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

The course and prognosis of chronic renal failure are much worse in hypertensive patients than in normotensive patients with otherwise similar basic disease. Therefore, antihypertensive measures with a combination of diuretics, beta-blockers, and vasodilators have clearly been shown to improve the progression of diabetic nephropathy. Treatment of hypertension with angiotensin-converting enzyme (ACE) inhibitors has also been shown to have a favorable effect on the prognosis of chronic renal failure. In the past few years, more knowledge about the pathogenesis of hypertension and the development of hypertension-induced organ damage has been followed by changing attitudes to antihypertensive therapy and the introduction of calcium antagonists for the treatment of hypertension, even in chronic renal failure. ACE inhibitors and calcium antagonists seem to be advantageous in the prognosis of chronic renal failure as they act on the humoral and trophogenic factors now known to be important in antihypertensive therapy.
J Cardiovasc Pharmacol 1992
PMID:The effect of antihypertensive therapy on the course of renal failure. 128 93

Roughly 40% of all diabetics, whether insulin dependent or not, develop persistent albuminuria, a decline in their glomerular filtration rate, and elevated blood pressure, i.e., diabetic nephropathy. Diabetic nephropathy is the single most important cause of end-stage renal disease in the Western world, accounting for over one-quarter of all end-stage renal disease. Systemic/glomerular hypertension plays a role in the initiation and progression of diabetic glomerulopathy. Angiotensin-converting enzyme (ACE) inhibitors are superior to conventional antihypertensive drugs in preventing the development of glomerular lesions in insulin-treated streptozotocin diabetic rats. Lowering of glomerular hypertension may be the crucial factor involved. Human studies suggest that ACE inhibitors postpone the progression to clinical overt diabetic nephropathy in normotensive diabetic patients with persistent microalbuminuria. ACE inhibitors combined with a diuretic reduce albuminuria and postpone renal insufficiency in hypertensive diabetics with overt nephropathy. No treatment modality other than antihypertensive treatment has yet been proven to be effective in protecting renal function in diabetic nephropathy. All previous reports dealing with the natural history of diabetic nephropathy have demonstrated a cumulative death rate between 50 and 77% 10 years after the onset of proteinuria. Effective antihypertensive treatment has reduced the cumulative death rate to 15-20% 10 years after the onset of nephropathy.
J Cardiovasc Pharmacol 1992
PMID:Renoprotective action of angiotensin-converting enzyme inhibition in diabetes mellitus. 138 60

Recent studies in animal models suggest that glomerular capillary hyperperfusion and hypertension, rather than ischemia, cause renal injury. Interventions that control glomerular capillary hypertension may protect against progressive injury, even in the presence of continued systemic hypertension. In the absence of systemic hypertension, diabetes mellitus is a prominent clinical example of glomerular hypertension. Animal studies have shown that glomerular hemodynamic abnormalities, especially elevations in glomerular pressure, play an important role in the pathogenesis of diabetic glomerulopathy. A number of clinical observations suggest that angiotensin converting enzyme (ACE) inhibitors may delay the progression of diabetic nephropathy by their effects on renal hemodynamics. In experimental animals, comparisons between calcium channel blockers and ACE inhibitors have shown the latter to be more effective in protecting the kidneys. Preliminary clinical studies indicate that ACE inhibitors may have advantages in preserving renal function in hypertensive and diabetic patients with renal failure.
J Cardiovasc Pharmacol 1990
PMID:Renal effects of converting enzyme inhibitors in hypertension and diabetes. 169 12

