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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mutual relationship between elevated blood pressure and structural changes in the kidney is still an area with more open questions than clear answers. Indirect evidence is available concerning one aspect: When hypertension is present it has a significant impact on the further progression of the structural changes. This evidence is available only in terms of the effect of antihypertensive treatment on the preservation of renal function. Since it has been shown that the demise in renal function in long-term diabetics is closely related to the development of advanced diabetic glomerulopathy, it seems likely that normalization of the blood pressure leads to a slowing of this development. Structural studies to elucidate these interactions are, however, not available. An intriguing question is whether the relationship is interactive also in the other direction. Focusing on the alterations within the glomeruli, the fact is that the glomerulopathy develops over several years before it come to the stage when clinical signs appear. Thus, diabetics with "incipient nephropathy" clearly demonstrate basement membrane (BM) accumulation, showing as increased BM-thickness and increase in mesangial matrix volume. Since this is the most likely point of time for hypertension to develop the necessary condition obtains, that the development of hypertension might be triggered by structural abnormalities in the kidney. The mechanisms of action at this point of time remain speculative. The relationship between structural parameters characterizing diabetic glomerulopathy and the blood pressure level was studied in a series of 14 IDDM patients, representing a span of renal functional impairment. Mean blood pressure in the group was 117 mmHg, with a range from 87-122 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Morphology of diabetic glomerulopathy and relationship to hypertension. 269 44

Although an elevated blood pressure has been proposed as one of the major risk factors for the development and acceleration of diabetic retinopathy, demonstration of an unequivocal association between high blood pressure and retinopathy is lacking. Recent epidemiologic, cross-sectional studies indicated a close relationship between elevated systolic blood pressure and diabetic retinopathy, particularly in NIDDM subjects. In IDDM patients, the association with diastolic blood pressure was more pronounced. In the few prospective studies with sufficient number of individuals and acceptable documentation of retinal changes, in addition to poor metabolic control elevated blood pressure emerged as one of the best predictors of the development of severe deterioration of diabetic eye disease. In the Joslin study the risk of progression to severe forms of diabetic retinopathy increased exponentially with hemoglobin A1c and was dramatically different in patients with diastolic blood pressure below versus above 70 mmHg. It was hypothesized that a very low diastolic blood pressure is associated with some mechanisms which are protective against progression of eye lesions. Treatment and adequate control of hypertension is strongly recommended in all diabetic patients, the optimal level of blood pressure reduction, however, is yet to be determined.
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PMID:Impact of blood pressure on diabetic retinopathy. 269 52

Approximately one third of patients with IDDM develop end-stage renal disease. About the same percentage, though not of certainty the same patients, have elevated GFRs and plasma flow rates early in their disease and probably have elevated capillary pressure. Arterial hypertension in the setting of this pattern of renal vasodilation may be particularly predisposing to glomerular injury. Treatment of established diabetic nephropathy with good antihypertensive control can dramatically reduce the rate of progression of the disease. However, blood pressure control should be targeted to near normal ranges, that is, mean arterial pressures less than 100 mmHg and preferably lower. Some agents may be particularly beneficial in slowing the progression of the disease, but even standard agents have very important effects.
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PMID:Antihypertensive therapy in diabetes. 273 23

Intraplatelet serotonin (5-HT) content was determined in 23 patients with type I (insulin-dependent) diabetes mellitus (IDDM), 23 patients with type II (non-insulin-dependent) diabetes mellitus (NIDDM), 29 patients with peripheral vascular disease (PVD) and 34 age-matched normal subjects. Intraplatelet 5-HT content in normal subjects showed an age-related decline (r = -0.45; P less than 0.008), as has been previously demonstrated. The median 5-HT content in platelets of the young normal subjects was 4.36 (range: 3.62-6.79) nmol 10(-9) platelets, while that in the elderly normal subjects was 3.87 (range: 2.8-6.0) nmol 10(-9) platelets and that in young + elderly subjects was 4.05 (range: 2.8-6.8) nmol 10(-9) platelets. The median intraplatelet 5-HT content was significantly lower (P less than 0.002) in IDDM patients: 3.0 (range 1.3-6.3), NIDDM patients: 2.5 (range 1.7-5.8), PVD patients: 2.42 (range 0.94-4.98) nmol 10(-9) platelets than that in all young + elderly healthy subjects. The presence of hypertension in DM patients caused a small but significant (P less than 0.05) decrease in intraplatelet 5-HT content, whilst its presence had no effect in PVD patients. In a smaller study, it was established that NIDDM and PVD patients have significantly (P less than 0.002) greater plasma 5-HT concentrations than controls. Insulin-dependent diabetes mellitus patients had greater plasma 5-HT concentrations but this did not achieve statistical significance despite a 66% increment in its value.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intraplatelet serotonin in patients with diabetes mellitus and peripheral vascular disease. 313 26

