Jean Ribstein | Université de Montpellier (original) (raw)
Papers by Jean Ribstein
HAL (Le Centre pour la Communication Scientifique Directe), Nov 11, 2016
Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Rad... more Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Radiographic Erosions. 2016 ACR/ARHP Annual Meeting
HAL (Le Centre pour la Communication Scientifique Directe), Nov 11, 2016
Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Rad... more Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Radiographic Erosions. 2016 ACR/ARHP Annual Meeting
HAL (Le Centre pour la Communication Scientifique Directe), Nov 11, 2016
Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Rad... more Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Radiographic Erosions. 2016 ACR/ARHP Annual Meeting
Journal of Hypertension, Jun 1, 2011
Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remo... more Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remodeling is an independent predictor of fatal and non-fatal cardiovascular events in patients with CKD stage 2-5.
Journal of Hypertension, Jun 1, 2011
Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remo... more Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remodeling is an independent predictor of fatal and non-fatal cardiovascular events in patients with CKD stage 2-5.
Journal of Hypertension, Jun 1, 2011
Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remo... more Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remodeling is an independent predictor of fatal and non-fatal cardiovascular events in patients with CKD stage 2-5.
Springer eBooks, 1998
Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary ... more Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary hypertension. In clinical practice, a search for renal disease (i.e., proteinuria, abnormal urinary sediment, increased serum creatinine) should be undertaken in the presence of any newly diagnosed hypertension; however, only selected patients should be screened for renovascular disease. In recent years, the challenge in the management of patients with renal parenchymal disease has focused on the influence of strict control of hypertension on the rate of deterioration of renal function with time. In several experimental models, the use of antihypertensive agents has proved efficient in preventing the decline in renal function as well as the extent of glomerulosclerosis; interestingly, all antihypertensive medications were not equally effective in this regard. A number of questions remain unsettled in humans: Can adequate control of blood pressure slow down renal deterioration? Which drug should be used? What is the optimal level of arterial pressure? Although ischemic renovascular disease has recently emerged as an important cause of renal failure, the potential of revascularization to improve or preserve renal function is still a matter of debate.
Springer eBooks, 1998
Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary ... more Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary hypertension. In clinical practice, a search for renal disease (i.e., proteinuria, abnormal urinary sediment, increased serum creatinine) should be undertaken in the presence of any newly diagnosed hypertension; however, only selected patients should be screened for renovascular disease. In recent years, the challenge in the management of patients with renal parenchymal disease has focused on the influence of strict control of hypertension on the rate of deterioration of renal function with time. In several experimental models, the use of antihypertensive agents has proved efficient in preventing the decline in renal function as well as the extent of glomerulosclerosis; interestingly, all antihypertensive medications were not equally effective in this regard. A number of questions remain unsettled in humans: Can adequate control of blood pressure slow down renal deterioration? Which drug should be used? What is the optimal level of arterial pressure? Although ischemic renovascular disease has recently emerged as an important cause of renal failure, the potential of revascularization to improve or preserve renal function is still a matter of debate.
Springer eBooks, 1998
Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary ... more Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary hypertension. In clinical practice, a search for renal disease (i.e., proteinuria, abnormal urinary sediment, increased serum creatinine) should be undertaken in the presence of any newly diagnosed hypertension; however, only selected patients should be screened for renovascular disease. In recent years, the challenge in the management of patients with renal parenchymal disease has focused on the influence of strict control of hypertension on the rate of deterioration of renal function with time. In several experimental models, the use of antihypertensive agents has proved efficient in preventing the decline in renal function as well as the extent of glomerulosclerosis; interestingly, all antihypertensive medications were not equally effective in this regard. A number of questions remain unsettled in humans: Can adequate control of blood pressure slow down renal deterioration? Which drug should be used? What is the optimal level of arterial pressure? Although ischemic renovascular disease has recently emerged as an important cause of renal failure, the potential of revascularization to improve or preserve renal function is still a matter of debate.
PubMed, Sep 1, 1989
Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension. Howev... more Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension. However, acute renal deterioration may occur in some conditions where angiotensin plays a crucial role in the regulation of the glomerular filtration rate (GFR), such as volume depletion, severe stenosis of both renal arteries and stenosis of the renal artery of a single functioning kidney. Acute renal failure induced by ACE inhibition may develop without a reduction in systemic blood pressure it is enhanced by prior sodium depletion and is reversible when treatment is withdrawn. The relative superiority of ACE inhibitors in slowing the progression of chronic parenchymal renal disease remains to be demonstrated, although promising results have been reported in patients with diabetic nephropathy.
