Parkinson Disease Manual
The dyslipidaemia of ESRF is an independent risk factor for atherosclerosis in ESRD (38). To date there are no convincing trials to show that the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statin) are equally as effective as they are for non-renal-compromised patients, and although widely used, their benefits are not unequivocally established (39,40). Dietary management of glycaemic control for diabetic patients on PD improves hypertriglyceridaemia and overall dyslipidaemia. The effectiveness of dietary manipulation of plasma lipids in PD patients is limited and it could be argued that if adhered to, properly constructed dialysis diets are close to optimal lipid-lowering recommendations (41,42). General healthy eating advice given to patients with normal renal function may not be appropriate, as many PD
Due to the metabolic problems associated with glucose as the main osmotic agent for inducing ultrafiltration in PD, alternative osmotic agents are now becoming available. High molecular weight glucose polymer solutions such as Icodextrin appear to be safe and effective. Icodextrin has the advantage of a reduced glucose and calorific load but requires dwell times of between 8-12 h and is therefore often left in situ overnight. No studies of use in diabetic patients have so far been published (24).
Controlled study) showed that in PD ESRD patients (42 diabetic) increases in peritoneal small-solute clearances within the National Kidney Foundation-Dialysis Outcomes Quality Initiative targets (21) have no effect on patient survival, even after controlling for a variety of factors (age, diabetes mellitus, serum albumin levels, normalized protein equivalent of total nitrogen appearance, and anuria) known to affect survival. Thus, it challenges us to focus on treating the entire patient to achieve optimal outcomes, including fluid control and nutrition management. Similarly, the Hemodialysis (HEMO) study concluded that patients undergoing HD three times a week appear to have no major benefit from a higher dialysis dose than that recommended by current guidelines or from the use of a high-flux membrane (22). Current efforts are being focused on, improving phosphate control, and lowering traditional and nontraditional risk factors for adverse cardiovascular events in these patients (23).
Similarly, neuroanatomic changes in the frontal lobes have been implicated in depressive disorders. Lesions of the orbitofrontal cortex increase the risk for developing depression, and metabolic activity is more reduced in this brain region in depressed vs. non-depressed Parkinson's patients. Lower cortical volume in the subgenual prefrontal cortex and orbitofrontal cortex occurs more often in depressed subjects compared to non-depressed controls (50, 51). Further, decreased glial cell counts, density, as well as smaller neuronal size have been reported in the prefrontal, anterior cingu-late, and orbitofrontal cortices of patients with MDD (52, 53). Reduction in the gray matter of the anterior subgenual cingulate cortex persists across illness episodes, correlates with illness severity, appears early in the course of illness, and has been found prior to illness onset in patients with significant family history of MDD.
The introduction of technological developments in HD treatment, the advent of volumetric HD machines, high-flux and high-efficiency dialyzers, along with computerization of the dialysis sessions have all contributed to better care for ESRD diabetic patients. Similarly, in PD treatment technological improvements such as the Y-set disconnect system have substantially decreased the incidence of peritonitis and improved CAPD technique survival, but still it is inferior to HD technique survival (55). Furthermore, during the last decade, there was a great effort toward improving the quality of care, under the development of clinical practice guidelines, focusing at adequacy of treatment, and patient outcomes. Additionally, there is now effective treatment of the anemia of CKD, which improves survival, (56) decreases morbidity, (57) and increases quality of life (58). Marcelli et al. (59) found that PD technique survival in diabetic patients, unadjusted for pretreatment prognostic...
And protein loss with the accompanying malnutrition are some of the shortcomings of PD. Furthermore, long-term studies in PD patients with DN have demonstrated that the micro- and macrovascular disease of diabetes continue to progress after initiation of CAPD, leading to ongoing problems with cardiovascular disease, malnutrition, autonomic neuropathy, retinopathy, and PVD (43).
Peritonitis and conventional PD solutions containing high glucose and glucose-degradation products are implicated in PD technique failure (54), whereas PD solutions without glucose or solutions containing low glucose degradation products may prevent or delay peritoneal membrane alterations and allow its long-time function in both diabetic and nondiabetic patients during long-term PD.
Both in clinical practice and in research settings, neuropsychological assessment typically has two aims the first is to contribute to the differential diagnosis of diseases or syndromes, the second is to provide information about cognitive strengths or weaknesses that can be used for decision-making with respect to treatment or care or educate the patient or his caregivers or significant others about neurocognitive changes that may be present. For making a reliable medical diagnosis, however, neuropsycholog-ical testing rarely contributes uniquely. While a low score on the MMSE is indicative for cognitive decline typically seen in Alzheimer dementia, a low performance may also be due to vascular cognitive impairments, Parkinson's disease, or even to problems in hearing. If cognitive tests or screening instruments are used for establishing medical diagnoses, information
ROS and RNS are closely linked to degenerative diseases such as Alzheimer's disease, Parkinson, neuronal death including ischemic and hemorrhagic stroke, acute and chronic degenerative cardiac myocyte death, diabetes mellitus type 2 and cancer. As a by-product of oxidative phosphorylation (mitochondrial respiration), a steady stream of reactive species emerges from our cellular energy plant, the mitochondria. ROS and RNS potentially cause damage to all cellular components. Structure alterations, biomolecule fragmentation, and oxidation of side chains are trade-offs of the cellular energy production. ROS and RNS production results in the activation of cyto-solic stress pathways, DNA damage, and the upregulation of JNK, p38, and p53. Incomplete scavenging of ROS and RNS, e.g. by the enzymes superoxide dismutase and catalase particularly, affects the release of mitochondria cytochrome c with subsequent activation of caspase 9 and 3 and ultimately induces the intrinsic death pathway.
There are further reasons to offer PD as the initial mode of RRT to the diabetic patient. During the first 2 yr of treatment, survival is better for patients treated with PD compared with HD (83) and this is also true for diabetic patients. The survival advantage was no longer demonstrable beyond the second year (presumably because by then residual renal function has decayed). Moreover, PD provides low and sustained ultrafiltration without rapid fluctuations of fluid volume and electrolyte concentrations (features that are advantageous for blood pressure control and prevention of heart failure).
NF, consisting of heavy, medium, and light subunits, form the major structural lattice of axon. The function of the neurofilaments (NF) is not clear, but abnormal phosphorylation of these proteins is associated with neurodegenerative diseases such as amyotrophic lateral sclerosis, Parkinson disease, Alzheimer disease, and diabetes (58,59). In diabetes, stress-activated protein kinases are thought to be involved in their aberrant phosphorylation (60,61). Further, abnormal NF accumulation was found in the proximal axon segments of diabetic dorsal root ganglia sensory neurons in human (62), whereas loss of NF in distal nerve terminals of sensory neurons was observed in long-term diabetic rats (63). Impairment in the transport of NF proteins was suspected (64). However, it is not clear whether these changes are the cause or consequences of diabetic lesion.
On starting dialysis sodium intake should be limited to below 100mmol, equivalent to 6 g salt day. When dialysis patients become anuric their fluid and sodium intake needs to be further restricted, to 1 litre fluid day and 80100 mmol sodium day. In patients able to maintain a urinary output above ll day, fluid restriction of 1.5-2 l day and more flexible sodium intake may be appropriate. Residual urinary excretion is maintained for longer in PD than HD patients and hence fluid and sodium intake can initially be more liberal in PD patients.
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