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)

From 1960 through 1972, 236 cases of amyloidosis with histologic proof were found. The amyloidosis was primary (without evidence of preceding or coexisting disease) in 132 cases (group 1) and associated with multiple myeloma in 61 (group 2). Secondary amyloidosis appeared in 19 cases (associated with rheumatoid arthritis or osteomyelitis in two-thirds of them). There were 22 patients with amyloid localized to a single organ (bladder, lung, skin, or larynx in more than half of them). Two patients had familial amyloidosis. In group 1 and group 2, the most common presenting symptoms were fatigue, weight loss, edema, dyspnea, light-headedness or syncope, and paresthesias. Symptoms of the carpal-tunnel syndrome were frequent. The liver was palpable in almost 50% of the series, but splenomegaly was an initial finding in less than 10%. Macroglossia was recorded in 26% of group 2 and in 12% of group 1. Enlargement of submandibular structures was noted in about 10% of cases; and purpura, particularly around the eyes, was a significant feature. Substantial numbers of the patients had carpal-tunnel syndrome, nephrotic syndrome, congestive heart failure, sprue, peripheral neuropathy, or orthostatic hypotension. Approximately 50% of patients had renal insufficiency at the time of diagnosis. Proteinuria was found in more than 90%. A monoclonal protein was found in the serum of 49% of group 1 and in 74% of group 2. Monoclonal proteins were found in the urine of 35% and 81%, respectively. Only 12% of patients in group 1 had no monoclonal protein when both serum and urine were analyzed, and all patients of group 2 had a monoclonal protein in the serum or urine when both were analyzed. Lambda light chains were more common than kappa. None of the patients in group 1 had more than 15% plasma cells in the marrow, whereas more than half of group 2 had more than 15% plasma cells. Roentgenograms showed no evidence of skeletal disease in 94% of group 1, but 50% of group 2 had skeletal abnormalities. Rectal biopsy was positive for amyloid in 84% of cases. Kidney, liver, and carpal-tunnel biopsies were positive in 90% or more. Follow-up of all 193 patients in groups 1 and 2 revealed that 80% of group 1 and 97% of group 2 had died. The median survival was 14.7 months in group 1 and 4 months in group 2. Cardiac failure was the most common cause of death, accounting for 30% of the fatalities. We also reclassified all cases by the method of Isobe and Osserman (105), which is based on clinical patterns: pattern I--principal involvement of tongue, heart, gastrointestinal tract, muscle, nerves, skin, and carpal ligaments; pattern II--principal involvement of liver, spleen, kidneys, and adrenals; and mixed pattern I and II. This analysis failed to reveal predictive value in the clinical pattern classification, and did not discern the survival differences between primary amyloidosis (group 1) and amyloidosis with myeloma (group 2). Consequently, for the present we prefer the classification used in this study.
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PMID:Amyloidosis: review of 236 cases. 115 71

A patient with a 10 year history of monoclonal gammopathy of undetermined significance and Bence Jones proteinuria, and a 44 year history of ankylosing spondylitis, developed a nephrotic syndrome secondary to renal amyloidosis. Clinically the amyloidosis was ascribed to Bence Jones proteinuria rather than to the burnt out ankylosing spondylitis. However, histochemical and immunofluorescence staining techniques used to type the amyloid fibrils showed AA amyloidosis, implicating ankylosing spondylitis rather than monoclonal gammopathy as the underlying cause of the patient's systemic amyloidosis and consequent nephrotic syndrome. It is recommended that immunostaining of amyloid become a routine procedure to detect occult or apparently inactive disease.
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PMID:Renal AA amyloidosis in a patient with Bence Jones proteinuria and ankylosing spondylitis. 143 Feb 70

Secondary amyloidosis is an important complication that may have a strong influence on the prognosis of patients with rheumatoid arthritis (RA). We studied 21 RA patients with secondary amyloidosis. The two major initial signs were gastrointestinal symptoms and renal involvement. When 15 of the 21 patients were diagnosed as having secondary amyloidosis, they displayed renal involvement including proteinuria, hematuria and hypercreatininemia. The 15 patients with amyloidosis were either subjected to dialysis or died within 35 months on the average. The causes of death in 13 patients were cardiac failure, gastrointestinal bleeding and infection, which were strongly implicated with renal failure. Dialysis was applied to seven patients. Three of them were maintained with chronic dialysis. We discussed the induction-time and the method of dialysis in patients with amyloidosis secondary to RA.
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PMID:[Clinical characteristics and prognosis of secondary amyloidosis in patients with rheumatoid arthritis--renal involvement and therapy]. 144 80

Of 103 patients with membranous glomerulonephritis proved by renal biopsy, 11 (10.7%) had rheumatoid arthritis. Nine of these 11 patients received systemic treatment with anti-rheumatic remedies including gold, D-penicillamine and bucillamine. Two others were administered only token of nonsteroidal antiinflammatory drugs. Renal function of the patients was well maintained and within normal limits. Four patients showed nephrotic syndrome, while mild to moderate proteinuria was found in the other 7. Hematuria was minimal to mild, and it was not a major symptom. Six patients resolved proteinuria completely and 2 patients incompletely after discontinuation of chrysotherapy. Nine cases of the membranous lesion in patients with rheumatoid arthritis were stage 1. Thus it was often difficult to identify the glomerular change only by light microscopy. IgA nephropathy and AA amyloidosis were associated in one patient respectively. Our data lead us to conclude that chrysotherapy would cause membranous lesions, but rheumatoid arthritis itself also induce membranous glomerulonephritis.
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PMID:[Clinicopathological study of membranous glomerulonephritis in patients with rheumatoid arthritis]. 163 32

