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Query: UMLS:C0011881 (
diabetic nephropathy
)
10,836
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The term
diabetic nephropathy
includes the Kimmelstiel-Wilson intercapillary glumerulosclerosis (1936), arterio-arteriolosclerotic changes and pyelonephritis. In principle,
diabetic nephropathy
becomes more frequent with increasing duration of diabetes mellituus. Pyelonephritis is 4 to 5 times more frequent in diabetics than in the general population. Elderly
overweight
women are particularly at risk. - Only the nodular intercapillary glomerulosclerosis and not the diffuse or exudative form is specific for diabetes mellitus. It is found in 20-40% of all diabetics who have had the disease for 10-15 years. Whether the microangiopathy is typical of diabetes mellitus remains to be seen. Due to the intense cardiovascular changes, possible disorders of brain and liver function and infection, the prognosis of renal insufficiency is considerably worse in diabetics than in non-diabetics.
...
PMID:[Diabetic nephropathy (author's transl)]. 81 41
Diabetes may be associated with systolic hypertension secondary to atherosclerosis, renal hypertension secondary to
diabetic nephropathy
, and essential hypertension. The latter is by far the most prevalent, and a wealth of epidemiologic data suggests that such an association is independent of age and obesity. Considerable evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive subjects, whether obese or of normal body weight, are compared to age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. With the use of the glucose clamp technique coupled with tracer glucose infusion and indirect calorimetry, it can be shown that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal, and is directly correlated with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms--sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and altered muscle fiber composition. Physiologic maneuvers such as caloric restriction in the
overweight
individual and regular physical exercise can improve tissue sensitivity to insulin; good preliminary evidence shows that these measures can also lower blood pressure in both normotensive and hypertensive individuals. A strong case can therefore be made for the use of physiologic intervention in the treatment of essential hypertension.
...
PMID:The association of essential hypertension and diabetes. 268 84
In July 1989, 230 non-insulin-dependent subjects were identified in the James Bay Cree population through medical chart review of physician diagnosed diabetes mellitus cases. Data extracted from the medical files included type and rate of complications, life-style, anthropomorphic and metabolic descriptors as well as clinical care practices. Mean age at diagnosis was 48.3 years and mean duration of illness at time of study was 60.4 months. Furthermore, 77.3% were
overweight
and 65.4% obese. Microvascular disease (
diabetic nephropathy
or retinopathy) was the most frequent group of complications (19.6%). Moreover, 76.4% of the Cree diabetics showed poor glycemic control. Diet combined with oral hypoglycemic medication was the current treatment of choice. A medical practice profile was produced in order to provide a comparison basis with recommended baseline care. Diabetes is becoming a major illness in the native population of Canada. Health promotion strategies are of some urgency in order to contribute to the control of diabetes.
...
PMID:Descriptive epidemiology of non-insulin-dependent diabetes mellitus in the James Bay Cree population of Quebec, Canada. 831 19
Hyperlipoproteinemia is one of the main coronary risk factors. Lipid metabolism disorders occur in about 40-60% of patients with NIDDM. Hyperlipidemia in diabetics is related to diabetes control, presence of
diabetic nephropathy
, diet, some drugs and genetic factors. Lipid metabolism disorders in NIDDM comprise qualitative changes--usually increase of serum triglyceride concentration and decrease of HDL--cholesterol, and qualitative changes of lipoprotein composition, glycation and oxidation. The first steps of hypolipemic therapy are good control of diabetes, reduction of
overweight
, hypolipidemic diet, and if a goal level is not achieved--farmacotherapy. Hypolipidemic treatment should be relevant in reduction of cardiovascular diseases in diabetic patients.
...
