Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperoxaluria is frequently seen in patients with inflammatory bowel disease, or after resection of the ileum. It is assumed to be responsible for the development of nephrolithiasis, nephrocalcinosis (oxalate nephrosis) and progressive renal impairment in these patients. Steatorrhea may aggravate the severity of hyperoxaluria. A 60-year-old male underwent massive resection of the jejunum and ileum 10 years prior to admission, due to strangulation of the small bowel, with occlusion of the superior mesenteric artery. He remained well except for steatorrhea which developed two-and-a-half years prior to admission, when microhematuria, proteinuria and oxaluria developed progressively. Since that time, the nephrolithiasis, nephrocalcinosis and renal failure have continued to worsen despite therapy with oxalate restriction and oxalate-binding agents. A renal biopsy, performed late in the clinical course, showed severe changes in the renal parenchyma. The decline in renal function proved irreversible. The unusual metabolic consequences of massive resection of the small intestine and their mechanisms are discussed.
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PMID:Hyperoxaluria, nephrolithiasis, nephrocalcinosis and renal failure after massive resection of the small intestine: report of a case. 136 95

From 1956 through 1989, 38 men and 26 women were seen at the Mayo Clinic with biopsy-proven AA. The underlying disorder was rheumatic disease in 42, infectious disease in 11, inflammatory bowel disease in 6, and other causes in 5. All patients were symptomatic at the time of diagnosis. Fifty-eight of the 64 patients had proteinuria or renal insufficiency. Fourteen also had significant symptoms of gastrointestinal amyloid, and 6 had amyloid goiter. None of the patients had symptomatic cardiac involvement, and only 3 had palpable hepatomegaly. Renal, gastric, rectal, fat, and marrow biopsies were positive for amyloid in 100%, 94%, 82%, 58%, and 46% of tested patients, respectively. The median survival of the entire group was 24.5 months. Thirty-five of the 47 deceased patients died as a direct result of their amyloidosis, primarily from complications of renal failure. Nine were successfully treated and had regression of the disease. Two with bronchiectasis responded to long-term cyclic antibiotic therapy, as did 1 patient with osteomyelitis. One patient with inflammatory bowel disease responded to surgical resection, and 1 with familial Mediterranean fever responded to colchicine. Four patients with rheumatic disease were treated with cyclophosphamide (in 2) and methotrexate (in 2), with complete resolution of their renal disease. All 9 successfully treated patients are alive, with a median follow-up of 58 months. Statistical analysis revealed that creatinine values greater than or equal to 2.0 mg/dl (P less than 0.003) and a serum albumin value less than 2.5 g/dl (P less than 0.02) were associated with a poorer survival. The single strongest variable associated with poor survival was a serum creatinine level greater than 2 mg/dl at presentation, with a median survival of 11.2 months compared to patients with a creatinine level less than 2.0 mg/dl, with a median survival of 56.9 months.
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PMID:Secondary systemic amyloidosis: response and survival in 64 patients. 206 9

A 13-year-old girl presented with a history of fever, arthritis, conjunctivitis, abdominal pain, and diarrhea. Colonoscopy and barium enema were consistent with Crohn's disease. A renal biopsy, performed because of persistent proteinuria and hematuria in the absence of obstruction to the urinary tract, revealed diffuse proliferative necrotizing glomerulonephritis: IgG, IgM, and C3 were deposited on the involved glomeruli. Circulating immune complexes were present in her serum. This immune-complex glomerulonephritis represents a previously unreported extraintestinal manifestation of inflammatory bowel disease.
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PMID:Immune-complex glomerulonephritis in Crohn's disease. 294 85

Retrospective analysis of 82 pregnancies in women with either ulcerative colitis or Crohn's disease suggested that, in general, neither disease had a major effect on pregnancy outcome. The birth-weights of babies born to women with inflammatory bowel disease were marginally lower than those born to women in a control group matched for age and parity, but the difference was statistically significant only in women with Crohn's disease. In both disease groups there was a higher frequency of low haemoglobin levels in pregnancy than in the matched control groups. There were no statistically significant effects of ulcerative colitis or Crohn's disease on duration of pregnancy, mode of delivery or raised blood pressure and/or proteinuria. In the absence of a relapse, a diagnosis of inflammatory bowel disease should not influence obstetric management.
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PMID:The effects of inflammatory bowel disease on pregnancy: a case-controlled retrospective analysis. 377 45

A 20 year old male patient with a four-years-history of moderately active ulcerative colitis was admitted due to extensive generalized edema. He suffered from a nephrotic syndrome, which was caused by secondary renal amyloidosis due to the colitis. Under continuous low dose therapy with colchicine in addition to the usual colitis therapy proteinuria decreased from values above 10 g/die to about 3 g/die and edema disappeared completely. Secondary amyloidosis following inflammatory bowel disease is a rare event, in case of ulcerative colitis a true curiosity. Cases published so far are discussed.
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PMID:[Secondary amyloidosis in ulcerative colitis--successful treatment with colchicine]. 904 37

There have been a wide variety of reported renal parenchymal diseases associated with inflammatory bowel disease, ranging from interstitial nephritis to amyloidosis to immune complex glomerulonephritis. Two pediatric cases of renal parenchymal pathology in association with Crohn disease are presented. The first is an 11-year-old child who presented with recurrent bouts of gross hematuria, biopsy-proven IgA nephropathy, and later developed Crohn disease 4 years after the initial presentation. Her renal function is normal with persistent isolated microscopic hematuria. The second case is that of a 9-year-old male who presented with the classic gastrointestinal manifestations of Crohn disease, later developed hematuria and proteinuria, and was found on a renal biopsy to have thin basement membrane disease. There have been several reported cases of IgA nephropathy associated with inflammatory bowel disease; but to our knowledge, this is the first case of thin basement membrane disease occurring in conjunction with Crohn disease. Discussion focuses on the relationship of IgA nephropathy with inflammatory bowel disease with additional comments on thin basement membrane disease.
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PMID:IgA nephropathy and thin basement membrane disease in association with Crohn disease. 932 97

