease,Glomerulonephritis, Hypocomplementemic,MPGNII,Membranoproliferative Glomerulonephritis Type II,Membranoproliferative Glomerulonephritis, Type I,Membranoproliferative Glomerulonephritis, Type II,Membranoproliferative Glomerulonephritis, Type III,Mesangiocapillary Glomerulonephritis, Type I,Mesangiocapillary Glomerulonephritis, Type II,Subendothelial Membranoproliferative Glomerulonephritis,Type II MPGN,DDD MPGNIIs,Glomerulonephritides, MPGN Membranoproliferative,Glomerulonephritides, Membranoproliferative,Glomerulonephritis, MPGN Membranoproliferative,Glomerulopathies, Complement 3,Glomerulopathy, Complement 3,Hypocomplementemic Glomerulonephritides,Hypocomplementemic Glomerulonephritis,MPGN Membranoproliferative Glomerulonephritides,MPGN, Type II,MPGNII, DDD,MPGNIIs,Membranoproliferative Glomerulonephritides,Membranoproliferative Glomerulonephritides, MPGN,Membranoproliferative Glomerulonephritis, MPGN,Membranoproliferative Glomerulonephritis, Subendothelial,Mesangiocapillary Glomerulonephritides,Type II MPGNs

Related Publications

J E Toblli, and A M Chirife, and A M Budani, and A Marcuzzi, and M C Digioia, and H Collado
January 1985, International urology and nephrology,
J E Toblli, and A M Chirife, and A M Budani, and A Marcuzzi, and M C Digioia, and H Collado
January 1986, Pathologica,
J E Toblli, and A M Chirife, and A M Budani, and A Marcuzzi, and M C Digioia, and H Collado
February 2014, Annals of hematology,
J E Toblli, and A M Chirife, and A M Budani, and A Marcuzzi, and M C Digioia, and H Collado
September 2016, Kidney international reports,
J E Toblli, and A M Chirife, and A M Budani, and A Marcuzzi, and M C Digioia, and H Collado
December 2003, Clinical and experimental nephrology,
J E Toblli, and A M Chirife, and A M Budani, and A Marcuzzi, and M C Digioia, and H Collado
June 1985, Annales de pediatrie,
J E Toblli, and A M Chirife, and A M Budani, and A Marcuzzi, and M C Digioia, and H Collado
October 2015, Kidney international,
J E Toblli, and A M Chirife, and A M Budani, and A Marcuzzi, and M C Digioia, and H Collado
October 2000, American journal of kidney diseases : the official journal of the National Kidney Foundation,
J E Toblli, and A M Chirife, and A M Budani, and A Marcuzzi, and M C Digioia, and H Collado
June 1987, Medicina clinica,
J E Toblli, and A M Chirife, and A M Budani, and A Marcuzzi, and M C Digioia, and H Collado
November 2010, Nephrologie & therapeutique,
Copied contents to your clipboard!