Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indentations of the glomerular basement membrane were observed by light microscopy in ultrathin Epon-embedded serial sections from the renal biopsies of patients who had membranous glomerulonephritis, minimal change glomerulonephrits, acute or resolving exudative glomerulonephritis and focal glomerulonephrits, interstitial nephritis, amyloidosis, rheumatoid arthritis, or ankylosing spondylitis. In patients with membranous glomerulonephritis, acute or resolving exudative glomerulonephritis, amyloidosis, or rheumatoid arthritis, the occurrence of indentations in the glomerular basement membrane differed significantly from that in controls. The presence of indentations did not correlate with proteinuria, hematuria, leukocyturia, arterial hypertension, or with the nephrotic syndrome or its treatment with steroids. Examination of alternate serial sections by light and be electron microscopy showed that the indentations that were light microscopically visible corresponded to craters on the epithelial surface of the glomerular basement membrane seen in the electron microscope. These craters contained protruding portions of the epithelial cells, extracellular electron-lucent material or electron-dense amorphous or striated membranous material. They were often surrounded by spikelike protrusions of the lamina densa. These indentations might represent solitary remnants of former subepithelial deposits.
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PMID:Indentations of the glomerular basement membrane in renal diseases. A light and electron microscopic study on ultrathin serial sections. 97 63

Antibodies to the collagen-like region of C1q have been described in patients with SLE and rheumatoid vasculitis. In this study the prevalence of both IgG and IgA C1qAb was assessed in serum samples of 385 patients with different systemic and renal diseases. The results demonstrate that the prevalence of IgG and IgA C1qAb is not restricted to the diseases in which they were originally described. C1qAb can also be demonstrated in patients with MCTD, Felty's syndrome, ankylosing spondylitis, polyarteritis nodosa, mixed cryoglobulinaemia, membranoproliferative glomerulonephritis, glomerulosclerosis, and patients with anti-glomerular basement membrane nephritis. The widespread occurrence of C1qAb of both immunoglobulin classes in systemic and renal diseases may provide insight into the mechanisms that lead to C1qAb formation.
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PMID:IgG and IgA autoantibodies to C1q in systemic and renal diseases. 134 21

We describe 2 patients with immunoglobulin A (IgA) nephropathy in association with ankylosing spondylitis. Renal biopsy demonstrated mesangial proliferative glomerulonephritis with prominent IgA, C3c, and less intense properdin deposition in the glomeruli. Intraglomerular clumps of virus-like particles were also observed in the kidney sample from one patient (case 2), who had an abnormal liver function. Our findings support the hypothesis that here is a possible common pathogenesis responsible for the concurrence of both IgA nephropathy and ankylosing spondylitis.
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PMID:Immunoglobulin A nephropathy and ankylosing spondylitis. Report of two patients in Taiwan and review of the literature. 304 83

A case of a 48 years old man with a combination of immunoglobulin A glomerulonephritis and ankylosing spondylitis is reported. The patient presents with the typical clinical and X-ray data of Bechterew's disease and the kidney biopsy shows diffuse mesangioproliferative glomerulonephritis with IgA precipitates. The rheumatic manifestations precede the hematuria and proteinuria. High serum IgA and arterial hypertension are present. It is suggested that the combination of these two diseases is more frequent since common pathogenetic mechanisms may play a leading role.
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PMID:[Immunoglobulin A glomerulonephritis in a patient with ankylosing spondylitis]. 343 23

There have been a few reports suggesting the association between glomerulonephritis (GN) and ankylosing spondylitis (AS). The reported glomerulonephritides include IgA nephropathy, mesangial proliferative GN and membranous nephropathy. From January 1983, through December 1984, we observed 5 cases of GN among 116 cases of definite AS. Three of them were IgA nephropathy. The other two were mesangial proliferative GN, with IgM deposit in one case and isolated C3 deposit in another. Microscopic hematuria was observed in all of them. The renal function and 24-hour urine protein excretion were all within normal limits. Serum IgA level increased in all but the case of mesangial proliferative GN with IgM deposit. All except one had the antigen of HLA-B27. Serum IgA level was determined in 78 cases (86 estimations) of AS. The mean value was 399.6 +/- 15.0 mg/dl (mean +/- SE) (normal range: 100-350 mg/dl). Fifty-four of them (63%) had a value higher than 350 mg/dl. The interrelationship of AS and IgA nephropathy was discussed.
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PMID:Glomerulonephritis in ankylosing spondylitis. 351 79

