Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UNIPROT:Q92565 (GFR)
4,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium antagonists are known to exert various effects on the kidney that might modulate their antihypertensive potential. This study evaluated the renal effects, along with the efficacy, of isradipine in two subgroups of patients with mild to moderate essential hypertension (EH), defined according to plasma renin activity (PRA). Twenty-six patients were randomly assigned to receive 12-week treatment with slow-release isradipine (2.5-5 mg) or placebo. Assessment of PRA related to concurrent 24-hour sodium excretion was used to define patients with high/medium (n=16) and low renin profile (n=10). Urinary albumin excretion (UAE), serum creatinine and glomerular filtration rate (GFR, as endogenous creatinine clearance) were measured. Blood pressure (BP) decrease with isradipine was greater in the low PRA group as compared with the high/medium PRA group (P<0.05), and normalization of BP was achieved in all low-renin patients compared with 57% in the high/medium PRA group. BP reduction in the placebo group was statistically not significant. Isradipine, but not placebo, induced significant reduction in UAE (P<0.05); the decrease was similar in both PRA groups. Treatment did not cause any significant changes in GFR, PRA, urinary sodium or creatinine excretion, or serum aldosterone or creatinine concentrations. The decrease of BP in the whole isradipine-treated group was inversely correlated with pretreatment serum creatinine as well as with basal urinary creatinine excretion. In conclusion, the antihypertensive effect of isradipine was more pronounced in low-renin EH patients, despite similar effects on renal function and UAE in both PRA groups.
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PMID:Antihypertensive and renal effects of isradipine in essential hypertension: focus on renin system activity. 937 50

In the general population, renal function linearly declines with age; hypertension may accelerate this decline. Because concentric left ventricular (LV) hypertrophy is a strong marker of the severity of hypertension, the influence of LV geometry on the age-associated decline in renal function was assessed in 195 normotensive subjects and 645 patients with never-treated essential hypertension with an average duration of 30 mo. According to LV mass and relative wall thickness, hypertensive patients were divided into normal LV (NL, 48%), concentric remodeling (CR, 19%), and concentric (CH, 22%) and eccentric (EH, 11%) hypertrophy. GFR and effective renal plasma flow (ERPF) were estimated by isotopic clearance technique. GFR and ERPF were inversely correlated with age in normotensive and hypertensive subjects, and no marked influence of the BP level or the presence of LV hypertrophy was detected. However, the slope of the regression line of GFR versus age was accentuated (P < 0.01) in patients with CH or CR (slope values of -0.95 +/- 0.11, -0.86 +/- 0.14 ml/min per yr, respectively) when compared with patients with EH or NL (slope values of -0.58 +/- 0.16 and -0.58 +/- 0.08 ml/min per yr, respectively). No such results were obtained when creatinine clearance was considered. Urinary albumin excretion was higher in patients with concentric or eccentric LV hypertrophy than in patients with concentric LV remodeling or normal LV. These results demonstrate that in never-treated essential hypertension, the age-associated decline in GFR is markedly influenced by the concentric pattern of LV response to hypertension rather than the level of BP and/or the presence of LV hypertrophy.
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PMID:Left ventricular remodeling and renal function in never-treated essential hypertension. 1266 Mar 22

