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Query: UMLS:C0011854 (
type 1 diabetes
)
20,749
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Diabetic nephropathy affects a subset of about 40% patients with
Insulin-Dependent Diabetes Mellitus
(
IDDM
); it also develops in a less defined percentage (30-50%) of patients with non
Insulin-Dependent Diabetes Mellitus
(NIDDM), after a period of 15-20 years. It is usually divided in 5 stages: the first 3 are characterized by renal hypertrophy and increased glomerular filtration surface area (I stage) followed by glomerular histological lesions (II stage) and early nephropathy with microalbuminuria (III stage). At these stages nephropathy is still reversible by medical treatment (
ACE
inhibitors) and good metabolic control. Aim of this study was to assess the usefulness of duplex sonography with Doppler wave form analysis in the evaluation of early diabetic nephropathy, in order to detected patients at risk for irreversible renal disease. Fifteen patients (10 males and 5 females) aged 28-46 years, affected by
IDDM
were studied; 15 healthy subjects (7 males and 8 females) aged 20-45 years composed the control group. All of them underwent duplex Doppler sonography of kidney; a scanner with a 3.5 MHz transducer (Toshiba 270 SSA) was used. All patients had renal function tests within normal range. Pulsatily Index (P.I.) and Resistive Index (R.I. of Doppler waveform were obtained at the interlobar arteries; the average value of 3 bilateral measurements was taken. Doppler sonography was done by the same authors without knowledge of the patient group (case or control). Both indexes (P.I. and R.I.) resulted to have higher values in patients with
IDDM
compared to controls: P.I. = 1.46 +/- 0.30 vs. 1.07 +/- 0.06, p < 0.05; R.I. = 0.77 +/- 0.09 vs 0.60 +/- 0.03, p < 0.05. Even if our data have to be confirmed by further studies, they suggest that duplex Doppler sonography may be a useful complementary test in the evaluation of diabetic nephropathy, even in the early stages.
...
PMID:[Pulsed-wave color Doppler echography of the intrarenal vessels in patients with insulin-dependent diabetes mellitus and incipient nephropathy]. 916 57
Diabetic nephropathy accounts for almost a third of all causes of ESRD. Microalbuminuria screening among diabetics can offer early detection of incipient nephropathy. Aggressive treatment with
ACE
inhibitors may delay the onset of overt renal failure or delay its progression. Furthermore, intensive control of blood glucose has also been proven to prevent the microvascular complications of diabetes and should be pursued in both
IDDM
and NIDDM. The high association of diabetes mellitus with hypertension presents another problem to the clinician. It is necessary to control blood pressure to prevent further progression of renal failure. The choice of antihypertensive medications, however, becomes a therapeutic dilemma because of the metabolic and lipid disturbances that some drugs can cause.
ACE
inhibitors, CCBs, alpha-agonists, and low-dose diuretics, alone or in combination, may be tried to normalize blood pressures. Although beta-blockers are widely used and effective in nondiabetics, these agents should be considered the drugs of last resort because of their adverse effects, which are particularly troublesome for diabetics. Moderate protein restriction should also be advocated as a helpful adjunct to therapy.
...
