[Atherosclerotic renovascular disease and renal function].
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Arteriosclerosis↗
Biomedical subjects
A Mimran
Publications and source records attributed to A Mimran.
Albuminuria predicts renal functional outcome after intervention in atheromatous renovascular disease.
BACKGROUND: Atheromatous renovascular disease is increasingly recognized as a cause of renal failure; however, the benefit of intervention on renal function outcome cannot be clearly anticipated. OBJECTIVE: To identify reliable predictor(s) of renal functional outcome after revascularization in patients with atheromatous renovascular disease. DESIGN: The effect of percutaneous transluminal renal angioplasty (n = 5) or surgery (n = 18) on glomerular filtration rate ([99mTc]-diethylene triaminopenta-acetic acid clearance) and renal haemodynamics was prospectively assessed in 23 patients with atheromatous renovascular disease (unilateral occlusion in five, unilateral stenosis in four, stenosis of a single kidney in five, unilateral occlusion associated with contralateral stenosis in six, bilateral stenosis in three). Renal function was altered in 18 patients. RESULTS: At early follow-up study (5 +/- 1 months) after intervention, glomerular filtration rate improved (i.e. increased by more than 15%) in six patients, deteriorated in five and remained unchanged in 12 patients. The change in glomerular filtration rate associated with intervention was inversely correlated with the pre-intervention level of urinary albumin excretion and positively with the change in effective renal plasma flow after intervention. Stepwise regression analysis showed that pre-intervention urinary albumin excretion was the only predictor of the glomerular filtration rate response to intervention. At late follow-up study (32 +/- 6 months, n = 13), glomerular filtration rate was stable compared with early follow-up determination in non-proteinuric patients whereas it had deteriorated further in proteinuric patients. CONCLUSION: In patients with atheromatous renovascular disease, albuminuria may be considered as a marker of pre-existing intra-renal vascular and glomerular damage and a reliable predictor of renal functional outcome after intervention.
Adult↗
Combined renal effects of overweight and hypertension.
The existence of a direct relationship between body mass and arterial pressure is well recognized; however, the effect of obesity on known target organs of hypertension is not clearly understood. We undertook the present studies to assess the influence of obesity on renal function and urinary albumin excretion in 40 normotensive subjects and 80 nevertreated hypertensive patients matched for age, sex, arterial pressure level, and known duration of hypertension in whom an oral glucose tolerance test was within normal limits. Glomerular filtration rate and effective renal plasma flow (expressed as absolute values or values normalized for height) were increased in overweight compared with lean subjects whether normotensive or hypertensive. Glomerular filtration rate was positively correlated with protein intake (as assessed from urinary excretion of urea) and fasting serum insulin level. Urinary excretion of albumin but not IgG and beta 2 microglobulin was higher in hypertensive patients compared with normotensive subjects. The overweight condition clearly enhanced the influence of arterial pressure on albuminuria; in fact, a steeper regression line between albumin excretion rate and arterial pressure was found in overweight compared with lean subjects. These results indicate that the overweight condition is associated with renal hyperfiltration and hyperperfusion, irrespective of the presence of hypertension, and that obesity magnifies the effect of hypertension on albuminuria, thus raising the possibility of an increased susceptibility of obese hypertensive patients to the development of renal damage.
Adolescent↗
Contrasting effect of antihypertensive treatment on the renal response to L-arginine.
We assessed the renal hemodynamic response to L-arginine infusion (30 g within 60 minutes) in normotensive subjects, patients with never-treated essential hypertension, and hypertensive patients controlled by long-term (more than 2 years) treatment with or without an angiotensin-converting enzyme inhibitor. The renal vasodilator response to L-arginine observed in normotensive subjects (15 +/- 4% increase in effective renal plasma flow) was abolished in untreated hypertensive patients and restored only in the group treated by angiotensin-converting enzyme inhibition. In the whole population a positive correlation between the change in effective renal plasma flow and the change in urinary cGMP was obtained. It is suggested that abnormalities of the renal nitric oxide pathway not corrected by increased availability of L-arginine and reversible only on long-term treatment by angiotensin-converting enzyme inhibition may underlie the abnormal renal resistance observed in essential hypertension.
Adrenergic beta-Antagonists↗
Left ventricular contractility and insulin resistance in essential hypertension.
