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)

5(18.5%) of a group 27 coppersmiths exposed to cadmium fume had stone disease. When compared with a control group of assembly workers in the same factory they had evidence of renal impairment as shown by blood biochemistry and proteinuria. A greater tendency to liver damage was found in the coppersmiths. There was evidence that restrictive airways disease was more common in the coppersmiths than in the control group. Blood-cadmium concentrations were significantly higher in the coppersmiths and in the assembly workers than in a reference population.
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PMID:Clinical and biochemical abnormalities in coppersmiths exposed to cadmium. 7 55

In 26 cases of myelofibrosis, the authors investigated for possible renal impairment that can be appraised from the usual clinical, laboratory, and roentgenographic signs. No anomalies were demonstrated in 12 of these cases. In 14 (or 53%) of the patients, some anomaly was discovered : essentially proteinuria with minor alteration of renal function, but also, two cases of poorly functioning left kidney evidenced on intravenous urograms, one case of acute anuric renal failure connected with hyperuricemia, one case of hypokalemic tubulo-interstitial nephritis, and one case of glomerulonephritis with, nephrotic syndrome. This study, when compared to the literature, indicates that besides nephropathy specific to myelofibrosis and attributed to myeloid metaplasia in the kidney, serious consideration must be given to lesions due to (1) compression of the left kidney by the enlarged spleen, (2) urate precipitation in the urinary passages, and (3) a possible glomerular disorder whose mechanism remains undefined.
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PMID:[Renal lesions in myelofibrosis (author's transl)]. 22 98

The case history of a patient having multiple myeloma with a remarkably high level of Bence Jones proteinuria (more than 20 g/day) is presented. The patient has responded well to therapy, and at no stage has he shown impairment of renal function as determined by creatinine clearance studies. A review of published reports has shown that such marked Bence Jones proteinuria at presentation is rare and is usually accompanied by renal impairment and a short survival. Additional presentation data from selected patients in the MRC First Myelomatosis Trial is presented. This suggests a higher incidence of marked Bence Jones proteinuria, and underlines the lack of correlation between the quantity excreted and the degree of renal impairment. The mechanisms by which Bence Jones protein may cause renal damage are discussed.
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PMID:Multiple myeloma with massive Bence Jones proteinuria and preservation of renal function. 26 96

Eighteen out of 57 patients (31-6 per cent) suffering from Familial Mediterranean Fever (FMF) were found to have the nephrotic syndrome, histologically proven amyloidosis and progressive renal failure. In 14 cases renal function deteriorated rapidly after the first appearance of significant proteinuria, and 12 cases (66-7 per cent) required regular haemodialysis. Seven of these patients, seen in the early stages of renal impairment, were subsequently diagnosed clinically as probably having developed renal vein thrombosis. There was radiological proof of intrarenal or major renal vein occlusion in five which in one patient progressed to inferior vena cave obstruction. Treatment with heparin, plasminogen activators and fibrinogenolytic agents was disappointing although renal function has stabilized in one patient on long term oral anticoagulant therapy. It is suggested that renal vein thrombosis is common in FMF with renal amyloidosis and usually causes rapid deterioration of function and irreversible renal failure requiring dialysis. Renal phlebography may delineate clot in the main renal veins or indicate areas of reduced blood flow due to thromboses in intrarenal venules. Treatment is only partially satisfactory but there is some evidence to suggest that renal phlebography should be undertaken promptly when renal function begins to fall followed by anticoagulant therapy to prevent further thromboembolic complications.
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PMID:Renal vein thrombosis as the major cause of renal failure in familial Mediterranean fever. 86 77

Glomerular disease is associated with a limited number of signs which are easily detected by routine clinical examination and urine tests. Haematuria, proteinuria, oedema, hypertension and renal impairment occur in various combinations including classical and predictable syndromes such as acute post streptococcal nephritis and the nephrotic syndrome in children. Apart from these classical syndromes clinico-pathological correlations in glomerular disease are poor. Early renal biopsy is required to determine the extent of the glomerular disease and the long term prognosis in most patients with prolonged proteinuria and haematuria.
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PMID:Glomerulonephritis in children and adults. 94 53

