TY - JOUR
T1 - Circulating anti-entactin antibodies in patients with glomerulonephritis
AU - Saxena, Ramesh
AU - Bygren, Per
AU - Cederholm, Bo
AU - Wieslander, Jörgen
N1 - Funding Information:
This study was supported by grants from Swedish Institute, Swedish Medical Research Council (MFR 16X-09487) and Medicinska Fakulte- ten Forskningsanslag. We are grateful to ProfesSor Ulla Bengtsson for her meticulous evaluation of this study. We also appreciate Dr. Peter Swedenborg for his critical comments on this study. We thank Prof. Birger Astedt, Dr. Archana Saxena, Dr. U. Srinivas, Dr. Jean-Henrik Braconier and Dr. Johan Rydberg for providing blood samples for our control groups.
PY - 1991/5
Y1 - 1991/5
N2 - Sera from 305 consecutive patients in a renal biopsy series were analyzed for the presence of anti-entactin antibodies by ELISA. Of these patients, 59% had primary glomerulonephritis, 21% had secondary glomerulonephritis. while 20% had other nephropathies (non-inflammatory conditions like amyloidosis. diabetic nephropathy, nephrosclerosis, etc.). Forty-one of these patients (13.4%) were positive for IgG/IgM antibodies against entactin; 60% of them had primary glomerulonephritis, 35% had secondary glomerulonephritis, while the remaining 3 patients had other nephropathies. Fifteen (70%) of the 23 patients with primary glomerulonephritis had proliferative glomerulonephritis (PGN), whereas 13 (87%) of the 15 patients with secondary glomerulonephritis were due to systemic connective tissue diseases (SCTD); 7 due to SLE, 4 due to SLE like SCTD and two due to other SCTD. There was a peak of incidence corresponding to the group aged 18 to 30 years. A majority of these patients (12 of the total 17) had primary glomerulonephritis and were associated with nephrotic or subnephrotic grade proteinuria, poorly or nonresponsive to immunosuppressive treatment and associated, in several cases, with progressive deterioration of renal function. In addition, there was a tendency to another peak in the age group 51 to 60 years. Most of these patients (6 of the total 8) had glomerulonephritis secondary, mainly, to SLE or SLE like SCTD with milder degree of proteinuria and better preserved renal functions. Anti-entactin antibodies were not found in certain glomerulonephritides like IgA nephropathy and those secondary to systemic vasculitides and in control subjects (healthy subjects, and patients with a variety of non-renal disorders including inflammatory diseases). There was a significant correlation between the presence of circulating anti-entactin antibodies and the deposition of corresponding class of immunoglobulin along the glomerular basement membrane. In addition, a significant correlation between the absence of immune deposits and negative results for anti-entactin antibodies by ELISA was also observed. Our observations suggest that anti-entactin antibodies are associated with certain definite categories of glomerulonephritides in human beings and may well be involved in their immunopathogenesis.
AB - Sera from 305 consecutive patients in a renal biopsy series were analyzed for the presence of anti-entactin antibodies by ELISA. Of these patients, 59% had primary glomerulonephritis, 21% had secondary glomerulonephritis. while 20% had other nephropathies (non-inflammatory conditions like amyloidosis. diabetic nephropathy, nephrosclerosis, etc.). Forty-one of these patients (13.4%) were positive for IgG/IgM antibodies against entactin; 60% of them had primary glomerulonephritis, 35% had secondary glomerulonephritis, while the remaining 3 patients had other nephropathies. Fifteen (70%) of the 23 patients with primary glomerulonephritis had proliferative glomerulonephritis (PGN), whereas 13 (87%) of the 15 patients with secondary glomerulonephritis were due to systemic connective tissue diseases (SCTD); 7 due to SLE, 4 due to SLE like SCTD and two due to other SCTD. There was a peak of incidence corresponding to the group aged 18 to 30 years. A majority of these patients (12 of the total 17) had primary glomerulonephritis and were associated with nephrotic or subnephrotic grade proteinuria, poorly or nonresponsive to immunosuppressive treatment and associated, in several cases, with progressive deterioration of renal function. In addition, there was a tendency to another peak in the age group 51 to 60 years. Most of these patients (6 of the total 8) had glomerulonephritis secondary, mainly, to SLE or SLE like SCTD with milder degree of proteinuria and better preserved renal functions. Anti-entactin antibodies were not found in certain glomerulonephritides like IgA nephropathy and those secondary to systemic vasculitides and in control subjects (healthy subjects, and patients with a variety of non-renal disorders including inflammatory diseases). There was a significant correlation between the presence of circulating anti-entactin antibodies and the deposition of corresponding class of immunoglobulin along the glomerular basement membrane. In addition, a significant correlation between the absence of immune deposits and negative results for anti-entactin antibodies by ELISA was also observed. Our observations suggest that anti-entactin antibodies are associated with certain definite categories of glomerulonephritides in human beings and may well be involved in their immunopathogenesis.
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U2 - 10.1038/ki.1991.126
DO - 10.1038/ki.1991.126
M3 - Article
C2 - 2067216
AN - SCOPUS:0025729382
SN - 0085-2538
VL - 39
SP - 996
EP - 1004
JO - Kidney International
JF - Kidney International
IS - 5
ER -