Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The NIDDM patient, willingly with high blood pressure and atheroma, has frequently an abnormal renal function. Must a renal artery stenosis (RAS) be searched as a determining or favorising cause? We have searched RAS by color duplex scan, in 60 consecutive NIDDM patients with altered renal function (creatinine clearance < or = 60 mL/min). Metabolic blood pressure (ABPM), cardiovascular and renal investigations have been realised. The population was composed of 22F/38M with middle age: 70.7 +/- 6.2 yrs, diabetic duration: 11.6 +/- 8 yrs, the plasma creatinine was: 161 +/- 78 mumol/L and clearance: 40 +/- 13 mL/min. Thirty eight had albuminuria, 28 had plasma creatinine > or = 150 mumol/L. All patients had high blood pressure. Significative RAS (> or = 70%) was detected in 15 patients (25%) by color duplex scan and proved with arteriography (n = 10) or angio NMR (n = 5). Twelve (80%) had unilateral stenosis (4 thrombosis), 3 (20%) bilateral stenosis. Renal US lead the diagnosis in 10 patients (66%): unilateral or bilateral hypotrophy. Those 15 patients had these following characteristics: 4F/11M (sex R : 0.36), middle age: 70.8 +/- 7.2 yrs, diabetic duration: 14.3 +/- 7.5 yrs, HbA1c was at 8.4 +/- 2%, 8 (53%) patients require insuline and 5 have retinopathy, plasma creatinine was at 169 +/- 6 mumol/L; 32% of patients with plasma creatinine > or = 150 mumol/L had RAS (n = 9/60%), creatinine clearance was at 38 +/- 12 mL/min (7/47% < or = 30 mL/min), 9 (60%) had macroalbuminuria and 5 (33%) microalbuminuria. All hypertensive patients were treated (mean SBP: 148 +/- 16, mean DBP: 82 +/- 7 mmHg) and had 62 +/- 28% SBP escape and 33 +/- 19% DBP escape. Ten had severe hypertension (at least 3 hypotensive drugs), 12 received CEI; 8 (53%) were smokers; 14 (93%) had one or more macroangiopathies (10/66% coronary heart diseases, 7/46% lower limbs arteritis, 6/40% carotid atheroma); 13 of these macroangiopathies are severe. In conclusion, renal failure (especially evolutive and/or treated with CEI) in NIDDM must call up a RAS (25%) specially in elderly males with a long diabetes duration, severe hypertension and macroangiopathies. This patient profile must lead to a color duplex scan to confirm the diagnosis already suspected by the renal echography.
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PMID:[Renal artery stenosis and chronic renal failure in NIDDM]. 974 69

Diabetic nephropathy (DN) appears in about 30% of patients with type 1 diabetes (D1) and 15 to 60% of patients with type 2 diabetes (D2). It is preceded by microalbuminuria. Microalbuminuria is defined as an albumin excretion rate between 30 and 300 mg/24 h (on a 24-hour urine collection) or between 20 and 200 micrograms/min (on an overnight collection) in at least two out of three consecutive collections made within a 6-month period. Alternative screening techniques use either dipstick (Micral-Test II) or the albumin to creatinine ratio on an early morning urine sample (30-300 mg/g creatinine). Once persistent microalbuminuria is confirmed, 80% of type 1 diabetic patients and 20 to 50% of type 2 diabetic patients will progress to DN. In D2, microalbuminuria also represents a powerful predictor of early mortality from cardiovascular disease. Macroalbuminuria (AER > 300 mg/24 h, corresponding to a total protein excretion > 500 mg/24 h) will eventually lead to a end-stage renal insufficiency within 10 to 20 years. In D2, numerous patients will die from cardiovascular disease before reaching end-stage renal failure. Angiotensin-converting enzyme inhibitors can slow down the evolution toward DN when prescribed when microalbuminuria appears. Screening for microalbuminuria should therefore be a part of the annual clinical assessment in every diabetic patient.
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PMID:[How I evaluate...diabetic nephropathy. First part: micro- and macroalbuminuria]. 981 Feb 12

