Search

In the general population aortic stiffening, assessed by carotid femoral pulse wave velocity (cf-PWV), is associated with cognitive dysfunction (CO/DY). Data in chronic kidney disease (CKD) are limited. This study tests the hypothesis that large artery stiffness and microvascular damage in CKD patients are related to the damage of brain microcirculation reflected by impaired cognitive function. A cross-sectional study enrolled 151 patients (mean age 58.4 years; 64.5% males; 44 patients with CKD stage 1; 47 with stage 2; 25 with stage 3; and 35 with stage 4). Cognitive impairment, assessed by the Mini Mental State Examination (MMSE), the Clock - drawing test (Clock-test), and the Instrumental Activity of Daily Living (IADL), was considered as primary outcome. We measured systolic and pulse pressures at the brachial and aortic sites and cf-PWV. Our patients revealed a significant linear deterioration in all the domains of cognitive function according to CKD stages. High values of cf-PWV (P = 0.029) and aortic pulse pressure (aPP) (P

Objectives: In the general population aortic stiffening assessed by carotid femoral pulse wave velocity (cf-PWV) is associated with cognitive dysfunction (CO/DY). Data in chronic kidney disease (CKD) are limited. Our study tests the hypothesis that large artery stiffness and microvascular damage in CKD patients are related to brain microcirculation changes reflected by impaired cognitive function. Methods: Among 244 patients, finally 44 with CKD stage 1; 47 stage 2; 25 stage 3; 35 stage 4, with mean age 58.4 years (64.5% males), were enrolled in a cross-sectional study. Cognitive impairment measured by Mini Mental State Examination (MMSE), Clock – drawing test (Clock-test), and Instrumental Activity of Daily Living (IADL) was considered as primary outcome. We directly measured brachial, aortic, systolic blood pressure, pulse pressure, mean blood pressure and cf-PWV. Results: Our patients revealed a significant linear deterioration in all the domains of cognitive function according to CKD stages, assessed by MMSE, Clock-test and IADL. The risk of cognitive dysfunction increased significantly from CKD stage 3 to 4 (p

Objective: Patients in hemodialysis frequently have cognitive dysfunction (CO/DY). Hemodialysis session often results in acute intravascular volume loss, fluid shifts, hypotensives episodes, decrease of cerebral perfusion and cerebral ischemia, all of which may cause transient deterioration of cognitive function. On the contrary, improvement in “uremic milieu” after a dialysis session can result in improved cognition. The aim of this study is to evaluate the effect of a single, random hemodialysis session on cognitive function, in absent of hypotensive episodes. Method: Global cognitive function was assessed, pre-and post-dialysis by using the Mini Mental State Examination. Results: Forty-eight patients participated in the study. The average age was 60.8±13.4 years. The mean dialysis vintage was 58±66 months. Patients received adequate renal replacement therapy and the mean urea reduction ratio was 72±6.6. At the onset and at the end of the study, no major hemodynamic changes were detecting (mean systolic/diastolic blood pressure (147.±20/78±11 vs 138±20/77±10 mmHg) according to our aforementioned criteria. Compared to pre- dialysis, an improvement in the test score was revealed after dialysis, paired t-test (p=0.03). Mean values of MMSE pre and post was 26.61 ± 3.24 and 28.86± 1.98 respectively (amelioration of 2.25 points). Conclusions: Our results illustrate the better performance of cognitive function that can be observed after a single dialysis session, in absent of hypotensives episodes. These results may be used as a starting point, in an effort to evaluate the best possible time, pre or post dialysis, to provide medical advice to these patients.

