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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In juvenile diabetes there is a renal hypertrophy: glomerular volume and capillary lumen of the individual glomeruli are about twice the size of healthy ones. The hypertrophy is associated with a hyperfunction (increased glomerular filtration and tubular reabsorption). If the diabetes is strictly controlled these changes may regress, which suggests a metabolically induced hypertrophy. Long-standing diabetes is characterized by a phase of intermittent proteinuria which gradually becomes permanent. Diabetic angiopathy is the result of many years of abnormal metabolism, presumably with involvement of the growth hormone and glucose. Whereas microangiopathy is considered specific for diabetes, it is still a matter for discussion whether a diabetic macroangiopathy exists. The results of numerous investigations suggest that it does.
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PMID:[Diabetic angiopathy. A new concept of pathogenesis (author's transl)]. 40 47

The effects of growth hormone (GH) on renal structure and function were investigated in rats aged 10-16 weeks bearing a tumour secreting GH. Body weight gain, food intake, urine volume, and urinary excretion of creatinine and urea nitrogen were significantly greater in tumour-bearing rats than in controls. The tumour-bearing rats presented progressive proteinuria, hyperproteinaemia, and hyperlipidaemia. Creatinine clearance was significantly higher in experimental animals during the early experimental stage, but decreased as the glomerular lesions progressed, associated with a rise in serum creatinine levels. The glomeruli became progressively enlarged with degenerative changes of the visceral epithelial cells and capsular adhesions. In advanced stages proteinaceous material invaded the subcapsular space and the capillary lumen collapsed finally leading to glomerulosclerosis. Except for the presence of proteinaceous material and damaged epithelial cells the glomerular lesions resemble those observed experimentally after reduction of renal mass, and in diabetes mellitus. We speculate that the pathological features described are due to effects of persistently high levels of circulating GH on the glomerular cells.
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PMID:Renal pathology in rats bearing tumour-secreting growth hormone. 191 Nov 34

We evaluated the efficacy of recombinant human growth hormone (r-hGH) on corticosteroid (CS)-induced growth-impaired rats with proteinuria (passive Heymann nephritis. R-hGH (2 IU twice daily) improved growth in rats treated with 20 mg/kg per day of prednisolone succinate in our 4-week study. Although plasma hGH was significantly increased in rats treated with r-HGH, plasma insulin-like growth factor-1 levels were not different between treated and untreated rats. The food utilization rate was significantly improved by r-hGH. R-hGH did not affect proteinuria, renal function, or calcium and phosphate metabolism. Our results suggest that r-hGH may be effective in improving growth impairment due to CS administration.
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PMID:Somatic growth in corticosteroid-treated rats with passive Heymann nephritis--effects of recombinant human growth hormone on growth impairment. 191 Nov 47

Recent experimental data has implicated growth hormone in the development of glomerular sclerosis. In this study, we have examined the development and progression of glomerular and tubulointerstitial scarring in Wistar and Dwarf rats, selectively growth hormone-deficient, following subtotal nephrectomy. Wistar rats showed progressive proteinuria, hypertension and renal failure as well as severe renal scarring 120 days after subtotal nephrectomy. In contrast, growth hormone-deficient Dwarf rats had minimal proteinuria, mild renal functional impairment and moderate renal histological scarring. The difference in these functional and structural parameters between the two strains is highly significant, although both experimental groups had comparable food consumption and systemic blood pressure. The significantly smaller glomeruli and limited kidney hypertrophy over 120 days observed in Dwarf rats may account for some of the protection against glomerular sclerosis and tubulointerstitial scarring observed in that strain.
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PMID:Role of growth hormone in the development of experimental renal scarring. 192 Nov 52

Insulinlike growth factor I (IGF-I) is the mediator of the growth-promoting effects of growth hormone and has been suspected of playing a role in the pathogenesis of proliferative diabetic retinopathy (PDR). However, previous attempts to correlate IGF-I levels with PDR have yielded conflicting results. We determined IGF-I levels in a large population-based study of 682 early-onset (diagnosed before 30 yr of age) adult (greater than or equal to 18 yr old) insulin-taking diabetic subjects. PDR was found in 25% of the population. IGF-I levels were measured by radioimmunoassay. The mean serum level of IGF-I was 277 +/- 108 micrograms/L (mean +/- SD). Spearman rank correlations showed statistically significant negative correlations between IGF-I levels and age (r = -0.51, P less than 0.0001), duration of disease (r = -0.36, P less than 0.0001), and glycosylated hemoglobin (r = -0.09, P less than 0.05). There was a significant trend (P less than 0.001) toward decreasing risk of PDR with increasing IGF-I. However, after controlling for duration of diabetes, glycosylated hemoglobin, diastolic blood pressure, and the presence of proteinuria and/or creatinine greater than or equal to 265 microM in a multiple logistic regression model, IGF-I was not significantly associated with PDR. These data suggest that IGF-I may not be a risk factor for the development of PDR.
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PMID:Is insulinlike growth factor I associated with diabetic retinopathy? 222 26

Intense proteinuria in rats bearing a functioning pituitary tumor MtT SA5 was considered to be evoked by overproduction of albumin due to elevated serum growth hormone (GH). The present study revealed a striking reduction of proteinuria by bilateral adrenalectomy. Supplementation for about 6 weeks with glucocorticoids to adrenalectomized tumor-bearing rats again induced marked proteinuria, but supplementation with mineralocorticoids failed to augment proteinuria. An analysis of systemic blood pressure and renal blood flow did not yield any conclusive result. In spite of an assumption that glucocorticoids enhance GH production of the tumor based on the presence of glucocorticoid receptor in the tumor tissue, no difference was found in serum GH levels between glucocorticoid- and mineralocorticoid-supplemented adrenalectomized rats. The mechanism remains to be clarified, but modification of glomerular permeability or a change in glomerular hydraulic pressure by glucocorticoids might be considered.
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PMID:Reduction of proteinuria by adrenalectomy and its restoration by glucocorticoids in rats bearing functioning pituitary tumor. 236 33

