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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1979 to 1989, continuous ambulatory peritoneal dialysis (CAPD) was undertaken for terminal renal failure in 104 patients (56 women and 48 men; average age 54 +/- 15.3 years at the onset of dialysis), for a total observation period of 175 patients years. Survival rate for patients and methods and dialysis effectiveness were analysed retrospectively, the incidence of peritonitis prospectively, 40 patients were aged 60 years and over. Diabetic nephropathy was the most common cause of terminal renal failure (44%). Cumulative patient survival rate was 80% in the first year of treatment; 57% of patients were still alive after two years. The cause of death in 45 of the 54 patients who had died was unrelated to CAPD, cardiac disease and cerebrovascular accident being the most frequent causes (n = 26). During the first treatment year 47% of patients contracted bacterial peritonitis, 59% during the first two years. In 9% of patients CAPD had to be discontinued within the first two treatment years because of CAPD-related complications. There was no case of sclerosing peritonitis or of ultrafiltration loss forcing CAPD termination. These data indicate that there is no plausible explanation from a medical viewpoint for the highly restrictive use of CAPD in the Federal Republic of Germany.
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PMID:[Continuous ambulatory peritoneal dialysis. Patient and method survival rate, peritonitis incidence and dialysis efficacy over 10 years]. 201 38

Haemostatic activation was measured in patients with either non-diabetic chronic renal failure (CRF) or diabetic nephropathy. We have investigated the relationship between these haemostatic markers and the rate of progression of renal failure. When compared with age- and sex-matched healthy controls, both patient groups showed significantly elevated plasma concentrations of D dimer, von Willebrand factor antigen (vWFAg), and C-reactive protein (CRP) (all P less than 0.001), as well as an increase in spontaneous platelet aggregation (P less than 0.01). Plasma concentration of platelet factor 4 was slightly but not significantly increased. Serum thromboxane was subnormal (P less than 0.01). Multiple regression analysis showed that in non-diabetic CRF proteinuria and serum TxB2 were independently related to the rate of progression of renal failure; in diabetic nephropathy proteinuria and vWFAg were independently related to the rate of progression. In both groups the relationship was stronger with proteinuria (standardised regression coefficients 0.56 and 0.45 respectively) than with serum TxB2 (0.29) or with vWFAg (0.37). We have found haemostatic activation in both non-diabetic and diabetic progressive renal failure. Proteinuria, and also in this study serum TxB2 and vWFAg, appear to be determining factors in the progression of renal failure, and their measurement may have prognostic value.
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PMID:Haemostatic activation and proteinuria as factors in the progression of chronic renal failure. 205 12

End-stage renal disease attributed to hypertension has increased annually for the last decade and will probably worsen through the year 2000. Patients with diabetic nephropathy and patients with hypertensive renal disease account for most new cases annually. Evidence reveals that all levels of untreated hypertension are associated with potentially declining renal function. Data from the Hypertension Detection and Follow-up Program and other studies show that antihypertensive treatment can prevent progressive renal failure. An ablation model demonstrates glomerular hyperfiltration as a possible mechanism for progressive renal failure. Human data on the renal effects of antihypertensive agents are limited and inconsistent. Despite the limitations, the Working Group on Hypertension and Chronic Renal Failure concludes that controlled hypertension to less than 140/90 mm Hg reduces the incidence of end-stage renal disease. Patients with established renal impairment may benefit from individualized treatment to 130/85 mm Hg or less.
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PMID:National High Blood Pressure Education Program Working Group report on hypertension and chronic renal failure. 206 78

The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain to be established. However, there is now evidence that renal disease clusters in families and that genetic factors are of central importance in determining liability. A predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Genetically controlled hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. This suggestion derives from the observation that the 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 sign of renal damage is the appearance of microalbuminuria and of a small elevation in arterial pressure, changes associated with significant mesangial expansion. Microalbuminuria is associated with abnormalities of lipoprotein profiles possibly as a consequence of insulin-resistance-induced hyperinsulinemia. It could be postulated that the environmental changes brought about by diabetes lead in susceptible individuals to increased systemic and intraglomerular pressure on the one hand and mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities would 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 of reduction in renal function, more hypertension, more proteinuria, more glomerular obsolence, more hyperlipidemia and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Mechanisms of diabetic renal and cardiovascular disease. 207 90