Three patients with paroxysmal nocturnal hemoglobinuria accompanied by chronic renal lesions were studied. All the cases had histories of severe hemolytic anemia and repeated hemoglobinuria. The biopsy specimen of the kidney of two patients (Case 1 and Case 2) showed interstitial nephritis. Renal glucosuria, tubular proteinuria, increased urate clearance (Case 2) and reduced tubular reabsorption of phosphate (Case 3) were revealed in Case 2 and Case 3, suggesting renal tubular impairment. From the nephrological point of view, hemodynamic alteration resulting from intravascular hemolysis and severe persistent chronic anemia may primarily be responsible for the renal impairment.
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PMID:Renal impairment in patients with paroxysmal nocturnal hemoglobinuria. 117 24

Membranous nephropathy is a histological appearance which indicates a particular immunopathogenesis, but may have many basic aetiologies and is probably not a single disease. It is predominantly an appearance seen in middle-aged and elderly individuals, and in general has a slow progression over years or even decades towards remission or renal impairment in almost equal proportions. An aggressive search for associated disease is worthwhile, and one should wait to see what the evolution of proteinuria and renal function may be. If a progressive course becomes evident, then a trial of treatment with corticosteroids is worthwhile, but if this is ineffective, a more aggressive approach involving the use of alkylating agents may be justified. Cyclosporin does not appear to have a major effect in the majority of patients, and intravenous gammaglobulin is under evaluation at the moment with some encouraging results. The best treatment regime remains to be determined.
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PMID:Membranous nephropathy and its treatment. 133 86

From 1983 to 1990, 32 patients with hemorrhagic fever with renal syndrome (HFRS) were admitted to our hospital. The diagnosis was confirmed by high IgM type titers of antibodies to Hantaan virus. All patients presented with serum and urine abnormalities suggesting renal involvement. Serum creatinine was elevated and ranged between 1.8 and 14.3 mg/dl. Proteinuria ranged between 0.5 and 6.4 g/24 h. Seven patients died due to shock or hemorrhage, while 6 patients were supported by hemodialysis or peritoneal dialysis. Five of them had a complete recovery. Two patients were discharged with some degree of renal impairment which remained stable 12-15 months later. Kidney biopsy in the first patient performed 1 year after his discharge revealed some degree of interstitial fibrosis and tubular atrophy as well as an area with ischemic and sclerosed glomeruli. We conclude that HFRS in Greece is a severe disease with a high mortality rate. The disease may cause chronic renal failure in a limited number of patients.
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PMID:Hemorrhagic fever with renal syndrome in an endemic area of Greece. 135 72

To investigate plasma renin and prorenin levels in non-insulin-dependent diabetes mellitus (NIDDM) and their relation with autonomic nervous function and renal impairment, we measured plasma renin and prorenin levels in 39 NIDDM patients. The patients included 21 males and 18 females, aged 56.3 +/- 6.2. Thirty-four normal age-matched subjects served as controls. Autonomic nervous function was evaluated in 23 patients by the performance of cardiovascular reflex tests. The plasma renin concentration was measured by angiotensin I generation after the addition of an exogenous substrate. Plasma prorenin was activated by trypsin. The results showed that the plasma renin concentration was similar between NIDDM patients and normal subjects, while plasma prorenin was higher in NIDDM patients. No correlation existed between the plasma renin or prorenin levels and autonomic nervous function. The patients with abnormally high levels of prorenin also had a similarly high plasma renin level but not a high creatinine clearance (Ccr) or daily proteinuria. The plasma renin level was correlated inversely with daily proteinuria but not with Ccr. These results suggest that the high plasma prorenin levels in some diabetic patients cannot be explained by renal impairment, poor prorenin conversion or autonomic dysfunction. The hyporeninemia in some patients may be related to microvascular involvement of the kidney.
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PMID:Plasma prorenin and renin levels in non-insulin-dependent diabetes mellitus. 136 16

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


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