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 a group of 75 patients with systemic lupus erythematosus (SLE), 30 patients with lupus nephropathy presenting concomitant changes of the CIC level, of the complement system (C3 and C1q factors) and proteinuria were chosen for the study. In these 30 patients, no statistically significant correlation was observed between CIC level and the value of serum complement. Low serum complement was observed in 89% of the cases while low complement values associated with increases of the CIC level were observed only in 57.8% of the cases. From the values of the C3 and C1 complement factors it results that in 76.6% of the cases of lupus nephropathy the activation of complement was achieved in the classical way. The value of proteinuria presented no significant correlation with any of the parameters investigated. The serum immunogram presented varied aspects and the components of the CIC structure revealed a great diversity of this structure.
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PMID:Circulating immune complexes and the complements system in lupus nephropathy. 149 64

In an uncontrolled trial, patients with IgA nephropathy (IgAN) were treated with drugs that can alter the intestinal mucosal permeability to food antigens. These drugs are known to ameliorate urinary abnormalities and histological lesions of IgAN associated with ulcerative colitis or Crohn's disease [5-aminosalicylic acid (5-ASA)] or to prevent, in mice, the induction of IgAN-like disease by oral immunization [disodium cromoglycate (SCG)]. Nine patients [serum creatinine (s-Cr) less than 2 mg/dl; 24-hour proteinuria higher than 1.5 g, but not nephrotic) were treated with 5-ASA (2.4 g/day for 6 months); 9 similar patients were treated with SCG (400 mg/day for 6 months); the follow-up extended to 6 months after stopping therapy. The 5-ASA group showed a slight but not significant decrease in s-Cr, 24-hour/proteinuria, IgA circulating immune complexes (IgA-CIC) and IgA rheumatoid factor (IgA-RF); serum beta 2-microglobulin and serum IgA were unchanged; 2 of 9 treated patients showed, after 6 months of therapy, a reduction in proteinuria of more than 50% that lasted for the subsequent 18 months. The SCG-treated group showed a slight but not significant increase in 24-hour proteinuria and a significant decrease in serum IgA; unchanged were s-Cr, IgA-CIC, IgA-RF, serum beta 2-microglobulin; no patient treated with SCG showed a reduction in proteinuria of more than 50%. At the dosages and for the periods used, 5-ASA and SCG did not show a significant influence on clinical and laboratory parameters of disease in IgAN; other trials with increased dosages are warranted to definitely ascertain the possible therapeutic role of these drugs in IgAN.
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PMID:Low doses of drugs able to alter intestinal mucosal permeability to food antigens (5-aminosalicylic acid and sodium cromoglycate) do not reduce proteinuria in patients with IgA nephropathy: a preliminary noncontrolled trial. 163 May 44

Sodium cromoglycate (SCG), an antiallergic agent, is an effective drug in an experimental model for IgA nephropathy. The present report concerns a preliminary trial of patients with IgA nephropathy and proteinuria (greater than 1.0 g/d), which was conducted to determine the therapeutic value of SCG. Thirty patients were divided into two groups: one group (n = 15) was given oral SCG (1,200 mg/d) for 16 weeks after an observation of 4 weeks (SCG group), and the other group (n = 15) was observed without the changes of prescription (control group). No fluctuations were noted in proteinuria during the observation period in both groups. Proteinuria in the SCG group slowly decreased throughout the time course; however, a significant reduction was observed at 16 weeks as compared with that of the control group. On the other hand, no significant changes were noted in creatinine clearance (Ccr), serum albumin (s-alb), serum IgA (s-IgA), and IgA-CIC between groups. Five of 15 patients, designated "responders", showed a reduction in proteinuria of more than 50% of the pre-value (average value of observations period). The responder and nonresponder groups were comparable in clinical and histopathological data at the beginning of the trial. Nevertheless, no significant correlations arose concerning any point. Short-term SCG therapy may be beneficial in reducing proteinuria in some patients with IgA nephropathy. Allergic reactions may participate in the pathogenesis of this disease.
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PMID:Sodium cromoglycate therapy in IgA nephropathy: a preliminary short-term trial. 210 38