PMID:Diabetic nephropathy. 916 51
Lisinopril, like other
ACE
inhibitors, lowers blood pressure and preserves renal function in hypertensive patients with non-insulin-dependent or insulin-dependent diabetes mellitus (NIDDM or
IDDM
) and early or overt nephropathy, without adversely affecting glycaemic control or lipid profiles. On available evidence, renoprotective effects appear to be greater with lisinopril than with comparator calcium channel blockers, diuretics and beta-blockers, despite similar antihypertensive efficacy. As shown by the EUCLID (EUrodiab Controlled trial of Lisinopril in Insulin-Dependent Diabetes) trial, lisinopril is also renoprotective in normotensive patients with
IDDM
and microalbuminuria. The effect in normotensive patients with normoalbuminuria was smaller than in those with microalbuminuria, and no conclusions can yet be made about its use in patients with normoalbuminuria. In complications other than nephropathy, lisinopril has shown some benefit. Progression to retinopathy was slowed during 2 years' lisinopril therapy in the EUCLID study. Although not yet fully published, these results provide the most convincing evidence to date for an effect of an
ACE
inhibitor in retinopathy. The drug may also improve neurological function, but this finding is preliminary. Lastly, post hoc analysis of the GISSI-3 trial indicates that lisinopril reduces 6-week mortality rates in diabetic patients when begun as early treatment after an acute myocardial infarction. The tolerability profile of lisinopril is typical of
ACE
inhibitors and appears to be similar in diabetic and nondiabetic individuals. Hypoglycaemia has occurred at a similar frequency with lisinopril and placebo, as shown in the EUCLID trial. In addition, the GISSI-3 study indicates that the incidence of persistent hypotension and renal dysfunction is increased with lisinopril in general, but the presence of diabetes does not appear to confer additional risk of these events in diabetic patients with acute myocardial infarction receiving lisinopril. In summary, lisinopril lowers blood pressure and produces a renoprotective effect in patients with
IDDM
and NIDDM without detriment to glycaemic control or lipid profiles. Like other
ACE
inhibitors, lisinopril should thus be viewed as a first-line agent for reducing blood pressure and preventing or attenuating nephropathy in hypertensive diabetic patients with
IDDM
or NIDDM and microalbuminuria or overt renal disease. The EUCLID study, using lisinopril, provides new data supporting an additional place in managing normotensive patients with microalbuminuria and
IDDM
. These findings, together with some evidence for an effect of lisinopril in delaying progression of retinopathy and in reducing mortality, suggest a broader role for the drug in managing diabetic vascular complications.
...
PMID:Lisinopril. A review of its pharmacology and use in the management of the complications of diabetes mellitus. 917 32
We postulated that nitric oxide (NO)-mediated endothelial function would be improved by acute and short-term treatment with an
angiotensin converting enzyme
(
ACE
) inhibitor in patients with
type I diabetes mellitus
, in whom endothelial function is depressed. Nine type I diabetic patients and eight healthy subjects underwent forearm blood flow measurement using strain gauge plethysmography during intraarterial infusion of incremental doses of endothelium-dependent (acetylcholine [ACh]) and endothelium-independent (sodium nitroprusside [SNP]) vasodilators. Pretreatment ACh responses were depressed in diabetic patients relative to the normal subjects (P < 0.05). No difference between the groups was evident in response to SNP. Acute
ACE
inhibition (with intrabrachial enalaprilat) enhanced ACh responses in the diabetic patients (P < 0.005), with a further improvement evident after 1 mo of oral therapy with enalapril (P < 0.001) when ACh responses were normalized.
ACE
inhibition did not affect SNP responses. We conclude that acute administration of the
ACE
inhibitor, enalaprilat, enhances NO-mediated endothelial function in type I diabetic patients, with further improvement evident after 4 wk of enalapril therapy.
...
PMID:Improvement in endothelial function by angiotensin converting enzyme inhibition in insulin-dependent diabetes mellitus. 923 16
The therapeutic advantage of the long acting
ACE
-inhibitor benazepril in a 12 weeks intervention period on 23 diabetic (3
IDDM
, 20 NIDDM) patients with essential hypertension was studied. Participants-giving informed consent before beginning the study-on the base of repeated casual blood pressure measurements were divided into "slightly" (n = 8) and "moderately" (n = 15) hypertonic groups. Type of diabetes, time elapsed since its manifestation, actual antidiabetic therapy, period of existence of the hypertension (newly discovered vs known and treated for a time) were independent from the point of view of entering the study. Initial dose of benazepril was 5-10 mg/day depending on the blood pressure level, followed by a stepwise dose elevation according to the control investigations (at weeks 2, 4, 8 and 12 casual blood pressure control, at weeks 4 and 12 ambulantory blood pressure monitoring, ABPM as well) to a maximal daily dose of 20 mg. In the majority of patients benazepril was given in a morning single dose, in some cases because of a better tolerability divided into two parts. 20 patients received benazepril in monotherapy, 3 patients combined with other antihypertensive preparations. Parameters indicating severity of hypertension-hypertonic time index, hyperbaric impact-showed significant improvement already at week 4 when analysed in the total of patients and the moderately hypertonic group respectively. As a tendence the same was observed also in the slightly hypertonic group. No remarkable side effects, or alterations of the metabolic state and in the investigated laboratory parameters appeared. Based on these results benazepril is an effective choice in the treatment of diabetic hypertensive patients.
