Long-Term Effects of Converting Enzyme Inhibitors on Split Renal Function in Renovascular Hypertension

Long-term effects of angiotensin converting enzyme inhibitors on split renal function were studied using a noninvasive radioisotopic method in five patients with renovascular hypertension. In the stenotic side the glomerular filtration rate which acutely decreased following captopril, tended to return toward pretreatment levels on prolonged captopril administration (up to 2 years), while the value remained unchanged in the nonstenotic side of the kidney. Effective renal plasma flow increased in both sides. During long-term captopril treatment, there were no significant changes in serum creatinine, sodium, potassium, and blood pressure control was maintained at the same level in an acute period. These results suggest that the glomerular filtration in the stenotic kidney of renovascular hypertension, which was acutely reduced, will not further deteriorate, but will increase after prolonged captopril treatment.     

Renal scintigraphic captopril test in the diagnosis of renovascular hypertension

Angiotensin converting enzyme (ACE) inhibitor-induced renal failure has been reported in bilateral renal artery stenosis and in stenosis in solitary kidneys, but not in unilateral renal artery stenosis. In these patients, however, a functional impairment of the kidney ipsilateral to the stenosis can often be detected after ACE inhibition by scintigraphic techniques employing glomerular radionuclide tracers like 99mTc-diethylenetriamine pentaacetic acid (DTPA). Dynamic renal scintigraphy with 99mTc-DTPA before and 1 hour after administration of captopril, 25 mg (renal scintigraphic captopril test; RSCT), was performed in a selected series of 39 hypertensive subjects with suspected renovascular hypertension. Changes in glomerular filtration rate induced by captopril on the individual kidney were estimated by assessing the early (120-180 seconds) DTPA uptake by the kidney. Values were expressed as the ratio between the kidney with the lower uptake and the contralateral one in 34 patients and as the ratio of the kidney counts to the injected dose in five patients with solitary kidneys, aortic coarctation, or both. Compared with precaptopril values, postcaptopril uptake decreased markedly in 14 subjects (-62.42 +/- 30.94 [SD]%; range, -25 to -100%) and decreased modestly or even increased in the other 25 (+0.57 +/- 9.83%; range, +28 to -13%). Of the 14 subjects considered to be RSCT-positive diagnostic workup revealed either established (10) or strongly suspected (2) renal artery stenosis in 12 and aortic coarctation in 2 subjects. In another patient with established renovascular hypertension, results of the RSCT were negative when performed in the supine position but became positive when repeated in the sitting position.(ABSTRACT TRUNCATED AT 250 WORDS)     

Renal insufficiency after administration of captopril in renal artery stenosis with a single kidney or bilateral stenosis is not compulsory

Acute renal failure has been reported during captopril therapy of hypertension due to renal artery stenosis with a single kidney or bilateral renal artery stenosis. Under low perfusion pressures inhibition of the renin-angiotensin system could disturb the autoregulation, decrease efferent arteriolar resistance and lead to a critical decrease in glomerular filtration. Renal function tests were repeated in a patient with hypertension due to 90 p. 100 renal artery stenosis with a single kidney, before and after captopril administration (sodium intake 100 mmol/24 h). (table; see text) Identical results have also been observed in a patient with bilateral renal artery stenosis. Both patients presented high risk renal haemodynamic states. The control of systemic blood pressure and the fall in filtration fraction were not associated with a critical, immediate or short term fall in glomerular filtration. The isolated administration of captopril is therefore not systematically contra-indicated in these two clinical situations.     

