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Query: UMLS:C0011881 (
diabetic nephropathy
)
10,836
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The evaluation and treatment of
hypertension
in the African-American patient with an elevated blood pressure presents a diagnostic challenge. We are less able to rely on young age and resistance to treatment as indications for more extensive evaluation of secondary causes of
hypertension
; thus, greater reliance on history, physical examination, and clinical judgment is required if we are to identify potentially treatable causes. The treatment of
hypertension
in the African-American patient also presents a therapeutic challenge. Thiazide diuretics remain the drugs of first choice for treating
hypertension
in the African-American hypertensive. The calcium channel blockers (CCBs) are attractive alternatives to thiazides in patients uncontrolled by or intolerant of thiazides or who have specific indications for these agents (eg, angina, severe diastolic dysfunction). Beta-blockers should not be denied to African-American hypertensives if indications for their use exist. Although beta-blockers may be less effective as monotherapy, 50% of African-American hypertensives can be so controlled. Resistance to beta-blockers may be eliminated by administering them with a diuretic. The angiotensin converting enzyme inhibitors (ACEIs), like CCBs, are well tolerated, but also lack long-term primary prevention data. As is the case with beta-blockers, ACEIs are less effective in African-American hypertensives when used as monotherapy. ACEIs have particular value in therapy for African-American hypertensives with concomitant congestive heart failure and may protect against progression of
diabetic nephropathy
. Finally, all hypertensives, especially African-American hypertensives, should have access to treatment prior to the development of end organ damage. The cost of early intervention is minimal compared with the economic consequences of neglect.
...
PMID:Hypertension in African Americans: evaluation and treatment issues. 168 47
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.
...
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)
...
PMID:Diabetes and coronary artery disease: what a coincidence? 171 Jul 45
In order to evaluate the influence of glycemic control and
hypertension
on the development of
diabetic nephropathy
, we measured urinary excretion of albumin (AER) and other microproteins in non-insulin-dependent diabetes mellitus (NIDDM), and reexamined the 103 patients who had had AER less than 300 micrograms/min at the initial study 12-18 months later. AER in the patients with HbA1c greater than or equal to 7.5% increased significantly in both the normoalbuminuric (AER less than 30 micrograms/min) and microalbuminuric (30-300 micrograms/min) groups, whereas no significant change in AER was observed in the patients with HbA1c less than 7.5%. In the microalbuminuric group, AER in both hypertensive and normotensive patients increased significantly. In this group, the change in AER correlated positively with the change in alpha 1-microglobulin (alpha 1M). These results indicate that glycemic control has a greater influence on the development of nephropathy in its early stage than
hypertension
and that alpha 1M is as a good predictor of nephropathy as albumin.
...
PMID:Influence of glycemic control and hypertension on urinary microprotein excretion in non-insulin-dependent diabetes mellitus. 172 5
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.
...
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.
...
PMID:Preservation of renal function in diabetic patients. 172 44
Increased urinary albumin excretion rate (AER) in the microalbuminuric phase of
diabetic nephropathy
has been attributed to intraglomerular
hypertension
. This could be caused by constriction of efferent glomerular arterioles, which carry alpha-adrenoceptors. We tested the hypothesis that insulin-dependent diabetes mellitus (IDDM) patients with microalbuminuria are hypersensitive to vasoconstriction induced by norepinephrine (NE). We studied 15 IDDM patients with microalbuminuria (AER 32-295 mg/24 h), 13 IDDM patients with normal AER (5-24 mg/24 h), and 9 nondiabetic subjects (AER 8-22 mg/24 h). All were normotensive. NE-induced vasoconstriction was measured in dorsal hand veins, which carry alpha-receptors similar to those of glomerular efferent arterioles. Vein diameter was measured with a linear displacement probe during a stepped NE infusion (1-32 ng/min) into the vein, and venoconstriction was expressed as a percentage of the maximum passively distended venous diameter. Microalbuminuric IDDM patients exhibited significantly greater vasoconstriction (P less than 0.005) at all NE infusion rates than both other groups. The NE infusion rate producing 50% of maximal venoconstriction (ED50) in the microalbuminuric IDDM group (median 1.1 ng/min, range 0.2-25.2 ng/min) was significantly less than in both the normoalbuminuric IDDM group (median 12.5 ng/min, range 4.9-40.5 ng/min, P = 0.00007) and the nondiabetic group (median 17.7 ng/min, range 5.9-42.2 ng/min, P = 0.0003). Dose-response curves and ED50 did not differ significantly between normalbuminuric IDDM and nondiabetic groups. IDDM patients with microalbuminuria are hypersensitive to NE-induced vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Exaggerated sensitivity to NE-induced vasoconstriction in IDDM patients with microalbuminuria. Possible etiology and diagnostic implications. 173 11
Late complications of diabetes mellitus include a variety of clinical pictures, mainly related to the involvement of the arterial wall both of large vessels (macroangiopathy) and small vessels (microangiopathy), and of the peripheral nervous system (neuropathy). Their presence in almost all types of diabetes indicates that there is a common pathogenetic mechanism, which can be substantially identified in high blood glucose levels and related alterations. Hyperglycemia, in fact, leads to some metabolic abnormalities, i.e. non-enzymatic glycosylation of proteins and polyol pathway activity; moreover it can negatively affect the pattern of some hormones, especially GH and sex steroids, and normal rheological and clotting properties of blood. These abnormalities, confirmed by experimental models, play a key role in the development of late diabetic complications. However some evidence indicates that a genetic background may predispose to their development or protect from their onset. The two main forms of diabetic retinopathy, non-proliferative and proliferative, show an incidence which increases with age and duration of diabetes, reaching 100% when diabetes lasts for more than 20 years. The risk of blindness, which is very high for the proliferative form, has been dramatically reduced by laser-photocoagulation.
