eGFR is a reliable preoperative renal function parameter in patients with gastric cancer

AIM: To evaluate the validity of the estimated glomerular filtration rate (eGFR) as a preoperative renal function parameter in patients with gastric cancer. METHODS: A retrospective study was conducted in 147 patients with gastric cancer. Preoperative creatinine clearance (Ccr), eGFR, and preand postoperative serum creatinine (sCr) data were examined. Preoperative Ccr and eGFR were then compared for their reliability in predicting postoperative renal dysfunction. RESULTS: Among 110 patients with normal preo...     

GLUT-1 overexpression: Link between hemodynamic and metabolic factors in glomerular injury?

Mesangial matrix deposition is the hallmark of hypertensive and diabetic glomerulopathy. At similar levels of systemic hypertension, Dahl salt-sensitive but not spontaneously hypertensive rats (SHR) develop glomerular hypertension, which is accompanied by upregulation of transforming growth factor beta1 (TGF-beta1), mesangial matrix expansion, and sclerosis. GLUT-1 is ubiquitously expressed and is the predominant glucose transporter in mesangial cells. In mesangial cells in vitro, GLUT-1 overexpression increases basal glucose transport, resulting in excess fibronectin and collagen production. TGF-beta1 has been shown to upregulate GLUT-1 expression. We demonstrated that in hypertensive Dahl salt-sensitive (S) rats fed 4% NaCl (systolic blood pressure [SBP]: 236+/-9 mm Hg), but not in similarly hypertensive SHR (SBP: 230+/-10 mm Hg) or their normotensive counterparts (Dahl S fed 0.5% NaCl, SBP: 145+/-5 mm Hg; and Wistar-Kyoto, SBP: 137+/-3 mm Hg), there was an 80% upregulation of glomerular GLUT-1 protein expression (P< or =0.03). This was accompanied by a 2.7-fold upregulation of TGF-beta1 protein expression in glomeruli of DSH compared with DSN rats (P=0.02). TGF-beta1 expression was not upregulated and did not differ in the glomeruli of Wistar-Kyoto and SHR rats. As an in vitro surrogate of the in vivo hemodynamic stress imposed by glomerular hypertension, we used mechanical stretching of human and rat mesangial cells. We found that after 33 hours of stretching, mesangial cells overexpressed GLUT-1 (40%) and showed an increase in basal glucose transport of similar magnitude (both P< or =0.01), which could be blocked with an anti TGF-beta1-neutralizing antibody. These studies suggest a novel link between hemodynamic and metabolic factors that may cooperate in inducing progressive glomerular injury in conditions characterized by glomerular hypertension.     

原发性高血压患者经颅多谱勒脑动脉血流变化特征分析

目的 探讨原发性高血压患者脑动脉血流变化特征及其影响因素,为高血压防治提供依据。方法 对29名原发性高血压患者和16名健康人进行了经颅彩色多普勒脑血流成像技术（TCI）监测分析,观察大脑中动脉（MCA）的收缩期血流速度（Vs)平均血流速度（Vm)、舒张期血流速度（Vd)、搏动指数（PI）、阻力指数（RI）的变化特征,并与收缩压（SBP）、舒张压（DBP）、平均动脉压（MBP）、脉压进行了直线相关分析。结果 与健康对照组相比,高血压组患者收缩压（SBP）、舒张压（DBP）、平均动脉压（MBP）、脉压和体重指数（BMI）及PI、RI均明显升高（P＜0．01）;高血压组中DBP与Vs,Vm,Vd,PI,RI呈明显正相关（P＜0．05）,脉压与Vs,Vm,Vd及PI呈明显正相关（P＜0．05）。SBP、MBP均与脑血流指标相关不明显（P＞0．05）。结论 高血压患者脑动脉血流变化特征主要表现为PI和RI的显著升高,舒张压和脉压是影响脑血流变化的两个主要因子。TCI是一种简便的、有价值的检查方法。     

Relationship of renal histological damage to glomerular hypertension in patients with immunoglobulin A nephropathy

