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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 prevalence of hypertension in patients with chronic renal insufficiency is high. In the stage of renal insufficiency it is 60% and in conservatively terminal renal failure it is as high as 90%. After the initiation of dialyzation treatment it declines temporarily, it is higher during chronic haemodialysis (50-80%) and lower in continuous ambulatory peritoneal dialysis (30%). After transplantation it is recorded in 70-80% recipients of a renal graft. Among the causes of renal hypertension in subjects with conservatively treated chronic renal insufficiency at present secondary renal impairment is increasing--in type 2 diabetes and also renal vascular affection due to atherosclerotic changes and essential arterial hypertension. Approximately 30% of patients where chronic dialyzation treatment is started, come "from the street". In the pathogenesis of renal hypertension sodium retention is involved with volume expansion and an impaired ratio of the formation of vasoactive (vasopressor and vasodepressor) substances. In chronic renal failure the volume component of hypertension predominates markedly. The causes of the development of hypertension after renal transplantation are multifactorial and are most closely associated with immunosuppressive treatment and graft rejection. Pharmacological treatment of renal hypertension prefers inhibitors of the angiotensin converting enzyme (possibly angiotensin II antagonists) because of their concurrent renoprotective action. In the stage of renal insufficiency they call for reduced doses and combination with other antihypertensive agents. The objective of treatment is to achieve a blood pressure < 130/80 mm Hg. In chronic dialyzation treatment the main therapeutic provision in hypertension is adjustment of the volume of extracellular fluid by regime provisions and effective haemoelimination treatment. Calcium blockers are useful in particular in the treatment of hypertension in haemodialyzed subjects and in hypertension after renal transplantation.
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PMID:[Hypertension and chronic renal insufficiency--chronic kidney failure]. 1290 74

Hypertension is common among patients with type 2 diabetes mellitus, increasing their risk of cardiovascular morbidity and mortality. Such patients are also at risk of renal impairment and end-stage renal disease. Long-term, tight blood pressure control (ideally to a target of < 130/85 mmHg) in patients with type 2 diabetes is a highly effective strategy for reducing the risk of cardiovascular complications and is now embodied in the many guidelines of hypertension and diabetes management. More recent studies indicate that the choice of antihypertensive agent is also important. Drugs that block the renin-angiotensin-aldosterone system, such as the angiotensin-II receptor blockers (ARBs), may prevent the onset of diabetes and confer greater cardiovascular benefit among patients who already have this disease compared with some older antihypertensive agents. For example, in type 2 diabetic patients with renal dysfunction, ARBs exert a renal protective effect that extends beyond blood pressure reduction and may retard diabetic nephropathy. Antihypertensive therapy, together with lifestyle modification to address obesity and physical inactivity, can significantly reduce the risk of cardiovascular complications in patients with type 2 diabetes. The challenge is to achieve beneficial, hygienic measures in populations with diverse backgrounds and improve compliance with proven treatments that inevitably involve multiple drugs. Combination therapies comprising agents that offer good tolerability and do not exacerbate existing metabolic disturbances, as well as demonstrating benefit in preventing events in diabetic patients beyond blood pressure reduction itself, seem a likely way forward.
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PMID:Benefits of blood pressure reduction in diabetic patients. 1451 49

The ability to assess renal function in diabetes patients rapidly and early is of major importance. This study was designed to determine whether cystatin C can replace serum creatinine as the screening marker for reduced glomerular filtration rate (GFR) in type 2 diabetes patients. The study was performed on 51 type 2 diabetic patients. GFR was estimated by the plasma clearance of (99m)Tc-DTPA. The correlation between (99m)Tc-DTPA clearance and levels of serum cystatin C, serum creatinine, and creatinine clearance was determined. Sensitivity and specificity for the diagnosis of renal impairment (defined as GFR<68 ml/min) were calculated by a receiver operating characteristic (ROC) curve for serum cystatin C, serum creatinine, and creatinine clearance. The correlation coefficients with (99m)Tc-DTPA clearance were -0.744 for serum cystatin C, -0.658 for serum creatinine, and +0.625 for creatinine clearance (P<0.001). With a cutoff value of 68 mL/min, the area under the ROC curve (AUC) was 0.891 for cystatin C, 0.77 for creatinine, and 0.753 for creatinine clearance. The AUC was statistically different between serum cystatin C and creatinine clearance (P<0.05). The ROC plot indicates that cystatin C is superior to serum creatinine and creatinine clearance for detecting impaired GFR. Serum cystatin C appropriately reflects GFR in diabetes, and is more efficacious than serum creatinine and creatinine clearance in detecting reduced GFR in type 2 diabetes patients.
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PMID:Serum cystatin C assay for the detection of early renal impairment in diabetic patients. 1473 May 55

