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Progress in our understanding diabetic angiopathy has been slow, but we are now learning a number of lessons of interest to the cardiologist. Diabetic angiopathy is a collective term for conditions specific to the diabetic state and related to its duration more than to patient age. The angiopathy produces calcification of the media of larger arteries, but its major effects are in the microcirculation. Intense interest in one feature, skeletal muscle capillary basement membrane thickening, has dominated the last decade. Capillary basement membrane thickening, while characteristic of diabetes, is associated with little direct impairment of the microcirculatin. It appears to play no role in the pathogenesis of diabetes itself. The pathology of diabetic retinopathy and diabetic nephropathy suggests that arteriolar changes may be the major mediator of diabetic angiopathy. This concept is supported by the interactions between hypertension and diabetes in the eye and kidney. The course of diabetes of youthful onset differs from that of maturity onset. The relative frequency of diabetic angiopathy is higher, and of atherosclerotic complications is lower. This has made it difficult to demonstrate the potential value of preventive measures. Benefit to one type of problem may become hidden by worsening of the other. If the diabetic benefits from what is learned about how ischemic heart disease risk can be reduced, he will require even more effective management to prevent or control diabetic angiopathy.
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PMID:Diabetic angiopathy--its lessons in vascular physiology. 35 70

The clinical course of diabetic nephropathy was evaluated in 150 patients and the effect of hemodialysis in 68 of them. Proteinuria was the first sign of renal disease. Once renal dysfunction becomes evident, there is a rapid deterioration leading to dialysis within 3.0 +/- 0.2 years. Hypertension and circulatory congestion are common complications. The hypertension is probably volume dependent. Retinopathy was not invariably present at the onset of renal insufficiency but appeared with progression of renal failure. The course during hemodialysis was complicated by continued progression of diabetic vascular disease manifested by vascular access difficulties, worsening of retinopathy and blindness, and cardio- and cerebrovascular deaths. Mortality was higher than in nondiabetic dialysis patients.
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PMID:Diabetic nephropathy: clinical course and effect of hemodialysis. 64 44

The most serious complication of diabetes mellitus is clinical nephropathy. The development of persistent proteinuria (urinary excretion of more than 300 mg albumin/24 hours) implies an extremely high risk of early death. Renal failure is the most frequent cause of death but the mortality of cardiovascular diseases is also increased. Besides the link between albuminuria (nephropathy) and atherosclerosis in coronary arteries, albuminuria is also a predictor of microangiopathy in other organs than the kidneys. The annual incidence of proliferative retinopathy in early nephropathy is 10-15% compared to only 1% in patients without nephropathy. Also signs of cardiomyopathy have been demonstrated in early nephropathy. Further we have described markers of universal endothelial damage in these patients, and we hypothesize that albuminuria not only is a predictor of renal disease but also of widespread vascular disease. Long-term improvement of metabolic control by use of insulin infusion pumps and early antihypertensive treatment seem to stop the further progression of early diabetic nephropathy and to significantly improve the prognosis of clinical nephropathy.
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PMID:Diabetic retinopathy, nephropathy and neuropathy. Generalized vascular damage in insulin-dependent diabetic patients. 149 Jun 95

Since the late 1970s patients with diabetic nephropathy have formed an increasing proportion of new entrants to the Hospital renal dialysis and transplantation programme, reaching 28% for the three year period to December 1988. Between 1 January 1975 and 31 December 1988, 87 diabetic patients were accepted for treatment. Fifty-one per cent were European, predominantly type I diabetics. Maori (9% of the total reference population) accounted for a disproportionately high 47% due to an over-representation by type II diabetic patients (34 of 41 Maori). These findings cannot be explained by the higher prevalence in Maori of type II diabetes but appear to be due to a more prevalent and/or aggressive diabetic renal lesion in this group. On commencing treatment, nearly all patients had retinopathy and the majority had evidence of peripheral vascular disease, hypertension and neuropathy. CAPD was the initial mode of renal replacement therapy in 70% of patients. Overall patient survival was 77% at one year and 42% at three years, and survival on CAPD was 76% and 37% at one and three years, respectively. Patient survival on transplantation was 63% at one year and 58% at three years. Graft survival was 51% at one year and 46% at three years. Although the short term outlook for diabetic patients on renal replacement therapy is encouraging, longer term survival compared to non-diabetic patients is poor. Vascular disease is the major cause of death and an important factor in patient morbidity.
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PMID:Diabetic end stage renal failure--the Wellington experience 1975-1988. 203 73