Renovascular hypertension identified by captopril-induced changes in the renogram

Radioisotope renography was performed in 21 patients with hypertension and unilateral renal artery stenosis with and without premedication with 25 mg of captopril, and the results were compared with the effect of percutaneous transluminal angioplasty on the blood pressure, assessed 6 weeks after angioplasty. Angioplasty caused a considerable decrease in blood pressure in 15 of the 21 patients. In 12 of these 15 patients, captopril induced changes in the time-activity curves of the affected kidney only, suggesting deterioration of the excretory function of that kidney, while the function of the contralateral kidney remained normal. After angioplasty the asymmetry in the time-activity curves diminished despite identical pretreatment with captopril. Such captopril-induced unilateral impairment of the renal function was not seen in the six patients with unilateral renal artery stenosis whose blood pressure did not change after percutaneous transluminal angioplasty or in 13 patients with hypertension and normal renal arteries. The functional impairment of the affected kidneys was characterized by a decrease of 99mTc-diethylenetriamine pentaacetic acid uptake and a delay of 131I-hippurate excretion, while the 131I-hippurate uptake remained unaffected. These data are in agreement with a reduced glomerular filtration rate and diuresis during preservation of the renal blood flow, changes that can be expected after converting enzyme inhibition in a kidney with low perfusion and an active, renin-mediated autoregulation of the glomerular filtration rate. These data suggest that functional captopril-induced unilateral changes, shown by split renal function studies with noninvasive gamma camera scintigraphy, can be used as a diagnostic test for renovascular hypertension caused by unilateral renal artery stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of angiotensin on renal transport of sodium in renovascular hypertension

Eleven patients with renovascular arterial hypertension were studied, 9 of whom had unilateral renal artery stenosis and 2 bilateral renal artery stenosis.

Angiotensin increased sodium excretion in the contralateral kidney and did not change it in the stenotic one.

In bilateral stenosis angiotensin increased sodium excretion significantly in both kidneys.

The difference in response to angiotensin between patients with unilateral stenotic kidney and those with bilateral stenosis is apparently unrelated to arterial blood pressure distal to the arterial stenosis.     

Furosemide augments the effects of captopril on nuclear studies in renovascular stenosis

Captopril facilitates detection of unilateral renovascular hypertension by selectively reducing glomerular filtration rate in affected kidneys. To determine if volume depletion augments this response, we compared the effects of captopril, furosemide, and combined furosemide plus captopril on individual kidney computer-derived clearances of 99mTc-diethylenetriamine pentaacetic acid (DTPA) and [131I]o-iodohippurate in two-kidney, one clip Goldblatt hypertensive rats and normal controls. In clipped kidneys, captopril reduced DTPA clearance significantly from baseline (from 0.31 +/- 0.02 to 0.19 +/- 0.04 ml/min/100 g; p less than 0.02) whereas furosemide alone had no effect (0.28 +/- 0.03 ml/min/100 g). Combined furosemide plus captopril further reduced clipped kidney DTPA clearance to a level significantly less than captopril alone (0.10 +/- 0.02 ml/min/100 g; p less than 0.02). Clipped kidney o-iodohippurate clearance was not changed from baseline by any treatment. In contralateral unclipped and normal kidneys, DTPA clearance did not decline from baseline following either captopril or furosemide plus captopril treatment. Since the dose of captopril used (3 mg/kg by intraperitoneal injection) did not reduce systolic blood pressure of hypertensive rats significantly, these changes probably reflect intrarenal rather than systemic hemodynamic effects of converting enzyme inhibition and are consistent with the hypothesis that captopril interferes with glomerular filtration in stenotic kidneys by reducing efferent arteriolar vascular resistance. Prior volume depletion accentuates the effect of captopril on stenotic kidney glomerular filtration rate, providing improved functional discrimination of stenotic kidneys from contralateral unclipped and normal kidneys. These results indicate that furosemide-induced volume depletion may increase the diagnostic sensitivity of captopril-enhanced 99mTc-DTPA renography in the detection of unilateral renovascular hypertension.     

Ramipril for hypertension secondary to renal artery stenosis. Changes in blood pressure, the renin-angiotensin system and total and divided renal function

The converting enzyme inhibitor, ramipril, 20 mg once daily, was given to 3 hypertensive patients with unilateral renovascular disease. At 1 month, 24 hours after the last dose of ramipril, blood pressure, plasma angiotensin II and converting enzyme activity remained low, and active renin and angiotensin I high. There was no tendency for converting enzyme inhibition to be overcome during 1 month of ramipril therapy. Ramipril caused slight increases in serum potassium and urea, no change in serum creatinine and no consistent changes in the renal vein renin ratio. Ramipril caused little change in renal plasma flow on the stenotic side, but filtration fraction was reduced in 2 patients. There was no serious deterioration in total or individual glomerular filtration rate during ramipril therapy. The drug was well tolerated and there were no serious side effects. Ramipril, given once daily, is likely to be effective in controlling hypertension with renal artery stenosis.     