The prevalence of chronic renal failure (CRF) in 460 patients with diabetes mellitus attending the diabetic outpatient clinic at the University Hospital of the West Indies in Jamaica was determined from a review of medical records. The prevalence of CRF was 10% (39/386) in the diabetic clinic population. Significant positive associations with CRF were found with male gender (20/98, 20% vs 19/287, 7%; odds ratio (OR), 3.24; p = 0.001); age 60 years and older (22/162; 14% vs 17/221, 8%; OR, 2.01; p = 0.04); fasting blood glucose concentrations exceeding 8.0 mmol/L (22/162, 13% vs 12/182, 7%; OR, 2.08; p = 0.05); the presence of significant proteinuria as a marker for outcome (13/39, 33% vs 48/346, 14%; OR, 3.60; p = 0.02) and peripheral vascular disease (6/20, 30% vs 139/386, 10%; OR, 4.75; p = 0.005). The prevalence of CRF did not differ significantly between patients with Type 1 and Type 2 diabetes mellitus. Also, the presence of CRF was not significantly associated with duration of diabetes mellitus, type of hypoglycaemic agents used, or history of hypertension. However, the presence of persistent proteinuria was significantly associated with duration of diabetes mellitus exceeding five years (46/255, 17% vs 11/149, 7%; OR, 2.52; p = 0.005) and a history of hypertension (41/235, 17% vs 20/198, 10%; OR, 1.88; p = 0.03) but not with age or gender. This study emphasizes the need to evaluate patients with diabetes mellitus for renal impairment so that intervention strategies may be adopted early to delay progression to endstage renal disease.
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PMID:Prevalence of chronic renal failure in the diabetic population at the University Hospital of the West Indies. 1519 17

The relationship between serum levels of beta-trace protein (BTP) or serum creatinine (s-Cr) and the prognostic stages of type 2 diabetic nephropathy was determined. Serum samples from 174 patients with type 2 diabetes were obtained from Juntendo University Hospital, Tokyo, and Juntendo Urayasu Hospital, Chiba, Japan. They were classified into four groups according to the Report of the Ministry of Health and Welfare of Japan (1991, p 251-256) as follows: Stage I (normoalbuminuric stage), Stage II (microalbuminuric stage), Stage IIIA (macroalbuminuric stage without renal dysfunction), Stage IIIB (macroalbuminuric stage with renal dysfunction), and Stage IV (renal failure stage). Among these patients, 68 were Stage I, 29 Stage II, 32 Stage IIIA, 17 Stage IIIB, and 28 Stage IV. Levels of serum BTP were measured using the nephelometric assay on a BNA II analyzer (Dade Behring Diagnostics, Marburg, Germany). The mean levels of serum BTP in Stage IIIA were significantly higher than those in Stage I or II (P < 0.00001, P < 0.002, respectively). However, the mean levels of s-Cr in Stage IIIA were not significantly higher than that in Stage I or II. In conclusion, serum BTP was a good marker for the identification of early renal impairment in type 2 diabetes.
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PMID:Beta-trace protein, a new marker of GFR, may predict the early prognostic stages of patients with type 2 diabetic nephropathy. 1520 16

Manidipine is a lipophilic, third-generation dihydropyridine calcium channel antagonist with a high degree of selectivity for the vasculature, thereby inducing marked peripheral vasodilation with negligible cardiodepression. In addition, manidipine does not significantly affect norepinephrine levels, suggesting a lack of sympathetic activation. It has a gradual onset of action and a long duration of action enabling once daily administration. Furthermore, manidipine dilates both the efferent and the afferent renal arterioles and appears to have beneficial renal effects unrelated to its antihypertensive effect. Once-daily oral manidipine is an effective and generally well tolerated antihypertensive agent for younger and elderly adult patients with mild-to-moderate hypertension. In particular, in a large double-blind trial, the incidence of ankle oedema was significantly lower in manidipine than in amlodipine recipients. Manidipine is also effective in hypertensive patients with comorbidities, such as type 2 diabetes mellitus and/or renal impairment, and appears to improve insulin sensitivity without affecting metabolic function. Thus, manidipine represents a first-line treatment option for patients with essential mild-to-moderate hypertension.
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PMID:Manidipine: a review of its use in the management of hypertension. 1532 44

