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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The adequacy of peritoneal dialysis should be defined by clinical outcomes. Studies using multivariate techniques to evaluate the effect of demographic and clinical risk factors on these clinical outcomes showed worse patient survival for age > 60 years, diabetes mellitus, history of cardiovascular disease, black race and prior ESRD therapy. The single study reporting a multivariate analysis of urea kinetics and these baseline prognostic factors on clinical outcome showed serum albumin to be the most powerful predictor of survival. A multicentre study (10 Canadian and 4 US Centres) has enrolled 374 consecutive new peritoneal dialysis patients. The target enrollment is 600 patients. Among these 374 patients are 217 males (58%), 71 patients age > 70 (19%), 106 with diabetic renal disease (28%), 95 with a history of cardiovascular disease (25%) and 60 with serum albumin values < 30 Gm/L (16%). There are 307 white patients (82%) and 26 black patients (7%). The 9 month probabilities were: for patient survival, 96%; for technique survival, 93%; peritonitis-free survival, 68%; exit site infection-free survival, 71%. Final statistical analysis will use multivariate techniques to evaluate the relationships among baseline prognostic factors, nutritional status and clinical outcomes.
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PMID:Canada-USA (CANUSA) multicentre study of peritoneal dialysis adequacy: description of the study population and preliminary results. CANUSA Peritoneal Dialysis Study Group. 136 61

To elucidate the presence of chronic hyperinsulinemia and its relation to clinical and biochemical parameters, 112 (53 females and 59 males) Chinese non-insulin-dependent diabetes mellitus (NIDDM) patients under chlorpropamide therapy were closely monitored for three years. Clinical and biochemical risk factors for chronic hyperinsulinemia were studied by regular monitoring of body weight, fasting insulin levels and various biochemical data. Chronic hyperinsulinemia was defined as a mean fasting level over 20 microU/mL (highest level observed in 35 non-diabetics). Among 112 diabetics, 52 cases (46.4%) showed chronic hyperinsulinemia. From simple linear regression analysis, female gender, high BMI and elevated triglyceride and uric acid levels were correlated with insulin levels (p < 0.05). The presence of diabetic complications (retinopathy, neuropathy and nephropathy) and the degree of glycemic control were not significantly different between the normoinsulinemic and hyperinsulinemic groups. In conclusion, 1) NIDDM patients treated with chlorpropamide showed higher fasting insulin levels with 46.4% of them meeting the criteria for chronic hyperinsulinemia; 2) female gender, uric acid, BMI and triglyceride were the risk factors correlated with chronic hyperinsulinemia; and 3) the presence of diabetic complications and diabetic control correlated poorly with chronic hyperinsulinemia.
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PMID:Risk factors for hyperinsulinemia in chlorpropamide-treated diabetic patients: a three-year follow-up. 136 15

In the follow-up of insulin-dependent diabetes mellitus patients with renal disease, a decline in glomerular filtration rate measured by an exact technique is the major primary end point in evaluating the progress of the disease. Abnormal albuminuria is considered an intermediate or secondary end point. All studies suggest that an increase in albuminuria indicates a decline or a risk of future decline in glomerular filtration rate. The main risk factor for progression appears to be the elevated blood pressure (which in itself may be a pathogenetic factor) that is associated with abnormal albumiuria from the microalbuminuric level. Abnormal albuminuria seems to always be associated with the risk of progression, and a reversal of abnormal albuminuria suggests a beneficial prognosis. Abnormal albuminuria is easily monitored by immunochemical procedures, including semiquantitative dipstick tests that may be important in renal screening procedures. Elevated blood pressure is important for the progression of abnormal albuminuria, but poor metabolic control seems to be the major initiating factor (although the mechanisms at a molecular biologic level are less clear). New studies confirm the strong predictive value of microalbuminuria for overt renal disease. At the same time, it is clear that microalbuminuria is associated with many cardiovascular abnormalities that cluster in some patients and is clearly associated with a poor prognosis. An intervention strategy is to achieve the best possible metabolic control without creating hypoglycemic problems or too difficult a lifestyle. Increasingly, studies underscore the value of early antihypertensive therapy, especially with angiotensin-converting enzyme inhibitors, in patients with microalbuminuria. This scenario of earlier and earlier antihypertensive treatment for microalbuminuric patients is evolving. Numerous studies indicate that microalbuminuria is stabilized or reversed by this treatment, and some new evidence suggests better preservation of glomerular filtration rate by this intervention program. Accumulating results also suggest considerable improvement in survival rate with this program in proteinuric insulin-dependent diabetes mellitus patients.
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PMID:Management of renal disease and hypertension in insulin-dependent diabetes, with an emphasis on early nephropathy. 136 21

