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Query: UMLS:C0033687 (
proteinuria
)
24,015
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
To determine whether each of glycemic control (GC), low protein diet (LPD) or administration of angiotensin converting enzyme inhibitor (ACEI) has beneficial effects on diabetic nephropathy through the different mechanisms, changes in charge and size selectivity of glomerulus and renal hemodynamics were analyzed in microalbuminuric type 2 diabetic patients after additive combination therapy (first period: GC only, second period: GC-LPD, third period: GC+LPD+ACEI). To detect improvement of the impairments of glomerular charge selectivity and size selectivity, changes in the ratio of the renal clearance of two plasma proteins with similar molecular radii and different isoelectric points (pIs) (ceruloplasmin and IgG: CRL/IgG) and changes in the ratio of the renal clearance of two plasma proteins with similar pIs and different molecular radii (
alpha2-macroglobulin
and albumin: alpha2/Alb) were examined before and after each therapy. Creatinine clearance decreased significantly in the first and third periods although slight but not significant decrease was detected in the second period. Filtration fraction was significantly decreased only in the third period. Although renal clearances of Alb, IgG and CRL were decreased in periods of all three therapies, that of
alpha2-macroglobulin
with a large molecular radius was decreased significantly only after the third therapy. Neither CRL/IgG nor alpha2/Alb changed during these three therapies. These findings suggest that each of three short-term therapies consisting of GC, GC+LPD and GC+LPD+ACEI, reduced
proteinuria
in microalbuminuric type 2 diabetic patients not through the improvement of renal size and charge selectivities, but through improvement of renal hemodynamics.
...
PMID:Effects of short-term glycemic control, low protein diet and administration of enalapril on renal hemodynamics and protein permselectivity in type 2 diabetic patients with microalbuminuria. 1077 55
Reactive oxygen species are generated during ischemia-reperfusion tissue injury. Oxidation of thymidine by hydroxyl radicals (HO*) causes formation of 5,6-dihydroxy-5,6-dihydrothymidine (thymidine glycol). Thymidine glycol excreted in urine can be used as a biomarker of oxidative DNA damage. The aim of this study was to investigate the oxidative DNA damage in patients showing immediate allograft function after kidney transplantation, and to find out whether this damage correlates with glomerular and tubular lesions. Time dependent changes in urinary excretion rates of thymidine glycol, but also of total protein, albumin, low molecular weight (alpha1-microglobulin, beta2-microglobulin) and high molecular weight proteins (transferrin, IgG,
alpha2-macroglobulin
) were analyzed quantitatively and by polyacrylamide-gel electrophoresis in six patients. Urinary thymidine glycol was determined by a fluorimetric assay in combination with affinity chromatography and HPLC. After kidney transplantation the urinary excretion rate of thymidine glycol increased gradually reaching a maximum within the first 48 hours (16.56+/-11.3 nmol/m mol creatinine, ref. 4.3+/-0.97). Severe
proteinuria
with an excretion rate of up to 7.2 g/mmol creatinine was observed and declined within the first 24 hours of allograft function (0.35+/-0.26 g/mmol creatinine). The gel-electrophoretic pattern showed a nonselective glomerular and tubular
proteinuria
. The initial nonselective glomerular
proteinuria
disappeared within 48 hours, changing to a mild selective glomerular
proteinuria
. In this period (12-48 hours) higher levels of thymidine glycol excretion were observed, when compared to the initial posttransplant phase (13.66+/-9.76 vs. 4.31+/-3.61 nmol/mmol creatinine; p<0.05). An increased excretion of thymidine glycol is seen after kidney transplantation and is explained by the ischemia-reperfusion induced oxidative DNA damage in the kidney. In the second phase higher levels of excretion were observed parallel to the change from a nonselective to a selective glomerular and tubular
proteinuria
. An explanation may be sought in the repair process of DNA in the glomerular and tubular epithelial cells, appearing simultaneously with functional recovery.
...
PMID:Urinary thymidine glycol as a biomarker for oxidative stress after kidney transplantation. 1090 Nov 87
Experimental and clinical studies show that
proteinuria
is an independent risk factor for the progression of chronic glomerular diseases and is associated with the extent of tubulo-interstitial damage. The accumulation of proteins in tubular cells induces the increased expression of a variety of inflammatory and fibrogenic cytokines, with the consequent development of interstitial inflammation, a proliferation of fibroblasts, the increased production of extracellular matrix, and the formation of interstitial fibrosis. Laboratory methods, such as immunonephelometry, can easily evaluate the glomerular component of
proteinuria
, due to the alteration of the structural integrity of the glomerular capillary wall. This alteration allows the tubular lumen to pass proteins of high and middle molecular weight (HMW and MMW proteins: IgM,
alpha2-macroglobulin
, IgG, transferrin, albumin). Using the same method and SDS-PAGE, it is possible to evaluate those tubular components of
proteinuria
that are composed of low molecular weight (LMW) proteins, such as alpha1-microglobulin (alpha1m) and beta2-microglobulin (beta2m), whose reabsorption by tubular cells-almost complete in physiological conditions-is impaired in pathological conditions. Recent studies clarified some aspects of the relationships between the components of
proteinuria
, histological lesions, prediction of outcome, and response to therapy. The extent of tubulo-interstitial damage is correlated with selectivity of
proteinuria
and IgG excretion, suggesting a possible tubulo-toxic role for IgG or for some other protein of similar molecular weight. The tubulo-interstitial lesions are also correlated with the excretion of LMW proteins, due to their impaired reabsorption. The remission of nephrotic syndrome, not predicted by the amount of
proteinuria
, is highly predicted by the selectivity index or IgG excretion in membranous glomerulonephritis (MGN) and focal segmental glomerulosclerosis (FSGS). Progression to chronic renal failure is better predicted both by the glomerular component (selectivity index, IgG excretion) and by the tubular component of
proteinuria
(alpha1m, beta1m, LMW proteins), than by 24-hour
proteinuria
. The response to therapy in MGN and FSGS is dependent on the excretion of IgG and alpha1m. In conclusion the composition of
proteinuria
can easily be assessed using automated methods, and it is useful to evaluate the relationship of
proteinuria
with histological lesions to predict the functional outcome and response to therapy in primary glomerulonephritis.
...
PMID:[Composition of proteinuria in primary glomerulonephritides: association with tubolo-interstitial damage, outcome and response to therapy]. 1452 95
Basal glomerular membrane represents mechanical and electrical barrier for passing of the plasma proteins. Mechanical barrier is composed of cylindrical pores and filtration fissure, and negative layer charge in exterior and interior side of basal glomerular membrane, made of heparan sulphate and sialoglycoprotein, provides certain electrical barrier. Diagnostic strategy based on different serum and urine proteins enables the differentiation of various types of
proteinuria
. Depending on etiology of
proteinuria
it can be prerenal, renal and postrenal. By analyzing albumin, alpha1-microglobulin, immunoglobulin G and
alpha2-macroglobulin
, together with total protein in urine, it is possible to detect and differentiate causes of prerenal, renal (glomerular, tubular, glomerulo-tubular) and postrenal
proteinuria
. The adequate and early differentiation of
proteinuria
type is of an immense diagnostic and therapeutic importance.
...
PMID:[Proteinuria: the diagnostic strategy based on determination of various urinary proteins]. 1530 17
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