Excretion of digoxin-like immunoreactivity (DLIS) was measured by RIA in timed overnight urine collections from 91 normotensive nondiabetic subjects and 104 normotensive insulin-dependent diabetic (IDDM) patients. The mean +/- SD DLIS excretion rate for the diabetic patients significantly exceeded that for the controls (73 +/- 41 vs 63 +/- 36 pg/min, P = 0.024). In both groups, the mean DLIS excretion rates for men were significantly higher (P = 0.0014, P = 0.006) than for women. In the controls, the DLIS excretion rate significantly correlated with the urinary excretion rate of creatinine (P less than 0.01), Na+ (P less than 0.05), and K+(P less than 0.05), and with the subjects' body weight (P less than 0.01), body mass index (P less than 0.05), and systolic blood pressure (P less than 0.05). In the diabetics, the DLIS excretion rate was significantly correlated with body weight (P less than 0.05) and with urinary excretion rates for albumin (P less than 0.01), creatinine (P less than 0.01), Na+ (P less than 0.05), and K+(P less than 0.05). Our data indicate that: (a) increased amounts of a cardiac glycoside-like substance (or a group of substances) are excreted in the urine of IDDM patients; (b) the urinary excretion of DLIS seems to depend on glomerular filtration rate and physiocochemical properties of glomerular membrane, as well as on subjects' body mass; and (c) because cardiac glycoside-like substances may increase peripheral vascular resistance, increased urinary excretion of DLIS by IDDM patients may indicate a tendency to develop hypertension.
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PMID:Increased urinary excretion of digoxin-like immunoreactive substance by insulin-dependent diabetic patients: a linkage with hypertension? 319 78

Diabetic retinopathy was studied in two cohorts of insulin-dependent diabetics (IDDs) from the Children's Hospital of Pittsburgh. The first cohort (n = 696) consisted of IDDs of long duration. Severe retinopathy was self-reported in 70% of this cohort by 30 years duration of diabetes. Associations between severe retinopathy, hypertension and smoking were observed. In order to examine the relationship between metabolic control and early diabetic retinopathy, a second cohort of adolescent IDDs (n = 58) were referred for standardized fluorescein angiography. Sixty-four percent had early retinopathy. None had proliferative changes. Significant differences in individual mean whole blood glycosylated hemoglobin (GHb), averaged over 3 years before angiography, were consistently seen between those with and without early retinopathy. Also, the number of microaneurysms was positively correlated with individual mean GHb. Before the advent of GHb testing, those IDDs who later had retinopathy were more likely to have experienced at least one hospitalization for diabetic ketoacidosis. These observations provide strong support that poor metabolic control preceded the development of diabetic retinopathy. Results are consistent with the hypothesis that improvement of metabolic control early in the course of IDDM may prevent or delay the development of the early changes of diabetic retinopathy.
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PMID:An epidemiologic approach to the study of retinopathy: the Pittsburgh diabetic morbidity and retinopathy studies. 334 36