The relationship between fasting insulin as well as the insulin response to an oral glucose tolerance test and echocardiographic cardiac geometry and function was assessed in 55 never-treated lean patients with essential hypertension and normal glucose tolerance and 31 age- and gender-matched normal subjects. The ratio of the area under the curve of the response of insulin and glucose to the oral glucose load was positively correlated with supine heart rate (r values of 0.37) or left ventricular contractility estimated by the end-systolic wall stress to end-systolic volume index ratio and the afterload-corrected fractional shortening (r = 0.59 and 0.36, respectively). No correlation between insulin and left ventricular mass index was observed. When hypertensive patients were divided into those without (n = 39) and with insulin resistance (n = 16), as defined by an elevated value of the ratio of the area under the curve of the response of insulin and glucose, it appeared that both heart rate, end-systolic wall stress to end-systolic volume index ratio and afterload-corrected fractional shortening were higher in patients with insulin resistance, whereas age, arterial pressure, left ventricular mass index, urinary electrolytes, and plasma renin activity were similar in the two groups. These results suggest that increased cardiac systolic performance and heart rate may be associated with insulin resistance in a subset of lean patients with never-treated essential hypertension.
Administration, Oral↗
[Sodium and left ventricular hypertrophy in patients with hypertension].
Dietary sodium is an environmental factor capable of amplifying or limiting the consequences of hypertension on the heart. In a given population of hypertensive subjects, recent clinical trials have shown a positive relationship between sodium intake and the degree of left ventricular hypertrophy, independently of the value of blood pressure and body weight. In addition, dietary sodium could play a role in modulating the myocardial response to a decrease in blood pressure by antihypertensive therapy. The logical consequence of these observations is to try and prove the possible advantages of restricting dietary sodium in reducing the blood pressure and reversing left ventricular hypertrophy. With this in mind, the evaluation of dietary sodium excretion is certainly an element to take into account in the initial evaluation and also the follow-up of hypertensive subjects and of the effects of antihypertensive therapy.
Animals↗
[Left ventricular hypertrophy and left atrial morphology in untreated hypertensive patients].
The level of arterial pressure is not the sole determinant of cardiac and vascular adaptation to hypertension. In order to identify other factors (such as preload) we categorized by echocardiography, 55 never treated hypertensive patients and 39 age and gender-matched normal subjects, according to values of relative wall thickness and left ventricular mass index. Normal left ventricular anatomy was found in 63% hypertensives, whereas among hypertensives 7% had "concentric left ventricular remodeling", 16% concentric left ventricular hypertrophy and 14% had eccentric left ventricular hypertrophy. Systolic left atrial area (LA) was obtained from the four-chamber views. Mitral peak early diastolic (E) and late diastolic (A) flow velocity was assessed by Doppler. Because clinical characteristics such age and sex differed among the 5 groups only results of ANCOVA were reported (means +/- SD). [table: see text] We conclude that eccentric left ventricular hypertrophy may be associated with a parallel increase of left atrial area. Thus the association of an increase of cardiac volume in hypertensive patients with normal diastolic function suggest that volume overload may modulate the effect of arterial pressure on cardiac morphology.
Adult↗
[Preservation of renal function by revascularization in renovascular disease].
Renovascular disease is the leading cause of surgically-curable arterial hypertension and one of the few cause of reversible chronic renal failure, but its exact prevalence remains unknown. Progression of atheromatous disease occurs in 50% of cases and it may result in bilateral stenosis (25%) or total occlusion (15%). By now, the main aim of renal revascularization is retrieval of impaired function or prevention of renal failure rather than control of hypertension. However, renal functional deterioration may result from cholesterol embolism or glomerulosclerosis in addition to ischemia. Correction of post-proximal stenosis is obtained by both surgery and percutaneous angioplasty. In favor of angioplasty are a higher acceptability and a modestly better cost-benefit ratio. Surgery may be preferred when the stenosis is proximal, complex or associated with aortic disease; in addition, analysis of published (mostly uncontrolled) series suggest that beneficial renal functional outcome is slightly better following surgery. Importantly, both diagnosis and prognosis of ischemic nephropathy are difficult to establish. Various predictors of recovery (renal size, renal vein renin ratio, alteration in scintigrams, angiography or biopsy) were shown to fail on an individual basis. Further controlled studies based on reliable methods of measuring renal function are warranted.