Blood rheology was investigated in patients with diabetic nephropathy and progressive renal insufficiency, and compared with similar non-diabetic patients and healthy control subjects. Plasma viscosity and whole blood viscosity at standardized haematocrit were elevated to a comparable degree in the two patient groups, but erythrocyte deformability was normal. In diabetic patients, the rate of progression of renal failure showed weak, but significant, correlations with plasma viscosity (rs = 0.50, p = 0.005), standardized whole blood viscosity (rs = 0.41, p = 0.021), plasma fibrinogen (rs = 0.46, p = 0.010), C reactive protein (rs = 0.40, p = 0.023), and proteinuria (rs = 0.52, p = 0.003). Both plasma viscosity and plasma fibrinogen correlated significantly with proteinuria (rs = 0.45, p = 0.012 and 0.40, p = 0.027, respectively). Rheological abnormality is probably a manifestation of increased acute phase proteins, but it remains to be determined whether these are the cause or the effect of the renal injury. Abnormal blood rheology may be a risk factor for the progression of renal failure in diabetic nephropathy.
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PMID:Blood hyperviscosity and its relationship to progressive renal failure in patients with diabetic nephropathy. 214 85

Optimal metabolic control, strict antihypertensive therapy and a low-protein diet may reduce renal functional disorders such as hyperfiltration and microalbuminuria in the initial and latent phase of diabetic nephropathy and may retard progression of renal functional loss in the clinically-manifest proteinuric, azotaemic phase. Increasing clinical experience with renal replacement therapy in the end-stage renal failure of diabetic nephropathy led to a worldwide rise in the percentage of diabetic patients in dialysis centres. However, full rehabilitation is not achieved and retinopathy may progress to complete blindness. As a result of better rehabilitation and possible stabilisation of diabetic neuropathy and retinopathy after renal transplantation, in diabetic patients a kidney graft should be available early in the course of progressing renal failure.
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PMID:[Diabetic nephropathy--recent therapeutic concepts]. 218 81

Medicare's End-Stage Renal Disease (ESRD) Program provides funding for life-saving renal replacement therapy for patients with irreversible chronic renal failure. Although more than 100,000 patients are currently alive due to dialysis and transplantation, mortality among ESRD patients is still much higher than in the general population. Gross mortality, calculated from aggregate statistics such as those available from the annual ESRD facility survey, is an extremely imprecise measure of mortality and can lead to misleading conclusions. Standard methods of survival calculation such as actuarial life-table analyses provide more accurate descriptions of variations and trends in mortality. The most important characteristic influencing mortality among ESRD patients on dialysis is the changing age and diagnostic distribution. The average age of dialysis patients has increased by over 5 years during the past decade. Patients whose renal failure is attributed to diabetic nephropathy currently account for 30% of all patients initiating renal replacement therapy each year and constitute the fastest growing group of ESRD patients. From 1982 to 1987, 1-year survival on dialysis was 72.7% for patients whose renal failure was attributed to diabetic nephropathy and 79.8% for all other patients. Survival decreases rapidly with advancing age at time of renal failure, from 95.1% among patients 15 to 24 years to 52.5% for patients over the age of 85 (for non-diabetics). Survival rates for whites are 5% to 6% lower than for other racial categories. There are no obvious trends in mortality among dialysis patients over the past decade. For patients whose renal failure is attributed to diabetic nephropathy, survival rates have remained constant despite overall aging in this group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mortality rates among dialysis patients in Medicare's End-Stage Renal Disease Program. 218 27