Diabetic nephropathy has become the single most important cause of endstage renal failure in most countries of the Western world. Against this background, the role of the renin-angiotensin system (RAS) and its blockade command considerable interest. In diabetic patients and in diabetic animals, the circulating components of the RAS are suppressed. Although the evidence is not completely uniform, there are indirect arguments (renal hemodynamic response to RAS blockade, AT1 receptor expression), however, which would be consistent with increased intrarenal action of angiotensin (ANG) II. There is solid evidence that ACE inhibitors effectively interfere with progression of micro-albuminuria both in IDDM and NIDDM. They also prevent progression of advanced renal failure in IDDM, while there is only preliminary evidence in this respect for NIDDM. ACE inhibitors are superior to conventional antihypertensive agents (with the possible exception of some calcium channel blockers), but such superiority is seen only when the levels of blood pressure are relatively high. In diabetic animals, treatment with ANG II receptor blockers interferes with the development of glomerular lesions. In acute and subacute studies on diabetic patients, ANG II receptor blockers reduced albuminuria (or proteinuria) more than beta-blockers. Head-on comparison of equipotent doses ACE inhibitors and ANG II receptor blockers in non-diabetic patients produced equal reductions in proteinuria. The long-term effects of ANG II receptor blockers on progression of advanced diabetic nephropathy is the object of two large international studies. The results will not be available before the year 2000.
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PMID:Diabetes--renal function--what are the special problems? 983 74

Type II diabetes mellitus has become the leading cause of end-stage renal failure in many countries of Western Europe. In all European countries, even in those with a relatively low prevalence of diabetic nephropathy, the number of patients with type II diabetes mellitus admitted for renal replacement therapy has recently increased continuously. Survival and medical rehabilitation of patients with type II diabetes on renal replacement therapy is significantly worse than in non-diabetic patients. It is obvious that in order to stem the tide, intense efforts are necessary (i) to inform the medical community about the renal risk of type II diabetes and the striking effectiveness of preventive measures, (ii) to provide better care for diabetic patients, and (iii) to reduce the high prevalence of diabetes in the population by modification of the Western life style.
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PMID:The drama of the continuous increase in end-stage renal failure in patients with type II diabetes mellitus. 987 Apr 18

The soluble form of the insulin-like growth factor II/mannose 6-phosphate (IGF-II/M6-P) receptor has been detected in serum from a variety of mammalian species. We report the development of a highly sensitive quantitative human IGF-II/M6-P receptor immunoassay. Antibodies raised to receptor purified from a human hepatoma cell line by phosphomannan affinity chromatography were used to develop a specific enzyme-linked immunosorbent assay. In this assay, the serum level of soluble receptor for healthy adult subjects was 0.70 +/- 0.23 mg/L. We have shown that soluble receptor is developmentally regulated, with levels in infant (1.12 +/- 0.28 mg/L) and prepubertal (1.18 +/- 0.6 mg/L) subjects dropping by 40% during adolescence (0.73 +/- 0.61 mg/L) and remaining constant throughout adulthood. Further, the receptor is gestationally regulated, with a highly significant association between gestational age and maternal serum receptor levels (r = 0.947; P < 0.0001). Noninsulin-dependent diabetes mellitus (0.98 +/- 0.25 mg/L) and insulin-dependent diabetes mellitus (0.98 +/- 0.25 mg/L) mildly elevated soluble receptor levels, whereas end-stage renal failure (0.75 +/- 0.23 mg/L) and acromegaly (0.79 +/- 0.25 mg/L) did not affect receptor levels. Additionally, we have shown that soluble receptor is present in amniotic fluid, but at a 100-fold lower concentration than serum levels. The ability to quantitate soluble IGF-II/M6-P receptor levels in serum and other fluids provides a valuable tool that will help to further elucidate the role of the receptor in human physiology and disease states.
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PMID:Regulation of soluble insulin-like growth factor II/mannose 6-phosphate receptor in human serum: measurement by enzyme-linked immunosorbent assay. 1002 25

Nephropathy may develop in patients with type 1 diabetes because poor glycemic control produces effects that eventually lead to glomerular scarring and renal failure. The worse and more prolonged the hyperglycemia, the greater the risk of diabetic nephropathy. In patients with type 2 diabetes, hyperglycemia, as well as insulin resistance and generalized vascular disease, is involved in the pathogenesis of nephropathy. The glomerular changes of early diabetic nephropathy can be identified only by renal biopsy or by testing for microalbuminuria. Once macroalbuminuria occurs (albumin excretion rate, > 300 mg/day), usually after type 1 diabetes has been present for 10 to 15 postpubertal years, end-stage renal disease is almost inevitable. However, aggressive control of hypertension in diabetic patients without microalbuminuria helps avoid nephropathy, and tight glycemic control in those with microalbuminuria can avoid or delay its onset. Even when macroalbuminuria is present, treatment can prolong renal function. Aggressive antihypertensive therapy, especially with ACE inhibitors, can reduce renal decline by half. Avoiding circumstances that may damage the kidneys (e.g., use of radiocontrast materials or nephrotoxic drugs, dehydration, hyperlipidemia, urinary tract infection, buildup of AGEs) is critical. Some treatment methods are controversial (dietary protein restriction) or still under investigation (use of injected or oral heparin) but may help delay renal transplantation or dialysis.
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PMID:Dealing with diabetic nephropathy. 1002 5

