Search

Background and Objective: Non-adherence to fluid intake restrictions is one of the leading problems in hemodialysis patients. The consequences of chronic volume overload and massive hypotensive episodes resulting from enhanced ultrafiltration lead to an increased mortality and incidence of vascular events. Telemetric body weight monitoring (TBWM) suggests itself as a successful way to reduce daily fluid intake, Patients and Methods: This monocentric, prospective, randomized open study includes 120 patients with end-stage renal failure undergoing chronic hemodialysis (for at least two months) three times a week. The mean interdialytic weight gain (IWG) was more than 1.5 kg/2 days over the four weeks immediately before start of the study. The effect of daily body weight telemonitoring on IWG, blood pressure, haemoglobin variability, hospital stay, vascular events and mortality were observed for three months. All monitored patients (group 1, n = 60) received a weekly report of their weight changes, the number of alarms (automatically sent by email to the study center when daily IWG was greater than 0.75 kg/d) and of the interventions by phone (conducted by the responsible nephrologist when IWG was > 2 kg/day). Hemodynamics (each hemodialysis procedure) and weekly laboratory data were recorded for all patients., Results: Preliminary data of 44 patients showed a significant reduction of daily IWG (weekly average, p = 0.0187) and a smaller number of alarm reports after the whole study period in group 1. Blood pressure monitoring during hemodialysis showed less hyper- and hypotensive episodes in patients with an IWG of less than 1.5 kg/2 days. In the control group there have so far been no changes of the analysed parameters., Conclusions: TBWM seems to be an effective method for optimizing adherence to fluid intake restrictions in patients on hemodialysis. Hemoglobin variability, mortality rates and the number of vascular events will still have to be analysed in detail for all patients once the entire study period has been completed.

Experimental and clinical studies give evidence for breakdown of membrane phospholipids during neurodegeneration. In the present study, we measured the levels of glycerophosphocholine (GPCh), phosphocholine (PCh), and choline, that is, water-soluble metabolites of phosphatidylcholine (PtdCho), in human cerebrospinal fluid (CSF). Among 30 cognitively normal patients the average CSF levels of GPCh, phosphocholine and choline were 3.64, 1.28, and 1.93 microM, respectively; metabolite levels did not change with increasing age. When compared with age-matched controls, patients with Alzheimer's disease had elevated levels of all choline metabolites: GPCh was significantly increased by 76% (P<0.01), phosphocholine by 52% (P<0.05), and free choline (Ch) by 39%. Six patients with vascular dementia had lower choline and elevated phosphocholine levels, when compared to controls, but normal levels of GPCh. These data demonstrate that Alzheimer's disease is accompanied by an increased PtdCho hydrolysis in the brain. PtdCho breakdown seems to be mediated by phospholipase A2 and leads to significantly elevated levels of GPCh in CSF.

Intestinal ischaemia is a major complication of shock syndromes causing translocation of bacteria and endotoxins and multiple organ failure in intensive care patients. The present study was designed to use microdialysis as a tool to monitor intestinal ischaemia after cardiac arrest and resuscitation in pigs. For this purpose, microdialysis probes were implanted in pig jejunal wall, peritoneum, skeletal muscle and brain, and interstitial fluid was obtained during circulatory arrest (induced by ventricular fibrillation) and after return of spontaneous circulation (ROSC). Cardiac arrest for 4 min caused a prolonged (60 min) reduction of blood flow in jejunal wall, muscle and brain as determined by the ethanol technique. This was accompanied by cellular damage in heart muscle and brain as indicated by increased levels of troponin-I and protein S-100, respectively. Plasma levels of glucose, lactate and choline were increased at 15-60 min following cardiac arrest. In contrast, cardiac arrest induced a rapid but variable decrease of interstitial glucose levels in all monitored organs; this decrease was followed by an increase over baseline during reperfusion. In the intestine, lactate, glutamate and choline levels were increased during ischaemia and reperfusion for 60-120 min; intestinal and peritoneal samples yielded parallel changes of lactate levels. Brain and muscle samples showed similar changes as in intestinum and peritoneum except for glutamate, which was increased in brain but not in muscle. We conclude that intestinal ischaemia occurs as a consequence of cardiac arrest and resuscitation and can be monitored by in vivo microdialysis. Comparative analysis by multi-site microdialysis reveals that the intestine is equally or even more sensitive to ischaemia than brain or muscle.