Diabetic nephropathy
affects a lesser number of diabetics but, after a silent or preclinical stage, leads to renal failure and subsequent replacement therapy. Strict metabolic control in the silent stage and later rigid anti-hypertensive treatment can prevent or retard the evolution of this complication. A close association has been observed between diabetes and
hypertension
, which can directly affect the onset and evolution of
diabetic nephropathy
, probably through a common genetic mechanism. Diabetic neuropathy has a wide variety of clinical manifestations, at somatic, autonomic and central levels and can greatly modify the quality and expectancy of life. However, the major cause of death in diabetic subjects is large vessel disease or macroangiopathy, which is similar to non-diabetic atherosclerosis regarding the main histopathological and clinical manifestations but has a much higher prevalence and severity. Finally, a specific cardiomyopathy has also been described in diabetes mellitus and can account for the high rate of heart failure observed in these patients.
...
PMID:The late complications of diabetes mellitus. 174 48
This Symposium includes 15 presentations and an editorial review dealing with prorenin activation and function. It comes 20 years after prorenin was first reported in various contexts and attracted attention because of its connection with renin--angiotensin, its high concentration relative to renin in the blood, and its presence in extrarenal, as well as renal, tissues. Intriguing changes in plasma prorenin have been reported after treatment with antihypertensive and other drugs, following various physiological stimuli, and in pathophysiological states such as Wilms' tumor, Bartter's syndrome, and
diabetic nephropathy
. Lately, very high prorenin concentrations have been found in human and animal ocular fluid, ovarian follicular fluid, and in association with angiogenesis and microangiopathy. High circulating prorenin concentrations and fulminant
hypertension
have been reported in rats harbouring the mouse Ren-2 gene. However, what prorenin does in all these extrarenal fluids, tissues, and conditions is not well understood. Among the reasons for this lack of understanding are the difficulties in measuring prorenin and in establishing good animal models. We have not answered the critical question as to whether prorenin itself is bioactive like a hormone, and if so, what its action(s) might be. Nor have we established the main alternative, i.e., whether the function of prorenin is indirect, through renin--angiotensin, be it in the circulation or in the extrarenal tissues. This Symposium provides only partial methodological advances and answers, but we hope it will stimulate the breakthrough work needed to supply more complete answers.
...
PMID:Activation and function of prorenin: different viewpoints. 175 30
The effects of the angiotensin converting enzyme inhibitor captopril on blood pressure, proteinuria, creatinine clearance and metabolic control in
diabetic nephropathy
have been evaluated. Captopril 144 mg per day was given to 8 longstanding, insulin-dependent, diabetic females with nephropathy. The blood pressure was significantly reduced (systolic 45.4, diastolic pressure 30.6 and mean arterial pressure 33.8 mm Hg after 24 weeks of treatment). Plasma renin activity rose significantly from a basal value of 1.60 to 6.71 ng.ml-1.h-1, and so did serum potassium (from 4.57 to 4.83 mEq.1-1). Serum aldosterone fell from 161 to 70.9 pgm.ml-1 and from 27.3 to 15.3 micrograms.24 h-1 in plasma and urine, respectively, after 6 months on captopril therapy. Urinary protein excretion was decreased by about 48% and creatinine clearance remained unchanged throughout the study. Plasma triglycerides and cholesterol also remained unchanged, and glycosylated haemoglobin was significantly reduced from 13.8 to 10.2% after captopril. The results suggest that captopril is a useful drug to treat
hypertension
in patients suffering from
diabetic nephropathy
, as the decline in kidney function can be reduced without impairing glucose tolerance or the lipid profile.
...
PMID:Effects of captopril on diabetic nephropathy in hypertensive women. 176 Oct 66
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