Radiocontrast-induced nephropathy (RCIN), a leading cause of in-hospital acute renal failure, is an acute decrease in renal function related to intravascular administration of iodinated radiocontrast agents. Though RCIN is relatively uncommon in patients without predisposing factors, patients with preexisting renal dysfunction, diabetes mellitus and severe congestive heart failure are at increased risk for acute renal failure following radiocontrast. Three recently developed animal models have provided important insights into the pathophysiology of RCIN. Specifically, these studies have implicated transient renal ischemia, direct renal tubular toxicity and changes in glomerular capillary permeability as possible mediators of RCIN, and these pathophysiologic mechanisms are not mutually exclusive. There is currently no effective treatment for RCIN. Assuring adequate hydration may reduce the risk of RCIN. In addition, synthetic atrial natriuretic factor and/or mannitol are promising, but as yet unproven, approaches to the prophylaxis of RCIN.
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PMID:Radiocontrast-induced nephropathy: current status and future prospects. 138 89

1. It has been suggested that hypertension may be an important determinant of the rate of progression of diabetic microangiopathy. 2. Renal microvascular disease as assessed by urinary albumin excretion and glomerular ultrastructure was evaluated in a model in which streptozotocin diabetes was induced in spontaneously hypertensive rats (SHR). 3. Diabetes was associated with increases in urinary albumin excretion, and hypertension resulted in a further increase in albuminuria. 4. Various antihypertensive regimens were administered to diabetic SHR, with the angiotensin-converting enzyme inhibitor perindopril and triple therapy (hydralazine, reserpine and hydrochlorothiazide) being more effective than the calcium antagonist (lacidipine) in retarding the increase in albuminuria in diabetic SHR. 5. Antihypertensive therapy appears to ameliorate the development of diabetic renal disease.
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PMID:Diabetic renal microvascular disease: the role of hypertension and ACE inhibitors. 139 13

Microalbuminuria is diagnosed when the UAER is greater than 20 but less than 200 micrograms/min. The prevalence of microalbuminuria among diabetic patients is 15-20%. Persistent microalbuminuria in diabetic patients is a risk marker not only of renal disease, but also of proliferative retinopathy and cardiovascular morbidity and mortality. Even among nondiabetic individuals, those with microalbuminuria tend to have an increased cardiovascular morbidity. The established cardiovascular risk factors, such as smoking, elevated plasma cholesterol, fibrinogen, and hypertension, are seen more frequently in diabetic patients with persistent microalbuminuria than in normoalbuminuric diabetic patients of similar age, sex, and diabetes duration. However, these risk factors cannot by themselves explain the cardiovascular overmortality in these patients. In addition, insulin resistance or genetic disposition to hypertension or cardiovascular disease fails to be the missing link. Accumulating evidence suggests a common pathogenetic mechanism for microalbuminuria and premature atherosclerosis (i.e., qualitative alterations of the extracellular matrix, including decreased density and sulfation of HS-PG). Decreased density of HS in the glomeruli may lead to albuminuria and mesangial proliferation. In the intima of large vessel walls, decreased density and/or sulfation of HS may enhance several of the processes involved in premature atherosclerosis. Diabetes affects the composition and structure of the extracellular matrix in many ways and leads to decreased density and sulfation of HS-PG by several mechanisms. Genetic differences in the sulfation of HS and/or genetic defects in the coordinated biosynthesis of HS-PG might contribute to decreased concentration and sulfation of HS-PG in susceptible individuals. It is hoped that susceptibility genes can be identified soon, thereby making prevention of severe late diabetic complications more successful.
Diabetes Care 1992 Sep
PMID:Microalbuminuria. Implications for micro- and macrovascular disease. 139 15

A number of risk factors associated with the development of diabetic nephropathy has been described, such as elevated blood pressure, poor metabolic control, hyperlipidemia, and smoking. Abnormal albuminuria also is associated with progression of renal disease, but has until recently been considered principally a marker of disease activity rather than a risk factor. This article discusses the role of elevated blood pressure versus abnormal albuminuria in a genesis and prediction of renal disease in diabetes. Controversy exists regarding parental disposition to hypertension and early blood pressure elevation in the course of diabetes, but all studies agree that elevated blood pressure--in the presence of abnormal albuminuria--constitutes a risk factor. Because abnormal albuminuria is associated with progression disease, it may itself be a risk factor because increased macromolecular traffic over the glomerular membrane may produce glomerulopathy. Problems related to blood pressure measurement are important, and 24-h recordings of blood pressure may be recommended in some situations. Regarding renal structure, preliminary results suggest that structural lesions precede blood pressure elevation. The solid end point for evaluation of renal disease progression is the fall rate of GFR, with abnormal albuminuria as an intermediate end point, also in drug trials. Abnormal albuminuria may constitute a new indication for antihypertensive treatment, being, as it is, a clear indicator of organ damage, whereas elevated blood pressure with normal AER may not increase risk substantially.
Diabetes Care 1992 Sep
PMID:Blood pressure elevation versus abnormal albuminuria in the genesis and prediction of renal disease in diabetes. 139 16