The incidence of coronary artery disease (CAD) is markedly increased in both insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). The background for this coincidence is as yet incompletely understood. In uncomplicated IDDM, the levels of cardiovascular risk factors do not show any substantial abnormalities if the metabolic control is good. However, when diabetic nephropathy ensues, even in its early microalbuminuric stage, blood pressure tends to become elevated and multiple atherogenic plasma lipid abnormalities appear. In juvenile-onset IDDM, increased occurrence of clinically manifest CAD emerges after the age of 30 years and becomes particularly marked in patients with diabetic nephropathy. Premenopausal female patients with IDDM develop CAD almost as often as male diabetics with IDDM of the same age--a situation in sharp contrast to that in nondiabetics, with a large excess of CAD in men. IDDM may act as a promoter of the progression of atherosclerotic lesions in subjects who are otherwise prone to develop them. This could explain why patients with IDDM have an increased risk of CAD, even in the absence of diabetic nephropathy, which enhances atherogenesis through several mechanisms. NIDDM is associated with multiple changes in cardiovascular risk factors, including abnormalities in the levels and composition of plasma lipids and lipoproteins and increased frequency of hypertension. These changes in cardiovascular risk factors are already present in subjects with impaired glucose tolerance (IGT), the precursor stage of NIDDM. In patients with NIDDM, the incidence of CAD is markedly increased compared to that in nondiabetic subjects of the same age, and more markedly in women than in men.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1990
PMID:Diabetes and coronary artery disease: what a coincidence? 171 Jul 45

Diabetes mellitus is associated with significant morbidity and mortality caused by the micro- and macro-vascular complications that all too frequently develop during the lifetime of the diabetic patient. In attempts to treat the complications of diabetes, several different treatment strategies have been investigated. The role of tight blood glucose control in the treatment of diabetic vascular complications has recently been challenged, as the existing data in support of this mode of therapy are currently inconclusive. Perhaps more effective in preventing many of the vascular complications is the rigorous treatment of hypertension that frequently accompanies diabetes mellitus. Epidemiological studies have demonstrated that the presence of hypertension significantly contributes to the development and progression of diabetic nephropathy, retinopathy, cardiovascular disease, and possibly neuropathy. Preliminary clinical studies demonstrate that the progression of diabetic renal disease can be slowed by vigorous antihypertensive therapy. Among the various antihypertensive agents used to treat the hypertension associated with diabetes mellitus, calcium channel blockers are emerging as one of the agents of first choice. This is because of their very low side effect profile and their absence of detrimental effects on serum lipid levels and glucose tolerance. Calcium channel blockers may be of additional potential benefit to the diabetic patient by slowing the progression of atherosclerosis, reversing the intracellular calcium defects that may contribute to the pathogenesis of diabetic cardiomyopathy, and protecting against the progression of chronic renal disease.
J Cardiovasc Pharmacol 1991
PMID:The future of calcium channel blocker therapy in diabetes mellitus. 172 50

Hypertension in type I diabetes appears to be causally related to nephropathy, whereas the relationship between hypertension and type II diabetes is more complex, hypertension being present in the absence of clinically overt nephropathy and even preceding the onset of diabetes. In the diabetic, hypertension is exquisitely sodium-sensitive. It is in diabetic nephropathy that the best evidence has been obtained that treatment of hypertension retards the progression of renal failure. Consensus is still lacking with respect to the point when antihypertensive treatment should be started and the target blood pressure that should be aimed at. Currently, there is no evidence in humans that converting enzyme inhibitors are superior to alternative antihypertensive agents in retarding progression, but tantalizing preliminary evidence on this has been reported in nondiabetic patients with renal failure.
J Cardiovasc Pharmacol 1991
PMID:Preservation of renal function in diabetic patients. 172 44

The autoregulation of blood flow in subcutaneous tissue was investigated at the level of the lateral malleolus by the local 133Xenon washout technique. We have investigated eight long-term insulin-dependent diabetics and seven healthy controls. All diabetics had moderate diabetic nephropathy and retinopathy. The blood flow remained constant in all normal subjects, when the arterial perfusion pressure was varied between 70 and 150 mm Hg. All diabetics had impaired or reduced autoregulation of the subcutaneous blood flow. The blood flow increased and decreased almost linearly with the changes in arterial perfusion pressure. The mechanism underlying the defect autoregulation of blood flow in diabetics is uncertain; possibilities include structural changes of the arterioles and/or alterations of local metabolic factors.
J Cardiovasc Pharmacol 1984
PMID:Loss of autoregulation of blood flow in subcutaneous tissue in juvenile diabetes. 608 9

