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

The epidemiological evidence that only a subset of diabetic patients are susceptible to renal damage and the demonstration of clear familiar clustering of diabetic nephropathy are consistent with the possibility that genetic factors may explain the liability to or protection from renal disease of diabetic patients. A predisposition to hypertension and cardiovascular disease may be an important determinant of susceptibility to renal disease and its cardiovascular complications in diabetes since raised blood pressure [1] and an increased frequency of cardiovascular disease [2] are more prevalent in parents of diabetic patients with nephropathy. These results have raised growing interest in the search for intermediate phenotypes significantly associated with diabetic nephropathy, poorly influenced by environment, stable with age, easy to quantify and possibly dependent upon a single major gene effect. Such intermediate phenotypes can be useful for early diagnosis and would help clarify the molecular mechanisms leading to diabetic nephropathy. An elevation of Na+/H+ antiporter activity has consistently been associated with diabetic renal disease both in insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) patients, making this cell membrane exchanger system an ideal intermediate phenotype for the study of diabetic nephropathy.
Nephrol Dial Transplant 1997 Apr
PMID:Sodium-hydrogen antiporter: its possible role in the genesis of diabetic nephropathy. 914 Sep 84

To determine whether the onset of coronary artery disease may precede the initiation of dialysis in patients with end-stage renal disease, we performed coronary angiography within 1 month of initiation of maintenance haemodialysis in 24 patients (age range 42-78 years; mean 63.7 +/- 11). Coronary angiography was performed regardless of the absence or presence of angina. Fifteen patients had diabetic nephropathy, and nine had non-diabetic nephropathy. Significant coronary stenosis was defined as at least 75% narrowing of the reference segment. Fifteen patients (62.5%) with a total of 49 lesions were classified as the coronary artery disease present group. Eleven of those 15 (73.3%) had multivessel disease. The average number of stenotic lesions was 3.3 per patient. The most common patterns of stenosis were complex (23 lesions; 47%), and diffuse lesions over 20 mm long (14 lesions; 29%). None of the clinical or haematological factors evaluated differed significantly between the groups with and without coronary artery disease. The prevalence of coronary artery disease was 72.7% in the symptomatic patients and 53.8% in the asymptomatic patients. The diagnosis of coronary artery disease at the start of maintenance haemodialysis based only on chest symptoms and clinical factors proved to be difficult. Coronary angiography is thus essential for evaluating coronary artery disease in uraemic patients. Many patients with end-stage renal disease had coronary artery disease prior to the start of haemodialysis.
Nephrol Dial Transplant 1997 Apr
PMID:Onset of coronary artery disease prior to initiation of haemodialysis in patients with end-stage renal disease. 914 Oct

Recently evidence has accumulated that diabetic nephropathy clusters in families, both in insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetic patients. Furthermore, hypertension and cardiovascular accidents are found more frequently in families of NIDDM with diabetic nephropathy. Some observations in offspring of NIDDM patients with diabetic nephropathy point to high urinary albumin excretion and slightly greater blood pressure values, both within the normal range compared to offspring of patients without diabetic nephropathy. Further follow-up is required to assess whether these findings are indicative of a possible genetic predisposition to diabetic nephropathy.
Nephrol Dial Transplant 1997
PMID:Risk factors for development of diabetic nephropathy: a review. 926 95

