Effect of captopril on renal function in patients with essential hypertension

The glomerular filtration rate (creatinine clearance), glomerular permeability (qualitative and quantitative proteinuria), tubular reabsorption (k-λ chains of immunoglobulins and lysozyme) and indexes of tubular cell lysis (alpha-glucosidase and gamma-glutamyltranspeptidase) were measured in the urine of 10 patients with moderate, uncomplicated essential hypertension during placebo therapy and after captopril given at increasing doses of 25, 50, 100 and 200 mg twice daily, the first three doses being given for 3 days and the last one for 4 weeks in all patients and for an additional 6 months in 5 patients. During placebo therapy, proteinuria was absent in eight patients and detectable (glomerular and selective) in two; selective proteinuria appeared in two and a decrease in selectivity was observed in two patients with previous proteinuria after 4 weeks of captopril therapy. No proteinuria was detectable in the five patients followed up for 6 months, not even in the one in whom a decrease in glomerular selectivity had occurred after 4 weeks. The glomerular filtration rate was unchanged as were lysozyme and gamma-glutamyltranspeptidase values, while light chains were always undetectable. Alpha-glucosidase showed some increase; however, increments were transient and always much lower than those observed with known tubular toxic drugs. These data show that under our experimental conditions captopril caused no evident changes in glomerular and tubular function.     

Effect of the ACE-inhibitor captopril on the blood pressure and kidney function of patients with essential and renal hypertension]

We retrospectively analysed the effects of a 12-month treatment with captopril (Tensiomin) in 46 patients. All of the patients had hypertension lasting for years (9 essential, 37 with chronic renal failure), 32 of them had proteinuria. Captopril was given in addition to, or in exchange for, other antihypertensive drugs. Under treatment with ACE-inhibitors, a small but significant decrease in diastolic blood pressure (0.4 torr/month) and in proteinuria (0.19 g/month) was seen (regression analysis). Discriminant analysis showed proteinuria and diastolic blood pressure to be the more modifiable, the younger the patients, the higher the proteinuria at the beginning and the longer the history of hypertension. Serum creatinine, blood urea nitrogen, serum protein and serum potassium did not change.     

Effect of intrarenal furosemide on renal function and intrarenal hemodynamics in acute renal failure

The ability of short-term furosemide administration to alter intrarenal hemodynamics and to modify the clinical course of acute renal failure was assessed in six patients 2 to 9 days after the onset of acute renal failure. Following renal arterial catheterization, the intraarterial administration of furosemide at a dose of 9.6 mg/min for 30 minutes failed to improve renal function as assessed either by an increase in urine output or a decrease in serum creatinine during the 4 days after administration in the five oliguric patients. In a sixth patient with nonoliguric acute renal failure, urine volume increased with a gradual decrease in blood urea nitrogen and creatinine during the week after study. Furosemide failed to alter either mean renal blood flow or its intrarenal distribution as determined at intervals of 3 to 40 minutes after its infusion. These studies demonstrate that the short-term administration of furosemide in large doses does not improve renal hemodynamics or alter the clinical course of patients with established acute oliguric renal failure.     

氨氯地平和苯那普利联合治疗对高血压患者肾功能的影响

目的探讨氨氯地平、苯那普利单独治疗和联合治疗对高血压病患者肾功能的影响。方法66例高血压病患者随机分为3组:氨氯地平组(5mg,qd,22例);苯那普利组(10mg,qd,22例);氨氯地平和苯那普利联合治疗组(氨氯地平5mg,qd,苯那普利10mg,qd,22例)。疗程24周。治疗前、后观察肾功能指标变化。结果①氨氯地平、苯那普利及联合治疗组高血压病患者治疗后均能显著降低血压(P<0.01)及尿蛋白的排泄量。但联合治疗组降低尿蛋白排泄的幅度比氨氯地平组、苯那普利组明显高,而氨氯地平组和苯那普利组之间差异无统计学意义(P>0.05)。②治疗后,肾小球滤过率在联合治疗及苯那普利组明显增高,而氨氯地平组无明显变化。③三组治疗后尿白蛋白下降幅度与血压下降幅度均无显著相关。结论氨氯地平、苯那普利长期单独治疗均可减少蛋白尿,保护肾功能,两药联合治疗对减少蛋白尿、保护肾功能有一定相加作用。     

