Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0033687 (
proteinuria
)
24,015
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The significance of
proteinuria
during febrile infectious diseases is widely underestimated, although the more marked
proteinuria
probably signalizes a parainfectious nephropathy rather than a functional disorder. This study shows that mild
proteinuria
of less than 0.65 g/24 h (normal range less than 0.3 g/24 h using the sensitive tannine-
FeCl3
-technique) might be caused by the elevated body temperature alone. 9 out of 18 volunteers without renal disease undergoing experimental hyperthermia of 40-41 degrees C for 1-2 h did not develop a
proteinuria
according to quantitative and qualitative (SDS-PAGE) measurements. In 6/18 the amount and composition of urinary proteins changed giving a glomerular type of
proteinuria
, possibly caused by temperature related transient glomerular alterations. In 3/18 a mild glomerulopathy existed before hyperthermia, as deduced from a glomerular pattern despite a quantitatively physiological
proteinuria
, leading in all 3 to pathological
proteinuria
during hyperthermia. In all 18 volunteers alterations reversed to normal within 12 h. Therefore, the degree of
proteinuria
during febrile diseases should be considered.
Proteinuria
of less than 0.5-1 g/24 h in adults might be explained by an altered glomerular function alone.
Proteinurias
exceeding this value, with a slow regressing tendency will indicate glomerular or tubulo-interstitial diseases, caused possibly by immunologic or toxic products resulting from underlying infectious disease.
...
PMID:[Does febrile proteinuria exist?]. 663 31
Proteinuria
has been invoked as a cause of tubulointerstitial injury in chronic renal disease, and in vivo studies have suggested indirectly the particular nephrotoxicity of one urinary protein holotransferrin (Tf-Fe). However, to date there has been no direct evidence for the nephrotoxicity of Tf-Fe. To examine the potential cytotoxicity of Tf-Fe and the mechanism involved, and to compare this to another urinary protein albumin, rat proximal tubule cells were studied in primary culture. Tf-Fe at pH 6.0 caused functional and ultrastructural injury, but no cytotoxicity was seen with cells exposed to albumin, apotransferrin (transferrin), or Tf-Fe at pH 7.4. The influence of pH on Tf-Fe-induced cytotoxicity was not due to pH per se, but could be explained by an effect on Tf-Fe uptake. At pH 6.0, uptake of 125I-Tf-Fe (3.55 +/- 0.05 versus 1.25 +/- 0.10 fmol/dish, P < 0.01) and intracellular iron concentration (1.14 +/- 0.25 versus 0.46 +/- 0.23 nmol/dish, P < 0.01) were increased compared with values at pH 7.4. In contrast, pH 6.0 did not increase iron uptake from
FeCl3
. Lysine (100 mM) inhibited Tf-Fe uptake, decreased intracellular iron concentration, and attenuated Tf-Fe-induced cytotoxicity. The iron chelator des-ferrioxamine (200 microM) and hydroxyl radical scavenger dimethylpyrroline N-oxide (32 mM) abolished lactate dehydrogenase leakage induced by Tf-Fe at pH 6.0. Lipid peroxidation, as assessed by production of malondialdehyde, preceded lactate dehydrogenase leakage. In summary, holotransferrin, but not albumin, is toxic to rat proximal tubule cells, a pH-dependent effect involving its uptake into tubule cells, its iron moiety, and its lipid peroxidation.
...
PMID:Toxicity of holotransferrin but not albumin in proximal tubule cells in primary culture. 944 90