OBJECTIVE: Studies of experimental animals show glomerular hypertension to be important in the progression of glomerular disease. We evaluated this connection clinically by examining the relationship between glomerular hemodynamics and histological changes in patients with immunoglobulin (Ig)A nephropathy. METHODS: The subjects were 23 patients with IgA nephropathy. All patients underwent renal biopsies. Glomerular hemodynamics, in terms of glomerular capillary hydraulic pressure (PGC) and the whole-kidney ultrafiltration coefficient, were calculated from the renal clearance, plasma total protein concentration, and pressure-natriuresis relationship. The severity of glomerulosclerosis, tubulointerstitial damage and mesangial matrix expansion was evaluated semiquantitatively. RESULTS: PGC ranged from 33-69 mm Hg, and the mean arterial pressure (MAP) from 79-112 mm Hg. Their correlation was not significant (r= 0.29, P= 0.18). PGC was significantly correlated with the glomerulosclerosis score, and also with the score for tubulointerstitial damage (r= 0.65, P < 0.001 and rs = 0.59, P = 0.007, respectively), but not with the score for mesangial matrix expansion (r= 0.08, P= 0.72). MAP was significantly correlated only with the score for tubulointerstitial damage (rs = 0.63, P = 0.004). In multiple linear regression analysis of the histological changes and hemodynamics, the glomerulosclerosis score and the score for tubulointerstitial damage were correlated with PGC, but not with MAP. CONCLUSION: These clinical results support the speculation that glomerular hypertension is involved in the glomerulosclerosis and tubulointerstitial damage that occurs in IgA nephropathy.     

Pathological regression by angiotensin II type 1 receptor blockade in patients with mesangial proliferative glomerulonephritis.

Although angiotensin II type 1 receptor blocker (ARB) therapy reduces proteinuria and retards the progression of renal injury in patients with glomerulonephritis, whether these drugs actually ameliorate pathological damages in human glomerulonephritis has not been determined. Fifteen patients with biopsy-proven mild-to-moderate mesangial proliferative glomerulonephritis (10 with immunoglobulin A [IgA] nephropathy and 5 with non-IgA mesangial proliferative glomerulonephritis) received ARB monotherapy. In these patients, repeated renal biopsy was performed after a mean of 28.1 months, and pathological changes (including the mesangial matrix expansion ratio and interstitial fibrosis expansion ratio) were quantitatively examined using an image analyzer. Clinical markers were also evaluated, including the serum creatinine, serum IgA, creatinine clearance (Ccr), 24-h urinary protein excretion, urinary N-acetyl-beta-D-glucosaminidase (NAG), and blood pressure. ARB therapy significantly reduced urinary protein excretion (0.68+/-0.63 to 0.20+/-0.32 g/day, p=0.016) and the blood pressure (systolic: 133.3+/-18.2 to 123.4+/-10.5 mmHg, p=0.041; diastolic: 79.4+/-11.9 to 72.0+/-8.2 mmHg, p=0.038). Although the global glomerular sclerosis ratio was unchanged (6.3+/-8.5% to 10.7+/-16.1%, p=0.33), the mesangial matrix expansion ratio (33.1+/-10.8% to 22.7+/-7.8%, p=0.001) and the interstitial fibrosis ratio (19.9+/-5.8% to 13.8+/-4.4%, p=0.034) were significantly reduced by ARB treatment. The levels of pathological improvement were similar between patients with IgA nephropathy and those with non-IgA mesangial proliferative glomerulonephritis. The results of the present study strongly suggest that ARB monotherapy can significantly reverse pathological changes, including mesangial matrix expansion and interstitial fibrosis, in human glomerulonephritis.     

Impact of hypertension and hypertension-related vascular lesions in IgA nephropathy.

It remains poorly understood whether vascular pathology plays an important role in the progression of renal parenchymal disease in humans. Moreover, in the case of hypertensive patients with mild proteinuria, nephrologists tend to make a diagnosis of benign nephrosclerosis without renal biopsy. Among 172 patients who were treated at our hospital for biopsy-proven IgA nephropathy, we performed quantitative histopathological analysis in 38 patients with mild proteinuria of less than 0.5 g/day. We related these histopathological parameters with clinical data at biopsy and also with follow-up data. The percentage of glomeruli showing global sclerosis exceeded 10% of total glomeruli in 15 of the patients (39.5%) and exceeded 20% in 9 (23.7%). Arteriosclerosis and tubulointerstitial changes significantly correlated with glomerular sclerosis, but mesangial cell proliferation did not. Among the 38 patients, the 12 with hypertension showed more severe glomerular sclerosis, tubulointerstitial changes and arteriosclerosis compared with the 26 without hypertension, but the mesangial cell proliferation was identical between the two groups. Stepwise multiple regression analysis revealed that hypertension and urinary protein excretion (UPE) were independent risk factors for arteriosclerosis. The follow-up data of a mean period of 27.6 months showed that 9 of the 38 patients (23.7%) had an increase in UPE. Hypertension, arteriosclerosis, age, and UPE at biopsy were selected as the important risk factors for an increase in UPE in the follow-up. Our results provide not only clinical but histopathological evidence that hypertension affects the prognosis of mild proteinuric nephropathy through vascular lesions.     

