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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic patients who develop proteinuria show a marked increase in cardiovascular morbidity and mortality. The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain, in part, obscure. However, there is now evidence that renal disease clusters in families and that genetic factors may be of central importance in determining susceptibility. Predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. Interestingly, fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first clinical signs of renal involvement are the appearance of microalbuminuria and a small elevation in arterial pressure. Mesangial expansion accompanies these changes. Microalbuminuria is associated with abnormalities of lipoprotein profiles and higher Na+/Li+ countertransport rates. The environmental changes brought about by diabetes could lead in susceptible individuals to increased systemic and intraglomerular pressures on the one hand and to mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities may further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered, involving reduction in renal function, further hypertension, proteinuria, glomerular obsolence and hyperlipidaemia, and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Risk factors for renal and cardiovascular disease in diabetic patients. 165 64

Elevated arterial pressure in patients with obesity-hypertension is associated with an increased cardiac output and total peripheral resistance. The elevated output is related to expanded intravascular volume that increases cardiopulmonary volume, venous return, and left ventricular preload; the elevated pressure and total peripheral resistance increase afterload. This dual ventricular overload promotes a dimorphic, concentric, and eccentric hypertrophy in response to the volume and pressure overload. Increased myocardial oxygen demand results from the elevated tension in the left ventricular wall, reflecting its increased diameter and pressure, and provides physiologic rationale for the greater potential of coronary arterial insufficiency and cardiac failure. There are greater renal blood flow and lower renal vascular resistance in patients with obesity-hypertension at any level of arterial pressure. This may be offset by an increased renal filtration fraction that may favor protein deposition and glomerulosclerosis, and predisposition of obese patients for diabetes may aggravate this problem. With weight reduction, these hemodynamic derangements may be reversed: intravascular volume contracts, cardiac output decreases, and arterial pressure falls.
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PMID:Obesity and hypertension. Hemodynamic aspects. 166 10

The purpose of the study was to investigate the development of microangiopathic complications in North African sand rats with diabetes induced by a long-term standard laboratory diet. Hyperinsulinaemic rats, whether non-diabetic obese or diabetic, developed capillary basement membrane (CBM) thickening in the skin; in insulin-dependent animals, this change was diffuse. Many PAS positive areas were demonstrated in skeletal muscle and myocardium, together with evidence of microangiopathy; the primary myocardial lesion in insulin-dependent disease was ischaemic fibrosis. The kidney was also affected with marked basement membrane thickening in Bowman's capsule and glomerular capillaries; glomerulosclerosis and tubular changes were found in insulin-dependent disease. No evidence of diabetic retinopathy was found, and there was a high incidence of cataract.
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PMID:Diabetes mellitus in sand rats (Psammomys obesus): microangiopathy during development of the diabetic syndrome. 174

The major renal pathologic changes of diabetes include thickening of all renal extracellular basement membranes and mesangial matrix and, to a lesser extent, mesangial cell expansion. Two renal lesions appear critical in diabetic nephropathy. Mesangial expansion out of proportion to the size of the glomerulus is closely and inversely related to measures of peripheral capillary wall filtration surface and to clinical features of proteinuria, hypertension, and decreasing glomerular filtration rate (GFR). Arteriolar hyalinosis is related to global glomerulosclerosis, and both are correlated with the clinical features of nephropathy. These lesions are markedly advanced by the time renal dysfunction is clinically detectable. Relationships of structure and function early in the course of the diabetes have not been examined satisfactorily.
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PMID:Structural-functional relationships in type I insulin-dependent diabetes mellitus in humans. 177 56