Angioplasty, Balloon↗
Renal function in one-kidney, one clip sodium-restricted rats: influence of enalapril and losartan.
BACKGROUND: Some observations have suggested that the harmful renal effects of angiotensin converting enzyme inhibitors might be partly mediated by non-angiotensin mechanisms under conditions in which a high intraglomerular pressure is required to maintain the glomerular filtration rate. MATERIALS AND METHODS: The effects of enalapril and losartan (10 and 30 mg/kg per 24 h for 6 days, respectively) on arterial pressure and renal function were assessed in one-kidney, one clip hypertensive rats subjected to dietary sodium depletion before treatment. RESULTS: Arterial pressure and renal vascular resistance were reduced to a similar extent in rats treated with enalapril and with losartan. However, the glomerular filtration rate (867 +/- 40 mu l/min per g kidney weight in untreated rats) decreased to a greater extent in enalapril than in losartan-treated rats (284 +/- 29 and 444 +/- 32 mu l/min per g kidney weight, respectively). In addition, the filtration fraction was reduced in treated compared with untreated rats; however, it was slightly but significantly lower in enalapril- than in losartan-treated rats. CONCLUSIONS: Despite similar final arterial pressure and renal vasodilation, angiotensin converting enzyme inhibitors may exert an effect on intrarenal forces contributing to the regulation of glomerular filtration rate, independently of blockade of the renin-angiotensin system.
Angiotensin-Converting Enzyme Inhibitors↗
Albuminuria in untreated patients with primary aldosteronism or essential hypertension.
AIM: The determinants and significance of urinary albumin excretion have been studied in normal subjects and in hypertensive patients; however, they are unknown in patients with primary aldosteronism. PATIENTS AND METHODS: From a population of 114 patients with documented primary aldosteronism, we selected 23 never-treated patients (12 males, 11 females; 11 tumoral, 12 non-tumoral) and compared them to patients with never-treated essential hypertension with low renin (supine plasma renin activity <1 ng/ml per h, n = 23) or normal renin (supine plasma renin activity between 1 and 4 ng/ml per h, n = 23), matched for age, body mass index, mean arterial pressure, renal function and known duration of hypertension. RESULTS: The patients with primary aldosteronism had lower serum potassium and higher plasma aldosterone concentrations than those with essential hypertension. Urinary albumin and beta2-microglobulin excretion were greater in untreated patients with primary aldosteronism than in those with low- or normal-renin essential hypertension. Among the patients with essential hypertension, the renin activity was not a determinant of albuminuria. CONCLUSIONS: These findings indicate that primary aldosteronism is associated with excessive urinary albumin excretion. This albuminuria could be due to impairment of proximal tubular reabsorption caused by hypokalemic nephropathy and/or by high levels of circulating aldosterone; however, it could be an indicator of target-organ damage associated with primary aldosteronism.
Albuminuria↗
[Renal hemodynamic anomalies related to arterial hypertension and overweight].
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Albuminuria↗
Angiotensin-converting enzyme inhibitors versus calcium antagonists in the progression of renal diseases.
In addition to factors such as protein intake or hyperlipidemia, hypertension contributes to the progressive deterioration of renal function in experimental animal models of renal disease, and has a prominent role in the imbalance of intrarenal hemodynamics. Reduction of arterial pressure was shown to alter the course of human chronic renal disease. In patients with diabetic as well as nondiabetic nephropathy, the lowering of proteinuria by angiotensin-converting enzyme inhibitors is greater than that observed with other antihypertensive drugs and appears to be independent of blood pressure control alone, whereas albuminuria may be unaffected or worsened during nifedipine treatment. Angiotensin-converting enzyme inhibitors may afford better protection than conventional treatment at various stages of diabetic nephropathy and prevent the evolution from incipient to overt nephropathy. In patients with nondiabetic renal disease, no unequivocal evidence exists for such a protective effect. In renal transplant recipients receiving cyclosporine, converting enzyme inhibitors and calcium antagonists are equally effective in the control of hypertension and both leave unaltered the glomerular filtration rate. It remains to be demonstrated, using adequate study designs, whether a particular class of agent is superior to another in patients with chronic renal disease.
Angiotensin-Converting Enzyme Inhibitors↗
Endogenous vasoactive systems and the pressor effect of acute N omega-nitro-L-arginine methyl ester administration.