Atherosclerotic vascular disease is a major cause of morbidity and mortality in insulin-dependent diabetes mellitus. The frequent coexistence in these patients of microangiopathy and coronary artery disease was observed more than 30 years ago and later verified in large epidemiological studies. Thus, the subgroup (30-40%) of patients who develop clinical nephropathy, also are at extremely high risk of early cardiovascular death. A number of established cardiovascular risk factors are present not only in advanced clinical nephropathy but also in its earliest stages. These include elevated blood pressure, atherogenic changes in the plasma concentrations of lipids and lipoproteins, elevated plasma levels of fibrinogen and probably hyperreactivity of platelets. However, it seems unlikely that these risk factors fully explain the excess cardiovascular morbidity and mortality in insulin-dependent diabetic patients with clinical nephropathy. Patients with slightly elevated urinary albumin excretion are at increased risk of developing not only clinical nephropathy and coronary heart disease but also proliferative retinopathy and cardiomyopathy. We have, therefore, hypothesised that elevated urinary albumin excretion is a marker of generalized disease in the vascular wall of small and large blood vessels. Findings of elevated transcapillary escape rate of albumin, elevated plasma concentration of von Willebrand factor and impaired fibrinolytic capacity in early diabetic nephropathy have supported this hypothesis. However, the initial pathophysiological mechanisms involved are still hypothetical and largely unknown. During recent years the incidence of clinical nephropathy has declined and the prognosis of insulin-dependent diabetic patients has improved. Whether intervention directed against the often clustered cardiovascular risk factors will further improve the prognosis in proteinuric patients is suggested but still unknown. However, the key question is still, why is the vascular wall, in small and large blood vessels, vulnerable in some but not all diabetic patients? In the future more studies of the initial pathophysiological mechanisms involved in this vulnerability are needed.
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PMID:Albuminuria--a marker of renal and generalized vascular disease in insulin-dependent diabetes mellitus. 206 Mar 21

The 497 members of the London Cohort of the WHO Multinational Study of Vascular Disease in Diabetics have been followed for mortality from 1975 to 1987. During this period 92 patients died. The most common cause of death was myocardial infarction: 36 (39.1%) deaths, heart disease was responsible for 51.1% of deaths and all cardiovascular disease for 55.4%. Neoplastic disease accounted for 25% of the deaths and diabetic nephropathy for 5.4%. Age-standardised mortality rates were higher in men than in women in both Type 1 (insulin-dependent) diabetes and Type 2 (non-insulin-dependent) diabetes. Standardised mortality ratios for the first and second five year follow-up periods were higher for men than for women in Type 2 diabetes but were higher for women than men in Type 1. The results suggest that the female survival advantage seen in the general population may persist in Type 2 but not in Type 1 diabetes.
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PMID:A prospective study of mortality among middle-aged diabetic patients (the London Cohort of the WHO Multinational Study of Vascular Disease in Diabetics) I: Causes and death rates. 225 30

The prevalence of smokers among patients with diabetes is found to be lower than in the population as a whole. Diabetic patients have increased morbidity and mortality from cardiovascular diseases and, in the majority of investigations, smoking is found to be a risk factor in this relationship which does not differ quantitatively from that found in non-diabetics. On the basis of the literature, it has not proved possible to quantitate smoking as a risk factor for the development of peripheral arteriosclerotic vascular disease. Smoking involves hormonal and metabolic changes which are of particular interest in relation to diabetes mellitus. Thus, smoking stimulates the secretion of the antiinsulin hormones, particularly catecholamines, resulting in subcutaneous vasoconstriction which may be unfortunate as it influences insulin absorption. Patients who smoke do not, however, appear to present poorer glycaemic control than non-smokers. A few investigations have shown that smokers have greater insulin requirements than non-smokers. In type 1 (insulin-dependent) diabetes, there is evidence to suggest that diabetic nephropathy and proliferative retinopathy occur more frequently in smokers than in non-smokers. Smoking aggravates the pre-existing more pronounced osteoporosis which occurs in female insulin-dependent patients. It is therefore advantageous to advise diabetic patients against smoking from the point of view of diabetes as such.
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PMID:[Smoking and diabetes mellitus]. 268 32