To elucidate the characteristics of diabetic nodular lesions and the process of progression of diabetic glomerulosclerosis, kidney specimens obtained from 185 patients with non-insulin-dependent diabetes mellitus (NIDDM) were observed using light, electron, and immunofluorescence microscopes. The results suggest the following. First, there are two distinct subtypes of nodular lesions: One is formed by the progression and expansion of diffuse lesions; the other, showing a concentrically layered structure, is probably formed in the process of reconstruction of mesangiolysis. Second, there are three phases in the process of progression of diabetic glomerulosclerosis: In the first phase, arteriolosclerosis and diffuse lesions appear; in the second phase, mesangiolysis and nodular lesions develop in association with moderately advanced arteriolosclerosis; and in the third phase, exudative lesions and hyalinized glomeruli appear in association with advanced arteriolosclerosis together with advanced interstitial lesions. In the progression of the phases and in the development of mesangiolysis and layered nodular lesions, disturbed blood flow into glomeruli in consequence of diabetic arteriolosclerosis could be essential.
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PMID:Pathogenesis of diabetic nephropathy in non-insulin-dependent diabetes mellitus. 177 60

Indices of thrombocytic hemostasis were determined in 40 patients with diabetic glomerulosclerosis. It was found that patients suffering of diabetic glomerulosclerosis with chronic renal insufficiency showed signs of hypercoagulemia while changes of the thrombocytic hemostasis become of diverse values. There was a high correlation of hemostasis changes and clinical manifestations of diabetes mellitus and diabetic glomerulosclerosis. Three tests are recommended for treatment choice: hemolysate-aggregation test, determination of soluble complexes of monomer fibrin and fibrin-splitting product.
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PMID:[Changes in thrombocytic hemostasis in patients with diabetic glomerulosclerosis]. 177 40

The fetoplacental system of 132 women with diabetes mellitus and 85 healthy women was studied during the third pregnancy trimester. Blood estradiol and urinary estriol levels were found-reduced in the diabetics, particularly in those with insulin-dependent diabetes. Blood progesterone and oxytocinase levels were found unchanged. These parameters lowered in diabetic glomerulosclerosis. If pregnant diabetics develop hydramnion, their blood estradiol, progesterone, prolactin, and oxytocinase levels increased.
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PMID:[Feto-placental system in diabetes mellitus and hydramnios]. 178 35

The effect of streptozotocin (STZ) treatment on blood pressure in adult spontaneously hypertensive rats (SHR) was compared with that in neonatal SHR. Three-month-old SHR were intravenously given 10, 30 or 50 mg/kg of STZ. When STZ was given in adult SHR, weight loss, overt hyperglycemia and the reduction of blood pressure occurred dose dependently. Two-day-old pups from SHR were subcutaneously injected with 100 mg/kg of STZ. Neonatal STZ treatment did not attenuate the development of hypertension in SHR. Since neonatally STZ-treated SHR develop mild diabetic symptom with hypertension and develop mild diabetic glomerulosclerosis, they are a good model for studying vascular complications or other disorder relating to the synergism between hypertension and diabetes mellitus.
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PMID:Hypertensive diabetic rats: different effects of streptozotocin treatment on blood pressure in adult SHR and in neonatal SHR. 183 61

It was found that patients with diabetic glomerulosclerosis showed an increased intensity of blood coagulation as well as essential diverse changes in the system of fibrinolysis. These changes were more pronounced in patients suffering of diabetes mellitus than in the diabetic patients without glomerulosclerosis. It is recommended to introduce into clinical practice the Lejen method with the purpose of determining indications to heparin therapy and dynamic control of patients during treatment with anticoagulants.
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PMID:[The fibrinolysis system in diabetic glomerulosclerosis]. 186 22

The summary fibrinolytic activity of the urine (SFAU) was studied in 39 patients with diabetic glomerulosclerosis (DGS), 12 patients with diabetes mellitus (DM) without renal involvement, 8 patients with reduced glucose tolerance and 20 healthy subjects. The level of plasmin, plasminogen activators, plasminogen activation inhibitors and antiplasmins in the concentrated urine were also determined. Diabetic patients without clinical manifestations of DGS revealed a significant reduction of SFAU, plasmin activity and plasminogen activators. A significant reduction of the fibrinolytic activity of the urine was found in DGS without chronic renal failure and especially in DGS with chronic renal failure. It is concluded that reduced levels of urinary plasminogen activators may be used as an index of preclinical stages of renal involvement.
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PMID:[Fibrinolytic activity of the urine in patients with diabetic glomerulosclerosis]. 189 54


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