Mesenchymal stem cells and chronic renal artery stenosis.

Renal artery stenosis is the main cause of renovascular hypertension and results in ischemic nephropathy characterized by inflammation, oxidative stress, microvascular loss, and fibrosis with consequent functional failure. Considering the limited number of strategies that effectively control renovascular hypertension and restore renal function, we propose that cell therapy may be a promising option based on the regenerative and immunosuppressive properties of stem cells. This review addresses the effects of mesenchymal stem cells (MSC) in an experimental animal model of renovascular hypertension known as 2 kidney-1 clip (2K-1C). Significant benefits of MSC treatment have been observed on blood pressure and renal structure of the stenotic kidney. The mechanisms involved are discussed.

Glomerular filtration rate measured by (51)Cr-EDTA clearance: Evaluation of captopril-induced changes in hypertensive patients with and without renal artery stenosis.

INTRODUCTION: Renal artery stenosis can lead to renovascular hypertension; however, the detection of stenosis alone does not guarantee the presence of renovascular hypertension. Renovascular hypertension depends on activation of the renin-angiotensin system, which can be detected by functional tests such as captopril renal scintigraphy. A method that allows direct measurement of the baseline and post-captopril glomerular filtration rate using chromium-51 labeled ethylenediamine tetraacetic acid ((51)Cr-EDTA) could add valuable information to the investigation of hypertensive patients with renal artery stenosis. The purposes of this study were to create a protocol to measure the baseline and post-captopril glomerular filtration rate using (51)Cr-EDTA, and to verify whether changes in the glomerular filtration rate permit differentiation between hypertensive patients with and without renal artery stenosis. METHODS: This prospective study included 41 consecutive patients with poorly controlled severe hypertension. All patients had undergone a radiological investigation of renal artery stenosis within the month prior to their inclusion. The patients were divided into two groups: patients with (n=21) and without renal artery stenosis, (n=20). In vitro glomerular filtration rate analysis ((51)Cr-EDTA) and (99m)Tc-DMSA scintigraphy were performed before and after captopril administration in all patients. RESULTS: The mean baseline glomerular filtration rate was 48.6+/-21.8 ml/kg/1.73 m(2) in the group wuth renal artery stenosis, which was significantly lower than the GFR of 65.1+/-28.7 ml/kg/1.73m(2) in the group without renal artery stenosis (p=0.04). Captopril induced a significant reduction of the glomerular filtration rate in the group with renal artery stenosis (to 32.6+/-14.8 ml/ kg/1.73m(2), p=0.001) and an insignificant change in the group without RAS (to 62.2+/-23.6 ml/kg/1.73m(2), p=0.68). Scintigraphy with technetium-99m dimercapto-succinic acid (DMSA) did not show significant differences in differential renal function from baseline to post-captopril images in either group. CONCLUSIONS: Captopril induced a decrease in the GFR that could be quantitatively measured with (51)Cr-EDTA. The reduction is more pronounced in hypertensive patients with RAS.

Glomerular filtration rate measured by 51Cr-EDTA clearance: evaluation of captopril-induced changes in hypertensive patients with and without renal artery stenosis

INTRODUCTION: Renal artery stenosis can lead to renovascular hypertension; however, the detection of stenosis alone does not guarantee the presence of renovascular hypertension. Renovascular hypertension depends on activation of the renin-angiotensin system, which can be detected by functional tests such as captopril renal scintigraphy. A method that allows direct measurement of the baseline and post-captopril glomerular filtration rate using chromium-51 labeled ethylenediamine tetraacetic acid (51Cr-EDTA) could add valuable information to the investigation of hypertensive patients with renal artery stenosis. The purposes of this study were to create a protocol to measure the baseline and post-captopril glomerular filtration rate using 51Cr-EDTA, and to verify whether changes in the glomerular filtration rate permit differentiation between hypertensive patients with and without renal artery stenosis. METHODS: This prospective study included 41 consecutive patients with poorly controlled severe hypertension. All patients had undergone a radiological investigation of renal artery stenosis within the month prior to their inclusion. The patients were divided into two groups: patients with (n=21) and without renal artery stenosis, (n=20). In vitro glomerular filtration rate analysis (51Cr-EDTA) and 99mTc-DMSA scintigraphy were performed before and after captopril administration in all patients. RESULTS: The mean baseline glomerular filtration rate was 48.6±21.8 ml/kg/1.73 m² in the group wuth renal artery stenosis, which was significantly lower than the GFR of 65.1±28.7 ml/kg/1.73m² in the group without renal artery stenosis (p=0.04). Captopril induced a significant reduction of the glomerular filtration rate in the group with renal artery stenosis (to 32.6±14.8 ml/kg/1.73m², p=0.001) and an insignificant change in the group without RAS (to 62.2±23.6 ml/kg/1.73m², p=0.68). Scintigraphy with technetium-99m dimercapto-succinic acid (DMSA) did...

Rat renal prorenin concentration in experimental hypertension.

The amount of renal prorenin in models of hypertension in rats was studied by using a novel enzyme (PreR-Co). Ten microgrames of PreR-Co promoted a complete conversion of inactive renin, and during the first 15-min incubation the reaction was under initial velocity conditions. The enzyme-substrate reaction obeyed Michaelis-Menten kinetics, with a Vmax of 0.97 x 10(-5) pmol Ang I/min and a Km of 5.03 x 10(-5) pmol prorenin. The difference between the total renin concentration (TRC) and active renin concentration (ARC) in the normal rat kidney (356.4 +/- 20.6 and 105.3 +/- 7.6 ng Ang I/mg tissue/h respectively), indicated that inactive renin comprised 70% of TRC. In the aortic coarctation model, inactive renin comprised 68 % of TRC in the right kidney and no or very little prorenin was found in the left kidney. In the Goldblatt 2-kidney, 1-clip rats, the right kidney prorenin comprised 61% of the TRC and 54% in the clamped left kidney. After DOCA-Salt treatment prorenin was almost absent in the rat kidneys. In conclusion, we have developed an easy and sensitive method to measure inactive renin in the kidney that may be useful to study the biochemical events of renin maturation in physiological and pathological states.