The contribution of the renin-angiotensin system (RAS) and various endogenous vasoconstrictors on the pressor response to acute N omega-nitro-L-arginine methyl ester (L-NAME) administration (200 micrograms/kg/min) was assessed in anesthetized Wistar rats. Activity of the endogenous RAS was suppressed either by chronic treatment by a nonpeptide angiotensin II (AII) receptor antagonist (losartan) or an angiotensin-converting enzyme inhibitor (ACEI: enalapril), DOCA-salt pretreatment (without previous uninephrectomy), and binephrectomy (36-40 hours before experiments). We also studied the influence of chronic dietary sodium restriction. The role of alpha 1-adrenoceptor activity, endothelin (ET), and eicosanoids was evaluated in rats pretreated by prazosin, phosphoramidon (a nonspecific blocker of the conversion of big ET to ET), indomethacin, and the thromboxane A2 (TXA2) prostaglandin H2 (PGH2)-receptor antagonist SQ 29548, respectively. Finally, we tested the influence of the calcium channel blocker nicardipine on the vasopressor effect of L-NAME. In nonpretreated animals, L-NAME infusion induced an increase in mean arterial pressure (MAP) of 38 +/- 4 mm Hg. Chronic suppression of the RAS by losartan, enalapril, or DOCA did not alter the response to L-NAME, but the effect of L-NAME was moderately blunted in binephrectomized rats. Moderate attenuation (approximately 25%) and to a similar extent of the pressor effect of L-NAME was afforded by the low-sodium diet, phosphoramidon, SQ 29548, and indomethacin, whereas nicardipine markedly blunted by 74% the effect of L-NAME. We conclude that the acute pressor effect of L-NAME is mediated (at least in part) by cyclooxygenase-dependent products (mainly TXA2) and ET, but not by the RAS.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenergic alpha-Antagonists↗
Effect of losartan and enalapril on renal adaptation sodium restriction in rat.
The influence of losartan (10 or 30 mg.kg-1.day-1), enalapril (10 mg.kg-1.day-1), and combined treatment by losartan and enalapril on the renal adaptation to dietary sodium withdrawal was assessed in normal rats. Treatments were given by gavage for 3 days before and during the 6-day period of low-sodium (LS) diet. Cumulative sodium excretion during LS was similar in untreated and low-dose losartan groups (0.62 +/- 0.07 and 0.75 +/- 0.07 mmol/6 days), whereas it was significantly increased in groups treated by the high dose of losartan and enalapril alone or combined with both doses of losartan (1.38 +/- 0.16, 1.50 +/- 0.10, 1.37 +/- 0.16, and 1.12 +/- 0.03 mmol/6 days, respectively). A decrease in conscious systolic arterial pressure was observed in all treated groups in response to LS. At the end of LS, conscious renal blood flow (microsphere method) was similarly increased in all treated groups. Creatinine clearance decreased to a similar extent with both doses of losartan, whereas a further reduction was observed with enalapril given alone or combined with losartan. These results demonstrate that the enalapril-induced disturbance in the response of renal sodium excretion to LS is mainly related to angiotensin-mediated mechanisms. However, non-angiotensin-related actions of enalapril may contribute to the deterioration of renal function in sodium-restricted animals. In addition, a high dose of losartan is required to impair renal sodium conservation, thus suggesting that the tubular renin-angiotensin system may play a crucial role in the renal adaptation to dietary sodium withdrawal.
Adaptation, Physiological↗
Anatomic pairing of afferent arterioles and renin cell distribution in rat kidneys.
Close afferent arteriolar (AA) connectivity is a prerequisite for hemodynamic interaction between superficial rat nephrons. Studies were conducted in rat, mouse, rabbit, and human renal vasculatures obtained by an HCl maceration-microdissection technique to document the extent of AA connectivity. In rat kidneys, we assessed the possibility for a slow component of internephron coupling, as reflected by arteriolar renin cell distribution after specific immunostaining for renin. In the four species examined, 51% (human) to 60% (mouse) of total AA populations were organized as vascular units consisting of mostly two AA sharing a common origin and a connecting arterial segment. In rat AA pairs, branch lengths were significantly correlated, suggesting coordinated arteriolar growth. The sum of AA branch lengths averaged 278 +/- 6 microns. Rat arteriolar renin status, ranging from no renin cells to renin-recruited midafferent arterioles, distributed in a significantly nonrandom fashion within AA pairs, and 52% of the pairs had equal renin status. Hence, AA pairing is a consistent anatomic characteristic of mammalian kidneys and may constitute an optimal vascular design for hemodynamic as well as endocrine interactions.