SHR和WKY大鼠血浆vasostatin-2水平的比较研究

目的 探讨自发性高血压（SHR）大鼠外周血vasostatin（VS）-2水平变化及阐明其意义。方法 采用ELISA方法检测14只SHR大鼠组和14只京都Wistar（WKY）大鼠组空腹外周血血浆VS-2水平,并利用清醒自由大鼠血流动力学动态检测技术检测大鼠血压、心动周期及压力感受性反射敏感性。结果 ①与WKY对照组相比,SHR组大鼠空腹血浆VS-2水平升高〔(0.43±0.05) pg/ml vs.(0.34±0.05) pg/ml,P<0.01〕;②Pearson相关分析显示,收缩压（SBP）、舒张压（DBP）、平均动脉压（MAP）与VS-2水平呈正相关（r=0.781,P<0.05;r=0.822,P<0.05;r=0.918,P<0.01）;HR与VS-2水平无关（r=0.350,P>0.05）;BRS与VS-2水平呈负相关（r=-0.959,P<0.01）;进一步使用多元线性逐步回归分析显示,MAP及BRS是VS-2水平的独立影响因子（P<0.05）。结论 SHR大鼠空腹血浆VS-2水平高于WKY大鼠,表明VS-2可能在动脉血压的调节过程中发挥作用。     

老年高血压患者亚临床甲状腺功能减退与血压变异性的关系

目的探讨亚临床甲状腺功能减退(亚甲减)的老年高血压患者每日血压变异性(BPV)指标特点及与亚甲减的关系。方法共纳入260例老年高血压患者,其中129例合并亚甲减,131例甲状腺功能正常者作对照,采集患者身高、体重、诊室坐位血压、血甲状腺功能指标、空腹血糖(FBG)、糖化血红蛋白、血脂、高敏C反应蛋白、血尿酸、同形半胱氨酸等指标,同时作24 h动态血压监测。结果亚甲减组与甲功正常组比较,夜间收缩压、清晨收缩压、反杓形节律构成比更高(P<0.05),杓形节律构成比、舒张压夜间下降率更低(P<0.05)。多元逐步回归分析显示:即便排除其他因素影响,清晨收缩压仍与游离三碘甲状腺原氨酸(FT3)负相关,与促甲状腺激素(TSH)正相关;清晨舒张压与年龄负相关,与体重、TSH正相关;夜间收缩压下降率与FBG负相关,与FT3正相关;夜间舒张压下降率与FT3正相关。结论老年高血压患者BPV增大与亚甲减密切相关。     

Nipradilol prevents L-NAME-exacerbated nephrosclerosis with decreasing of caspase-3 expression in SHR.

The proliferative cell nuclear antigen (PCNA) is an auxiliary protein of DNA polymerase delta and appears to be required for both DNA synthesis and repair. Previously, we showed that prolonged NO synthase (NOS) inhibition produced severe nephrosclerosis with an increase of glomerular cell DNA fragmentation (apoptosis), glomerular ischemia and hypertension in spontaneously hypertensive rats (SHR). The objective of the present study was to investigate the effects of the vasodilating, nonselective, NO-releasing beta-adrenoceptor blocker nipradilol on DNA fragmentation and synthesis/repair of glomerular cells in this prolonged NOS blockaded SHR. Twenty-week-old SHR were administered an NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME, 80 mg/l in drinking water) or co-treated with the same dose of L-NAME and nipradilol (20 mg/kg/day) for 3 weeks. After this treatment, expression of apoptosis was histologically examined using caspase-3, an apoptosis inducer, in addition PCNA (DNA synthesis/repair), and examination of glomerular morphometric changes, including cell number and tuft area. Nipradilol reduced blood pressure and preserved creatinine clearance reduction in L-NAME/SHR. These effects were associated with normalization of the glomerular cell apoptosis index and caspase-3 score, an increase in PCNA index, and increases in glomerular cell numbers and glomerular tuft area, resulting in a decreased glomerular injury score. Thus, in SHR administered an NOS inhibitor, nipradilol improved nephrosclerosis in association with a decrease in apoptosis and an increase in DNA synthesis/repair of glomerular cells. These findings may provide important insights into DNA repair/repair and apoptosis in nephrosclerosis.     