Diabetes is associated with changes in plasma lipids and lipoproteins into atherogenic direction. In IDDM these changes are small or absent if good metabolic control can be maintained. Diabetic nephropathy is, however, associated with the appearance of dyslipoproteinemia. In NIDDM plasma total and VLDL triglyceride levels are elevated, and HDL-cholesterol level is decreased, and this pattern of dyslipoproteinemia does not always respond to improved control of hyperglycemia. Abnormalities of lipoprotein metabolism, not reflected in conventional plasma lipid and lipoprotein level measurements, and glucosylation of lipoproteins and resulting alterations in lipoprotein catabolism may be of importance in the enhanced atherogenesis in diabetes. Both IDDM and NIDDM are associated with an increased frequency of hypertension, but the underlying mechanisms appear to be different. In IDDM hypertension is usually associated with the development of diabetic nephropathy and thus with a long duration of the disease. In NIDDM hypertension is often present already at the time of diagnosis, and also in IGT, the precursor stage of NIDDM, the prevalence of hypertension is already increased. Obesity explains only in part the high prevalence of hypertension in patients with NIDDM. Diabetes is known to be associated with multiple abnormalities in hemostatic factors and, although these abnormalities may contribute importantly to the increased risk of ASVD in diabetic patients, information about their real role is scanty and conflicting. The impact of general major risk factors for ASVD, elevated plasma cholesterol, elevated blood pressure, and smoking, on the risk of ASVD appears to be similar in diabetics and nondiabetics. Only a relatively small proportion of the excessive occurrence of ASVD in diabetics can, however, be explained by the effects of diabetes on the levels of general risk factors for ASVD. This proportion mediated through the effects of diabetes on risk factors is larger in female diabetics than in male diabetics. The major proportion of the excess of ASVD in diabetics remains, however, unexplained and must be due to effects of diabetes itself through mechanisms that are incompletely understood.
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PMID:Diabetes and atherosclerosis: an epidemiologic view. 355 30

Eighteen individuals with IDDM (type I) and diabetic nephropathy in whom the initial glomerular filtration rate (GFR) was reduced but not below 60 ml/min per 1.73 m2 were observed for an average of 3 yr. The rate of further decline of GFR was found to range between -2 and 21 ml/min/yr. The duration of diabetes until the GFR was first found to be reduced varied between 14 and 33 yr and was not correlated to the ensuing rate of decline in GFR (r = -0.13). In 10 individuals who developed uremia 40 yr or more after onset of IDDM, the development of persistent proteinuria was followed by hypertension and increased serum creatinine 2 yr later and by terminal uremia after an average of 8 yr. This is also the normal time span for individuals who develop terminal uremia after shorter duration of diabetes. We conclude that the course of clinical diabetic nephropathy is not more favorable in individuals with late onset of this complication and that there is no point at which a person with diabetes can be considered to be spared from developing diabetic nephropathy.
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PMID:Time as a risk factor in diabetic nephropathy. 407 45

The prevalence of arteriosclerosis obliterans (ASO) of the legs was determined by a battery of noninvasive tests in 141 insulin-dependent and 289 non-insulin-dependent diabetic subjects and in 64 other subjects. The prevalence of detectable ASO ranges from 18% in the younger IDDM group to 41% in the diet-treated NIDDM group. The prevalence of ASO increases 7.5% per decade, appears to increase 6.5% in the age-adjusted IDDM group, 9% in males, 19% in those with hypertension, and 12% in smokers. No consistently significant correlations with fasting glucose, glycosylated hemoglobin, or obesity were found. After accounting for the effect of smoking, the increased risk for ASO in males becomes nonsignificant.
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PMID:Arteriosclerosis obliterans and associated risk factors in insulin-dependent and non-insulin-dependent diabetes. 742 28

Diabetic nephropathy is a progressive renal disease and represents a serious late complication of diabetes. There are familial clustering and huge ethnic differences in the occurrence of diabetic nephropathy, which point to a genetic predisposition. Diabetic nephropathy is defined by persistent albuminuria (albumin excretion rate [AER] > 300 mg/day), declining glomerular filtration rate and rising blood pressure. Several years of incipient nephropathy, characterized by worsening microalbuminuria (AER 30 to 300 mg/day or 20 to 200 micrograms/min), which is Albustix-negative and detectable by special assays only, are followed by established nephropathy. The natural history of nephropathy differs between insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) diabetes mellitus. In IDDM, nephropathy develops in 30 to 40% of cases. The incidence peaks after 15 to 16 years of diabetes. In NIDDM, estimates of prevalence range from 15 to 20%, and nephropathy often supervenes after a shorter known duration of diabetes than in IDDM. GFR is often increased above normal (hyperfiltration) from the onset of IDDM due to increased renal blood flow, glomerular capillary hypertension and increased filtration surface. The glomeruli are hypertrophied and the kidneys enlarged. In both IDDM and NIDDM, GFR begins to decline irreversibly, when AER has risen to 100 to 300 mg/day at an average rate of 10 ml/min. per year. This is due to progressive reduction of the filtration surface area through mesangial expansion. Serum creatinine levels begin to rise when GFR falls below 50 ml/min, and then end-stage renal failure follows after an average of five years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diabetic nephropathy: significance of microalbuminuria and proteinuria in Type I and Type II diabetes mellitus]. 749 50


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