End-stage renal failure (ESRF) in diabetic patients, mostly type 2, has become the most frequent cause of renal replacement therapy in western Europe. The majority of patients with type 2 diabetes and renal failure suffer from diabetic glomerulosclerosis, but nondiabetic renal disease and atypical presentations, e.g. as irreversible acute renal failure or ischaemic nephropathy, play an increasingly important role. Known risk factors for the onset of diabetic nephropathy include (1) genetic predisposition (indicated by a history of hypertension and cardiovascular events in first-degree relatives), (2) quality of glycaemic control, (3) level of blood pressure, and (4) smoking. At the time when type 2 diabetes is diagnosed, an abnormal blood pressure profile is found in approximately 80%. In patients with established diabetic nephropathy, hypertension is the most important factor which promotes progression, and this is susceptible to intervention. Although less data are available for type 2 diabetes (compared with type 1 diabetes), ACE inhibitors appear to be the antihypertensive agent of first choice, but monotherapy is rarely sufficient to achieve the blood pressure goal. Although, at least in principle, diabetic nephropathy is a preventable condition, currently only a minority of type 2 diabetic patients in western Europe receives adequate medical treatment to prevent onset or progression of diabetic nephropathy. Consequently, novel approaches to patient management and interdisciplinary interaction are necessary to fulfil the postulate of the St Vincent declaration concerning prevention of diabetic complications.
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PMID:Nephropathy in type 2 diabetes. 1008 14

Diabetic nephropathy was first described in patients with non-insulin-dependent diabetes mellitus (NIDDM, type II diabetes) by Kimmelstiel and Wilson in 1936. It is a classical, late diabetic complication, diagnosed by measurement of the urinary albumin or total protein excretion, and typically develops after more than 15 years of diabetes. As most studies of patients with type II diabetes have been performed in White, European or North American populations in which the highest incidence of this disease is recorded in individuals aged over 70 years, a low prevalence has generally been found in these patients. Nephropathy has been considered a rare complication in type II diabetes patients. Other ethnic groups such as Pima Indians in the USA or Pacific Islanders have totally different incidence patterns of type II diabetes, with a high incidence in the 20- to 50-year age group. These patients live long enough to develop nephropathy, and they do so at the same rate as insulin-dependent diabetes mellitus (IDDM, type I diabetes) patients. Since the prevalence of type II diabetes is increasing worldwide, particularly in the developing world, diabetic nephropathy will be a growing problem in patients with this disease. From our experience in the treatment of type I diabetes patients, we know that prevention of end-stage renal failure is possible in most patients, but that treatment of end-stage renal disease is very expensive. In this paper, some of the major risk factors for the development of nephropathy are discussed together with the potential for treatment. It is shown that, in type I diabetes patients, early detection by screening for microalbuminuria and immediate recourse to antihypertensive treatment are likely to increase life-expectancy significantly while at the same time reducing the total costs to healthcare. Whether this is also the case in patients with type II diabetes is less clear, as most of the controlled clinical trials of the effect of strict metabolic control or antihypertensive treatment have been performed in patients with type I diabetes. Thus, clinical trials in patients with type II diabetes should be performed, and further epidemiological data relating to these patients are needed.
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PMID:The costs of nephropathy in type II diabetes. 1015 2

Diabetes mellitus is one of the most common chronic diseases in the developed countries and is a major cause of blindness, renal failure or amputations, all of which require expensive health-care resources. Diabetes is also associated with the increased risk of cardiovascular and cerebrovascular diseases and a substantial reduction in life expectancy. Therefore, prevention of diabetes is desirable. Recently, epidemiological studies have provided a basis of understanding the environmental determinants of diabetes and several prospective studies have shown that in the aggregate, intensive therapy improves health-care status by improving not only microvascular disease but also macrovascular disease in both type 1 and type 2 diabetes.
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PMID:[Prevention of diabetes mellitus]. 1019 48

Good evidence exists that genetic predisposition is a major determinant in the development of renal and cardiovascular complications of diabetes. In particular, the role of familial predisposition is well established in diabetic nephropathy which may cluster within families, both in type I (IDDM) and in type II (NIDDM) diabetes. The genes responsible for predisposition to renal and cardiovascular complications are not known, but those of the renin-angiotensin system (RAS) are plausible candidates. Beside the large number of studies aimed at evaluating the role of polymorphisms in these genes, particularly in angiotensin-converting enzyme (ACE) gene, in development of renal disease, no clear-cut evidence has been provided until now. Furthermore, a number of trials have shown that ACE-inhibitors (ACEi) may reduce the rate of progression of renal failure. If the RAS genotype were able to foresee the response to ACEi it would provide new strategies for a specific treatment of subjects at higher risk.
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PMID:Gene polymorphism of the renin-angiotensin system and progression of diabetic nephropathy. 1020 97


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