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MeSH Review

Proteinuria

 
 
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Disease relevance of Proteinuria

 

Psychiatry related information on Proteinuria

  • ESRD risk reduction was predicted by basal proteinuria (P < 0.01) and GFR (P < 0.0001) and was strongly dependent on treatment duration (P < 0.0001) [5].
  • The clinical and laboratory features were not significantly different from those reported in large series of patients with SLE, except for less pleuritis and a trend toward less proteinuria, hallucinations, thrombopenia, and leukopenia [6].
  • Four months after a booster injection of 16/6 Id, the young mice developed clinical manifestations of SLE, including proteinuria and leukopenia, which were seen, in milder form, in the aged mice [7].
 

High impact information on Proteinuria

 

Chemical compound and disease context of Proteinuria

  • Blood glucose levels and proteinuria [13].
  • All control patients treated with prednisone alone continued to relapse at the same rate, with all patients experiencing a return of proteinuria by seven months [14].
  • Nineteen of 24 patients in whom proteinuria developed were positive for HLA-B8 and HLA-DRW3 antigens; 14 of 15 episodes of aurothiomalate-induced proteinura and nine of 13 episodes of penicillamine-induced proteinura occurred in patients with these antigens [15].
  • The rate of development of proteinuria and mortality were significantly retarded in these conditioned mice relative to untreated controls and nonconditioned animals that received unpaired treatment with saccharin and cyclophosphamide [16].
  • Ribavirin was effective in prolonging survival, reducing the titer of antibodies to DNA, and reversing proteinuria [17].
  • Compared to no sirolimus, sirolimus use was associated with higher prevalence of proteinuria (40% vs. 76%, p < 0.0001) and higher protein excretion (378 + 997 vs. 955 + 1986 mg/day, p < 0.0001) [18].
 

Biological context of Proteinuria

  • The decrease in proteinuria did not coincide with a fall in systemic blood pressure or in the blood glucose concentration [12].
  • Similarly, patients with AGT MT and TT genotypes had higher maximal values of proteinuria than those with the MM genotype (i.e., median values, 2.5 and 3.5 vs. 2.0 g/d, respectively; P < 0.02 by Kruskal-Wallis test) [19].
  • Furthermore, administering Gas6(-/-) mice recombinant wild-type Gas6, but not Gas6 lacking a previously characterized N-terminal gamma-carboxyl group, induced massive proteinuria, glomerular cell proliferation, and glomerulosclerosis, comparable to responses seen in wild-type mice [20].
  • Lowering renal plasma flow by 24% during indomethacin therapy in seven patients resulted in a 74% reduction in proteinuria accompanied by a corresponding diminution of filtrate formed through the shunt pathway [21].
  • Cyclooxygenase inhibition resulted in normalization of glomerular eicosanoid generation rates, amelioration of proteinuria, afferent vasoconstriction, and normalization of SNPF, delta P, Kf, and GFR [22].
 

Anatomical context of Proteinuria

  • Deleting MCP-1 dramatically reduces macrophage and T cell recruitment but not proliferation, protects from kidney, lung, skin, and lymph node pathology, reduces proteinuria, and prolongs survival [23].
  • Preliminary results showed that the rats developed moderate proteinuria (100 mg/ml protein in urine), which was associated with the presence of hyaline droplets in renal tubules, on the third day [24].
  • A role for Mac-1 (CDIIb/CD18) in immune complex-stimulated neutrophil function in vivo: Mac-1 deficiency abrogates sustained Fcgamma receptor-dependent neutrophil adhesion and complement-dependent proteinuria in acute glomerulonephritis [25].
  • Also, bFGF induced proteinuria and podocyte damage in rats injected with 10% of the regular PHN-serum dose [26].
  • Disappearance of this plasma cell subset during treatment was associated with decreases in anti-double-stranded DNA (anti-dsDNA) Ab levels, proteinuria, and SLE disease activity index [27].
 

Gene context of Proteinuria

 

Analytical, diagnostic and therapeutic context of Proteinuria

References

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  12. Effect of captopril on heavy proteinuria in azotemic diabetics. Taguma, Y., Kitamoto, Y., Futaki, G., Ueda, H., Monma, H., Ishizaki, M., Takahashi, H., Sekino, H., Sasaki, Y. N. Engl. J. Med. (1985) [Pubmed]
  13. Blood glucose levels and proteinuria. Silva, F.G., Weber, C.J., Pirani, C.L., Hardy, M.A., Reemtsma, K. N. Engl. J. Med. (1979) [Pubmed]
  14. Chlorambucil treatment of frequently relapsing nephrotic syndrome. Grupe, W.E., Makker, S.P., Ingelfinger, J.R. N. Engl. J. Med. (1976) [Pubmed]
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  18. Proteinuria after kidney transplantation, relationship to allograft histology and survival. Amer, H., Fidler, M.E., Myslak, M., Morales, P., Kremers, W.K., Larson, T.S., Stegall, M.D., Cosio, F.G. Am. J. Transplant. (2007) [Pubmed]
  19. Association of angiotensinogen gene T235 variant with progression of immunoglobin A nephropathy in Caucasian patients. Pei, Y., Scholey, J., Thai, K., Suzuki, M., Cattran, D. J. Clin. Invest. (1997) [Pubmed]
  20. Essential role of Gas6 for glomerular injury in nephrotoxic nephritis. Yanagita, M., Ishimoto, Y., Arai, H., Nagai, K., Ito, T., Nakano, T., Salant, D.J., Fukatsu, A., Doi, T., Kita, T. J. Clin. Invest. (2002) [Pubmed]
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  26. Basic fibroblast growth factor augments podocyte injury and induces glomerulosclerosis in rats with experimental membranous nephropathy. Floege, J., Kriz, W., Schulze, M., Susani, M., Kerjaschki, D., Mooney, A., Couser, W.G., Koch, K.M. J. Clin. Invest. (1995) [Pubmed]
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