To elucidate the pathophysiologic significance of circulating endothelin-1 (ET-1) to the vascular lesions in diabetic patients, ET-1 levels in plasma and peritoneal dialysis fluid were measured in 11 patients receiving continuous ambulatory peritoneal dialysis (CAPD) [five with diabetic nephropathy (group A); six with chronic renal failure without diabetes mellitus (group B)]. ET-1 levels were determined by a highly sensitive and specific enzymeimmunoassay. Plasma ET-1 levels in group A were not significantly different from those in group B (3.3 +/- 0.9 versus 3.5 +/- 0.9 pg/ml). However, the amounts of ET-1 in peritoneal dialysis fluid in group A were significantly greater than those in group B (19.2 +/- 13.2 versus 10.4 +/- 6.3 ng/day). These results suggest that abdominal capillary vessels in diabetic patients are hyperpermeable to ET-1.
J Cardiovasc Pharmacol 1993
PMID:Hyperpermeability of abdominal capillary vessels to endothelin-1 in patients with diabetes mellitus. 750 87

A number of changes in intrarenal hemodynamics and morphology are characteristic of diabetic nephropathy. These changes include: increases in intraglomerular pressure and volume, glomerular capillary permeability to macromolecules, and mesangial matrix expansion. Most antihypertensive drugs attenuate some of the increases in these parameters. Certain antihypertensive agents, however, have effects on all these parameters. Studies in animal models of diabetes demonstrate that the angiotensin-converting enzyme (ACE) inhibitors reduce both intraglomerular volume and pressure, mesangial matrix expansion, and albuminuria. The calcium antagonists TA-3090 (diltiazem-like) and verapamil recently have been shown to have most of these effects. Conversely, the dihydropyridine calcium antagonists (nifedipine, felodipine, nitrendipine) do not attenuate increases in most of these parameters. In several clinical studies, nifedipine either did not affect or increased urinary albumin excretion in diabetic patients with renal insufficiency. Moreover, in animal models of diabetes, most dihydropyridine compounds do not prevent progression of glomerulosclerosis in spite of blood pressure control. Although the majority of clinical studies support the concept that reduction of arterial pressure preserves renal function, recent long-term clinical studies show that ACE inhibitors and heart-rate-lowering calcium antagonists (diltiazem, verapamil) attenuate progression of diabetes to a greater extent than most other agents do.
J Cardiovasc Pharmacol 1994
PMID:Antihypertensive therapy and progression of diabetic renal disease. 751 95

Endothelin-1 (ET-1) causes dramatic vasoconstriction and reduction of renal blood flow, with a decreased glomerular filtration rate (GFR). Early diabetic nephropathy is characterized by elevation of GFR and the formation of intrarenal microaneurysms. However, the mechanisms are unclear. To elucidate the pathophysiologic significance of urinary ET-1 in early diabetic nephropathy, the 24-h urinary excretion of ET-1 in 12 normal subjects and 20 patients with newly diagnosed type 2 diabetes mellitus were determined by a highly sensitive radioimmunoassay. The 24-h urinary ET-1 excretion in patients with diabetes mellitus (14.2 +/- 3.1 pmol, mean +/- SEM) was significantly lower (p < 0.05) than that of normal subjects (25.0 +/- 3.7 pmol). This decrease in urinary excretion of ET-1 in patients with recent-onset diabetes mellitus suggests a possible role of ET-1 in the pathogenesis of early diabetic nephropathy.
J Cardiovasc Pharmacol 1995
PMID:Does endothelin play a role in the pathogenesis of early diabetic nephropathy? 858 52


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