Diabetic nephropathy is now the leading cause of renal failure in patients referred for uremia therapy. The diabetic patient is a complicated treatment problem from the first detection of microalbuminmuria, at which time decisions regarding choice of antihypertensive and strictness of metabolic control assume increasing importance. At present, our policy is to advocate strict control of blood pressure, aiming for a systolic blood pressure of less than 140 mm Hg and a diastolic blood pressure of less than 80 mm Hg. We attempt to maintain hemoglobin Alc levels at less than 8%, if the patient does not develop frequent episodes of hypoglycemia. We extend these recommendations to the patient with frank proteinuria, nephrotic syndrome and early uremia, understanding that strict metabolic control may be impossible as patients lose GFR. In addition, we recommend avoidance of a high protein diet in the early nephropathic diabetic, with diet of approximately 1 gm/kg/d. As renal failure progresses, we embark on an analysis of the patient's abilities, lifestyle, and social support. At a GFR of approximately 10 mL/min, we initiate preparations for uremia therapy. If a willing and appropriate living related kidney donor is available, the patient is referred for cardiovascular evaluation and kidney transplantation performed subsequently. If no donor is immediately available, we refer the patient for vascular access placement and/or insertion of a Tenckhoff peritoneal catheter, if preferred. Most of these predialysis patients also undergo screening for placement on the cadaveric kidney transplant list, including cardiac work-up as is done for the patients who receive living-related renal transplants. Because of the long waiting list in Brooklyn, and the universal shortage of organ donors, many of these patients eventually end up on dialysis for some period of time. Other extrarenal problems (urologic, ophthalmologic) are addressed at initial referral and followed up, in hopes of maintaining the patient in optimal physical shape as uremia progresses. The care of the diabetic patient with ESRD ideally involves a consortium of caregivers. We include a nurse-educator familiar with options for uremia therapy, a podiatrist, a cardiologist, and often a urologist, an endocrinologist, and a gastroenterologist. In addition, a social worker is helpful to assess psychologic difficulties in adjustment to uremia, socioeconomic considerations, and rehabilitation status. Finally, the nephrologist, as coordinator of this team works with the vascular or transplant surgeon, to facilitate the transition to ESRD and its therapy.
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PMID:Care of the diabetic patient with end-stage renal disease. 219 Feb 84

Today the clinical picture of diabetes mellitus is often determined by its late complications. Diabetic nephropathy appears in about 40% of all diabetic patients with type 1 (insulin-dependent) diabetes mellitus within a period of 10-15 years. Early diagnosis is crucial for the prognosis as appropriate therapy may delay or even arrest the reduction of filtration fraction and terminal renal failure. Most important for the early diagnosis is the measurement of albumin and protein excretion.
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PMID:[Diabetic nephropathy. Pathogenetic, diagnostic and therapeutic concepts]. 220 99

The objective of the work was to evaluate the basic parameters of zinc metabolism, i.e. serum levels and urinary excretion of zinc (Zn) in insulin dependent diabetes. The authors investigated a group of diabetics with normal renal function (DM) and with chronic renal insufficiency as a result of diabetic nephropathy (RIDM). Two control groups were formed by healthy volunteers (C) and non-diabetic subjects with chronic renal insufficiency (RI). In diabetics without impaired renal functions (DM) the Zn serum levels did not differ significantly from controls, urinary excretion was significantly raised. The authors did not reveal a correlation of serum Zn levels with parameters of compensation of diabetes nor with the insulin dose. Urinary Zn output correlated positively with proteinuria and the average blood sugar level during the collection of urine. The authors did not find a correlation with diuresis, fractional water excretion, glycosuria or urea excretion. The fractional Zn clearance in diabetic subjects was significantly raised and correlated with the mean blood sugar level. This finding suggests a decline of the tubular Zn absorption in hyperglycaemia. In diabetics with renal failure (RIDM) the results did not differ from non-diabetics with the same degree of renal insufficiency: serum Zn levels were, as compared with healthy controls, in both groups significantly reduced, the urinary excretion being normal. Thus insulin dependent diabetes nor its metabolic compensation do not influence in a marked way serum Zn levels but lead to higher urinary Zn losses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serum levels and urinary excretion of zinc in patients with insulin-dependent diabetes]. 220 24


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