Mild renal dysfunction, defined as GFR <60 to 70 ml/min and/or the presence of increased urinary albumin excretion, is associated with higher cardiovascular morbidity and mortality in primary hypertension. The aim of the present study was to investigate the relationship between renal dysfunction and target organ damage (TOD), namely left ventricular hypertrophy (LVH), retinal vascular changes, and carotid atherosclerosis, in a large cohort of unselected middle-aged hypertensive patients with normal serum creatinine. A group of 934 untreated patients with primary hypertension (543 men, 391 women; mean age 50 +/- 11 yr) was studied. Renal function was estimated by the creatinine clearance using the Cockcroft-Gault formula and by the presence of albuminuria, measured as the albumin to creatinine ratio (A/C) in first morning urine samples. LVH was determined according to electrocardiographic criteria, and retinal vascular changes were evaluated by direct ophthalmoscopy in all patients. In a subgroup of patients (n = 340; 208 men, 132 women; mean age 47 +/- 9), the presence and extent of cardiac and vascular organ damage was also assessed by ultrasound techniques. Creatinine clearance was on the average 82 +/- 20 ml/min. The overall prevalence of ECG-detected LVH and retinopathy was 12 and 49%, respectively. Creatinine clearance was inversely related to duration of disease, systolic BP, serum glucose, total cholesterol, LDL cholesterol, and early signs of TOD, namely retinal vascular changes and LVH. Patients in the bottom quintile of creatinine clearance showed higher prevalence of both ECG-determined LVH (P = 0.04) and retinal vascular changes (P = 0.02). In the subgroup of patients who underwent ultrasound evaluation of cardiovascular structures, the prevalence of mild renal dysfunction was 18%, whereas the prevalence of LVH and carotid plaque was 49 and 26%, respectively. Patients with mild renal dysfunction showed higher left ventricular mass and increased intima-media thickness (P < 0.0001), as well as higher prevalence of LVH and carotid plaque as compared with those with normal renal function. Controlling for duration of hypertension and mean BP, the risk of TOD in our cohort increased by 20% for each 10 ml/min decrease in creatinine clearance and by 30% for each 0.2 mg/mmol increase in Log A/C. In conclusion, mild renal dysfunction is associated with preclinical end-organ damage in patients with primary hypertension. These data may help to explain the observed increase in cardiovascular mortality reported in these patients. The evaluation of creatinine clearance and urinary albumin excretion could be useful for identifying patients who are at higher cardiovascular risk.
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PMID:Mild renal dysfunction and cardiovascular risk in hypertensive patients. 1468 81

The existence of a significant percentage of treated hypertensive patients presenting a diminished renal function has been recently described. Mild renal function abnormalities are recognized as powerful predictors of cardiovascular morbidity and mortality. However, longitudinal data demonstrating this association are lacking. The objectives of this study have been analysis of the evolution of GFR, assessed as creatinine clearance (CrCl), during long-term follow-up of hypertensive patients and evaluation of the impact of the development of chronic kidney disease (CKD) on cardiovascular prognosis. A historical cohort of 281 patients attending our Hypertension Unit was selected according to the following criteria: essential hypertension, more than 5 yr of follow-up, and normal GFR at baseline (CrCl > 90 ml/min per 1.73 m(2)). Patients had an average follow-up of 13.2 +/- 4.8 yr. Forty-one patients (14.6%) developed CKD (CrCl < 60 ml/min per 1.73 m(2)) attributed to hypertensive nephrosclerosis. Initial serum creatinine, age, systolic BP at baseline, and average total cholesterol during follow-up were independent predictors of CKD development. Forty-nine (17.4%) of 281 patients presented a cardiovascular event during follow-up: 17 patients (40.6%) who developed CKD and 32 patients (13.3%) with preserved renal function (log rank test P < 0.001). After adjustment in a Cox multivariate analysis, age, development of CKD during follow-up, and male gender were independent predictors of the appearance of cardiovascular events. In essential hypertensive patients with normal renal function at baseline, the development of CKD during the follow-up is strongly and independently related with poor cardiovascular prognosis.
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PMID:Development of chronic kidney disease and cardiovascular prognosis in essential hypertensive patients. 1515 73

Changes in renal function related with essential hypertension are associated with an elevated cardiovascular morbidity and mortality. Indices of altered renal function (e.g., microalbuminuria, increased serum creatinine concentrations, decrease in estimated creatinine clearance or GFR, and overt proteinuria) are independent predictors of cardiovascular morbidity and mortality. The Framingham Heart Study documented the relevance of proteinuria for cardiovascular prognosis in the community. The INSIGHT Study assessed the role of proteinuria as a risk factor in essential hypertension. The presence of proteinuria at baseline turned out to be a very potent predictor for the development of cardiovascular events and death in patients with essential hypertension and one or more associated cardiovascular risk factors. Recent data indicate that minor derangements of renal function, including proteinuria, are associated, both in the community and in the hypertensive population, with the clustering of cardiovascular risk factors observed in metabolic syndrome that promote progression of atherosclerosis. Renal function has to be routinely evaluated in every hypertensive patient, and the presence of minor alterations considered in the stratification of cardiovascular risk in hypertensive patients.
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PMID:Effect of proteinuria and glomerular filtration rate on cardiovascular risk in essential hypertension. 1548 17