The incidence of renal abnormalities is increased in patients with ankylosing spondylitis (AS). Possible mechanisms include the effects of nonsteroidal anti-inflammatory drugs (NSAIDs), an increased incidence of glomerulonephritis and the deposition of amyloid. We assessed renal function in 51 patients with AS randomly selected from those attending routine rheumatology clinics. Five patients were found to have a definite renal abnormality and three of them underwent renal biopsy. These showed one case each of IgA glomerulonephritis, focal segmental glomerulosclerosis and nonspecific tubulo-interstitial damage. A sixth patient had recurrent haematuria and borderline renal functional impairment but refused further investigation. The urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) was elevated in four patients; two had other biochemical evidence of renal damage while the other two patients appeared normal, although they had both received spinal irradiation in the past. The finding of a significant renal abnormality in 10% of AS patients suggests that evidence of renal involvement should be actively sought in this disease.
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PMID:Renal abnormalities in ankylosing spondylitis. 366 58

The ability of human sera to prevent the precipitation of antigen-antibody complexes has been investigated. The early complement components including C3 are required for optimal prevention of immune precipitation, whereas the later components are not required. The sera of 36 of 75 patients with seropositive rheumatoid arthritis (RA), 14 of 32 with SLE and four of 17 with glomerulonephritis exhibited reduced capacities to prevent immune precipitation. In contrast sera from patients with seronegative RA, ankylosing spondylitis, psoriatic arthritis or degenerative joint disease were normal in this respect. In SLE and GN sera hypocomplementaemia was frequently associated but not always with failure to prevent immune precipitation, whereas only a small proportion of the patients with seropositive RA and reduced capacity to retain complexes in a soluble form were hypocomplementaemic. Thus the failure of sera to prevent the precipitation of antigen-antibody complexes is not always associated with hypocomplementaemia.
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PMID:Complement-mediated inhibition of immune precipitation in patients with immune complex diseases. 622 Aug 48

2 patients with ankylosing spondylitis (A Sp) were found to have renal lesions similar to those seen in IgA nephropathy. In 1 patient the changes were extremely severe and progressive and in the other they were mild. Vascular changes were also noted in 1 patient. The findings suggest an immune complex mediated glomerulonephritis and support an earlier report that there may be a specific renal lesion in patients with A Sp. The significance of IgA deposition in the mesangium, and of an increase in the serum levels of IgA in some patients with A Sp is unclear.
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PMID:A renal lesion in ankylosing spondylitis. 644 64

A retrospective analysis of our patients with ankylosing spondylitis revealed a 17.8% incidence of recurrent hematuria. Two of the five patients with recurrent hematuria had previously undergone renal biopsies showing a focal proliferative glomerulonephritis. The only specimen examined by immunofluorescent staining showed the typical changes of IgA nephropathy. A control group of patients with rheumatoid arthritis did not show recurrent hematuria. Recurrent hematuria may be a frequent occurrence in ankylosing spondylitis and may signify the presence of one of the glomerulonephritides such as IgA nephropathy.
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PMID:Increased incidence of recurrent hematuria in ankylosing spondylitis: a possible association with IgA nephropathy. 671 51

Three patients with a seronegative spondylarthropathy were found to have IgA nephropathy. Two patients had ankylosing spondylitis (one with psoriasis), and one had incomplete Reiter's syndrome. All three had a focal proliferative glomerulonephritis with IgA-dominant mesangial immune deposits. One patient had a leukocytoclastic vasculitis. This association of IgA nephropathy with seronegative spondylarthropathies raises the possibility of a common or related pathogenesis. There is evidence to suggest that both diseases are mediated by genetically controlled immune responses to mucosal contact with etiologic antigens.
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PMID:IgA nephropathy associated with seronegative spondylarthropathies. 706 44


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