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

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

A case of definite ankylosing spondylitis (AS), classical rheumatoid arthritis (RA) and membranous nephropathy is presented. Concurrent presence of the HLA-B27 and HLA-DR4 antigens was demonstrated. The association of AS and RA as well as RA and membranous nephropathy are discussed and the literature reviewed.
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PMID:Coexistence of HLA-B27 ankylosing spondylitis and DR4 seropositive nodular rheumatoid arthritis in patient with membranous nephropathy. 697 78

Eleven patients with amyloidosis were treated for terminal renal failure by transplantation, receiving 12 cadaver allografts. In one patient the amyloidosis was primary and in the remaining 10 it was secondary to a chronic inflammatory disease. All of the patients were subjected to one or two fine-needle aspiration biopsies of the kidney graft during a followup of 11 to 68 months. The biopsies of three patients, one with primary amyloidosis and two with ankylosing spondylitis, revealed amyloid recurrence in the graft. These recurrences were diagnosed at 11, 28, or 37 months, respectively. The risk of amyloid recurrence is thus by no means negligible. The present study revealed no factors determining the development of recurrence. In two additional cases, membranous glomerulonephritis was observed in transplant biopsy. Both of these patients had rheumatoid arthritis as the underlying disease and were treated with gold salts before transplantation. It is suggested that an impaired immune response, related to amyloidosis and/or immunosuppressive therapy, may have favored the formation and deposition of circulating immune complexes.
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PMID:Recurrence of renal amyloid and de novo membranous glomerulonephritis after transplantation. 702 98

Infliximab is a chimeric tumor necrosis factor-alpha (TNF-alpha) monoclonal antibody, which has been used extensively in patients with rheumatoid arthritis and inflammatory bowel disease. It also appears to be effective in other conditions such as psoriasis and ankylosing spondylitis. The major side effect of infliximab is infection. Renal complications are uncommon and not well recognized. This report describes a probable case of infliximab-induced membranous nephropathy.
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PMID:Infliximab and nephrotic syndrome. 1620 73

Ankylosing spondylitis is a chronic inflammatory disease of the vertebral joints and soft tissues. Renal involvement, apart from amyloidosis, is rare in this disorder. Of the various glomerulonephritides reported in association with ankylosing spondylitis, IgA nephropathy is the most common. Membranous glomerulonephritis occurs very rarely in patients with ankylosing spondylitis, and only four such cases have been reported in the available English literature. Due to the rarity of this association, membranous glomerulonephritis may not initially be considered in patients with ankylosing spondylitis and proteinuria. We report the case of a 29-year-old man with ankylosing spondylitis who presented with pedal edema and was detected to have nephrotic syndrome. A percutaneous renal biopsy showed features of membranous glomerulonephritis with capillary wall granular deposits of IgG and C3 on immunofluorescence and subepithelial immune complex deposits on electron microscopy. No other secondary cause of membranous glomerulopathy was found on extensive investigations. Membranous glomerulonephritis is extremely rare in association with ankylosing spondylitis, the present case being the fifth such report. The exact relationship of these two entities (etiological or coincidental) still needs to be elucidated. The occurrence of this rare association needs to be recognized and differentiated from other more common causes of renal involvement in ankylosing spondylitis.
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PMID:Membranous glomerulonephritis in a patient with ankylosing spondylitis: a rare association. 1965 3

Biological therapeutics (biologics) that target autoimmune responses and inflammatory injury pathways have a marked beneficial impact on the management of many chronic diseases, including rheumatoid arthritis, psoriasis, inflammatory bowel disease, and ankylosing spondylitis. Accumulating data suggest that a growing number of renal diseases result from autoimmune injury - including lupus nephritis, IgA nephropathy, anti-neutrophil cytoplasmic antibody-associated glomerulonephritis, autoimmune (formerly idiopathic) membranous nephropathy, anti-glomerular basement membrane glomerulonephritis, and C3 nephropathy - and one can speculate that biologics might also be applicable to these diseases. As many autoimmune renal diseases are relatively uncommon, with long natural histories and diverse outcomes, clinical trials that aim to validate potentially useful biologics are difficult to design and/or perform. Some excellent consortia are undertaking cohort studies and clinical trials, but more multicentre international collaborations are needed to advance the introduction of new biologics to patients with autoimmune renal disorders. This Review discusses the key molecules that direct injurious inflammation and the biologics that are available to modulate them. The opportunities and challenges for the introduction of relevant biologics into treatment protocols for autoimmune renal diseases are also discussed.
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PMID:Biologics for the treatment of autoimmune renal diseases. 2694 77