Rapid growth in the number of dialysis patients over the age of 65 is occurring coincidentally with the overall aging of the general population. Elderly patients are often poor and physically incapacitated, needing family or social support. These patients may also be susceptible to malnutrition and have multiple complicating medical disorders in addition to end-stage renal disease (ESRD). Thus the selection of an appropriate dialysis modality is particularly critical in elderly patients. Continuous ambulatory peritoneal dialysis (CAPD) offers many advantages to elderly patients, including hemodynamic stability, steady-state chemistries, and no need to create a vascular access. However, little data are available in the literature documenting the use of CAPD in this setting. Therefore, to evaluate the efficacy of CAPD in elderly patients, we retrospectively reviewed the clinical outcomes of 23 patients 65 years of age or older at the start of CAPD (elderly group). Then for each of these patients, 23 comparison subjects younger than 65 were chosen from CAPD patients at our hospital (control group). The control group was matched for sex, CAPD duration, cause of ESRD, and initial connection device. In the elderly group, 23 patients (12 male, 11 female) with a mean age of 70 +/- 4 years (range 65-86 years) were treated with CAPD for 15 +/- 17 months. In the control group, 23 patients (12 male, 11 female) with a mean age of 41 +/- 11 (range 18-57) were treated with CAPD for 16 +/- 17 months. Diabetic nephropathy was the cause of ESRD in 35% of patients. The negative CAPD selection of patients was higher in the elderly group (61% vs 17%, p = 0.0025) as well as in the group that needed a helper (61% vs 17%, p = 0.0025). The exit-site infection and peritonitis rates were not statistically different between the two groups (0.43 vs 0.91 episodes/patient-year and 1.46 vs 2.03 episodes/patient-year). The dialysate leakage and bleeding rates were comparable (13% vs 22% and 9% vs 9%). One-year catheter survival was similar in the elderly and younger patients (87.5% vs 84.0%). Although the negative CAPD selection of patients was higher in the elderly group, outcomes were similar to those seen in younger patients. Therefore, CAPD is an acceptable form of therapy for the elderly ESRD patients, particularly if a helper can participate.
Adv Perit Dial 1997
PMID:CAPD, an acceptable form of therapy in elderly ESRD patients: a comparative study. 936 Jun 73

The vast majority of animal data derived from models of either remnant kidney or diabetes demonstrate that dihydropyridine (nifedipine-like) calcium-channel blockers (DHPCCBs) effectively reduce arterial pressure but do not significantly affect proteinuria nor prevent development of glomerular scarring. Conversely, the non-DHPCCBs such as diltiazem and verapamil blunt both the rise in proteinuria as well as mesangial matrix expansion and subsequent glomerular scarring in diabetes. Additionally, the non-DHPCCBs markedly attenuate development of glomerular scarring in the remnant kidney model. The primary reasons for these differences between subclasses of CCBs relates to a lack of the following attributes by DHPCCBs: (1) they fail to reduce glomerular membrane permeability which is increased in these models; (2) they fail to affect the synthesis of certain key matrix proteins that perpetuate development of glomerular scarring (this effect may be due to the differential expression of calcium channels within the glomerular mesangium); and (3) the DHPCCBs totally abolish renal autoregulation in these models, an effect not observed with non-DHPCCBs. Taken together with long-term (> 3 year) clinical studies, primarily in diabetic nephropathy, it is clear that the non-DHPCCBs seem to offer protection to the kidney not available with DHPCCBs alone, unless systolic arterial pressure is reduced to levels of < or = 110 mmHg.
Nephrol Dial Transplant 1997 Nov
PMID:Preservation of renal function: the spectrum of effects by calcium-channel blockers. 976 40

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.
Nephrol Dial Transplant 1998
PMID:The drama of the continuous increase in end-stage renal failure in patients with type II diabetes mellitus. 987 Apr 18

This brief review will focus on the major factors leading to incipient diabetic nephropathy (i.e. microalbuminuria) progressing to overt nephropathy (i.e. macroalbuminuria) and particularly on the role of glycaemic control and hypertension. Both experimental and cohort studies support the role of hyperglycaemia in the development of diabetic nephropathy. Some recent long-term interventional studies in microalbuminuric patients show conflicting results regarding the role played by good metabolic control in reducing the incidence of overt nephropathy. However, strict metabolic control, which is fundamental in normoalbuminuric patients, is of little use even in microalbuminuric patients. In general, levels of glycosylated haemoglobin less than two standard deviations above the upper normal range, commonly <7.5-8%, seem to protect patients from developing nephropathy. The results of many cross-sectional studies have shown that the progression of renal damage regularly is accompanied by arterial hypertension both in insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). Many long-term interventional studies have been performed in order to understand the effect of antihypertensive treatment on the incidence of proteinuria in both normotensive and hypertensive patients with IDDM or NIDDM. These data show a marked effect of antihypertensive therapy in preventing the onset of overt nephropathy, and suggest the superiority of angiotensin-converting enzyme (ACE) inhibitors. We believe that optimal blood pressure values are approximately 120/70-75 mmHg in younger patients and 125-130/80-85 mmHg in older patients. In conclusion, antihypertensive treatment, ACE inhibitors per se and possibly strict metabolic control reduce the development of nephropathy, thus playing a striking role in the secondary prevention of renal failure.
Nephrol Dial Transplant 1998
PMID:Diabetic nephropathy: from micro- to macroalbuminuria. 987 Apr 19