N- and L-type calcium channel antagonist improves glomerular dynamics,reverses severe nephrosclerosis,and inhibits apoptosis and proliferation in an l-NAME/SHR model

OBJECTIVE : To determine the responses of the new dihydropyridine N- and L-type calcium antagonist, cilnidipine, on systemic and renal hemodynamics, glomerular dynamics, renal function, and histopathology in an Nomega-nitro-l-arginine methylester spontaneously hypertensive rat (l-NAME/SHR) model of nephrosclerosis. METHODS : Five groups of 20-week-old male SHR were studied using renal micropuncture techniques and histopathological analyses: group 1, control; group 2, cilnidipine (10 mg/kg per day) by gavage, for 3 weeks; group 3, l-NAME (50 mg/l) in drinking water, for 3 weeks; group 4, combination of l-NAME and cilnidipine, for 3 weeks; group 5, l-NAME for 3 weeks, followed by cilnidipine for a subsequent 3 weeks. RESULTS : Cilnidipine significantly reduced mean arterial pressure, total peripheral resistance and renal vascular resistance, while increasing effective renal blood flow and glomerular filtration rate (P < 0.01) in l-NAME/SHR. These hemodynamic changes were associated with significantly increased single nephron glomerular filtration rate (SNGFR) and plasma flow (SNPF) and decreased afferent glomerular arteriolar resistances when cilnidipine was used alone, and with increased SNGFR and SNPF, but decreased glomerular capillary pressure, afferent and efferent arteriolar resistances, urinary protein excretion, serum creatinine and uric acid concentrations (at least P < 0.05) in l-NAME-exacerbated SHR nephrosclerosis. In addition, glomerular and arteriolar injuries were markedly reversed (both P < 0.01), and glomerular apoptosis and cellular proliferation were inhibited and associated with glomerular tuft enlargement and an increase in cell number. CONCLUSION : Cilnidipine not only prevented, but reversed, the severe renal hemodynamic and glomerular dynamic changes, including apoptosis and glomerular cellular proliferation, in l-NAME/SHR-exacerbated nephrosclerosis. This dual-channel calcium antagonist thus exerted renoprotective pathophysiological effects in the l-NAME/SHR.     

Morning blood pressure surge varies with age and gender in hypertensive individuals

Many studies revealed that most cardio-cerebrovascular events were closely related to morning blood pressure surge (MBPS). The aim of our study was to investigate the relationship of MBPS with age and gender in hypertensive individuals, morning blood pressures of a total of 1100 cases with primary hypertension were analyzed. In our study, the morning systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP) of hypertensives with MBPS were all higher (P<0.01). MBPS values were correlated with age (r=0.061, P<0.05). In hypertensive individuals with MBPS, morning SBP and PP increased while morning DBP decreased (P<0.01) as patients aged. Morning DBP and MAP of female patients were lower while morning PP was higher (P<0.01). These results indicated that MBPS was associated with both age and gender in hypertensive individuals.     

原发性高血压患者血压水平与早期肾损害的相关性研究

目的探讨原发性高血压患者脉压(PP)、SBP、DBP及平均动脉压(MAP)与早期肾损害的关系。方法选择180例初诊或停药2周以上的原发性高血压患者进行PP、SBP、DBP和MAP检查,以血β2微球蛋白(β2-MG)水平>2.6mg/L作为肾损害的标准,分为肾损害组和非肾损害组,其中肾损害组84例,非肾损害组96例。将两组血压参数进行比较,并与血β2-MG水平进行相关性分析。结果(1)肾损害组PP[(59±10)mmHg]及SBP[(168±28)mmHg]较非肾损害组[(41±8)mmHg,(151±10)mmHg]明显增高。(2)相关分析显示血β2-MG与PP、SBP呈正相关,尿β2-MG与PP、SBP、DBP、MAP呈正相关。其中与PP、SBP相关性较好。结论PP与SBP、DBP、MAP增高均可导致高血压患者早期肾损害,而PP、SBP增大是导致高血压患者早期肾损害的主要因素。     

Calcium antagonist inhibits glomerular cell apoptosis and injuries of L-NAME exacerbated nephrosclerosis in SHR.

