Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tenascin (TN), a large oligomeric glycoprotein, is a recently described component of the extracellular matrix (ECM). Previous reports focusing largely on the role of TN in nephrogenesis have documented the strong expression of TN in embryonic kidney tissue and implied an important role for TN in nephrogenesis. However, the expression of TN in normal and pathologic kidneys in adults has not been systematically evaluated. In this study immunohistochemical staining for TN was applied to 184 renal specimens diagnosed as: normal kidney (23 cases); minimal change disease and its variants (8); mesangial proliferative glomerulonephritis (GN) including IgA nephropathy and mesangial proliferative lupus nephritis (9); endocapillary proliferative GN including membranoproliferative GN, lupus nephritis, and post-infectious GN (25); crescentic GN (11); membranous GN (19); focal segmental sclerosis (15); thrombotic microangiopathy (8); amyloidosis (5); diabetic nephropathy (9); primary tubulointerstitial nephritis (14); transplant rejection (14); and ischemia (24). It was found that: (a) there was unequivocal global diffuse staining limited to the mesangium in normal kidney; (b) regardless of the etiologies and the morphologic types of glomerular disease, whenever there was expansion of the ECM, whether in the mesangial, endocapillary, or extracapillary spaces, there was a concomitant and proportional in situ increase in the TN staining; (c) globally sclerotic glomeruli, regardless of causes, showed diffuse, strong staining, especially in the subcapsular fibrous deposition seen in ischemic sclerosis; (d) non-sclerotic glomeruli showing early ischemic change uniformly displayed a marked decrease or complete loss of staining; (e) in cases of thrombotic microangiopathy, there was segmental or global staining of the capillary wall, probably corresponding to the enlarged lamina rara interna; (f) all nodular lesions in diabetic glomerulosclerosis showed strong staining, but in several of them this staining was much more pronounced in the periphery than in the center of the lesion. Our study proves that TN is probably a component of the normal mesangial matrix, that TN is an ubiquitous component of the expanded glomerular ECM in pathologic conditions regardless of morphologic subtypes, and that further studies on the cell types and mechanisms responsible for TN synthesis may provide a new venue for the understanding of the process of glomerular sclerosis.
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PMID:Tenascin is an important component of the glomerular extracellular matrix in normal and pathologic conditions. 751 Mar 49

A number of changes in intrarenal hemodynamics and morphology are characteristic of diabetic nephropathy. These changes include: increases in intraglomerular pressure and volume, glomerular capillary permeability to macromolecules, and mesangial matrix expansion. Most antihypertensive drugs attenuate some of the increases in these parameters. Certain antihypertensive agents, however, have effects on all these parameters. Studies in animal models of diabetes demonstrate that the angiotensin-converting enzyme (ACE) inhibitors reduce both intraglomerular volume and pressure, mesangial matrix expansion, and albuminuria. The calcium antagonists TA-3090 (diltiazem-like) and verapamil recently have been shown to have most of these effects. Conversely, the dihydropyridine calcium antagonists (nifedipine, felodipine, nitrendipine) do not attenuate increases in most of these parameters. In several clinical studies, nifedipine either did not affect or increased urinary albumin excretion in diabetic patients with renal insufficiency. Moreover, in animal models of diabetes, most dihydropyridine compounds do not prevent progression of glomerulosclerosis in spite of blood pressure control. Although the majority of clinical studies support the concept that reduction of arterial pressure preserves renal function, recent long-term clinical studies show that ACE inhibitors and heart-rate-lowering calcium antagonists (diltiazem, verapamil) attenuate progression of diabetes to a greater extent than most other agents do.
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PMID:Antihypertensive therapy and progression of diabetic renal disease. 751 95

Glomerular hyperfiltration is a candidate marker for diabetic nephropathy in insulin-dependent diabetic patients since it can reflect elevated glomerular capillary pressure, a cause of glomerulosclerosis. We studied the potential contribution of several dietary components to glomerular hyperfiltration during a cross-sectional study of 110 consecutive normotensive, non-proteinuric insulin-dependent patients with respect to glomerular filtration rate (GFR) and food intake. GFR was measured using the 51Cr-EDTA plasma disappearance technique. Glomerular hyperfiltration was defined as GFR > 137 ml.min-1 1.73 m-2 (mean +2 SD of age-matched healthy controls). Food intake was recorded with a computer-assisted programme. Thirteen patients displaying glomerular hyperfiltration ingested more protein (1.60 +/- 37 vs 1.38 +/- 0.34 g.kg-1 body weight.day-1; p = 0.032) and more fat (1.70 +/- 0.54 vs 1.39 +/- 0.44 g.kg-1 body weight.day-1; p = 0.022) than other subjects, although their total energy intakes were similar. Univariate regression analysis showed that GFR was positively related to both protein (r = 0.28; p = 0.003) and fat (r = 0.25; p = 0.007) intakes and negatively related to age (r = -0.29; p = 0.002). Stepwise multivariate regression analysis indicated 2 independent determinants for GFR: age (F = 15.26) and fat intake (F = 13.15). Excess fat intake may contribute to glomerular hyperfiltration in insulin-dependent diabetes.
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PMID:Relationship between fat intake and glomerular filtration rate in normotensive insulin-dependent diabetic patients. 755 7