Recently, clinical trials evaluating cardiovascular outcomes with antihypertensive drugs that target the renin-angiotensin-aldosterone system have been dramatically increasing in size. The CONSENSUS trial in 1987 enrolled 253 patients, while Val-HeFT in 1999 enrolled 5,010 patients; indeed, the Val-HeFT subgroup of patients not receiving angiotensin-converting enzyme inhibitors was bigger than the whole CONSENSUS trial even though the 366 patients were only 7% of the total trial population. More recent and ongoing cardiovascular trials have even greater patient numbers with 14,703 patients enrolled in VALIANT, 15,314 in VALUE, 23,400 in ONTARGET and 33,357 in ALLHAT. Part of the reason is that in modern trials, patients in the control group are already receiving optimal therapy. Therefore, in order to be adequately powered to detect any benefit of new drugs, trials must recruit thousands of patients. This expanding trend cannot continue forever because of time and economic constraints and as a result, trials are shifting their design to include composite and surrogate endpoints. In addition, more predefined substudies are being carried out to analyze possible benefits in specific patient populations such as those with type 2 diabetes or renal impairment. Modern trials are also placing more emphasis on protection as a long-term strategy to control cardiovascular risks. Examples of these points, particularly regarding the size of modern cardiovascular trials to have the power to show protective effects, are illustrated by Val-HeFT, LIFE, ELITE II, VALIANT, VALUE, CHARM and NAVIGATOR.
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PMID:RAAS inhibitors in the cardiovascular continuum: what is still missing? 1536 29

Manidipine is a third-generation dihydropyridine calcium antagonist, which causes systemic vasodilation by inhibiting the voltage-dependent calcium inward currents in smooth muscle cells. In clinical studies, manidipine has been shown to significantly lower office and 24-h blood pressure compared with placebo in patients with essential hypertension. The resulting reduction in blood pressure is maintained over 24 h, with preservation of the circadian blood pressure pattern; its blood pressure-lowering capacity appears to be similar to that of other calcium antagonists. In elderly patients with mild-to-moderate essential hypertension, manidipine is able to significantly decrease blood pressure compared with placebo for up to 3 years of treatment. The drug also significantly lowers blood pressure in patients with hypertension and concomitant Type 2 diabetes mellitus or renal impairment, and is devoid of adverse metabolic effects. It is well-tolerated with few untoward adverse effects related to vasodilation. In particular, manidipine appears to have less potential for pedal edema than other calcium channel blockers.
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PMID:Role of manidipine in the management of patients with hypertension. 1550 Apr 27