Increased apoptosis of glomerular cells, with progression of glomerulosclerosis, overactivity of the renin-angiotensin system and elevation of glomerular pressure, follows chronic nitric oxide synthase (NOS) inhibition in spontaneously hypertensive rats (SHR). To gain insight into the regulation of glomerular cell apoptosis in severe nephrosclerosis, we investigated apoptosis, the expression of proliferative cell nuclear antigen (PCNA) in glomeruli, and glomerular morphometric changes in 20-week-old SHR, SHR treated with NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 80 mg/l in drinking water), and SHR treated with L-NAME and the calcium antagonist, efonidipine (20 mg/kg per day), for 3 weeks. Apoptosis in non-sclerotic glomeruli was quantified by terminal deoxynucleotide transferase-mediated dUTP nick-end labeling. The increase in systolic blood pressure and the severe proteinuria with severe nephrosclerosis induced by chronic NOS inhibition were completely prevented by efonidipine. Furthermore, the glomerular area and capillary tuft area were markedly increased in rats treated with efonidipine compared with both control rats (+30 and +42%, respectively, p<0.01) and rats treated with L-NAME (+35 and +56%, respectively, p<0.01)-treated rats. This calcium antagonist also significantly inhibited the both increases of the glomerular cell apoptosis index (-72%) and the PCNA index (+44%), therefore the alteration between apoptosis and proliferation slightly increased the number of glomerular cells (subcapsular, +22%, p<0.01; juxtamedullary, +2%, not significant). Thus, the calcium antagonist efonidipine seems to play an important role in the regulation of apoptosis and proliferation of glomerular cells and may be effective in preventing nephrosclerosis exacerbated by NOS inhibition.     

ACLF相关AKI患者的血清集聚蛋白多糖C端片段水平及其诊断价值

目的探讨并发急性肾损伤(acute kidney injury,AKI)的慢加急性肝功能衰竭(acute-chronic liver failure,ACLF)患者血清集聚蛋白多糖C端片段(C-terminal agrin fragment,CAF)水平用于AKI诊断的价值。方法 HBV相关ACLF患者347例,其中AKI患者165例,无AKI患者182例。记录患者一般信息及常规实验室指标,检测血清CAF水平。分析CAF与各项指标的相关性,ROC曲线分析CAF用于ACLF患者AKI诊断的效能。结果 AKI组CAF水平[1243.3(678.4,210)5.9)pg/mL]显著高于无-AKI组[250.2(135.7,436.5)pg/mL],差异有统计学意义(P0.01);不同AKI分期CAF水平由高至低依次为:AKI-3期AKI-2期AKI-1期。AKI组患者血清CAF水平与MAP呈显著负相关(R=-0.242,P=0.004)、eGFR(R=-0.480,P0.01),与ALT(R=0.222,P=0.004)、WBC(R=0.212,P=0.006)、sCr(R=0.392,P0.01)及MELD评分(R=0.272,P0.01)。CAF用于诊断ACLF并发AKI的AUC为0.859(95%CI:0.819~0.898),而CAF联合sCr的AUC为0.923(95%CI:0.894~0.951)。结论 CAF反映ACLF患者并发AKI时的肾功能损害严重程度,并可与sCr联合用于提高AKI的诊断效能。     

Renal sodium handling and renal dopaminergic activity in overweight normotensive subjects