Differential renal function during angiotensin converting enzyme inhibition in renovascular hypertension

Renal function was measured sequentially in 32 patients with proven renovascular hypertension who were treated with the oral angiotensin converting enzyme inhibitor captopril. Renal function was assessed by serial measurement of serum creatinine. Six patients showed acute rises in serum creatinine concentration compatible with acute renal failure. Acute renal failure was confined to those patients with stenosis to a solitary kidney (transplant or native, occurring in 3 of 8 patients) or bilateral renal artery stenosis (occurring in 3 of 13 patients). No rise in serum creatinine concentration was observed in 11 patients with unilateral renal artery stenosis during long-term angiotensin converting enzyme inhibitor therapy. Acute renal failure during angiotensin converting enzyme inhibitor therapy was not related to the degree of blood pressure fall or the plasma angiotensin II level. Eleven patients with renovascular hypertension were followed prospectively with estimation of renal function by 99mTc-diethylenetriaminepentaacetic acid (DTPA) clearance (determined by computer analysis of scintillation camera renography). In six patients with unilateral renal artery stenosis, total 99mTc-DTPA clearance and serum creatinine level remained constant following angiotensin converting enzyme inhibitor therapy, while in five patients with bilateral renal artery stenosis 99mTc-DTPA clearance fell from 40 +/- 9 to 27 +/- 5 ml/min (p less than 0.05). Split renal function studies revealed that 99mTc-DTPA clearance fell in most kidneys with stenosed arteries during angiotensin converting enzyme inhibition, including the stenosed kidney from patients with unilateral renal artery stenosis (16 stenosed kidneys studied; change in Tc-DTPA clearance, -7.5 +/- 2.7 ml/min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Release of immunoassayable prostaglandin E by the human ischemic kidney.

Immunoassayable prostaglandin E concentration in renal venous plasma was measured in eight patients with renovascular hypertension. Two subjects with bilateral renal artery stenosis had similar concentrations from both renal veins. The six subjects with unilateral artery stenosis had greater concentration on the stenotic side in each case, suggesting that the human ischemic kidney produces increased amounts of prostaglandins.     

Usefulness and limits of distal echo-Doppler velocimetric indices for assessing renal hemodynamics in stenotic and non-stenotic kidneys

BACKGROUND: Distal echo-Doppler velocimetric indices are widely used for revealing the presence of a renal artery stenosis but there is scarce information as to whether they reflect the renal hemodynamics in stenotic and nonstenotic kidneys. OBJECTIVES AND METHODS: We evaluated the pulsatility and resistive indices (PI and RI), acceleration (A) and acceleration time (At) and correlated their values with those of effective renal plasma flow (ERPF), glomerular filtration rate (GFR), renal vascular resistance (RVR) and filtration fraction (FF) estimated by single kidney scintigraphy in 24 kidneys with 70-95% renal artery stenosis (atherosclerotic n = 17, fibromuscular n = 7) and in 27 non-stenotic kidneys (11 contralateral to renal artery stenosis and 16 of patients with essential hypertension). In patients with stenotic kidneys, these measurements were repeated within 7 days after a successful percutaneous transluminal renal angioplasty (PTRA) (in 11 arteries performed in combination with stent implantation). RESULTS: Prior to dilation we found that the stenotic kidneys had significantly lower values of ERPF, GFR and higher RVR than the non-stenotic kidneys and that these hemodynamic alterations were associated with those, also statistically significant, of the four velocimetric indices. In non-stenotic kidneys, there were highly significant relationships between PI and ERPF, and RVR (r = -0.68 and 0.81 respectively P < 0.01); similar relationships were found for RI (r = -0.67 and 0.78 P < 0.01) whereas no such correlations were found between these two velocimetric indices and GFR and FF; also no correlations were found between A and Atand ERPF, GFR, RVR and FF. In stenotic kidneys no significant correlations were found between any of the velocimetric and the hemodynamic indices. Renal artery dilation induced clear cut increments in ERPF, GFR and reduction in RVR in post-stenotic kidneys, which were associated with normalization of all four velocimetric indices. No relationships were observed between the renal hemodynamic and the velocimetric changes induced by dilation; however in post-stenotic kidneys the relationships between PI and RI, ERPF and RVR were restored as in nonstenotic kidneys. CONCLUSIONS: These data indicate that PI and RI can be used to assess ERPF and RVR both in non-stenotic and post-stenotic kidneys; however, none of the velocimetric indices examined in this study can provide valid informations on the renal hemodynamics of stenotic kidneys and on their changes induced by PTRA.     