Objective It has been suggested that aliskiren has a longhalf-life and maintains a blood pressure (BP)-loweringeffect following a missed dose. We tested the hypothesisthat every otherday (eod) administration of aliskiren has thesame effects as the once daily (od) dosing in albuminurichypertensive patients.Methods Fifteen hypertensive patients, after a 4-weekwash-out period on clonidine, received 300mg aliskiren odas the sole treatment. In patients who remained out oftarget, other nonrenin–angiotensin system blockers wereadded. Patients who completed a 24-week (w24) treatmentperiod were switched to eod administration of aliskiren foran additional period of 24 weeks (w48).Results Thirteenpatients completed the full study protocol.The mean office BP was reduced at the end of w24(−9/3mmHg), a reduction that continued to be observedat w48 (−11/1mmHg). At the end of the study, the 48hambulatory BP monitoring was divided into two 24hperiods. The mean 24h systolic BP, and the mean daytimesystolic and diastolic BP were significantly lower (P

Introduction: Blockade of the renin-angiotensin system (RAS) is a critical approach to the management of hypertension, especially in proteinuric patients. It is well proven that the direct renin inhibitor aliskiren shows comparable clinical efficacy to the angiotensin II receptor blocker valsartan on blood pressure control and albuminuria. However, there is only limited data on the hand-to-hand effectiveness of these two RAS blockers in improving arterial stiffness. We tested whether aliskiren or valsartan would improve arterial stiffness in hypertensive patients with albuminuria who are already on antihypertensive therapy. Material and methods: Thirty-four patients with hypertension and albuminuria < 1 g, after a wash-out period of three weeks, were randomized to aliskiren or valsartan in a 24-week randomized parallel-group study. Results: A nonsignificant difference in blood pressure was seen between the two treatment groups. Albuminuria was significantly reduced in both groups (56% for the aliskiren group, p < 0.05, and 38% for the valsartan group, p < 0.05). Only valsartan but not aliskiren significantly reduced carotid-femoral pulse wave velocity (–1.1 ± 0.8 m/s ( p = 0.02) for valsartan and +0.1 ± 0.7 m/s (ns) for aliskiren). Conclusion: The results of our study showed that valsartan improves arterial stiffness to a significantly greater extent than aliskiren, despite a similar antihypertensive and antiproteinuric effect.

The sympathetic nervous system has a profound effect on the kidney's ability to regulate blood pressure and, vice versa, the kidney has an important effect on the overall sympathetic tone. As a result, renal sympathetic nerves are crucial for initiation and the maintenance of systemic hypertension. It is fairly well established that efferent renal sympathetic nerve activity contributes significantly to homeostatic regulation of renal blood flow, glomerular filtration rate, renal tubular epithelial cell solute and water transport, and hormonal release. The afferent nerves from the kidney activate central sympathetic nervous system activity, participate in a reflex control system via reno-renal reflexes and are involved in cardiovascular regulation and pathogenesis of hypertension in CKD patients whose kidney ischemia also seems to play a key role. Sympathetic nerve modulation in hypertension had been considered as a therapeutic strategy long before the advent of modern pharmacological therapies. Renal sympathetic denervation with a percutaneous, catheter-based approach results in significant and sustained blood pressure reduction in patients with resistant hypertension. This procedure has also beneficial effects in multiple organs function. However, renal physiology and the long term observed benefits with the use of renal sympathetic denervation have not completely elucidated.

Cognitive dysfunction (CO/DY) in chronic kidney disease (CKD) patients has long been recognized. Hypertension is also associated with CO/DY. The study describes associated factors with CO/DY in CKD patients compared to hypertensive subjects.Ninety-six hypertensive subjects without CKD, 19 patients with CKD stages I-II, 33 with CKD III, 42 with CKD stage IV, 33 on hemodialysis (HD) and 33 on peritoneal dialysis (PD) were included in our study. Cognitive impairment measured by MMSE, clock-drawing test and IADL was considered as primary outcome.In all groups tested, age was significantly associated with CO/DY by almost all cognitive function tests. Among CKD patients, CKD stage and DM were significantly associated with CO/DY by all three cognitive function tests. PTH levels were also associated with CO/DY by MMSE and clock-drawing tests. In hypertensives, pulse pressure (PP) was associated with CO/DY by clock-drawing and IADL tests, while those receiving CCBs as monotherapy were less likely to have CO/DY by IADL test. For dialysis patients, DM was significantly related to CO/DY by MMSE and clock-drawing tests. In the same group of patients Hb11 g/dl was significantly correlated with CO/DY by MMSE, dialysis modality and Kt/V1.2 by IADL test. PD patients were less likely to present with CO/DY by clock-drawing test.In every CKD stage, the risk of CO/DY increased significantly. Low Hb levels (Hb11 g/dl) and increased serum PTH levels were associated with CO/DY while DM plays also a significant role in cognitive function deterioration. Among hypertensive subjects, those with PP ≤60 mmHg or receiving CCBs showed a better executive function.