Recently, we reported that the blunted natriuretic ability related to an attenuation of renal dopaminergic activity might play an important role in the hypertensive mechanisms of overweight patients with essential hypertension. On the other hand, the interrelationships between obesity, blood pressure and renal sodium handling in normotensives (NT) have not been clear. The purpose of the present study is to reveal the role of renal dopaminergic activity on renal sodium handling in overweight NT. The study consisted of 52 hospitalized NT receiving a regular diet containing 200mEq of sodium, 75mEq of potassium, 2400kcal/day, who were divided into two groups of 31 non-obese (NNT) and 21 obese (ONT) subjects. NNT was categorized as the body mass index (BMI) less than, and ONT as the BMI equal to or more than, 25kg/m2. In the early morning, after overnight fasting, all subjects remained in a supine state and were examined for renal clearance. During the clearance period, mean arterial pressure (MAP), heart rate (HR), endogenous creatinine clearance (Ccr), urinary excretion of sodium (UNaV), fractional excretion of sodium (FENa) and of inorganic phosphorus (FEP) and urinary excretion of free dopamine (uDA) were determined. There were no significant differences in age, HR, Ccr or UNaV between the two groups. Higher MAP and lower FENa) were observed in ONT than in NNT, but the differences in these parameters were not statistically significant. However, FENa in ONT was significantly lower than in MAP-and Ccr-matched NNT. In addition, FENa correlated negatively with BMI in ONT, unlike in NNT. MAP was correlated positively with FENa, and a similar tendency was found between MAP and FEP in NNT, but not in ONT. On the other hand, there was no significant correlation between BMI and uDA in either NNT or ONT. This result was different from our previous data in patients with essential hypertension (EHT) in which BMI correlated with uDA positively in non-obese EHT and negatively in obese EHT. These findings suggest that blunted natriuretic ability may exist in ONT, and the role of renal dopaminergic activity related to the attenuated natriuretic ability in ONT may be less important than in obese EHT.     

Determination of optimal blood pressure for patients with IgA nephropathy based on renal histology.

To evaluate the optimal BP control for patients with IgA nephropathy (IgAN) based on the histologic severity of the nephropathy and the degree of renal dysfunction. We analyzed 332 consecutive renal biopsy specimens and clinical data from patients with IgAN. Patients were divided into three groups based on their BP at the time of biopsy: an optimal BP (SBP<120 mmHg and DBP<80 mmHg), a hypertensive BP (SBP > or = 140 mmHg and/or DBP > or = 90 mmHg), and an intermediate BP group. Each biopsy specimen was evaluated for mesangial proliferation, degree of sclerosis and/or hyalinosis of the arterioles and the interlobular artery using a semiquantitative method. Creatinine clearance and the percentage of sclerosed glomeruli were also determined. Both the degree of renal dysfunction and the histologic changes correlated significantly with BP, even in patients with a BP <140/90 mmHg. The patients with an optimal BP at the time of biopsy had significantly less histologic damage with respect to mesangial proliferation and vessel changes than those with an intermediate or hypertensive BP. In the patients with a hypertensive BP, the percentage of sclerotic glomeruli was significantly higher and the creatinine clearance was significantly lower. The optimal BP proposed by the WHO in 1999 prevents histologic evidence of renal damage for patients with IgAN.     

Effect of Blood Pump Flow and Arteriovenous Fistula Blood Flow on the Blood Pressure and Cardiac Function in Patients Undergoing Maintenance Hemodialysis

The effect of blood pump flow rate on the cardiac functions of hemodialysis patients with arteriovenous fistula (AVF) is largely unknown. This study aimed to investigate if blood pump flow rate (Qb) and AVF access flow rate (Qa) can affect the cardiac function of Chinese hemodialysis patients. A total of 72 patients undergoing AVF hemodialysis were included from March 2010 to June 2014 and dichotomized into the high‐ and low‐flow groups using the medians of Qb (220 mL/min) and Qa (1000 mL/min) as the cutoffs. The cardiac function parameters were measured by ultrasound dilution technique within the first (t + 30) and the last (t ? 30) 30 min of dialysis. At t + 30, Qb‐high group had significantly higher systolic blood pressure (SBP) and mean arterial pressure (MAP) than Qb‐low group. At t ? 30, Qb‐high group had higher SBP, diastolic blood pressure (DBP), and MAP than Qb‐low group. Qa‐high group had higher SBP, MAP, cardiac output (CO), cardiac index (CI), central blood volume (CBV), and lower peripheral resistance than Qa‐low group. Multiple linear regression showed that at t ? 30, Qb was positively correlated with SBP and MAP. Qa was positively correlated with CO, CI, CBV, and PR but negatively correlated with heart rate. Although Qb > 220 mL/min and Qa >1000 mL/min would elevate some parameters, the means of SBP, DBP, MAP remain within the normal range, indicating that appropriate increase in blood pump flow rate has little effect on the cardiac function of hemodialysis patients.     