Predicting cardiac morbidity

Captopril was administered for 6 days to 26 severely hypertensive hospitalized patients, 17 with essential hypertension and 9 with renovascular hypertension. All the patients were on a low sodium diet and were treated after the 3rd day in the hospital with progressively increasing doses of captopril (75 to 450 mg/day). Mean blood pressure decreased from 142 ± 20 to 117 ± 18 mm Hg in essential hypertension and from 136 ± 11 to 106 ± 10 mm Hg in renovascular hypertension. Plasma renin activity and aldosterone as well as urinary aldosterone and vasopressin were higher in renovascular hypertension than in essential hypertension. In both groups, captopril decreased similarly plasma aldosterone and urinary aldosterone and vasopressin, whereas plasma renin activity increased.These identical changes in blood pressure and hormonal variables were accompanied by different modifications in urinary sodium excretion, plasma volume and plasma creatinine. Urinary sodium excretion was higher (3.06 ± 1.38 mmol/mmol of urinary creatinine) in treated essential hypertension than in treated renovascular hypertension (1.77 ± 1.01, p < 0.05). Plasma volume was unchanged in essential hypertension and increased by 7.75 ± 7 percent of the normal values (p < .0.2) in renovascular hypertension. Plasma creatinine was slightly but significantly increased in essential hypertension (+6.7 ± 10.7 μmol/liter, p <0.02) and was much more elevated in renovascular hypertension (+45.2 ± 38.3 μmol/liter, p < 0.01).These data demonstrate that captopril is able to decrease similarly the activity of the renin-angiotensin-aldosterone-vasopressin system in essential and renovascular hypertension, whereas its renal effects are different. Marked increases in plasma creatinine were observed among patients with renal artery stenosis. These observations suggest caution in the use of converting enzyme inhibitors in patients with renovascular hypertension, especially those on a low sodium diet.     

Effect of captopril on 99mTc-diethylenetriaminepentaacetic acid renograms in two-kidney, one clip hypertension

In an effort to improve on the noninvasive detection of renal artery stenosis, we investigated the effect of angiotensin converting enzyme inhibition on computer-assisted 99mTc-diethylenetriaminepentaacetic acid (DTPA) renal flow studies in a canine model of two-kidney, one clip hypertension and compared these findings with clearances of inulin and p-aminohippuric acid in the stenotic and contralateral kidney before and after converting enzyme inhibition. The 99mTc-DTPA renal flow study with the converting enzyme inhibitor captopril (1.5 mg/kg bolus with 1.5 mg/min infusion) showed an increased sensitivity in the detection of unilateral renal artery stenosis over the use of the 99mTc-DTPA study alone. Captopril induced striking alterations that were most evident in the 15-minute 99mTc-DTPA renal flow study, in which all nine curves exhibited severely blunted uptake and excretion of the radionuclide. These changes were reversed during a recovery study without converting enzyme inhibition and were not seen when blood pressure was lowered with nitroprusside to a level similar to that observed during converting enzyme inhibition. The changes shown by the 99mTc-DTPA study during converting enzyme inhibition correlated with a decrease in the glomerular filtration rate of the stenotic kidney. Captopril infusion significantly decreased the glomerular filtration rate of the stenotic kidney (16.0 +/- 3.1 vs 11.0 +/- 2.5 mg/min, p less than 0.03) but not of the contralateral kidney (32.4 +/- 2.6 vs 28.4 +/- 2.8 mg/min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Use of the converting enzyme inhibitor enalapril in renovascular hypertension. Effect on blood pressure, renal function, and the renin-angiotensin-aldosterone system