Experimental and clinical data suggest that primary aldosteronism (PA) may be associated with cardiovascular hypertrophy and fibrosis, in part independent of the BP level. Whether PA may also result in specific deleterious effects on the kidneys was less studied. In 25 patients with tumoral PA, renal studies (urinary excretion of proteins, GFR, and effective renal plasma flow [ERPF], as clearances of technetium-labeled diethylene triaminopentaacetic acid and 131I-ortho iodohippurate, respectively) were performed both before and 6 mo after surgical cure. A control group consisting of patients with essential hypertension (EH) was studied before and after 6 mo of antihypertensive therapy. At baseline, PA and EH patients were similar with respect to demographic data, duration and level of hypertension, and GFR and ERPF. Urinary excretion of albumin and beta2 microglobulin were higher in PA than EH (88 +/- 26 versus 39 +/- 12 and 0.91 +/- 0.23 versus 0.26 +/- 0.19 mg/24 h, respectively; both P < 0.05). Adrenalectomy was followed by a decrease in arterial BP (by 28 +/- 3/13 +/- 2 mmHg), urinary excretion of albumin and beta2 microglobulin (by 48 +/- 19 and 0.53 +/- 0.21 mg/24 h, respectively), and GFR and ERPF (by 15 +/- 3 and 54 +/- 15 ml/min per 1.73 m(2), respectively). In EH, a similar decrease in pressure was associated with a decrease in albuminuria but no change in GFR or ERPF. In 17 of the 25 PA patients who received a 6-mo treatment of spironolactone, both GFR and ERPF decreased in parallel with BP, similar to what was observed after surgery. These data suggest that PA was associated with relative hyperfiltration, unmasked after suppression of aldosterone excess.
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PMID:Relative glomerular hyperfiltration in primary aldosteronism. 1580 Jan 24

Renal insufficiency in essential hypertension represents the expression of a medium- and small-size arteriolopathy characterized by intimal hyperplasia, hyalinosis, and smooth muscle cell hypertrophy (nephroangiosclerosis). Because in animal models endothelial dysfunction plays a role in this alteration, nephroangiosclerosis and the attendant renal insufficiency may be the expression of a systemic dysfunction of vascular endothelium. Endothelial function in the kidney vasculature of hypertensive individuals has been investigated little because studies on the hemodynamic response of the kidney to nitric oxide activation and blockade are laborious to perform. There is no direct proof that endothelial dysfunction in the forearm or in the coronary circulation is paralleled by a similar hemodynamic dysfunction in the kidney. A recent study in a large population of patients with essential hypertension showed that, independent of other risk factors, the GFR in these patients is strongly related to the forearm blood flow response to acetyl choline (an established test of endothelial function). Furthermore, in this study, C-reactive protein was inversely related to the GFR and with the vasodilatory response to acetyl choline, pointing to inflammation as a likely mechanism to explain the association between endothelial dysfunction and impaired renal function in essential hypertension. A dysfunctional endothelium may represent a critical link accounting for the risk for both renal impairment and cardiovascular complications in essential hypertension.
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PMID:Endothelial dysfunction and the kidney: emerging risk factors for renal insufficiency and cardiovascular outcomes in essential hypertension. 1656 49