Imidapril improves L-NAME-exacerbated nephrosclerosis with TGF-beta 1 inhibition in spontaneously hypertensive rats

OBJECTIVE: This study was designed to investigate whether chronic angiotensin-converting enzyme (ACE) inhibition prevents hypertensive glomerular injury and inhibits increases in the mRNA levels and immunohistological expression of the apoptosis inducer caspase-3, and transforming growth factor (TGF)-beta 1 during prolonged nitric oxide synthase (NOS) inhibition with N-nitro-L-arginine methyl ester (L-NAME) in spontaneously hypertensive rats (SHR). METHODS AND RESULTS: For 3 weeks, we studied three groups of 20-week-old male SHR: a control group, a l-NAME group, and a group treated with L-NAME and the ACE inhibitor imidapril. L-NAME rats developed severe hypertensive nephrosclerosis with significantly elevated blood pressure, markedly increased urinary protein excretion and serum creatinine levels, and more severe glomerulosclerosis and tubulo-interstitial changes. Levels of TGF-beta 1 mRNA in the renal tissue was also significantly increased in L-NAME rats compared with control SHR. Addition of imidapril significantly lowered blood pressure, inhibited nephrosclerosis and attenuated the mRNA level of TGF-beta 1 in comparison with L-NAME/SHR. Histologically, the glomerular cell apoptosis labeling index, terminal doxynucleotidil transferase-mediated dUTP nick-end labeling of fragmented DNA (TUNEL) and active caspase-3, and TGF-beta 1 positive areas were also reduced by imidapril. CONCLUSION: These data suggest that imidapril prevents glomerular and arteriolar damages and renal functions, through inhibiting both TGF-beta 1 production and apoptosis induction.     

老老年人群动态血压参数与动脉僵硬度的相关性

目的探讨老老年人群动态血压参数与动脉僵硬度的相关性。方法筛选年龄≥80岁的老老年人238例,以血压≥160/95 mm Hg(1 mm Hg=0.133 kPa)为标准,分为高血压组(134例)和对照组(104例),并进行臂-踝脉搏传导速度(baPWV)和24 h动态血压监测。用Pearson分析动态血压各参数与动脉僵硬度的相关性。结果高血压组baPWV高于对照组(P<0.05)。高血压组偶测收缩压,24 h、昼间和夜间收缩压、舒张压、脉压,收缩压负荷及舒张压负荷均高于对照组.夜间收缩压下降率、舒张压下降率低于对照组,差异有统计学意义(P<0.05,P<0.01)。baPWV与偶测血压;24 h收缩压、舒张压、脉压;昼间收缩压、舒张压、脉压、心率;夜间收缩压、舒张压、脉压;收缩压负荷、舒张压负荷呈正相关(P<0.05,P<0.01),而与夜间收缩压下降率呈负相关(P<0.01)。结论高血压是老老年人群动脉僵硬度增加的一个重要因素,动脉僵硬度与动态血压、脉压、心率及血压负荷相关。     

Effects of nitrendipine and atenolol on blood pressure and intracellular sodium in hypertensive blacks

Thirty-five hypertensive black patients were randomized in a double-blind fashion to receive either atenolol 100 mg per day (n = 17) or nitrendipine 20 mg daily (n = 18) for six weeks. Atenolol and nitrendipine significantly reduced blood pressure (P less than 0.05 or less). However, the magnitude of the decrease in supine systolic blood pressure (SBP) and diastolic blood pressure (DBP), and in standing diastolic pressure was more pronounced (P less than 0.05 or less) in the nitrendipine than in the atenolol group. Neither of the drugs significantly affected the erythrocyte sodium and potassium concentrations or the ouabain-sensitive efflux of sodium. In multiple regression analysis the changes in supine SBP and DBP with nitrendipine were independently and negatively correlated with the patients' age and initial blood pressure, and positively with the change in supine pulse rate; the change in supine SBP was also negatively correlated with initial erythrocyte sodium concentration. Our results suggest that nitrendipine is more efficient than atenolol in hypertensive blacks and that besides older age and higher pre-treatment. BP levels, a higher intracellular sodium concentration could predict a greater response to nitrendipine.