Renal and intrarenal blood flow in non-cirrhotic portal hypertension

The effect of portal hypertension or the consequent portal circulatory changes on renal haemodynamics was studied using the (133)xenon washout technique. Renal blood flow was reduced in nine of 11 patients with non-cirrhotic portal hypertension and this was accompanied by a redistribution of intrarenal blood flow, the distribution to and flow rate through the outer cortex being reduced while juxtamedullary and medullary flow was maintained. With slight or moderate decreases in cortical flow glomerular filtration was normal but poor cortical perfusion was associated with low creatinine clearances. These findings raise the possibility that portal hypertension or portal circulatory changes may play a role in the pathogenesis of the renal haemodynamic changes and functional renal failure which frequently complicate advanced hepatic cirrhosis.     

Effects of propranolol on renal blood flow and renal function in patients with cirrhosis

Systemic and splanchnic hemodynamics, renal blood flow, and renal function were studied in 13 patients with cirrhosis both before and 1 h after oral administration of 40 mg of propranolol (acute administration) and 1 mo after continuous administration of this substance at doses reducing the heart rate by 25% (chronic administration). Cardiac output and the gradient between wedged and free hepatic venous pressures significantly decreased after acute and chronic administration of propranolol; mean arterial pressure did not change significantly and systemic vascular resistance significantly increased. Renal blood flow and renal vascular resistance did not change significantly after acute administration of propranolol and renal function did not change significantly after acute or chronic administration of propranolol. We conclude that propranolol does not alter renal function in patients with cirrhosis who are in good physical condition.     

Effect of intrarenal renin-angiotensin-aldosterone system on renal function in patients after cardiac surgery

The aim of the study was to investigate the influence of intrarenal RAS on the decrease of renal function in patients undergoing cardiac surgery with cardiopulmonary bypass. This observational study investigated the activation of intrarenal RAS in 24 patients with AKI after cardiac surgery with cardiopulmonary bypass. The activation of intrarenal RAS was determined by urinary angiotensinogen (uAGT), which was measured at 12 hours before surgery, 0 and12 hours after surgery. The results were compared with those of 21 patients without AKI after cardiac surgery with cardiopulmonary bypass. Clinical and laboratory data were collected. Compared with baseline, all patients with cardiac surgery had activation of intrarenal RAS at 0 and 12 hours after surgery. The activation of intrarenal RAS was found significantly higher at both 0 and 12 hours after surgery in AKI group versus non AKI group (6.18 ± 1.93 ng/mL vs 3.49 ± 1.71 ng/mL, 16.38 ± 7.50 ng/mL vs 6.04 ± 2.59 ng/mL, respectively). There was a positive correlation between the activation of RAS at 0 hour after surgery and the decrease of renal function at 48 hours after surgery (r = 0.654, P = .001). These findings suggest that uAGT might be a suitable biomarker for prediction of the occurrence and severity of AKI after cardiac surgery. Inhibition of intrarenal RAS activation might be one the path of future treatment for this type of disease.     

Effect of nifedipine on renal function in patients with essential hypertension

Twenty-six essential hypertensive patients were entered into a protocol to assess the blood pressure and renal effects of the dihydropyridine calcium antagonist nifedipine (30-120 mg/day given in divided doses) administered for 4 weeks. Nifedipine monotherapy effectively lowered blood pressure in 73% of the patients. Glomerular filtration rate and effective renal plasma flow were increased 13.3 and 19.6%, respectively. The filtration fraction and urinary albumin excretion remained unchanged. Renal vascular resistance was markedly reduced (25.2%). Changes observed in renal function were independent of the patients' initial glomerular filtration rate. Furthermore, there was no correlation between the systemic and renal effects of nifedipine monotherapy. Patients with a poor systemic blood pressure response exhibited increases in both glomerular filtration rate (+13%) and effective renal plasma flow (+20%), changes comparable with increases in glomerular filtration rate (+13%) and effective renal plasma flow (+19%) observed in patients achieving a goal blood pressure response (diastolic blood pressure less than or equal to 90 mm Hg, or a greater than or equal to 10 mm Hg decrease in diastolic blood pressure, or both). These results suggest that nifedipine monotherapy has the potential to improve renal function abnormalities encountered in the essential hypertensive state independently of its effect on systemic blood pressure.     