PubMed, Sep 1, 1989
Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension. Howev... more Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension. However, acute renal deterioration may occur in some conditions where angiotensin plays a crucial role in the regulation of the glomerular filtration rate (GFR), such as volume depletion, severe stenosis of both renal arteries and stenosis of the renal artery of a single functioning kidney. Acute renal failure induced by ACE inhibition may develop without a reduction in systemic blood pressure it is enhanced by prior sodium depletion and is reversible when treatment is withdrawn. The relative superiority of ACE inhibitors in slowing the progression of chronic parenchymal renal disease remains to be demonstrated, although promising results have been reported in patients with diabetic nephropathy.
Acta Ophthalmologica, Feb 14, 2013
To assess the relation between retinal vascular caliber and renal function. Patients and methods:... more To assess the relation between retinal vascular caliber and renal function. Patients and methods: Eighty apparently healthy subjects screened for cardiovascular risk factors (mean age 47 years, 51% female, 36% hypertensive, without diabetes or renal dysfunction) were recruited. Retinal vascular calibers were measured from fundus photographs and expressed as central retinal artery and venular equivalent. Renal function was assessed by measurement of glomerular filtration rate (urinary clearance of 99mTc-DTPA) and urinary albumin ⁄ creatinine ratio. Results: Mean glomerular filtration rate was 117 ml ⁄ min ⁄ 1.73m 2. Overall, central retinal artery and venular equivalent were positively correlated with glomerular filtration rate (r = +0.31, p = 0.005 and r = +0.30, p = 0.006, respectively). In addition, central retinal artery equivalent was negatively correlated with urinary albumin ⁄ creatinine ratio (r =)0.34, p = 0.002). No significant relationship was found between central retinal venular equivalent and urinary albumin ⁄ creatinine ratio (r = +0.12, p = 0.32). The observed relations between retinal vascular calibers and renal function parameters remained significant after adjusting for potential confounding factors. Conclusion: In apparently healthy subjects with normal renal function, retinal arteriolar and venular calibers were negatively correlated with kidney function, suggesting common determinants of these preclinical target organ damages.
Acta Ophthalmologica, Feb 14, 2013
To assess the relation between retinal vascular caliber and renal function. Patients and methods:... more To assess the relation between retinal vascular caliber and renal function. Patients and methods: Eighty apparently healthy subjects screened for cardiovascular risk factors (mean age 47 years, 51% female, 36% hypertensive, without diabetes or renal dysfunction) were recruited. Retinal vascular calibers were measured from fundus photographs and expressed as central retinal artery and venular equivalent. Renal function was assessed by measurement of glomerular filtration rate (urinary clearance of 99mTc-DTPA) and urinary albumin ⁄ creatinine ratio. Results: Mean glomerular filtration rate was 117 ml ⁄ min ⁄ 1.73m 2. Overall, central retinal artery and venular equivalent were positively correlated with glomerular filtration rate (r = +0.31, p = 0.005 and r = +0.30, p = 0.006, respectively). In addition, central retinal artery equivalent was negatively correlated with urinary albumin ⁄ creatinine ratio (r =)0.34, p = 0.002). No significant relationship was found between central retinal venular equivalent and urinary albumin ⁄ creatinine ratio (r = +0.12, p = 0.32). The observed relations between retinal vascular calibers and renal function parameters remained significant after adjusting for potential confounding factors. Conclusion: In apparently healthy subjects with normal renal function, retinal arteriolar and venular calibers were negatively correlated with kidney function, suggesting common determinants of these preclinical target organ damages.