PMID:[Lipid disorders in non-insulin dependent diabetes--principles of treatment]. 899 31
Early detection and adequate treatment of complications of diabetes mellitus (DM) are important for many patients in maintaining independence and ability to work. Diabetic retinopathy cannot be prevented. Limitation of damage is possible by aiming for normoglycaemia and normotension. While exudative as well as proliferative retinopathy can occur without any visual symptom, regular ophthalmological examination is necessary for timely laser coagulation. Fundus photography for screening is applicable under certain conditions; fluorescence angiography can be useful in patients with understood deterioration of visual acuity or diabetic maculopathy. In many patients foot disease can be prevented by simple measures: examining the foot at least once a year, recognition of the foot with a high level of risk, education of patient and family, adapted shoes and preventive foot care. Treatment of a foot ulcus consists of relief of mechanical pressure, repair of disturbed skin circulation, treatment of infection and oedema, optimal metabolic control, frequent local wound care and education. Patients with a diabetic foot have to be thoroughly followed up for the rest of their lives. For patients with
diabetic nephropathy
cardiovascular complications are the main causes of morbidity and mortality. Of all patient with DM older than 10 years urine has to be examined for loss of albumin at least once a year. Treatment of nephropathy consists of non-smoking, sufficient physical exercise, reduction of
overweight
, well-composed nutrition and particularly treatment of hypertension. Diagnosing cardiovascular diseases in patients with DM is in principle the same as for other patients. Treatment of hypercholesterolaemia has to be based on an absolute risk of 20% for cardiovascular disease in the following 10 years. The limit for treatment will be reached earlier in the presence of microalbuminuria, persistent high HbA1c > 8.5%, triglyceride concentration > 2.0 mmol/l, or a positive family history with myocardial infarction < 60 years. In proven cardiovascular disease one needs to strive for optimalization of the glucose metabolism, non-smoking and if necessary drug therapy.
...
PMID:[CBO guidelines on diagnosis, treatment, and prevention of complication in diabetes mellitus: retinopathy, foot ulcers, nephropathy and cardiovascular diseases. Dutch Institute for Quality Assurance]. 1071 45
Experimental studies have demonstrated that proteins filtered by the glomerulus induce a proliferation of proximal tubular cells accompanied by an increased synthesis of many vasoactive and proinflammatory substances. The appearance of interstitial cellular infiltrates, a well-known finding in proteinuric diseases, precedes progressive tubulointerstitial fibrosis. Activation of the transcription factor kappaB (NF-kappaB) plays a pivotal role in the renal damage induced by proteinuria. In this scenario, any therapeutic intervention that reduces proteinuria should be beneficial for the kidney. Drugs that block the renin-angiotensin system [angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists (ARA)] have repeatedly shown striking antiproteinuric and renoprotective properties, both in experimental and clinical studies. Studies in patients with type 1 and type 2
diabetic nephropathy
as well as in non-diabetic nephropathies have confirmed that the renoprotection obtained with ACEI/ARA is closely related with their antiproteinuric effect and is largely independent of blood pressure changes. However, resistance to the antiproteinuric effect of ACEI/ARA is a common clinical observation. Several therapeutic measures (that is, adequate blood pressure control, early introduction of ACEI/ARA, dietary protein restriction, low salt diets, weight loss in
overweight
patients, addition of a diuretic, increasing ACEI/ARA dose titrated against proteinuria levels, combined therapy ACEI plus ARA, addition of drugs with antiproteinuric effect such as non-dihydropiridine calcium channel blockers or NSAIDs) may increase the proteinuria reduction induced by ACEI and ARA.
...
PMID:Renal damage associated with proteinuria. 1241 Aug 54
The red cell membrane Li+/Na+exchange is a heteroexchange that operates in either direction across the cell membrane. It binds either Li+ or Na+ on one side of the membrane and it exchanges the transported species for either Li+ or Na+ on the opposite side in a stoichiometric ratio of 1:1. In the population, Li+/Na+exchange is unimodally distributed but skewed to the right. Such distribution results from superimposition of two normal distributions. Many laboratories have shown that red-cell Li+/Na+ exchange is increased in patients with essential hypertension, compared with normotensive controls. Among the various alterations of cell membrane cation transport reported in hypertension, the increase of red-cell Li+/Na+ exchange has been most widely investigated and confirmed. Moreover, increased Li+/Na+ exchange has been found in some clinical conditions related to hypertension, such as
overweight
and diabetes. Among diabetic patients, Li+/Na+ exchange is particularly high in patients with nephropathy, hypertension, and microalbuminuria, leading to the hypothesis that it can be considered a cellular marker of the risk of developing
diabetic nephropathy
. Furthermore, it is associated with severe and drug-resistant hypertension, insulin resistance, vascular and cardiac hypertrophy, hyperlipidemia, obesity, family history of hypertension, and of major cardiovascular accidents suggesting that high Li+/Na+ exchange could be a biochemical marker for increased cardiovascular risk. Regardless of its the pathophysiological significance, its measurement could be of clinical use as an intermediate phenotype of increased cardiovascular risk.
...