Abnormal albumin excretion in the range not previously detectable by routine clinical methods can now be readily quantified, and has been shown to predict the development of clinically significant nephropathy in insulin-dependent diabetes mellitus (IDDM) and to predict excess mortality in non-insulin-dependent diabetes mellitus (NIDDM). Albuminuria of this degree has been inappropriately called "microalbuminuria," a misleading term which should be abandoned. In IDDM, persistent minimal elevation of albumin excretion predicts the development of more severe proteinuria and clinical diabetic nephropathy, which frequently progresses to renal failure. In NIDDM, the predictive value for renal failure remains to be established, but excess mortality occurs in those with abnormal albumin excretion, suggesting that it is an indicator of generalized vascular disease. However, the normal range of albumin excretion in older subjects is not well established. The relationship of glomerular injury to mildly elevated albumin excretion is uncertain. Several means of reducing the excretion rate have been described, but whether these can halt or prevent progression of glomerular injury is unknown. Thus, at the present time detection of mildly elevated albumin excretion and intervention to reduce the incidence of diabetic nephropathy or other diabetes-related complications fail to meet generally accepted criteria for prescriptive screening. However, such measurements of albumin excretion provide an important tool for research into the natural history and pathogenesis of diabetic nephropathy.
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PMID:'Microalbuminuria' and diabetes: a critique--assessment of urinary albumin excretion and its role in screening for diabetic nephropathy. 291 62

Beta-thromboglobulin (beta TG) is a platelet-specific protein and since its concentration in plasma rises when platelets are activated, it has been used as an indicator of platelet involvement in vascular disease. Since platelets might be involved in the pathogenesis of diabetic microvascular disease we measured urinary beta TG in 20 insulin-dependent diabetics with nephropathy and compared the results with those from 20 normal subjects. Measurement of beta TG in urine was undertaken to avoid errors induced by blood sampling and to gain information over a prolonged period using a single assay. Measurements were made of beta TG, beta 2-microglobulin and total protein in urine collected for 24 h and creatinine and beta 2 microglobulin in plasma. Survival of indium-111-labeled platelets was measured in nine patients. Urinary beta TG was significantly (p less than 0.02) increased in the 20 patients compared with 20 normal volunteers (median value 1.3 vs 0.8 microgram/24 h). There was a strong correlation between urinary beta TG excretion and plasma creatinine concentration (r = 0.8, p less than 0.0001) and plasma beta 2-microglobulin concentration (r = 0.9, p less than 0.0001). Urinary beta TG concentration did not correlate with platelet survival. The results indicate that although urinary beta TG is significantly increased in patients with diabetic nephropathy its concentration in urine correlates with indicators of glomerular filtration rather than with a test of platelet activation.
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PMID:Urinary beta-thromboglobulin correlates with impairment of renal function in patients with diabetic nephropathy. 294 92

Twenty-three patients with end-stage renal failure due to diabetic nephropathy received renal replacement treatment. All patients had insulin-dependent diabetes mellitus. Nineteen transplants were performed in seventeen patients. Two-year graft survival for all transplants was 74% with a two-year patient survival post-transplantation of 81%. Overall two-year patient survival was 73%, compared with 82% in non-diabetic patients receiving renal replacement treatment. In diabetic patients accepted for treatment there was a high incidence of non-renal complications, particularly vascular disease. An aggressive approach to the treatment of vascular disease in these patients may improve overall survival rates.
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PMID:Renal replacement treatment for diabetic nephropathy in Northern Ireland 1979-1987. 304 56


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