Not all patients with diabetes develop clinically significant nephropathy and, for this reason, attention has begun to focus on the risk factors for development of this serious complication. These risk factors have not been quantified to the same degree as those factors associated with more common progressive vascular diseases, such as atherosclerosis. However, studies of pathogenesis and clinical and epidemiological surveys of diabetic nephropathy point to numerous risk categories. Glycemic control, genetic and familial predispositions, renal and glomerular enlargement, glomerular hyperfiltration, and capillary and systemic hypertension can be invoked as contributors to this disease process. This review focuses on hemodynamic alterations and their role in the development and progression of diabetic nephropathy. Increases in GFR, largely driven by increases in plasma flow and capillary pressure, appear in early IDDM and NIDDM. This abnormality of renal vascular control probably is derived from alterations in several vasoactive control systems. In addition, the elevations in capillary pressure may be damaging to the glomerular capillaries. Arterial hypertension is not necessarily present before clinical nephropathy appears; however, it is a usual concomitant of progressive diabetic renal disease. The strongest evidences for the roles of altered systemic and renal hemodynamics in the progression of diabetic renal disease are clinical and experimental studies demonstrating attenuation of the disease process by lowering systemic and capillary pressures with antihypertensive agents, and dietary and glycemic modifications. Thus, although multiple factors probably interact to determine risk for the development of diabetic nephropathy, hemodynamic forces are a particularly important contributor and are especially amenable to therapeutic intervention.
Diabetes Care 1992 Sep
PMID:Diabetic nephropathy. Metabolic versus hemodynamic considerations. 139 17

Diabetes mellitus has become the leading cause of ESRF in the United States. Patients with diabetic nephropathy suffer high cardiovascular morbidity and mortality. Because only 40% of diabetic patients eventually develop diabetic kidney disease, it may be possible to devise primary prevention measures targeted at the subset of patients at risk. Recently, a predisposition to hypertension, a family history of diabetic nephropathy, and a family history of CVD disease each have been associated independently with the development of diabetic renal complication in IDDM. Risk factors for macrovascular damage, including raised arterial BP, dyslipidemia, and insulin resistance, can be detected early in the course of progression to diabetic nephropathy. These risk indicators recently have been shown to be already present at the stage of normoalbuminuria in those patients who eventually will progress to microalbuminuria. Treatment of established renal disease can only delay the onset of ESRF, and lowering of microalbuminuria has been shown to retard the onset of persistent proteinuria. However, no study to date has demonstrated prevention of renal disease in these patients. The ultimate aim should, therefore, be the prevention of the transition from normoalbuminuria to microalbuminuria in individuals who are at higher risk of diabetic renal disease and CVD.
Diabetes Care 1992 Sep
PMID:Diabetic nephropathy. Future avenue. 139 18

Diabetic nephropathy is caused primarily by advanced glomerulopathy, the renal expression of diabetic microangiopathy. With stereological methods a quantitative description of the structural changes is achieved. The glomerulopathy is characterized by an increase in basement membrane material: thickening of the capillary wall and an increase in mesangial volume relative to glomerular volume, comprising increase in matrix. Among groups of patients conformity between renal function stage and structure exists. The parameters measuring glomerulopathy are normal at the onset of diabetes; patients with normoalbuminuria may show slight basement membrane thickening, or normal parameters; the microalbuminuric group shows a measurable, but moderate glomerulopathy; patients with overt nephropathy have advanced lesions; at this stage heterogeneity among glomeruli makes the estimates weaker. Recent data indicate that the changes in peripheral basement membrane and in mesangial matrix develop in concert and both contribute to the early stage of glomerulopathy in patients with microalbuminuria. As to the consequences of the structural changes the mechanism of albuminuria is not clear. It is suggested that the early glomerulopathy entails other structural modifications, including formation of new vessels which may be the site of leakage. The marked deviations in glomerular filtration rate correspond well with estimates of filtration surface area: in the early hyperfunction state it is increased; in advanced nephropathy it is decreased, due to advanced glomerulopathy in conjunction with glomerular occlusion. The diabetic state is the necessary condition for the glomerulopathy. In relating structural changes to presumed contributing causes no supporting evidence of a relationship with glomerular hyperfunction or hypertrophy was observed. The structural parameters may be useful tools in clinical trials aiming at arresting the development of glomerulopathy, and thereby providing a prevention of diabetic nephropathy.
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PMID:Glomerular structural changes in type 1 (insulin-dependent) diabetes mellitus: causes, consequences, and prevention. 139 74


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