De bloedsomloop door de nieren bij essentiële hypertensie

De nier neemt een sleutelpositie in bij de volumeregulatie in het menselijk lichaam. Door de uitscheiding van water en zout aan de omstandigheden aan te passen, kunnen dreigende veranderingen van het extracellulaire volume worden voorkomen. De vullingsgraad van een systeem bepaalt in hoge mate de daarin heersende druk. Vergroting van het extracellulaire volume zal mogelijk een rol kunnen spelen bij het ontstaan van bloeddrukverhoging. Onmisbaar in deze voorstelling van zaken is het optreden van water- en zoutretentie door de nier. Bij de volumeregulatie lijkt er in de nier een regionale taakverdeling te bestaan. De nefronen in de buitenste nierschors zouden vooral van betekenis zijn voor de water- en zoutuitscheiding, terwijl de juxtamedullaire nefronen door de lange lissen van Henle meer geschikt zijn voor volumeretentie. De nier kan ook als endocrien orgaan bij de regulering van de bloeddruk betrokken zijn. Door productie van renine wordt angiotensine !I vrijgemaakt. Dit peptide is de sterkst bloeddrukverhogende stof bekend in de fysiologie. Het renine-angiotensine systeem is door het stimuleren van de aldosteronproductie nauw verbonden met de volumeregulatie. Vele gegevens wijzen op het bestaan van een wisselwerking tussen het renine-angiotensine systeem en de haemodynamische verhoudingen in de nier. Terwijl de renineproductie vooral plaats vindt in de buitenste nierschors, wordt in het niermerg prostaglandine A2 gemaakt, een stof met bloeddrukverlagende eigenschappen

The effect of the initiation of renal replacement therapy on lipid profile and oxidative stress during the first 6 months of treatment.

Contains fulltext : 48369.pdf (publisher's version ) (Closed access)BACKGROUND: Disturbed lipoproteins and increased oxidative stress are two of the "non-traditional" cardiovascular risk factors in chronic renal failure. There are very few prospective data of the influence of dialysis on these two factors. In the present study we investigated the effects of the initiation of both hemo- and peritoneal dialysis therapy on lipoproteins and parameters of LDL oxidation. METHODS: In this prospective cohort study, we assessed lipoproteins, plasma lipid peroxides and in vitro copper-induced LDL oxidation in 46 patients with end-stage renal disease prior to the start of dialysis and after 6 months of treatment with either hemodialysis (n=33) or peritoneal dialysis (n=13). RESULTS: After 6 months of treatment with hemodialysis there was an increase in total cholesterol (4.6+/-1.1 vs. 5.0+/-1.3 mmol/l; p<0.05) and triglycerides (2.0+/-0.9 vs. 2.8+/-1.6 mmol/l; p<0.03). In the peritoneal dialysis group the lipoproteins did not change. Regarding lipid peroxides and in vitro copper-induced LDL oxidation, also no changes were observed after 6 months of treatment in both groups. CONCLUSION: Dyslipidemia aggravates after 6 months of hemodialysis but not after 6 months of peritoneal dialysis. During this period, no net effects on oxidative stress were demonstrated

Oxidative stress in patients with end-stage renal disease prior to the start of renal replacement therapy.

Item does not contain fulltextBACKGROUND/AIM: In patients with end-stage renal disease (ESRD), cardiovascular complications are the main cause of death. Increased oxidative stress is one of the risk factors for enhanced atherosclerosis in this population. Literature data vary partially dependent on differences in methodology. The present study compares three different methods: plasma lipid peroxides, the newly developed measurement of circulating oxidized LDL (Ox-LDL) particles and the frequently used copper-induced LDL oxidation lag time. METHODS: We assessed plasma lipid peroxides, circulating Ox-LDL and in vitro copper-induced LDL oxidation lag time in 47 non-diabetic patients with ESRD, at the start of renal replacement therapy, and compared these with 41 age- and sex-matched controls. RESULTS: In ESRD, total cholesterol (4.6 +/- 1.1 vs. 5.6 +/- 0.9 mmol/l; p < 0.001), LDL cholesterol (2.8 +/- 0.8 vs. 3.5 +/- 0.7 mmol/l; p < 0.001) and HDL cholesterol (1.0 +/- 0.3 vs. 1.4 +/- 0.4 mmol/l; p < 0.001) were lower compared to controls. Plasma lipid peroxides were higher (1.1 +/- 0.5 vs. 0.8 +/- 0.5 micromol/l; p = 0.003) in ESRD. No differences were observed in plasma Ox-LDL (63.1 +/- 62.0 vs. 55.3 +/- 48.0 mg/l). However, due to the lower plasma LDL cholesterol in ESRD, LDL oxidation level was increased in ESRD (7.1 +/- 0.1 vs. 4.2 +/- 0.3%; p = 0.03). LDL lag time was slightly longer (89 +/- 11 vs. 84 +/- 11 min; p = 0.04) in ESRD. There were no significant differences regarding the amount and rate of dienes produced. CONCLUSIONS: Elevated levels of lipid peroxides and higher LDL oxidation levels support the theory that ESRD is associated with increased oxidative stress, which may explain the accelerated atherosclerosis. The measured amount of oxidative stress is not reflected by in vitro oxidizability of LDL

Effects of atorvastatin and vitamin E on lipoproteins and oxidative stress in dialysis patients: a randomised-controlled trial.

Contains fulltext : 47649.pdf (publisher's version ) (Closed access)OBJECTIVES: The objective of this study was to examine the effects of treatment with atorvastatin, alpha-tocopherol and the combination of both, on lipoproteins and oxidative stress in dialysis patients. DESIGN AND SETTING: This double-blind randomised placebo-controlled trial was performed at the dialysis department of a non-university hospital. SUBJECTS, INTERVENTION AND MEASUREMENTS: A total of 44 clinically stable, non-diabetic patients on dialysis therapy (23 on haemo- and 21 on peritoneal-dialysis) without manifest cardiovascular disease were included in this study. They were randomised for treatment during a period of 12 weeks with 40 mg atorvastatin + placebo alpha-tocopherol (group 1) once daily, 800 IU alpha-tocopherol + placebo atorvastatin once daily (group 2), 40 mg atorvastatin + 800 IU alpha-tocopherol once daily (group 3), or placebo atorvastatin + placebo alpha-tocopherol once daily (group 4). Assessment of lipid profile and oxidative stress was performed at the start of the study and after 12 weeks of treatment. RESULTS: Treatment with atorvastatin reduced total cholesterol, triglycerides (TG), low-density lipoprotein (LDL) cholesterol, apolipoprotein B (apoB) and levels of oxidised LDL (oxLDL) with 30-43%. It had no influence on LDL oxidisability. Additional supplementation with alpha-tocopherol had no effect on lipid profile and oxLDL levels but decreased in vitro LDL oxidisability. No side-effects were observed. CONCLUSIONS: Treatment with atorvastatin is effective in lowering plasma total cholesterol, TG, LDL, apoB and oxLDL in a population of stable dialysis patients and might therefore be an effective tool in improving the poor cardiovascular outcome in these patients. Supplementation of alpha-tocopherol to atorvastatin had beneficial effects on in vitro LDL oxidisability and might therefore be of additional value. Further research on the clinical effects of treatment with atorvastatin in combination with alpha-tocopherol is necessary