Forty seven patients with IgA glomerulonephritis (GN) were studied. The males predominated among them--the ratio males-female--2,9:1. The first clinical manifestations were macroscopic hematuria (in 2/3 of the cases) or only urine changes--low-degree proteinuria and microscopic erythrocyturia. As early as the establishment--38,2 per cent of the patients had elevated arterial pressure, and it reached, 59,5 per cent during the follow-up period. Anemia was rare. Manifestations of nephrotic syndrome were absent. ESR was normal in 1/3 of the employees or slightly accelerated. Chronic renal insufficiency developed 6,31 per cent of the patient all of them males. Terminal renal insufficiency developed 8 patients. The elevated arterial pressure, proteinuria over 2g/24 h, accelerated ESR, high serum levels of IgA, the longer duration of the disease and higher age of the patients to a certain extent--were unfavourable prognostic criteria. The basic immune deviations of IgA GN are the high serum levels of IgA (in 53,1% of the patients) and to a lower extent of IgG (in 17% of the patients) as well as the reduced serum levels of C3 (in 31,9% of the patients). CIC are not a frequent finding. The percentage of ERF is lower than in the healthy subjects. The treatment with a combination of azathioprine (acenocoumarol, indomethacin or levamisole) has no effect on the clinical manifestations and evolution.
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PMID:[Clinical, immunological and therapeutic research in mesangial immunoglobulin-A glomerulonephritis]. 653 70

Dent's disease, an X-linked renal tubular disorder, is a form of Fanconi syndrome which is characterized by proteinuria, hypercalciuria, nephrocalcinosis, kidney stones and renal failure. Previous studies localised the gene responsible to Xp11.22, within a microdeletion involving the hypervariable locus DXS255. Further analysis using new probes which flank this locus indicate that the deletion is less than 515 kb. A 185 kb YAC containing DXS255 was used to screen a cDNA library from adult kidney in order to isolate coding sequences falling within the deleted region which may be implicated in the disease aetiology. We identified two clones which are evolutionarily conserved, and detect a 9.5 kb transcript which is expressed predominantly in the kidney. Sequence analysis of 780 bp of ORF from the clones suggests that the identified gene, termed hCIC-K2, encodes a new member of the CIC family of voltage-gated chloride channels. Genomic fragments detected by the cDNA clones are completely absent in patients who have an associated microdeletion. On the basis of the expression pattern, proposed function and deletion mapping, hCIC-K2 is a strong candidate for Dent's disease.
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PMID:Isolation and partial characterization of a chloride channel gene which is expressed in kidney and is a candidate for Dent's disease (an X-linked hereditary nephrolithiasis). 787 26

Mutations in ClC-5 (chloride channel 5), a member of the ClC family of chloride ion channels and antiporters, have been linked to Dent's disease, a renal disease associated with proteinuria. Several of the disease-causing mutations are premature stop mutations which lead to truncation of the C-terminus, pointing to the functional significance of this region. The C-terminus of ClC-5, like that of other eukaryotic ClC proteins, is cytoplasmic and contains a pair of CBS (cystathionine beta-synthase) domains connected by an intervening sequence. The presence of CBS domains implies a regulatory role for nucleotide interaction based on studies of other unrelated proteins bearing these domains [Ignoul and Eggermont (2005) Am. J. Physiol. Cell Physiol. 289, C1369-C1378; Scott, Hawley, Green, Anis, Stewart, Scullion, Norman and Hardie (2004) J. Clin. Invest. 113, 274-284]. However, to date, there has been no direct biochemical or biophysical evidence to support nucleotide interaction with ClC-5. In the present study, we have expressed and purified milligram quantities of the isolated C-terminus of ClC-5 (CIC-5 Ct). CD studies show that the protein is compact, with predominantly alpha-helical structure. We determined, using radiolabelled ATP, that this nucleotide binds the folded protein with low affinity, in the millimolar range, and that this interaction can be competed with 1 muM AMP. CD studies show that binding of these nucleotides causes no significant change in secondary structure, consistent with a model wherein these nucleotides bind to a preformed site. However, both nucleotides induce an increase in thermal stability of ClC-5 Ct, supporting the suggestion that both nucleotides interact with and modify the biophysical properties of this protein.
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PMID:Nucleotides bind to the C-terminus of ClC-5. 1668 97