Recently, the tubulo-interstitial lesions in diabetes mellitus (DM) have become of greater interest, as well as, glomerulosclerosis. From the view points of tubular function, a variety of changes, including tubular proteinuria and transport of sodium, glucose, and divalent ions have been known until the present time, although the details remain to be elucidated. Morphologically the interstitial fibrosis and the thickening of tubular basement membrane were pointed out to be important features in incipient or overt diabetic nephropathy of insulin-dependent DM patients. We found the expansion of interstitium even in the area without hyalinized glomeruli and atrophic tubules in normo- and microalbuminuric non-insulin dependent DM patients by semiquantitative evaluation of biopsy specimens. Further studies of the mechanisms will be necessary to clarify the mechanism of the development of diabetic nephropathy.
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PMID:[The renal tubulointerstitium in diabetes mellitus]. 756 38

We examined the effect of two endogenous antioxidant agents, taurine and vitamin E, on renal function in experimental diabetes. Male Sprague-Dawley rats, rendered diabetic with streptozocin (STZ), were assigned to one of the following groups: 1) untreated; 2) insulin treatment with 6 U Ultralente insulin/day in two doses; 3) taurine supplementation by 1% taurine in drinking water; and 4) vitamin E supplementation at 100 IU vitamin E/kg chow. Animals were kept for 52 wk. The survival rate was similar (70-90%) in all groups except vitamin E-treated animals, of which 84% died by 6 mo. At 52 wk, glomerular filtration rate was elevated in untreated and taurine-treated STZ rats compared with normal or insulin-treated diabetic rats. Taurine supplementation reduced total proteinuria and albuminuria by nearly 50%. This treatment also prevented glomerular hypertrophy, preserved immunohistochemical staining for type IV collagen in glomeruli, and diminished glomerulosclerosis and tubulointerstitial fibrosis in diabetic animals. The changes in renal function and structure in taurine-treated diabetic rats were associated with normalization of renal cortical malondialdehyde content, lowering of serum free Fe2+ concentration, and decreased formation of the advanced glycooxidation products, pentosidine, and fluorescence in skin collagen. Administration of the vitamin E-enriched diet exacerbated the nephropathy in STZ-diabetic rats. In addition, vitamin E supplementation increased serum free Fe2+ concentration, enhanced renal lipid peroxidation, and accelerated the accumulation of advanced glycosylation end products (AGEs) in skin collagen. We conclude that administration of taurine, but not vitamin E, to rats with STZ-diabetes ameliorates diabetic nephropathy. The beneficial effect of taurine is related to reduced renal oxidant injury with decreased lipid peroxidation and less accumulation of AGEs within the kidney.
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PMID:Taurine ameliorates chronic streptozocin-induced diabetic nephropathy in rats. 757 92

The magnitude of type II diabetic nephropathy dilemma is observable in the growing number of diabetic patients with end-stage renal lesion receiving various modalities of treatment. Progressive glomerulopathy associated with proteinuria and hypertension is strongly causative of renal failure and mortality in diabetic patients. Besides hypertension, diabetes exceeds all other glomerulopathies in causing end-stage renal failure. Alterations in glomerular structure and function observed in diabetic patients are implicated in the development and progression of renal derangement. Diabetic glomerulosclerosis, an aggregate of structural and functional perturbations of the kidney, is indicated by alterations in the accumulation of extracellular matrix components, The pathology, epidemiology, risk factors, and other dependent variables may throw some light in the pathogenetic mechanisms and the prevention, treatment, and management modalities of type II diabetic nephropathy.
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PMID:Type II diabetic nephropathy in perspective. 773 45