Diabetic nephropathy is one of the leading causes of renal failure in Western countries, where diabetic patients account for nearly half of all patients on haemodialysis. Progressive expansion of the mesangial matrix, and thickening of the glomerular and tubular basement membranes without signs of major cell proliferation are hallmarks of human and experimental diabetic nephropathy. These lesions eventually lead to glomerular fibrosis, a central pathological feature in many human acute and chronic kidney diseases, which progressively destroys the renal filtration unit, and may finally cause renal failure. Indeed, structure function relationship studies have shown that mesangial matrix expansion is strongly related to the clinical manifestation of diabetic nephropathy.
Nephrol Dial Transplant 1998
PMID:Molecular biology of diabetic glomerulosclerosis. 987 Apr 21

The progressively growing number of patients with end-stage renal failure (ESRF) associated with diabetes mellitus and requiring renal replacement therapy (RRT) stimulated both nephrologists and diabetologists to investigate the mechanisms linking hyperglycaemia to diabetic renal failure and to set up measures to prevent the onset and slow the progression of diabetic nephropathy. Over the last few decades, a large number of studies have investigated both the incidence of diabetic nephropathy and the relationship between metabolic control and the development of diabetic nephropathy. Chronologically, the first type of diabetes and diabetic nephropathy to be studied was type I, and it is only in recent years that metabolic control has been proven to be a contributor to the development of nephropathy in such patients. Recently, the DCCT demonstrated that metabolic control in the prealbuminuric phase was effective in reducing the incidence of microalbuminuria, even if it was unable to reduce the incidence of overt proteinuria in patients with type I diabetes and established proteinuria. On the other hand, in type II diabetes, the number of studies demonstrating a favourable effect of metabolic control on onset and progression of diabetic nephropathy is only slightly greater than those that failed to show a favourable effect. This feature may suggest that in type II patients, genetic and ethnic differences, nutritional aspects, lifestyle and other confounding factors may play a relevant role in the course of the disease. However, the trials performed and the retrospective analyses generally agree that glycated haemoglobin two standard deviations greater than the mean is related to a worsening in progression of diabetic nephropathy and to an enhanced risk of other complications. In general, a glycated haemoglobin < or =8% seems advisable. Moreover, in both type I and type II, greater emphasis should be placed on the major risk factors such as hypertension, smoking habits and hyperlipidaemia.
Nephrol Dial Transplant 1998
PMID:The effect of metabolic control on development and progression of diabetic nephropathy. 987 Apr 24

Thirty-two patients with diabetes mellitus (22 IDDM and 10 NIDDM, 21 males and 11 females, age 44+/-11.8 years) were followed for 5.2+/-3.8 years after the onset of chronic renal failure, with the aim of evaluating the effect of low protein diets on the rate of decline of the residual renal function. During the 1.8+/-1.6 year follow-up period on free or uncontrolled low protein diet the mean rate of decline of creatinine clearance was 0.9+/-0.6 ml/min/month, significantly greater than that observed during 3.7+/-3.1 years on low or very low protein diets. The reduction of protein intake was followed by a significant decrease in daily urinary protein loss. A better glycaemic control was obtained on the low protein diet, and the daily insulin requirement decreased. The anthropometry, as well as the serum concentrations of rapid turnover proteins, did not change, in spite of the low or very low protein dietary supply for a long duration. The values of mean arterial pressure were quite similar during the follow-up period on free or uncontrolled low protein diet and during the study period on the low protein diet. A good compliance with reduced dietary intake (as demonstrated by the measurement of the daily urea excretion) was obtained in a large number of patients. In conclusion, our study confirms the protective effect on the residual renal function of low protein diets in IDDM and NIDDM patients with chronic renal failure due to diabetic nephropathy, in the absence of any sign of protein malnutrition.
Nephrol Dial Transplant 1998
PMID:Dietary treatment of diabetic nephropathy with chronic renal failure. 987 Apr 26


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