American Journal of Hypertension, Oct 1, 1993
American Journal of Hypertension, Oct 1, 1993
PubMed, Jul 1, 1989
Many factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of ... more Many factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of sodium has recently been suggested. In the present study, we assessed the influence of dietary sodium on the degree of left ventricular hypertrophy (LVH) in 41 patients aged 38 +/- 10 (mean +/- SD) with mild essential hypertension (casual blood pressure 149 +/- 17/91 +/- 11 mmHg). Patients had never been given antihypertensive drugs before and ingested ad libitum sodium intake. Posterior wall thickness (PWT) and left ventricular mass (LVM) were measured by M-mode echocardiography and sodium intake was estimated from urinary sodium excretion rate (UNa, mmol/24h). Both PWT and LVM, and not telediastolic diameter or LV fractional shortening, were directly correlated with UNa (r = 0.47 and 0.46; p less than 0.02 and 0.002, respectively. A stepwise multiple regression analysis confirmed that UNa was a determinant of LVM independently of sex, age, body weight, blood pressure and duration of hypertension. No correlation was found between LVM and plasma renin activity, whilst a positive one existed between PWT and hematocrit (r = 0.42; p less than 0.007). These results suggest that dietary sodium may play a role in modulating left ventricular mass in untreated hypertensives, possibly in expanding volume or activating the adrenergic system.
PubMed, Jul 1, 1989
Many factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of ... more Many factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of sodium has recently been suggested. In the present study, we assessed the influence of dietary sodium on the degree of left ventricular hypertrophy (LVH) in 41 patients aged 38 +/- 10 (mean +/- SD) with mild essential hypertension (casual blood pressure 149 +/- 17/91 +/- 11 mmHg). Patients had never been given antihypertensive drugs before and ingested ad libitum sodium intake. Posterior wall thickness (PWT) and left ventricular mass (LVM) were measured by M-mode echocardiography and sodium intake was estimated from urinary sodium excretion rate (UNa, mmol/24h). Both PWT and LVM, and not telediastolic diameter or LV fractional shortening, were directly correlated with UNa (r = 0.47 and 0.46; p less than 0.02 and 0.002, respectively. A stepwise multiple regression analysis confirmed that UNa was a determinant of LVM independently of sex, age, body weight, blood pressure and duration of hypertension. No correlation was found between LVM and plasma renin activity, whilst a positive one existed between PWT and hematocrit (r = 0.42; p less than 0.007). These results suggest that dietary sodium may play a role in modulating left ventricular mass in untreated hypertensives, possibly in expanding volume or activating the adrenergic system.
HAL (Le Centre pour la Communication Scientifique Directe), Nov 11, 2016
Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Rad... more Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Radiographic Erosions. 2016 ACR/ARHP Annual Meeting
HAL (Le Centre pour la Communication Scientifique Directe), Nov 11, 2016
Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Rad... more Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Radiographic Erosions. 2016 ACR/ARHP Annual Meeting
HAL (Le Centre pour la Communication Scientifique Directe), Nov 11, 2016
Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Rad... more Sodium Intake Is Increased in Patients with Early Rheumatoid Arthritis and Is Associated with Radiographic Erosions. 2016 ACR/ARHP Annual Meeting
Journal of Hypertension, Jun 1, 2011
Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remo... more Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remodeling is an independent predictor of fatal and non-fatal cardiovascular events in patients with CKD stage 2-5.
Journal of Hypertension, Jun 1, 2011
Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remo... more Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remodeling is an independent predictor of fatal and non-fatal cardiovascular events in patients with CKD stage 2-5.
Journal of Hypertension, Jun 1, 2011
Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remo... more Conclusion: This study provides the first direct evidence that aortic stiffness not arterial remodeling is an independent predictor of fatal and non-fatal cardiovascular events in patients with CKD stage 2-5.
Springer eBooks, 1998
Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary ... more Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary hypertension. In clinical practice, a search for renal disease (i.e., proteinuria, abnormal urinary sediment, increased serum creatinine) should be undertaken in the presence of any newly diagnosed hypertension; however, only selected patients should be screened for renovascular disease. In recent years, the challenge in the management of patients with renal parenchymal disease has focused on the influence of strict control of hypertension on the rate of deterioration of renal function with time. In several experimental models, the use of antihypertensive agents has proved efficient in preventing the decline in renal function as well as the extent of glomerulosclerosis; interestingly, all antihypertensive medications were not equally effective in this regard. A number of questions remain unsettled in humans: Can adequate control of blood pressure slow down renal deterioration? Which drug should be used? What is the optimal level of arterial pressure? Although ischemic renovascular disease has recently emerged as an important cause of renal failure, the potential of revascularization to improve or preserve renal function is still a matter of debate.