Effects of captopril on renal function in patients with cirrhosis and ascites

Blockade of angiotensin-converting enzyme has been variously reported to increase or to decrease sodium excretion in patients with cirrhosis and ascites. We administered captopril (50-150 mg) to 11 patients with cirrhosis and ascites to determine the effects on blood pressure, renal blood flow and sodium excretion. Plasma renin activity increased and mean blood pressure fell (by 14 mm Hg). Para-aminohippurate clearances increased from 321 +/- 53 to 559 +/- 83 ml/min (P less than 0.005), but inulin clearances were minimally altered (73 +/- 8 to 76 +/- 7 ml/min), suggesting preferential dilation of glomerular efferent arterioles. Despite unchanged glomerular delivery of sodium, urinary sodium excretion fell in all subjects (from 2.70 +/- 1.00 to 0.48 +/- 0.21 mEq/h), urinary volume was reduced (377 +/- 55 to 182 +/- 42 ml/h, P less than 0.005), and the natriuretic effect of furosemide was blunted. The antinatriuretic effect of captopril may be mediated by reduced angiotensin II-mediated sodium excretion, by decreased prostaglandin production, and/or by indirect effects of reduced blood pressure. Captopril impairs rather than promotes sodium excretion.     

Combined actions of isradipine and captopril on renal function in hypertension.

The object of this study was to test the hypothesis that the natriuretic and uricosuric effect of calcium-entry blockers could be mediated through antagonism of angiotensin II dependent intrarenal mechanisms. The antihypertensive efficacy, haemodynamic and excretional effects of superimposed calcium blockade with isradipine were investigated in seven hypertensives with unsatisfactorally controlled blood pressure with captopril 50 mg twice daily. Glomerular filtration rate (GFR) and renal plasma flow (RPF), clearances (C) of sodium (Na), potassium (K), uric acid (UA) and lithium (Li), were measured before and after a low-dose bolus of isradipine, i.v. Subsequently, measurements were repeated during constant i.v. infusion of a higher dose with definite systemic haemodynamic effects. After 4 months of combined treatment with isradipine and captopril renal investigations were carried out again. The low isradipine dose induced a slight but statistically significant increment in CNa (22% +/- 28) and heart rate (4% +/- 4), whereas no other variables changed significantly. Infusion of the high isradipine dose caused a pronounced fall in renal vascular resistance (27% +/- 14), systolic (8% +/- 2) and diastolic blood pressure (17% +/- 5). RPF increased significantly (15% +/- 18) whereas no changes were noted in GFR, filtration fraction and urinary albumin excretion rate. In spite of the pronounced fall in BP during the high dose infusion, significant increments in natriuresis (91% +/- 63) and diuresis (41% +/- 27) were induced. The natriuresis was caused by a proximal tubular action as indicated by increased CLi and CLi/GFR.(ABSTRACT TRUNCATED AT 250 WORDS)     

糖尿病肾血流变化的彩色多普勒超声观察

用彩色多普勒血流显象（ＣＤＥＩ）和脉冲多普勒超声心动图（ＰＤＥ）检测２６例肾功能正常的非胰岛素依赖型糖尿病病人及２０例正常人的双侧肾动脉血流，以探讨糖尿病肾病血流动力学改变。糖尿病病人与正常人对照，肾动脉内径增宽（Ｐ〈０．０１），血流量增加（Ｐ〈０．０１），搏动指数及阻力指数降低（Ｐ〈０．０５）。结果表明，糖尿病临床肾病前期呈高灌注、低阻力改变。提示ＣＤＦＩ和ＰＤＥ可为临床异期发现糖尿糖尿病肾病提     

糖尿病家庭病床规范化管理的效果

目的:寻求一种减轻糖尿病高血压患者症状,有效控制其对心、脑、肾和视网膜等重要器官的影响,改善生活质量的途径。方法:52例糖尿病并高血压患者(建床组)建立家庭病床前查血脂、血糖等参数,建床后监测血压、血糖,建立疾病管理档案,每二周上门巡检随访,进行疾病健康教育及指导,共同制定药物治疗方案及康复锻炼计划,并根据病情及时调整。对照组(50例)接受常规门诊治疗。结果:建床组52位患者血糖(餐前、餐后2h)、血压控制、糖基化血红蛋白、血脂水平均有显著改善(P<0.05~<0.01),且优于对照组(P<0.05)。结论:对糖尿病高血压患者进行较系统宣教工作,规范管理,辅以饮食及康复锻炼,可更有效控制血压、血糖及血脂水平,减少住院率。     

Effects of captopril on renal function in hypertensive patients

The effects of captopril (SQ 14225) on renal function were studied in 10 hypertensive patients. After 7 weeks of treatment (75 to 500 mg/day) renal plasma flow was practically unchanged and glomerular filtration rate was only slightly decreased despite a significant decrease in blood pressure. All indexes of glomerular capillary permeability and of tubular anatomic integrity remained normal during the treatment period.     