Records and pedigrees of Soft Coated Wheaten Terriers (SCWT) with protein-losing enteropathy (PLE) or protein-losing nephropathy (PLN) were studied retrospectively. Criteria for inclusion were defined based on analysis of blood (panhypoproteinemia for PLE, hypoalbuminemia for PLN) and urine (proteinuria for PLN) and histopathologic examination of tissue. Two hundred twenty-two affected dogs (female:male ratio = 1.6, P < .001) were clinically identified. Dogs were diagnosed with PLE earlier (P < .005; mean +/- SD age: 4.7+/-2.6 years, n = 76) than with PLN (6.3+/-2.0 years, n = 84) or with both diseases (5.9+/-2.2 years, n = 62). Clinical signs included vomiting, diarrhea, weight loss, pleural and peritoneal effusions, and less commonly thromboembolic disease. Dogs with PLE generally had panhypoproteinemia and hypocholesterolemia; intestinal lesions included inflammatory bowel disease, dilated lymphatics, and lipogranulomatous lymphangitis. Dogs with PLN generally had hypoalbuminemia, proteinuria, hypercholesterolemia, and azotemia; renal lesions typically showed chronic glomerulonephritis/glomerulosclerosis, and less commonly endstage renal disease. Dogs with combined PLE/PLN had intermediate mean values (P < .001) for serum total protein, albumin, globulin, and cholesterol but had a higher mean urine protein:creatinine ratio than did PLN dogs (P < .05); intestinal and renal lesions in these dogs were similar to those in the other groups. Two dogs had incidental mild renal dysplasia. Pedigree analysis from 188 dogs demonstrated a common male ancestor, although the mode of inheritance is unknown. Both PLE and PLN are common diseases in this small breed population. The prognosis is poor. Compared with previously reported intestinal and renal diseases in dogs, a new, distinctive familial predisposition for both PLE and PLN has been recognized in the SCWT breed.
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PMID:Familial protein-losing enteropathy and protein-losing nephropathy in Soft Coated Wheaten Terriers: 222 cases (1983-1997). 1066 20

A case of glomerulonephritis in a 35-year-old man with Crohn's disease is described here. The patient presented with severe diarrhea, nephrotic range proteinuria, hematuria, microangiopathic hemolytic anemia, thrombocytopenia, hypocomplementemia, acute renal failure requiring hemodialysis, cryoglobulinemia, and extensive thrombotic gangrene of the distal upper and lower limbs. The patient did not respond to plasmapheresis and steroid therapy and died of upper gastrointestinal bleeding. Renal tissue obtained at autopsy showed IgA-mediated antiglomerular basement membrane crescentic glomerulonephritis. Linear staining of the glomerular basement membrane by non-IgG antibodies is quite unusual with only 11 cases previously reported in the worldwide literature, 8 caused by IgA. Glomerulonephritis is a rarely reported extraintestinal manifestation of inflammatory bowel disease, and there are only 24 previously described cases that are reviewed and summarized in this report. Glomerulonephritis occurred in the setting of active bowel inflammation in all cases, circulating immune complexes were found in nearly half the cases, and serum complements usually were normal. Renal insufficiency and nephrotic range proteinuria were typically present at the time of diagnosis of glomerulonephritis and most often improved in parallel with treatment of the gastrointestinal disorder. The histologic findings were varied and included membranoproliferative glomerulonephritis, mesangioproliferative glomerulonephritis, membranous nephropathy, IgA nephropathy, and IgM nephropathy. Thus, the authors present the first case of glomerulonephritis caused by antiglomerular basement membrane disease in association with inflammatory bowel disease.
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PMID:IgA antiglomerular basement membrane nephritis associated with Crohn's disease: a case report and review of glomerulonephritis in inflammatory bowel disease. 1272 45

GI protein loss can result from a heterogeneous group of diseases, including lymphangiectasia, IBD, neoplasia, ulceration, intussusception, and histoplasmosis. PLE should be suspected in any hypoalbuminemic patient with no evidence of exudative protein loss, proteinuria, or HI. A minimum laboratory database for the suspected PLE patient should include a complete blood cell count, a biochemical and electrolyte profile, urinalysis (+/- urine protein:cretinine ratio), and pre- and postprandial bile acid determinations. Fecal alpha 1-PI concentrations may be used to confirm the presence of GI protein loss in cases with concurrent renal or hepatic disease. Because PLE is a syndrome and not a specific disease, the most effective therapy must be directed at the underlying cause. Multiple high-quality endoscopic biopsies are sufficient to diagnose most patients with PLE, although full-thickness biopsies are required in some cases. Patients with PLE are often clinically "fragile," and careful symptomatic therapy must be integrated with dietary and medical management strategies in most cases.
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PMID:Protein-losing enteropathies. 1455 61

We report the case of a 37 year old man who suffered from Crohn's Disease (CD), and was receiving treatment with mesalazine (5-ASA). Nine years after the diagnosis, because of detecting a slight proteinuria, a renal biopsy is made, being the anatomo-pathologic result compatible with membranous glomerulonephritis (MGN). Checking previous literature we have only found two cases reported of MGN in coincidence with Inflammatory Bowel Disease (IBD), one in association with Ulcerative Colitis and the other with Crohn's Disease in a 12 years old boy. This is, therefore, the second case presenting MGN associated with CD and the first in an adult patient.
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PMID:[Association between membranous glomerulonephritis and Crohn's disease]. 1545 98


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