Animals↗
Is microalbuminuria a marker of early intrarenal vascular dysfunction in essential hypertension?
The relation between basal intrarenal hemodynamics and the renal response to acute inhibition of angiotensin-converting enzyme by captopril and albuminuria was assessed in 106 lean patients with essential hypertension without detectable proteinuria. It was observed that the microalbuminuric group (24.5% of the total population) was characterized by a higher systemic arterial pressure, a lower level of high-density lipoprotein cholesterol, and similar mean values of age, duration of hypertension, glomerular filtration rate, renal plasma flow, filtration fraction, and plasma renin activity when compared with normoalbuminuric subjects. In response to captopril, a significant renal vasodilatation without a change in glomerular filtration rate or a fall in filtration fraction was observed in normoalbuminuric patients only. In contrast, the renal vasodilator response was abolished in microalbuminuric subjects, together with blunting of the rise in plasma renin activity associated with captopril. This occurred despite similar indexes of activity of the endogenous renin-angiotensin system. It is suggested that microalbuminuria may be a marker of early functional or fixed intrarenal vascular dysfunction in never-treated lean patients with essential hypertension.
Adolescent↗
Influence of dopamine and angiotensin II blockade on the acute response to unilateral nephrectomy in rats.
Unilateral nephrectomy (UNX) is followed by a prompt functional adaptation (as well as initiation of compensatory growth) in the contralateral kidney. We assessed the possibility that dopamine (DA) receptor antagonism and angiotensin-converting enzyme inhibition may influence the acute natriuretic response to UNX of the remaining kidney in euvolemic anesthetized Sprague-Dawley rats with or without pretreatment by haloperidol or enalapril. Twenty to 80 min after UNX, urinary excretion of sodium and potassium approximately doubled and fractional excretion of lithium (an index of proximal tubular handling of sodium) increased by about one third in untreated rats, whereas glomerular filtration rate, renal plasma flow and mean arterial pressure (MAP) did not change significantly. Haloperidol infusion blunted the post-UNX increase in fractional excretion of lithium without affecting the natriuretic/kaliuretic response of the remaining kidney. Enalapril pretreatment resulted in lower MAP and marked renal vasodilation at baseline but no significant alteration in the response to UNX. These results indicate that the magnitude of post-UNX natriuresis is not affected by suppression of angiotensin II (AII) generation or blockade of DA receptors. The lithium clearance data suggest that the immediate natriuretic response to UNX can be ascribed to both a proximal and a distal tubular phenomenon.
Angiotensin II↗
[Left ventricular performance and morphologic myocardial changes in untreated hypertensive patients].
Left ventricular contractile performance and geometric adaptation to hypertension were investigated in 255 patients with untreated essential hypertension and 160 normotensive subjects by M-mode echocardiography. Because all "ejection-phase" measurements are affected by changes in afterload, ventricular performance was estimated at the operating level of systolic wall stress by the afterload-corrected fractional shortening. Mitral regurgitation was excluded in all patients by Doppler echocardiography. Patients were categorized according to values of end-diastolic relative wall thickness and left ventricular mass index. Among hypertensive patients, ventricular mass and relative wall thickness were normal in 44%, whereas 20% had increase relative wall thickness with normal ventricular mass "concentric remodeling", 22% had concentric hypertrophy (increase both ventricular mass and relative wall thickness) and 14% had increased ventricular mass with normal relative wall thickness (eccentric hypertrophy). Arterial pressure and body mass index were higher in patients with concentric hypertrophy. Left ventricular contractile performance paralleled ventricular geometry, with a decrease of the afterload-corrected fractional shortening in the group with concentric remodeling and hypertrophy, whereas systolic function was normal in the eccentric group despite higher level of systolic wall stress. This study suggests a strong dependence of left ventricular mass with chamber size and myocardial contractility. Thus arterial pressure was not the sole determinant of left ventricular hypertrophy in essential hypertension. The respective role of this factors remains to be determined.
Adaptation, Physiological↗