Hyperphosphatemia is a well-recognized complication of chronic kidney disease, and phosphorus kinetics during hemodialysis (HD) remains a vague area of investigation. We studied the inorganic phosphorus homeostasis during the first hour of an HD session.Twelve patients were studied twice, in two consecutive HD sessions. Total (TPR), extracellular (EPR), and intracellular (IPR) phosphorus mass removal was determined using the direct dialysate quantification (DDQ) method. Alterations of serum inorganic phosphorus (sP), erythrocyte intracellular phosphorus (P(ERY)), and 2,3-diphosphoglycerate (2,3-DPG) concentrations were measured before HD initiation and at 1, 2, 3, 4, 5, 10, 30, and 60 min.The contribution of IPR to TPR was negative in the first 10 min of both HD sessions (-27.2 ± 6.5 and -26.4 ± 58 mmol, respectively, p = ns) while the contribution of the IPR to TPR increased as the time elapsed. Intracellular phosphorus and 2,3-DPG remained almost unchanged during the 60 min of HD session.Unchanged P(ERY) concentration during the first hour of an HD session does not reject the hypothesis of a simultaneous efflux and influx of phosphorus from/to intracellular compartment.

AIM: To access the association between albuminuria levels and arterial stiffness in non-diabetic patients with hypertension and chronic kidney disease (CKD) stages 1-2, treated with renin angiotensin blockade agents plus other hypertensive drugs when needed. METHODS: One hundred fifteen patients [median age 52 years (68% males)] were consequently enrolled in the study. For each patient, we recorded gender, age, body mass index (BMI), peripheral systolic blood pressure (pSBP), peripheral diastolic blood pressure, peripheral pulse pressure, central systolic blood pressure (cSBP), central diastolic blood pressure (cDBP), central pulse pressure (cPP), hematocrit, hemoglobin, hsCRP, total cholesterol triglycerides, high-density lipoprotein-C, low-density lipoprotein-C, calcium, phosphorus, parathormone, and albumin, as well as 24 h urine albumin excretion. According to 24-h urine albumin collection, patients were then classified as those with moderately increased albuminuria (formerly called macroalbuminuria) (≤ 300 mg/d) and those with severely increased albuminuria (formerly called macroaluminuria (> 300 mg/d). We considered aortic stiffness (AS) indices [carotid femoral pulse wave velocity (PWVc-f) and augmentation index (AIx)] as primary outcomes of the study. We explored potential correlations between severely increased albuminuria and AS indices using a multiple linear regression model. RESULTS: Fifty-eight patients were included in the moderately increased albuminuria group and 57 in the severely increased albuminuria. Blood pressure measurements of the study population were 138 ± 14/82 ± 1.3 mmHg (systolic/diastolic). There were no significant differences in age, sex, and BP measurements between the two groups. Patients with severely increased albuminuria had higher PWV and AIx than patients with moderately increased albuminuria (P < 0.02, P < 0.004, respectively). In addition these patients exhibited higher BMI (P < 0.03), hsCRP (P < 0.001), and fibrinogen levels (P < 0.02) compared to patients with moderately increased albuminuria. In multivariate linear regression analysis, severely increased albuminuria (β = 1.038, P < 0.010) pSBP (β = 0.028, P < 0.034) and Ht (β = 0.171, P = 0.001) remained independent determinants of the increased PWVc-f. Similarly, severely increased albuminuria (β = 4.385, P < 0.012), cSBP (β = 0.242, P < 0.001), cPP (β = 0.147, P < 0.01) and Ht levels (β = 0.591, P < 0.013) remained independent determinants of increased AIx. CONCLUSION: These findings demonstrate an independent association between AS indices and severely increased albuminuria in non-diabetic, hypertensive patients with CKD stages 1-2 treated with renin angiotensin aldosterone system blockers.