The relationship among inflammation (plasma high-sensitivity C-reactive protein [CRP]), endothelial function (hemodynamic response to acetylcholine [ACh] in the forearm), and renal function (serum creatinine and GFR [Modification of Diet in Renal Disease formula]) was investigated in 264 never-treated individuals with uncomplicated essential hypertension and serum creatinine within the normal range. Multiple regression models of renal function (creatinine) were constructed in sequence including Framingham risk factors as well the hemodynamic response to ACh and plasma CRP. The inclusion of endothelial function into a model based on Framingham risk factors added highly significant (P < 0.001) power to this model (+5%). Of note, in an alternative model that included CRP (instead of endothelial function), the creatinine variance explained by this factor was two times higher (+10%) than that associated with endothelial function in the first model. In the full model that included both endothelial function and CRP, CRP maintained a much stronger independent link with the outcome measure than endothelial function. In individuals with untreated, uncomplicated essential hypertension, multivariate modeling indicated that inflammation is a crucial mechanism mediating the endothelial-renal function link. The proatherogenic potential of inflammation associated with subtle impairment in renal function may contribute to the cardiovascular risk of essential hypertension.
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PMID:Inflammation as a mediator of the link between mild to moderate renal insufficiency and endothelial dysfunction in essential hypertension. 1656 50

Peripheral pulse pressure (PP) is a marker of aging-associated arterial stiffening after the fifth decade. In addition, PP has emerged as a strong predictor of cardiovascular morbidity and mortality. A study of the relationship between renal function and aging of the arterial system using reliable methods of estimating renal haemodynamics (effective renal plasma flow) and function (glomerular filtration rate; GFR) was thus undertaken in a large number of never-treated individuals with essential hypertension. In 212 patients with isolated systolic hypertension, there was an inverse correlation between GFR and PP, but the correlation did not persist after adjustment for age. In fact, the deleterious effect of PP on GFR was observed, independent of age and mean arterial pressure, only in patients aged 60 years and over. In contrast, no clear influence of PP on GFR was detected in patients aged 40 years and over but less than 60 years and in those younger than 40 years. It is thus proposed that PP may have a detrimental influence on the age-related decline in GFR. Prospective studies on the influence of antihypertensive agents with possible effects on peripheral and central PP on the progressive decline of GFR are required.
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PMID:Consequences of elevated pulse pressure on renal function. 1672 63

Genomewide linkage analyses were conducted of serum creatinine, estimated GFR (eGFR), and urine albumin-creatinine ratio (UACR) in search of genetic susceptibility loci for chronic kidney disease in 1351 black (median age 63 yr, 70% women, 79% hypertensive) and 1022 white individuals (median age 61 yr, 56% women, 75% hypertensive) from sibships in which two or more members had essential hypertension diagnosed before age 60 yr. After adjustment for gender, age, diabetes, and use of angiotensin inhibitors, the logarithm-transformed measure of serum creatinine was heritable in both ethnic groups (0.45 in black individuals [P < 0.001]; 0.39 in white individuals [P < 0.001]), as was eGFR (0.52 in black individuals [P < 0.001]; 0.39 in white individuals [P < 0.001]). Log UACR was heritable in black individuals (0.30, P < 0.001) but not in white individuals (0.12; P = 0.059). In black individuals, the univariate maximum multipoint logarithm of odds scores (MLS) were observed on chromosome 7 for log serum creatinine (MLS = 3.65, at 43 cM from pter; P = 0.00002) and eGFR (MLS = 2.52, at 45 cM from pter; P = 0.00033) and for log UACR (MLS = 2.91, at 112 cM from pter; P = 0.00012). In white individuals, only one MLS for log serum creatinine and one for eGFR achieved the logarithm of odds score criterion for "suggestive" evidence of linkage (2 < or = MLS < 3), both on chromosome 3 (at 211 and 209 cM, respectively); however, none did so for log UACR. In black individuals, bivariate linkage analyses of log serum creatinine and pulse pressure (i.e., systolic-diastolic BP) provided "suggestive" evidence of a region on chromosome 5 with pleiotropic effects on both traits (MLS = 3.62, at 85 cM from pter; P = 0.00023). These findings support the utility of genetic linkage analyses for identification of novel risk factors that influence measures of chronic kidney disease, particularly among black individuals.
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PMID:Influence of genomic loci on measures of chronic kidney disease in hypertensive sibships. 1677 34


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