Springer eBooks, 1998
Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary ... more Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary hypertension. In clinical practice, a search for renal disease (i.e., proteinuria, abnormal urinary sediment, increased serum creatinine) should be undertaken in the presence of any newly diagnosed hypertension; however, only selected patients should be screened for renovascular disease. In recent years, the challenge in the management of patients with renal parenchymal disease has focused on the influence of strict control of hypertension on the rate of deterioration of renal function with time. In several experimental models, the use of antihypertensive agents has proved efficient in preventing the decline in renal function as well as the extent of glomerulosclerosis; interestingly, all antihypertensive medications were not equally effective in this regard. A number of questions remain unsettled in humans: Can adequate control of blood pressure slow down renal deterioration? Which drug should be used? What is the optimal level of arterial pressure? Although ischemic renovascular disease has recently emerged as an important cause of renal failure, the potential of revascularization to improve or preserve renal function is still a matter of debate.
Springer eBooks, 1998
Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary ... more Renal parenchymal disease and renovascular abnormalities are the most common causes of secondary hypertension. In clinical practice, a search for renal disease (i.e., proteinuria, abnormal urinary sediment, increased serum creatinine) should be undertaken in the presence of any newly diagnosed hypertension; however, only selected patients should be screened for renovascular disease. In recent years, the challenge in the management of patients with renal parenchymal disease has focused on the influence of strict control of hypertension on the rate of deterioration of renal function with time. In several experimental models, the use of antihypertensive agents has proved efficient in preventing the decline in renal function as well as the extent of glomerulosclerosis; interestingly, all antihypertensive medications were not equally effective in this regard. A number of questions remain unsettled in humans: Can adequate control of blood pressure slow down renal deterioration? Which drug should be used? What is the optimal level of arterial pressure? Although ischemic renovascular disease has recently emerged as an important cause of renal failure, the potential of revascularization to improve or preserve renal function is still a matter of debate.
PubMed, Sep 1, 1989
Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension. Howev... more Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension. However, acute renal deterioration may occur in some conditions where angiotensin plays a crucial role in the regulation of the glomerular filtration rate (GFR), such as volume depletion, severe stenosis of both renal arteries and stenosis of the renal artery of a single functioning kidney. Acute renal failure induced by ACE inhibition may develop without a reduction in systemic blood pressure it is enhanced by prior sodium depletion and is reversible when treatment is withdrawn. The relative superiority of ACE inhibitors in slowing the progression of chronic parenchymal renal disease remains to be demonstrated, although promising results have been reported in patients with diabetic nephropathy.
PubMed, Sep 1, 1989
Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension. Howev... more Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension. However, acute renal deterioration may occur in some conditions where angiotensin plays a crucial role in the regulation of the glomerular filtration rate (GFR), such as volume depletion, severe stenosis of both renal arteries and stenosis of the renal artery of a single functioning kidney. Acute renal failure induced by ACE inhibition may develop without a reduction in systemic blood pressure it is enhanced by prior sodium depletion and is reversible when treatment is withdrawn. The relative superiority of ACE inhibitors in slowing the progression of chronic parenchymal renal disease remains to be demonstrated, although promising results have been reported in patients with diabetic nephropathy.
Acta Ophthalmologica, Feb 14, 2013
To assess the relation between retinal vascular caliber and renal function. Patients and methods:... more To assess the relation between retinal vascular caliber and renal function. Patients and methods: Eighty apparently healthy subjects screened for cardiovascular risk factors (mean age 47 years, 51% female, 36% hypertensive, without diabetes or renal dysfunction) were recruited. Retinal vascular calibers were measured from fundus photographs and expressed as central retinal artery and venular equivalent. Renal function was assessed by measurement of glomerular filtration rate (urinary clearance of 99mTc-DTPA) and urinary albumin ⁄ creatinine ratio. Results: Mean glomerular filtration rate was 117 ml ⁄ min ⁄ 1.73m 2. Overall, central retinal artery and venular equivalent were positively correlated with glomerular filtration rate (r = +0.31, p = 0.005 and r = +0.30, p = 0.006, respectively). In addition, central retinal artery equivalent was negatively correlated with urinary albumin ⁄ creatinine ratio (r =)0.34, p = 0.002). No significant relationship was found between central retinal venular equivalent and urinary albumin ⁄ creatinine ratio (r = +0.12, p = 0.32). The observed relations between retinal vascular calibers and renal function parameters remained significant after adjusting for potential confounding factors. Conclusion: In apparently healthy subjects with normal renal function, retinal arteriolar and venular calibers were negatively correlated with kidney function, suggesting common determinants of these preclinical target organ damages.
