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)

Chronic hyperglycemia is the single most important pathogenic factor in the diabetic triad: retinopathy, glomerulopathy and neuropathy. But at equal serum glucose balance, diabetics are not equally at risk of microangiopathy. Hence the importance of timely screening of patients who should be convinced to accept the constraints and risk of perfect serum glucose balance or to whom specific therapy independent from serum glucose balance could be proposed. But at present, there is no genetic or immunologic marker allowing for the individual identification of at risk patients. Attention is thus directed towards factors which may be directly involved in the pathogenesis of diabetic microangiopathy: --Special sensitivity of vascular collagen to protein glycosylation which could be reflected in the involvement of tendon and aponeurotic collagen, --platelet abnormalities of which the exacerbating role appears to be confirmed by the significant efficacy of aspirin in the treatment of nonproliferative retinopathy in insulin-independent diabetics, --rheological abnormalities which might essentially be secondary to chronic hyperglycemia, --hormonal abnormalities, in particular hypersecretion of growth hormone and/or somatomedin C, whose role has long been suspected and could be established by therapeutic trials with new somatostatin analogues. But the most recent advances concern the study of hemodynamic factors. Irreversible organic diabetic microangiopathy is thought to be preceded by a phase of reversible functional microangiopathy, characterized by increased capillary blood flow, vascular dilatation, hyperpermeability and altered regulation of flow. Thus, diabetic glomerulopathy with decreased glomerular filtration is preceded by a phase of renal "hyperfunctioning" and irreversible proteinuria is the outcome of a progressive increase in microalbuminuria, reversible at least while the levels are not too high.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Screening of subjects at high risk for diabetic microangiopathies]. 264 89

Hyperlipidemic Imai rats spontaneously develop proteinuria and glomerulosclerosis, especially in males. We investigated the effect of castration on spontaneous proteinuria and progressive renal injury in male Imai ats. Male Imai rats (n = 16) were castrated at 5 weeks of age. Body weight, blood pressure, urinary protein excretion and serum constituents were checked and compared with sham-operated control rats (n = 16) up to 24 weeks. Sham-operated group 1 (n = 5) and castrated group 2 (n = 6) underwent morphological study after 16 weeks of observation and sham-operated group 3 (n = 11) and castrated group 4 (n = 10) were followed for an additional 8 weeks and used for morphological study. Growth rate was significantly stunted in castrated rats as compared with the controls. Castration significantly reduced proteinuria almost throughout the experiment (167 +/- 84 vs. 46 +/- 24 mg/kg/day, p < 0.001, at 8 weeks and 688 +/- 211 vs. 458 +/- 97, p < 0.01, at 20 weeks). The glomerulosclerosis index was significantly higher in sham-operated control rats than in castrated rats (28.8 +/- 18.0 vs. 7.3 +/- 3.1, p < 0.01, at 16 weeks, and 92.1 +/- 35.5 vs. 39.5 +/- 8.9, p < 0.001, at 24 weeks). There were no significant differences in blood pressure, serum cholesterol, plasma renin activity, plasma somatomedin C levels between the two groups. These results raise the possibility that sex hormones may partly contribute to spontaneous proteinuria and progressive renal injury in male Imai rats.
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PMID:Castration attenuates proteinuria and glomerular injury in hyperlipidemic male Imai rats. 834 89

To determine the contribution of the ovary to the development of glomerulo-sclerosis, we investigated the effect of ovariectomy on glomerulosclerosis, using the unilaterally nephrectomized (Nx) female Sprague-Dawley rat. At 6 weeks of age, groups 2 and 3 underwent unilateral right nephrectomy and group 3 was simultaneously ovariectomized, while group 1 underwent a sham operation. Body weight, blood pressure, urinary protein, serum albumin, cholesterol, blood urea nitrogen and serum creatinine were checked every 2 months from 2 to 12 months after right nephrectomy. Control group 1, the Nx group 2 and the ovariectomized (Nx + ovariectomized) group 3 were studied morphologically at 6 and 12 months after nephrectomy. Body weight significantly increased in ovariectomized rats as compared with control and Nx rats. Nx rats became proteinuric with age. Ovariectomy significantly reduced proteinuria to the same levels in the controls. The glomerulosclerosis index was significantly higher in Nx rats than in either controls or ovariectomized rats. Ovariectomy attenuated glomerular injury in Nx rats, though not to the same levels in the control rats. Three groups showed no significant differences in either blood pressure or plasma somatomedin C. Growth hormone (GH) was significantly decreased by ovariectomy. The severity of glomerular injury and the glomerular tuft volume correlated with GH levels. Our results suggested that a decrease in plasma GH may contribute to the attenuating effect of ovariectomy on the development of glomerular injury in aging unilaterally Nx female Sprague-Dawley rats.
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PMID:Ovariectomy attenuates proteinuria and glomerular injury in unilaterally nephrectomized female Sprague-Dawley rats. 877 52

To clarify the pathogenesis of focal-segmental glomerulosclerosis, we investigated the sex-related difference and the effect of castration in Adriamycin (ADR) induced nephropathy of Sprague-Dawley rats. At 5 weeks of age, group 1 female and group 2 male rats were sham operated, and group 3 male rats were castrated. ADR 2 mg/kg was intravenously administered to all rats at 8 weeks of age twice at a 20-day interval. Body weight, blood pressure, urinary protein, and serum constituents were investigated every 4 weeks, 4-20 weeks after the second ADR injection. Each group was studied morphologically 12 and 20 weeks after the second ADR injection. ADR induced massive proteinuria in male rats, whereas it induced significantly lower proteinuria in female rats, and castration significantly reduced proteinuria of male rats to an extent equal to the levels seen in female rats. Control male rats had significantly lower serum albumin levels and a significantly greater impairment of renal function (blood urea nitrogen and creatinine levels) than the female rats or the castrated male rats at 20 weeks. The glomerulosclerosis index was significantly higher in control male rats than in female rats, and castration attenuated glomerular injury of male rats to an extent close to the levels seen in female rats, though there was a significant difference in the glomerulosclerosis index between female rats and castrated male rats. The three groups did not differ in blood pressure and plasma somatomedin C and serum growth hormone levels, whereas the plasma testosterone levels were decreased to undetectable in female and castrated male rats, resulting in a reduction of sex-related low molecular weight protein in urine. These observations suggest that sex hormones such as testosterone and estrogen and/or sex-related low molecular weight protein regulated by testosterone and estrogen may play a contributory role in sex differences in the progression of glomerulosclerosis in ADR-treated rats.
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PMID:Sex difference in progression of adriamycin-induced nephropathy in rats. 895 69