Urokinase (u-PA) dissolves and removes fibrin deposits in the renal secretory pathways in various renal diseases. During pregnancy nephropathy creates a problem in preeclampsia and diabetes, but the underlying mechanism of glomerular damage is different. Preeclamptic nephropathy is characterized as 'glomerular endotheliosis' with hypertrophy of the intracapillary cells, and diabetic nephropathy as 'glomerulosclerosis' with hyaline deposits. The role of fibrin deposition for the etiology of renal damage in preeclampsia is controversial. Changes of the urinary secretion of u-PA may reflect the type of glomerular damage. Our hypotheses were that renal insufficiency is associated with a low u-PA activity in both conditions, and that severe disease is parallel to declining concentrations of u-PA. We compared the glomerular filtration rate, S-Creatinine and S-Urate with urinary u-PA excretion in 24 hypertensive and 20 diabetic pregnant women. In diabetic patients, a low u-PA concentrations was associated with an impaired renal function. In hypertensive pregnancy, the u-PA excretion did not reflect the severity of the hypertensive disease or renal function. No association was found between u-PA excretion and renal function post partum in any group. We conclude that renal urokinase activity plays a role for renal function in diabetic but not in hypertensive pregnancy.
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PMID:Renal function and urinary urokinase in hypertensive and diabetic pregnancies. 782 57

Formation of diabetic glomerulosclerosis was followed by the electron microscopy of 21 puncture renal biopsy and 12 incisive pancreatic biopsies from patients with insulin-dependent diabetes mellitus. The influence of the B-cell destruction and the decrease or absence of their activity (the presence of serum C-peptide) on the degree of renal damage and clinical symptoms of the diabetic nephropathy (proteinuria, hypertension) is noted. Dynamics of the diabetic glomerulosclerosis formation is as follows: 1st group--thickening of capillary basal membrane in the glomeruli, mesangial ectopy, formation of nodules at the periphery of loops; 2nd group--increase of the mesangial matrix, doubling of the glomerular capillary basal membrane, hyalin droplets in the capsule membrane. 4 stages in the development of diabetic glomerulopathy are distinguished: diabetic segmentary mesangioproliferative glomerulonephritis, mesangiolysis, two stages of glomerulosclerosis progression. Duration of the disease more than 15 years predetermines the development of diabetic glomerulosclerosis.
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PMID:[Diabetic glomerulosclerosis--a prolonged stage of diabetic glomerulopathy]. 784 6

We present a 23-year-old woman with a 7-year history of insulin-dependent diabetes mellitus (IDDM) who became pregnant. At the 23rd week of pregnancy she exhibited the signs and symptoms (hypertension, edema, proteinuria) of both diabetic nephropathy and preeclampsia. A cesarean section was successfully performed. The proteinuria persisted for more than 3 months after delivery. Renal biopsy confirmed the diagnosis of diabetic glomerulosclerosis together with the renal findings attributable to preeclampsia. The rapid acceleration of diabetic nephropathy in this patient was attributed to preeclampsia. We therefore recommend that patients with DM be followed closely during pregnancy in an attempt to prevent the acceleration of renal damage by preeclampsia.
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PMID:Renal complications during pregnancy in a patient with diabetes mellitus. 785 67

The characteristic features of OLETF rats are: (1) late onset of hyperglycemia (after 18 weeks of age); (2) a chronic course of disease; (3) mild obesity; (4) clinical onset of diabetes mellitus (DM) mostly in males; (5) hereditary trait: (a) multiple recessive genes are involved in the induction of DM; (b) rat MHC, RT1 has no diabetogenic effect; (c) control strain, LETO appears to share some of diabetogenic genes with OLETF rats; (d) female OLETF rats also carry diabetogenic genes; and (e) one of the diabetogenic genes, designated as odb-1, is transmitted linked with the X-chromosome of OLETF rats, however testosterone is an important factor involved in developing diabetes; (6) the changes of pancreatic islets can be classified into three stages: (1) an early stage (at less than 9 weeks of age) mild lymphocyte infiltration; (2) a hyperplastic stage (10-40 weeks of age); hyperplastic change and fibrosis in or around islets; (3) a final stage (at more than 40 weeks of age) showing atrophy of islets; (7) diabetic nephropathy; (a) diffuse glomerulosclerosis; (b) nodular lesion (thickening of basement membranes, mesangial proliferation, fibrin cap). These clinical and pathologic features of disease in OLETF rats resemble those of human NIDDM.
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PMID:OLETF (Otsuka Long-Evans Tokushima Fatty) rat: a new NIDDM rat strain. 785 27


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