Thirteen patients were entered into a protocol to assess the safety and efficacy of enalapril (MK 421), 5 to 20 mg b.i.d., and hydrochlorothiazide, 50 to 100 mg daily, for the treatment of renovascular hypertension. Specifically monitored were the effects of therapy on blood pressure and pulse, renal function, and the renin-angiotensin-aldosterone axis. Enalapril and hydrochlorothiazide therapy produced excellent control of blood pressure with no adverse side effects. After approximately 8 weeks of therapy, renal vascular resistance was decreased and no adverse effects on glomerular filtration rate or renal blood flow were noted, except in one patient with a functional unilateral stenotic kidney. Patients receiving enalapril and hydrochlorothiazide showed stimulation of plasma renin activity and suppression of plasma angiotensin II, although the initial degree of suppression was not sustained in all patients during prolonged therapy. Although plasma aldosterone concentration was initially suppressed, the degree of suppression was not sustained. Nine patients have been followed for an additional 6 months; none have experienced further progression of renal disease, as assessed by repeated measurements of glomerular filtration and effective renal plasma flow. These results suggest that combined enalapril and hydrochlorothiazide therapy is safe and effective in the medical management of renovascular hypertension and that blood pressure control may be achieved in the absence of sustained interruption of the renin-angiotensin-aldosterone system.     

Atherosclerotic renal artery stenosis

Opinion statement The clinical diagnosis of renal artery stenosis relies on a high index of suspicion and confirmation by noninvasive imaging modalities. There are three distinct clinical syndromes associated with renal artery stenosis: renin-dependent hypertension, essential hypertension, and ischemic nephropathy. Clinical features that should heighten suspicion for renal artery stenosis include abrupt-onset or accelerated hypertension at any age, unexplained acute or chronic azotemia, azotemia induced by angiotensin-converting enzyme (ACE) inhibitors, asymmetric renal dimensions, and congestive heart failure with normal ventricular function. Patients with true renin-dependent (renovascular) hypertension are typically young or middle-age women with renal fibromuscular dysplasia (FMD). Initial therapy for renovascular hypertension associated with FMD is an ACE inhibitor; refractory hypertension responds readily to balloon angioplasty without stenting. Elderly patients with generalized atherosclerosis and hypertension often have atherosclerotic renal artery stenosis (ARAS); hypertension in these patients is usually not renin dependent (ie, essential hypertension). Hypertension alone, even if treated with multiple medications, is not a compelling indication for renal artery revascularization; these patients should be treated aggressively with antihypertensive medical therapy. Renal artery revascularization with stenting may be considered for refractory severe hypertension, and would be expected to improve blood control and modestly reduce medication requirements. Renal revascularization rarely cures hypertension in patients with ARAS. Patients with ARAS, hypertension, and end-organ injury should be considered for renal revascularization. Manifestations of end-organ injury include nonischemic pulmonary edema; hypertensive crisis associated with acute coronary syndrome, aortic dissection, or neurologic impairment; and renal insufficiency. Ischemic nephropathy is best treated before the development of advanced renal failure. The best candidates for revascularization are those with baseline serum creatinine less than 2.0 mg/dL, bilateral renal artery stenosis, normal renal resistive indices, no proteinuria, and one or more manifestations of end-organ injury. In these patients, renal revascularization is best accomplished by stenting, although surgical revascularization may be considered in patients with concomitant severe aortic aneurysmal or occlusive disease.     

Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease

We studied renal plasma flow and glomerular filtration rate during graded blood pressure reduction induced with sodium nitroprusside infusion in 16 hypertensive patients with atherosclerotic renovascular disease. Eight patients with unilateral disease tolerated pressure reduction from 205 +/- 9 (SE)/103 +/- 2 mm Hg to 146 +/- 6/84 +/- 3 mm Hg (p less than 0.01) with no change in total renal function. In 8 other patients with bilateral renal arterial stenosis (all arteries 70% or more stenosed), similar pressure reduction produced marked but reversible decrements in plasma flow (152 +/- 28 mL/min to 66 +/- 13 mL/min; p less than 0.01) and glomerular filtration rate (38 +/- 8 mL/min to 16 +/- mL/min; p less than 0.01). In 4 patients restudied after revascularization, sensitivity of renal function to pressure changes was no longer present. These data indicate that vascular stenosis to the entire renal mass may limit function and provide a means for evaluating patients at risk for loss of renal function during antihypertensive therapy.     

Nephrotic-range proteinuria in patients with renovascular disease

PURPOSE: Proteinuria is usually considered a manifestation of glomerular disease. We sought to describe the characteristics of patients with nephrotic-range proteinuria resulting from renovascular disease and to compare them with those of patients who had glomerulonephritis. SUBJECTS AND METHODS: We identified 14 patients with nephrotic-range proteinuria and renovascular disease and compared them with 14 patients who had nephrotic-range proteinuria and biopsy-proven glomerulonephritis, matched for sex, age, and glomerular filtration rate. RESULTS: Patients with renovascular disease were more likely to have known atherosclerotic vascular disease [13 of 14 (93%) vs 3 of 14 (21%), P < 0.0001) and were usually smokers [12 of 14 (85%) vs 3 of 14 (21%), P < 0.0001]. They also had a greater mean (+/- SD) difference between the lengths of their kidneys (29 +/- 10 vs 5 +/- 5 mm, P < 0.001); greater systolic blood pressure (203 +/- 22 vs 174 +/- 25 mm Hg, P < 0.005), plasma renin activity (17 +/- 19 vs 2 +/- 2 ng/mL/h, P = 0.005), and plasma aldosterone concentration (40 +/- 23 vs 11 +/- 10 ng/dL, P = 0.0001); and lower serum potassium levels (3.3 +/- 0.5 vs 3.8 +/- 0.5, P <0.05). Effective renal plasma flow was lower (139 +/- 68 vs 307 +/- 185 mL/min/1.73 m3) and filtration fraction was markedly greater (0.28 +/- 0.04 vs 0.15 +/- 0.07, P = 0.0001) in the patients with renovascular disease. After the oral administration of captopril, blood pressure, effective renal plasma flow, and glomerular filtration rate decreased only among patients with renovascular disease. Of the 14 patients with renovascular disease, 13 had evidence of renal artery thrombosis seen at angiography; 2 patients required dialysis, and 3 others died during follow-up. CONCLUSION: Our findings suggest that the patients with nephrotic-range proteinuria resulting from renovascular disease have distinct characteristics and a poor prognosis.     

Severe reversible azotemia from captopril therapy. Report of three cases and review of the literature

We saw three cases of severe reversible azotemia secondary to captopril therapy in hypertension. All patients had extensive peripheral vascular disease involving the renal arteries, and two patients (patients 2 and 3) had high levels of peripheral plasma renin activity. The azotemia occurred approximately two weeks after exposure to captopril, and fever, a maculopapular pruritic cutaneous rash, and eosinophilia developed in two patients (patients 2 and 3). The cause of the azotemia in our patients is not clearly known, since renal biopsies were not performed. The most likely cause for the azotemia was volume contraction with reduction in the glomerular filtration rate, although a direct insult to the kidney could not be excluded.     