Acta Ophthalmologica, Feb 14, 2013
To assess the relation between retinal vascular caliber and renal function. Patients and methods:... more To assess the relation between retinal vascular caliber and renal function. Patients and methods: Eighty apparently healthy subjects screened for cardiovascular risk factors (mean age 47 years, 51% female, 36% hypertensive, without diabetes or renal dysfunction) were recruited. Retinal vascular calibers were measured from fundus photographs and expressed as central retinal artery and venular equivalent. Renal function was assessed by measurement of glomerular filtration rate (urinary clearance of 99mTc-DTPA) and urinary albumin ⁄ creatinine ratio. Results: Mean glomerular filtration rate was 117 ml ⁄ min ⁄ 1.73m 2. Overall, central retinal artery and venular equivalent were positively correlated with glomerular filtration rate (r = +0.31, p = 0.005 and r = +0.30, p = 0.006, respectively). In addition, central retinal artery equivalent was negatively correlated with urinary albumin ⁄ creatinine ratio (r =)0.34, p = 0.002). No significant relationship was found between central retinal venular equivalent and urinary albumin ⁄ creatinine ratio (r = +0.12, p = 0.32). The observed relations between retinal vascular calibers and renal function parameters remained significant after adjusting for potential confounding factors. Conclusion: In apparently healthy subjects with normal renal function, retinal arteriolar and venular calibers were negatively correlated with kidney function, suggesting common determinants of these preclinical target organ damages.
American Journal of Hypertension, Oct 1, 1993
American Journal of Hypertension, Oct 1, 1993
PubMed, Jul 1, 1989
Many factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of ... more Many factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of sodium has recently been suggested. In the present study, we assessed the influence of dietary sodium on the degree of left ventricular hypertrophy (LVH) in 41 patients aged 38 +/- 10 (mean +/- SD) with mild essential hypertension (casual blood pressure 149 +/- 17/91 +/- 11 mmHg). Patients had never been given antihypertensive drugs before and ingested ad libitum sodium intake. Posterior wall thickness (PWT) and left ventricular mass (LVM) were measured by M-mode echocardiography and sodium intake was estimated from urinary sodium excretion rate (UNa, mmol/24h). Both PWT and LVM, and not telediastolic diameter or LV fractional shortening, were directly correlated with UNa (r = 0.47 and 0.46; p less than 0.02 and 0.002, respectively. A stepwise multiple regression analysis confirmed that UNa was a determinant of LVM independently of sex, age, body weight, blood pressure and duration of hypertension. No correlation was found between LVM and plasma renin activity, whilst a positive one existed between PWT and hematocrit (r = 0.42; p less than 0.007). These results suggest that dietary sodium may play a role in modulating left ventricular mass in untreated hypertensives, possibly in expanding volume or activating the adrenergic system.
PubMed, Jul 1, 1989
Many factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of ... more Many factors have been implicated in the pathogenesis of myocardial hypertrophy, and the role of sodium has recently been suggested. In the present study, we assessed the influence of dietary sodium on the degree of left ventricular hypertrophy (LVH) in 41 patients aged 38 +/- 10 (mean +/- SD) with mild essential hypertension (casual blood pressure 149 +/- 17/91 +/- 11 mmHg). Patients had never been given antihypertensive drugs before and ingested ad libitum sodium intake. Posterior wall thickness (PWT) and left ventricular mass (LVM) were measured by M-mode echocardiography and sodium intake was estimated from urinary sodium excretion rate (UNa, mmol/24h). Both PWT and LVM, and not telediastolic diameter or LV fractional shortening, were directly correlated with UNa (r = 0.47 and 0.46; p less than 0.02 and 0.002, respectively. A stepwise multiple regression analysis confirmed that UNa was a determinant of LVM independently of sex, age, body weight, blood pressure and duration of hypertension. No correlation was found between LVM and plasma renin activity, whilst a positive one existed between PWT and hematocrit (r = 0.42; p less than 0.007). These results suggest that dietary sodium may play a role in modulating left ventricular mass in untreated hypertensives, possibly in expanding volume or activating the adrenergic system.