...
PMID:[Experience with benazepril, a long-acting ACE inhibitor, in the management of diabetic hypertension]. 927 85
Although the evolution of diabetic nephropathy is brought about mostly by persistent hyperglycemia, its progression may be influenced by various other factors such as hypertension and dietary protein intake. It has been recently suggested in the literature that the gene polymorphism of
angiotensin converting enzyme
(
ACE
) might be associated with the development of diabetic nephropathy, because the DD genotype of
ACE
gene is closely associated with the presence of nephropathy in diabetic subjects. However, in our present analysis the frequency of the DD genotype in patients with non-
insulin dependent diabetes
is not significantly related to the presence or absence of nephropathy. It remains to be clarified by multi-center analysis using large numbers of patients whether the gene polymorphism of
ACE
is related to the progression of diabetic nephropathy to renal failure. Furthermore, it has been postulated that the interstitial fibrosis evaluated in renal biopsy specimens is significantly correlated with the declining of renal function in diabetic patients. However, it is not possible to clinically quantitate the interstitial fibrosis without performing renal biopsy. We have recently found that the urinary excretion of type IV collagen is significantly increased in diabetic patients. Moreover, the increase in urinary type IV collagen is well correlated with the amount of urinary albumin. Since type IV collagen in the urine is probably derived from tubulointerstitial tissue, it is likely that the increased amount of type IV collagen in the urine may reflect the fibrotic change in diabetic kidneys. Whether the increase in urinary type IV collagen is able to predict for the progression of diabetic nephropathy in the future should be examined.
...
PMID:Mechanism of the progression of diabetic nephropathy to renal failure. 935 Jun 77
The complementary action of
angiotensin converting enzyme
inhibitors and diuretics in the treatment of hypertension has been demonstrated in a number of studies of fosinopril and hydrochlorothiazide (HCTZ). The combination provides a clinically significant reduction in blood pressure while minimizing the dose-dependent adverse effects of HCTZ, such as hypotension and its metabolic effects on plasma lipoproteins, by keeping the dose of each agent to the minimum. Fosinopril has a unique dual mechanism of elimination and can therefore be used in patients with renal impairment. The efficacy of the combination of fosinopril and hydrochlorothiazide compared with placebo and other agents is reviewed in this article. Studies have demonstrated that the combination is effective in the elderly and in renally impaired patients, regardless of severity. In addition, in non-
insulin dependent diabetes
, antihypertensive effect is achieved without further affecting carbohydrate and lipid metabolism, which is often the case when thiazide diuretics alone are used. A matrix study was performed to evaluate the optimum dose combination to produce blood pressure normalization and minimize side effects. This study evaluated 17 different dose combinations and demonstrated that the lowest dose combination to produce a clinically significant effect was fosinopril 10 mg and HCTZ 12.5 mg. However, a dose-related antihypertensive effect can be seen, giving the option for the use of 20 mg fosinopril for moderately hypertensive patients. Both combination therapy and fosinopril were significantly more effective than HCTZ alone or placebo. The fosinopril/HCTZ combination has also been shown to have a comparable effect to sustained-release nifedipine and propanolol + HCTZ. The studies reviewed here demonstrate that fosinopril/HCTZ combination treatment has a number of advantages over either agent used alone, providing blood pressure normalization in a broad range of hypertensive patients, including diabetic patients and the elderly.