A 54 year-old woman who had had 4 years history of ulcerative colitis (UC) was admitted to our hospital because of recently developed proteinuria and leg edema. On admission, laboratory findings disclosed massive proteinuria, hypoalbuminemia, acceleration of ESR and elevated of CRP. Her abdominal symptom was remitted. Renal biopsy showed amyloid deposition in glomeruli and arteriole. Amyloid deposition was also found on rectal biopsy. She had no evidence of familial amyloidosis and multiple myeloma. In this case, amyloid deposition might be developed after UC. Secondary amyloidosis due to UC was extremely rare, only 3 cases including ours were reported in Japan.
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PMID:[A case of secondary amyloidosis complicated with ulcerative colitis]. 237 13

A case of histologically documented renal amyloidosis occurring in a boy who had juvenile rheumatoid arthritis is presented. The presenting problem was massive proteinuria resulting in nephrotic syndrome. Secondary amyloidosis is a serious complication of juvenile rheumatoid arthritis and it indicates very poor prognosis.
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PMID:Amyloidosis secondary to juvenile rheumatoid arthritis: a case report from Saudi Arabia. 243 36

The histological location of amyloid within various organs in 25 cases of systemic AA amyloidosis was studied with a view to determine whether different morphological patterns exist in this category of amyloidosis. Although morphological variations due to progressive severity of disease were observed, there were appreciable variations in the patterns of amyloid deposition in the kidney and spleen that could not be simply explained on those grounds. Eleven (61%) of 18 kidneys examined showed severe glomerular involvement with mild degrees of vascular deposition while the remaining seven showed predominantly vascular involvement. The glomerular pattern appeared to be more ominous, being significantly associated with severe proteinuria or chronic renal failure. In nine (69%) of 13 spleens examined, amyloid was confined to the walls of small and medium-sized arteries while in the remaining four, vascular involvement was less severe and amyloid was deposited mainly along the reticulin of the white pulp. Possible explanations for these different patterns included resorption and redistribution of amyloid within the body during the course of the disease, and variation in tissue deposition as a manifestation of polymorphism of amyloid proteins. The latter appeared more feasible in view of the recent demonstration of SAA polymorphism and AA heterogeneity in man.
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PMID:Histomorphological variations in systemic AA amyloidosis: clues of AA protein polymorphism. 270 47

The authors have studied 6 cases of systemic AA amyloidosis associated with ankylosing spondylitis. Renal failure occurred in all patients a mean of 19 years after the clinical onset of the rheumatic disease. Three patients progressed rapidly (between 3 months and 3 years) to end-stage renal failure. Such an outcome did not depend upon early onset of the renal impairment, degree of inflammation or treatment with colchicine. All patients were alive 2 to 10 years later, and this confirms a better prognosis than with AL amyloidosis. The utility of combining Wright's permaganate reaction with immunological methods to characterize the amyloid deposits was also confirmed. It is concluded that amyloidosis is a rare complication of ankylosing spondylitis and probably depends on a genetic predisposition. The possibility of amyloidosis should be kept in mind when proteinuria or renal failure appear in the course of ankylosing spondylitis.
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PMID:[Ankylosing spondylitis with type AA amyloidosis. 6 cases]. 297 71

Secondary amyloidosis is a rare complication of Crohn's disease, especially in pediatric patients. This report describes an 11-year-old child with Crohn's disease who developed intermittent proteinuria and thyroid enlargement at 14 years of age as the initial manifestations of secondary amyloidosis. Deterioration in renal function resulted in her death at 20 years of age. Published reports that discuss the occurrence of systemic amyloidosis in Crohn's disease and the pediatric age group are reviewed.
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PMID:Secondary amyloidosis in Crohn's disease of childhood. 376 Nov 15

A 22-year-old woman, who had been diagnosed as having rheumatoid arthritis (RA) 2 years before, was admitted to our hospital complaining of watery diarrhea (several times/day). She had been treated with low dose prednisolone (PSL) and auranofin in out-patient clinic. On admission, laboratory data showed moderate proteinuria (0.3 g/day) and positive CRP (2.7 mg/dl). Although the activity of RA was controlled by the administration of low dose methotrexate (7.5 mg/week) in addition to PSL, watery diarrhea and proteinuria did not improve. The biopsy of the stomach, rectum and kidney revealed the deposition of AA type amyloid protein, resulting in the diagnosis of secondary amyloidosis. Secondary amyloidosis has been reported as one of the common complications in RA patients, especially in old patients with a long history of RA. To our knowledge, however, there have been few reported cases who developed secondary amyloidosis so early during the course of RA as our case. We should be careful for the development of secondary amyloidosis even in young RA patients with short history of RA, when the disease is active.
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PMID:[A young woman with rheumatoid arthritis who rapidly developed secondary amyloidosis]. 755 43


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