Effect of 6-month therapy with simvastatin on lipid transport function of the blood and the state of endothelium in patients with diabetes and hypertension

The state of lipid transport function of the blood, blood contents of stable nitrogen metabolites, and proinflammatory cytokines (TNF-a and IL-1b) during therapy with simvastatin were studied in 29 patients receiving combination antihypertensive therapy with angiotensin converting enzyme inhibitors (ACEI) and verapamil. Lipid lowering action of simvastatin was realized just in 1 month of treatment and remained sustained for half a year (average duration). 6 months after addition of simvastatin to antihypertensive therapy substantial (58.4%, p=0.044) rise of plasma content of stable nitrogen metabolites took place. At the same time therapy with metoprolol in a similar group of patients exerted no considerable effect on blood plasma concentration of nitrate and nitrite anions. Lowering of median values of TNF-alpha from 20.13 (12.67-52.80) to 11.34 (3.31-31.29) pg/ml (p<0.0038) was also noted at the background of combination antihypertensive therapy. This happened without distinct affair with degree of lipid lowering action of simvastatin. The results of the study document positive effect of half year treatment of patients with concomitant hypertension and diabetes with simvastatin (10-20 mg/day) in combination with ACEI and verapamil on metabolism of nitric oxide and plasma content of TNF-alpha which realizes independently from degree of hypolipidemic action of simvastatin.     

Asymmetry of renal blood flow in patients with moderate to severe hypertension

It is generally assumed that renal blood flow is symmetric in the absence of renal artery stenosis. The aim of the present study was to evaluate whether this is really the case. From a group of consecutive hypertensive patients who had undergone renal angiography, we selected those with patent renal arteries. In all of them selective renal blood flow (RBF) measurements (133Xenon washout technique) had been performed with blood sampling from aorta and both renal veins (n=148). Asymmetry of RBF, defined as > or =25% difference in RBF between left and right kidney, was present in 51% of the patients. Subjects with and without asymmetry did not differ in age, body mass index, blood pressure, creatinine clearance, renal volume, or activity of the renin-angiotensin system. The presence of asymmetry coincided with an increased rate of false-positive results on renal scintigraphy. Preliminary data suggest that there may be a relation between asymmetry and renal sympathetic nerve activity. This study demonstrates that asymmetry of RBF is a frequent finding in essential hypertension, which may confound the results of diagnostic tests for renal artery stenosis. Furthermore, the present results underscore the importance of studying the function of both kidneys separately, because it cannot be assumed that they are functionally equal.     

Coronary blood flow function in patients with chronic postembolic pulmonary hypertension

Variations in coronary blood flow and cardiac output were studied using dopplerography throughout rationed exercise in 16 patients with chronic postembolic pulmonary hypertension. All patients showed reduced coronary flow during exercise, an evidence of early signs of coronary insufficiency. A correlation was demonstrated between coronary flow disorders and the severity of pulmonary hypertension, the extent of pulmonary vascular bed lesion and right-ventricular hypertrophy.     

Effect of captopril on plasma prolactin in patients with essential hypertension

The effects of the angiotensin-converting enzyme inhibitor captopril on blood pressure, heart rate, plasma prolactin, and renin activity were examined in a single-blind, placebo-controlled trial on 30 patients with essential hypertension (15 given drug, 15 placebo). Captopril, 25 mg administered orally, reduced the blood pressure and increased the plasma renin activity. Captopril decreased mean plasma prolactin from 17.5 +/- 1.4 ng/mL to 9.1 +/- 1.0 ng/mL (p less than 0.001). Significant correlation was found between captopril-induced change from control values of plasma prolactin (delta plasma prolactin) vs delta plasma renin activity (r = -0.688, p less than 0.001). These results suggest that acute administration of captopril was accompanied by a reduction in plasma prolactin and that this reduction may be of clinical significance during therapy of hypertension.