...
PMID:Management of hypertension: the role of combination therapy. 936 83
In a 63-year-old woman with longstanding
type I diabetes mellitus
, CAD and chronic heart failure, a subacute myocardial infarction developed, together with decompensation of cardiac function and diabetes and concurrent pneumonia. Acute heart failure with acute renal failure on top of diabetic nephropathy, and interstitial pulmonary edema was initially treated with hemofiltration and catechol amines together with antibiotic and perfusor-regulated insulin therapy, and systemic heparinization. Subsequent chronic treatment with digitalis, acetyl salicylic acid, insulin and a combination of an
ACE
inhibitor and a loop diuretic resulted in an improvement of heart failure to NYHA functional class II where PTCA of coronary multi-vessel disease could be performed with low risk.
...
PMID:[Heart failure after myocardial infarct in decompensated diabetes mellitus. Acute therapy with catecholamines--long-term therapy with ACE inhibitor-loop diuretic combination]. 937 33
Diabetic nephropathy is one of the main causes of chronic renal failure in developed countries. The genesis and development of diabetic nephropathy is associated in both types of diabetes with a more rapid progression of other secondary complications and an increased mortality, in particular cardiovascular mortality. The main causes of development of diabetic nephropathy are prolonged hyperglycaemia along with a so far not elucidated inborn disposition. The course of diabetic nephropathy is characterized more clearly in
type 1 diabetes
. The clinically manifest stage is already irreversible and in the course of years it develops into chronic renal failure. Preventive and curative measures include maintenance of optimal metabolic control, systematic control of blood pressure, in particular by
ACE
-inhibitors, and a reduction of protein intake. Systematic multidisciplinary collaboration in care for patients with diabetic nephropathy helps to prevent the progression of other secondary complications such as diabetic foot and diabetic retinopathy. At present in the Czech Republic dialysis methods substituting renal function are available to practically all patients with diabetic nephropathy. As regards survival time and quality of life the optimal method of renal function replacement for patients in the terminal stage of diabetic nephropathy is transplantation.
...
PMID:[Care of patients with diabetic nephropathy]. 947 80
Nephropathy is a frequent complication of long term diabetes. Diabetic nephropathy is the major determinant of premature morbidity and mortality both in insulin-dependent (
IDDM
) and in non-insulin dependent-diabetes mellitus (NIDDM). There is good evidence that genetic predisposition plays a major role in development of diabetic nephropathy. This hypothesis is based on the observation that diabetic nephropathy clusters within families, both in
IDDM
and NIDDM. Components of the renin-angiotensin system (RAS) are plausible candidate genes to examine for a association with microalbuminuria and diabetic nephropathy. In this study we compared the distribution of PstI melting polymorphism at the
ACE
locus among NIDDM patients with diabetic nephropathy and in patients who, despite long duration of NIDDM, remain without this complication. The 220 NIDDM patients for whom DNA was available were classified into two groups according to their renal status: normoalbuminuric control subjects (n = 80) who are NIDDM patients with an A/C ratio < 2.5 and nephropathy cases (n = 140) who are NIDDM patients with A/C ratio > 2.5. Albumin excretion rate was assayed by radioimmunoassay. HbA1c was assayed using HPLC methods, creatinine--using Jaffe methods and DNA analysis using PCR reaction, and then after the amplification product was digested with PstI enzyme. The study revealed that PstI sequence differences ("+/= and -") in the
ACE
gene do not contribute to genetic susceptibility to diabetic nephropathy in NIDDM.
...
PMID:[Is PstI polymorphism of the angiotensin I converting enzyme gene associated with nephropathy development in non-insulin-dependent diabetes mellitus (preliminary study)]. 949 4
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