Type 2 diabetes mellitus is a progressive and complex disorder that is difficult to treat effectively in the long term. The majority of patients are overweight or obese at diagnosis and will be unable to achieve or sustain near normoglycaemia without oral antidiabetic agents; a sizeable proportion of patients will eventually require insulin therapy to maintain long-term glycaemic control, either as monotherapy or in conjunction with oral antidiabetic therapy. The frequent need for escalating therapy is held to reflect progressive loss of islet beta-cell function, usually in the presence of obesity-related insulin resistance. Today's clinicians are presented with an extensive range of oral antidiabetic drugs for type 2 diabetes. The main classes are heterogeneous in their modes of action, safety profiles and tolerability. These main classes include agents that stimulate insulin secretion (sulphonylureas and rapid-acting secretagogues), reduce hepatic glucose production (biguanides), delay digestion and absorption of intestinal carbohydrate (alpha-glucosidase inhibitors) or improve insulin action (thiazolidinediones). The UKPDS (United Kingdom Prospective Diabetes Study) demonstrated the benefits of intensified glycaemic control on microvascular complications in newly diagnosed patients with type 2 diabetes. However, the picture was less clearcut with regard to macrovascular disease, with neither sulphonylureas nor insulin significantly reducing cardiovascular events. The impact of oral antidiabetic agents on atherosclerosis--beyond expected effects on glycaemic control--is an increasingly important consideration. In the UKPDS, overweight and obese patients randomised to initial monotherapy with metformin experienced significant reductions in myocardial infarction and diabetes-related deaths. Metformin does not promote weight gain and has beneficial effects on several cardiovascular risk factors. Accordingly, metformin is widely regarded as the drug of choice for most patients with type 2 diabetes. Concern about cardiovascular safety of sulphonylureas has largely dissipated with generally reassuring results from clinical trials, including the UKPDS. Encouragingly, the recent Steno-2 Study showed that intensive target-driven, multifactorial approach to management, based around a sulphonylurea, reduced the risk of both micro- and macrovascular complications in high-risk patients. Theoretical advantages of selectively targeting postprandial hyperglycaemia require confirmation in clinical trials of drugs with preferential effects on this facet of hyperglycaemia are currently in progress. The insulin-sensitising thiazolidinedione class of antidiabetic agents has potentially advantageous effects on multiple components of the metabolic syndrome; the results of clinical trials with cardiovascular endpoints are awaited. The selection of initial monotherapy is based on a clinical and biochemical assessment of the patient, safety considerations being paramount. In some circumstances, for example pregnancy or severe hepatic or renal impairment, insulin may be the treatment of choice when nonpharmacological measures prove inadequate. Insulin is also required for metabolic decompensation, that is, incipient or actual diabetic ketoacidosis, or non-ketotic hyperosmolar hyperglycaemia. Certain comorbidities, for example presentation with myocardial infarction during other acute intercurrent illness, may make insulin the best option. Oral antidiabetic agents should be initiated at a low dose and titrated up according to glycaemic response, as judged by measurement of glycosylated haemoglobin (HbA1c) concentration, supplemented in some patients by self monitoring of capillary blood glucose. The average glucose-lowering effect of the major classes of oral antidiabetic agents is broadly similar (averaging a 1-2% reduction in HbA1c), alpha-glucosidase inhibitors being rather less effective. Tailoring the treatment to the individual patient is an important principle. Doses are gradually titrated up according to response. However, the maximal glucose-lowering action for sulphonylureas is usually attained at appreciably lower doses (approximately 50%) than the manufacturers' recommended daily maximum. Combinations of certain agents, for example a secretagogue plus a biguanide or a thiazolidinedione, are logical and widely used, and combination preparations are now available in some countries. While the benefits of metformin added to a sulphonylurea were initially less favourable in the UKPDS, longer-term data have allayed concern. When considering long-term therapy, issues such as tolerability and convenience are important additional considerations. Neither sulphonylureas nor biguanides are able to appreciably alter the rate of progression of hyperglycaemia in patients with type 2 diabetes. Preliminary data suggesting that thiazolidinediones may provide better long-term glycaemic stability are currently being tested in clinical trials; current evidence, while encouraging, is not conclusive. Delayed progression from glucose intolerance to type 2 diabetes in high-risk individuals with glucose intolerance has been demonstrated with troglitazone, metformin and acarbose. However, intensive lifestyle intervention can be more effective than drug therapy, at least in the setting of interventional clinical trials. No antidiabetic drugs are presently licensed for use in prediabetic individuals.
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PMID:Oral antidiabetic agents: current role in type 2 diabetes mellitus. 1566 80

Development of microalbuminuria increases the risk for cardiovascular disease (CVD) in type 2 diabetes. The nature of this relationship is unclear but may involve arterial stiffness, an independent risk marker for CVD mortality. Aortic pulse wave velocity (Ao-PWV) and albumin creatinine ratio (ACR) were measured in 134 consecutive patients with type 2 diabetes without overt renal impairment (serum creatinine <150 micromol/L). ACR ranged from 0.2 to 153 mg/mmol. Patients with raised ACR (>/=3 mg/mmol) had higher Ao-PWV, poorer diabetic control, and higher pulse pressure (PP) and systolic BP (SBP) (all P < 0.05) than those with normal ACR. The closest univariate associations of Ao-PWV were positively with age, duration of diabetes, SBP, PP, ACR, and insulin treatment and negatively with GFR and weight (all P < 0.01). In a multiple linear step-down regression analysis, the significant predictors of Ao-PWV were age, SBP or PP, duration of diabetes, gender, number of antihypertensive medications, and use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, which together explained 55% of the variance of Ao-PWV. When ACR was offered in place of arterial pressure to a separate model, ACR emerged as a significant predictor of Ao-PWV. After age adjustment, patients with lower, below median GFR had higher Ao-PWV than those with GFR above the median (P = 0.043). In patients with type 2 diabetes without overt renal impairment, raised ACR is associated with higher Ao-PWV, a relationship most likely mediated by raised BP. The association of Ao-PWV with reduced GFR suggests that even modest renal dysfunction may affect the viscoelastic properties of large arteries.
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PMID:Aortic pulse wave velocity and albuminuria in patients with type 2 diabetes. 1574 96


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