PMID:The Li+/Na+ exchange in hypertension. 1270 53
Overweight
/obesity represent an underestimated risk factor of renal disease. The incidence of obesity-related glomerulopathy (ORG) tremendously increased within the last decade. The first sign of renal damage in
overweight
conditions is microalbuminuria or proteinuria, indicating the potential risk of its progression to renal insufficiency and the development of premature cardiovascular events. In the early stage of obesity renal hemodynamics are characterized by a renal hypercirculation and glomerular hyperfiltration, particularly in the presence of hypertension. The hyperfiltration is especially harmful in patients with pre-existing inflammatory and metabolic renal disease, or under the conditions of reduced renal mass. Histopathologically, ORG is characterized by glomerulomegaly with/without signs of focal segmental glomerulosclerosis. Pathogenetically, numerous factors are involved, e.g. enhanced glomerular capillary pressure, adrenergic nerve overactivity, inappropriate activation of the renin-angiotensin-aldosterone system, insulin resistance, hyperinsulinemia and hyperleptinemia, dyslipidemia, enhanced clotting tendency and sodium retention.
Diabetic nephropathy
is one of the most serious complications of obesity-induced diabetes. In the industrial nations type 2 diabetes is the single most frequent cause of end-stage renal disease. After kidney transplantation,
overweight
/obesity is associated with a less favourable prognosis for the survival of the graft and the patient. Incidence of renal cell carcinomas is enhanced in
overweight
/obesity. Obesity-related renal disease may be prevented/postponed by an early weight reduction, by dietary intervention combined with physical exercise. In the advanced stages of renal disease benefits of weight reduction are minimal. Concomitant administration of angiotensin-converting-enzyme inhibitors or angiotensin II receptor 1 blockers exerts antiproteinuric effects and thereby aid in retarding the disease progression. Aimed prevention and treatment of obesity represent a challenge for the healthcare system. The concerted action of physicians, patients and the public health authorities is needed.
...
PMID:[Overweight and obesity--risk factors in the development and progression of renal disease]. 1532 63
Few large-scale epidemiologic studies have quantified the possible link between obesity and chronic renal failure (CRF). This study analyzed anthropometric data from a nationwide, population-based, case-control study of incident, moderately severe CRF. Eligible as cases were all native Swedes who were aged 18 to 74 yr and had CRF and whose serum creatinine for the first time and permanently exceeded 3.4 mg/dl (men) or 2.8 mg/dl (women) during the study period. A total of 926 case patients and 998 control subjects, randomly drawn from the study base, were enrolled. Face-to-face interviews, supplemented with self-administered questionnaires, provided information about anthropometric measures and other lifestyle factors. Logistic regression models with adjustments for several co-factors estimated the relative risk for CRF in relation to body mass index (BMI).
Overweight
(BMI>or=25 kg/m2) at age 20 was associated with a significant three-fold excess risk for CRF, relative to BMI<25. Obesity (BMI>or=30) among men and morbid obesity (BMI>or=35) among women anytime during lifetime was linked to three- to four-fold increases in risk. The strongest association was with
diabetic nephropathy
, but two- to three-fold risk elevations were observed for all major subtypes of CRF. Analyses that were confined to strata without hypertension or diabetes revealed a three-fold increased risk among patients who were
overweight
at age 20, whereas the two-fold observed risk elevation among those who had a highest lifetime BMI of >35 was statistically nonsignificant. Obesity seems to be an important-and potentially preventable-risk factor for CRF. Although hypertension and type 2 diabetes are important mediators, additional pathways also may exist.
...
PMID:Obesity and risk for chronic renal failure. 1667 17
Insulin resistance (IR) plays a larger role in the type 1 diabetes mellitus (T1DM) disease process than commonly recognized.
Overweight
and physical inactivity have increased steadily for the last 20-30 years in children and adolescents in many populations, concurrently with a rising incidence of T1DM. The role of IR in T1DM has only recently been gaining acceptance. This review will focus on how IR influences our current understanding of disease development and metabolic syndrome (MS) in T1DM. Increases in IR by weight gain and sedentarism, associated to decreased beta cell mass by autoimmune process, may disrupt normoglycemia in pre-T1DM individuals. IR may reflect a more aggressive form of autoimmune disease mediated by immuno-inflammatory factors that also mediate beta cell destruction (TNF-alpha and IL-6). These concepts are included in the "accelerator hypothesis". Moreover, family history of T2DM and chronic hyperglycemia (glucotoxicity), occurring after T1DM diagnosis, contribute to decrease peripheral glucose uptake. The onset of
diabetic nephropathy
(DN) might also contribute to IR and metabolic syndrome (MS) via low-grade inflammation and increased oxidative stress. MS is found between 12 to 40% in T1DM, especially in patients with advanced DN and poor glycemic control. These findings have therapeutic and cardiovascular prognostic implications as children make the transition toward adolescence and young adulthood T1DM.
...
PMID:[Insulin resistance and metabolic syndrome in type 1 diabetes mellitus]. 1676 91
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