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

In 107 patients with non-insulin dependent diabetes(NIDDM), plasma growth hormone(GH) responses during standard arginine test (0.5 g/kg of body weight) were studied and analyzed in comparison with those in 17 normal subjects. The indices of the responsiveness of GH, peak value of GH, sum of GH values(sigma GH), area of GH curve(integral of GH), sum of GH values above fasting level(sigma delta GH) and area of GH curve above fasting level(integral of delta GH) during the test (2 hr) were calculated. Data were also analyzed with multiple regression analysis using stepwise method for variable selection. Basal level of GH was significantly higher in diabetic patients than in normal subjects (2.1 +/- 1.7 vs. 1.6 +/- 0.5 ng/ml, mean +/- SD, p less than 0.05), and sigma GH and integral of GH were also higher in diabetic patients. There was a significantly positive correlation between fasting plasma glucose(FPG) and basal level of GH (r = 0.24, n = 107, p less than 0.05), and the indices of GH responses except delta GH and GH peak value (r = 0.24 to 0.31, p less than 0.05 to 0.01). Some indices of GH responses (sigma delta GH, sigma GH, integral of delta GH and integral of GH) were significantly higher in the poor control group (patients with FPG above 180 mg/dl, n = 29) of diabetic patients than in the good control group (patients with FPG below 140 mg/dl, n = 59), or in the group with no abnormal findings of retinopathy (n = 46). During the follow-up of retinopathy for 2.5 years on the average, progression of retinopathy was found in 21 out of 107 patients. Significantly higher GH, and GH in the patients with increasing severity of retinopathy were revealed retrospectively compared to the patients without it. However, there were no significant differences in these parameters between both groups matched by FPG or severity of retinopathy. Multiple regression analysis to the basal GH level and GH responses during arginine infusion as criterion variables of various predictor variables (total 44 factors: biochemical laboratory data, indices of glucose and insulin response to oral glucose load, indices of glucose response to arginine, age, age of the onset, obese index, duration of retinopathy, neuropathy, and therapy) were performed in 86 patients using forward and backward method for variable selection. Basal plasma level of GH showed close positive association with therapy and proteinuria and negative association with age and obesity. Five of 6 indices of GH responsiveness showed significant relationship with retinopathy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Growth hormone response to arginine administration in diabetics--with special reference to the multiple regression analysis in association with diabetic retinopathy]. 279 59

Growth factors such as growth hormone and insulin-like growth factor 1 (IGF-1) may be important in the pathogenesis of diabetic retinopathy. We measured serum IGF-1 in 371 diabetic patients attending a diabetic retinopathy clinic and in 73 non-diabetic control subjects. No significant difference was observed in IGF-1 level between the diabetic and control groups (168 +/- 3.9 vs 177 +/- 7.4 micrograms/l [mean +/- SE]). Within the diabetic group, there was no difference between patients with no retinopathy and those with proliferative change (198.7 +/- 8.8 vs 190.5 +/- 11 micrograms/l). After adjusting for differences in age, duration of diabetes, and presence of proteinuria, only the inactive previously proliferative group showed any significant difference from the other patient subgroups (151.8 +/- 11.5 micrograms/l; p less than 0.05). Serum IGF-1 correlated with age in the control group (r = 0.49; p less than 0.001) and to a lesser extent in the diabetic group (r = -0.23; p less than 0.05). IGF-1 levels were higher in patients with proteinuria than in those without proteinuria (196.8 +/- 10.3 vs 138.8 +/- 4.4 micrograms/l; p less than 0.001).
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PMID:Serum IGF-1 concentration in diabetic retinopathy. 296 86

Intensive proteinuria accompanied by marked renal enlargement occurs in rats bearing functioning pituitary tumor MtT SA5. Urinalysis showed that protein excretion was up to 700 mg/day, and that the excreted protein consisted mostly of albumin. However, serum total protein and albumin levels remained almost unchanged. Histological examination revealed glomerular lesions, hyaline casts in the tubules, and proliferation of the tubular epithelium. The glomerular lesions consisted of accumulation of proteinaceous material in the subcapsular space; its organization and formation of fibrous crescents was with or without epithelial crescents. Electron microscopy revealed loss of foot processes and accumulation of absorption droplets in glomerular epithelial cells. Removal of the tumor resulted in a rapid reduction in urinary protein excretion. However, proteinuria persisted for at least 4 weeks after tumor removal with levels of approximately one-fourth of those before tumor removal. Histological changes of the kidneys resolved to some extent but damage still remained in the glomerular epithelial cells 4 weeks after tumor removal. Although proteinuria in animals bearing functioning pituitary tumors has long been implicated in hyperprolactinemia, the present study suggests that proteinuria in tumor-bearing rats is a control mechanism for overproduction of albumin in the liver stimulated by elevated serum growth hormone since hyperalbuminemia and possibly the hyperfibrinogenemia would cause the elevation of blood viscosity, resulting in thrombosis, unless control mechanisms were present. This proteinuria may serve for studies of glomerular permeability disorders as a model for homologous protein-overload proteinuria.
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PMID:Proteinuria induced by transplantable rat pituitary tumor MtT SA5. Model for homologous protein-overload proteinuria. 371 38


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