Hemodynamic effects of captopril in essential hypertension, renovascular hypertension and cardiac failure: correlations with short- and long-term effects on plasma renin

The hemodynamic effects of captopril were investigated in 22 patients with essential hypertension, 22 with hypertension and renal artery stenosis and 14 with refractory chronic heart failure. The effects of a first dose of captopril, 50 mg orally, were observed for 2 hours, and the effects of repeated doses, 450 mg/day in combination with mild dietary sodium restriction, for at least 4 weeks.Short-term captopril treatment caused similar reductions in blood pressure in the three patient groups, that is, 21 ± 3 mm Hg in essential hypertension, 29 ± 6 mm Hg in renovascular hypertension and 21 ± 2 mm Hg in heart failure (mean ± standard error of the mean) despite large differences in pretreatment plasma renin. Heart rate and cardiac output did not change in hypertensive patients, and cardiac filling pressures decreased. The changes in right atrial pressure, pulmonary artery pressure and pulmonary capillary wedge pressure in essential hypertension and in renovascular hypertension did not differ. Heart rate decreased and cardiac output increased in heart failure, whereas cardiac filling pressures decreased. Blood pressure responses to long-term captopril therapy in essential and in renovascular hypertension were similar and, as with short-term treatment, changes in blood pressure were largely determined by changes in peripheral resistance. Several measurements of extracellular fluid volume showed no evidence of fluid retention by the kidneys.Short-term but not long-term blood pressure responses were correlated with pretreatment plasma renin (percent change in mean arterial pressure, short-term, versus log renin, r = 0.47, p < 0.001, n = 14). Both short- and long-term responses of total peripheral resistance were correlated with plasma renin (percent change in resistance, short-term versus log renin, r = 0.64, p < 0.001, n = 40; percent change in resistance, long-term versus log renin, r = 0.56, p < 0.001, n = 31). The correlations were weak and probably not important for clinical practice. These data indicate that other factors besides circulating renin are important in captopril's hypotensive effect. The favorable hemodynamic effects of converting enzyme inhibition warrant further consideration of this principle of therapy in the clinical management of most forms of hypertension and also in the treatment of chronic heart failure.     

Diagnostik der Nierenarterienstenose

If clinical signs suggest the presence of renal artery stenosis, screening methods should be employed to confirm or exclude the diagnosis. Ideally a screening method should not only be able to detect the presence of stenosis but should also be able to estimate its functional relevance. Frequently used screening methods in order of increasing cost are color-coded duplex ultrasonography, captopril scintigraphy, spiral CT and MR angiography. Invasive intra-arterial digital subtraction angiography should only be used for treatment and not solely to diagnose renal artery stenosis. All methods can be used for detection of renal artery stenosis but duplex ultrasonography is preferred for patients with impaired renal function (grade III or higher). A functional relevance of renal artery stenosis (renovascular hypertension and azotemia) may be estimated with Doppler ultrasonography (resistance index) but at present data are contradictory.     

Prospective evaluation of aggressive medical therapy for atherosclerotic renal artery stenosis, with renal artery stenting reserved for previously injured heart, brain, or kidney

Sixty-six patients with atherosclerotic renal artery stenosis (RAS) and serum creatinine < or =2.0 mg/dl were treated with antihypertensive therapy, a statin, and aspirin. Renal stenting was reserved for patients with injuries to the heart, brain, or kidneys. The primary end point was stenotic kidney glomerular filtration rate (GFR) at 21 months; secondary end points included major adverse clinical events, serum creatinine, total GFR, and blood pressure (BP). After baseline evaluation, 26 of 66 patients underwent renal stenting because of injuries to the heart, brain, or kidneys. After 21 months, 6 medical patients required renal stenting, and 5 patients experienced late clinical events (2 medical patients, 3 stent patients). There was no difference in final BP between groups. Whereas medical patients experienced 6% and 8% decreases in total and stenotic kidney GFR, stent patients experienced 7% and 11% increases in total kidney (p = 0.006) and stenotic kidney (p = 0.02) GFR. There was no difference in final serum creatinine. In conclusion, patients with atherosclerotic RAS and baseline creatinine < or =2.0 mg/dl can be safely managed with aggressive medical therapy, with a small decrease in GFR. For patients who develop injuries to the heart, brain, or kidneys, renal artery stenting may further reduce hypertension and improve renal function.