Background and Purpose —The goal of the present study was to examine a series of putative risk factors of poststroke dementia (PSD), especially those factors usually associated with cerebrovascular disease and degenerative dementia, in a series of 251 consecutive unselected stroke patients. Methods —A standard protocol was prospectively applied at admission and 3 months after stroke; this protocol included clinical, functional, and cognitive assessments, hemogram and serum biochemistry, ECG and CT exams, apolipoprotein E and angiotensin-converting enzyme genotype, and neuropsychological examination. After a neuropsychological examination and an interview with a relative, the following diagnostic criteria were used: the Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV for dementia after stroke, DSM-III-R for previous dementia and dementia stage, and Association Internationale pour la Recherche et l’Enseignement en Neurologie (NINDS-AIREN) for vascular dementia. Results —Seventy-five cases (30%) demonstrated dementia at 3-month follow up; 25 of them (10%) had demonstrated dementia before the stroke. Dementia was unrelated to type (ischemic/hemorrhagic) or location of stroke, vascular factors (hypertension, diabetes, ischemic heart disease, or hypercholesterolemia), apolipoprotein E or angiotensin-converting enzyme genotype, and serum homocysteine. Age (odds ratio [OR] 1.1, 95% CI 1.03 to 1.2), previous nephropathy (OR 6.1, 95% CI 1.5 to 24.3), atrial fibrillation (OR 4.4, 95% CI 1.4 to 13.9), low Canadian Neurological Scale score at discharge (OR 0.5, 95% CI 0.4 to 0.6), and previous mental decline assessed by the shortened Spanish version of the Informant Questionnaire on Cognitive Decline in the Elderly (SS-IQCODE; OR 1.2, 95% CI 1.1 to 1.4) were the correlates of dementia in logistic regression analyses. The same risks factors were found when cases with previous dementia and with hemorrhagic stroke were excluded. Conclusions —Dementia is frequent after ischemic or hemorrhagic stroke. Age, nephropathy, atrial fibrillation, previous mental decline, and stroke severity independently contribute to the risk.

Poststroke dementia : clinical features and risk factors

Stroke is a major cause of death in the elderly, and risk of dementia increases after stroke. Poststroke dementia （PSD） covers all types of dementia after stroke, and is an important cause of disability in the elderly. The prevalence of PSD varies from 31.4% to 21.5% in 3 months to 4 years after the stroke. Its incidence increases with time after the stroke. Stroke and dementia share a number of risk factors. Stroke can be the direct cause of dementia and may also produce dementia by precipitating the onset of degenerative disease.

Key words: 
stroke ;  dementia ;  Alzheimer＇s disease ; risk factor

Poststroke Dementia

Advanced glycation end products (AGEs) are produced through the non enzymatic glycation and oxidation of proteins, lipids and nucleic acids. Enhanced formation of AGEs occurs particularly in conditions associated with hyperglycaemia such as diabetes mellitus (DM). AGEs are believed to have a key role in the development and progression of cardiovascular disease in patients with DM through the modification of the structure, function and mechanical properties of tissues through crosslinking intracellular as well as extracellular matrix proteins and through modulating cellular processes through binding to cell surface receptors [receptor for AGEs (RAGE)]. A number of studies have shown a correlation between serum AGE levels and the development and severity of heart failure (HF). Moreover, some studies have suggested that therapies targeted against AGEs may have therapeutic potential in patients with HF. The purpose of this review is to discuss the role of AGEs in cardiovascular disease and in particular in heart failure, focussing on both cellular mechanisms of action as well as highlighting how targeting AGEs may represent a novel therapeutic strategy in the treatment of HF.

/pdf/role-of-advanced-glycation-end-products-in-cardiovascular-59nfj22gal.pdf

Role of advanced glycation end products in cardiovascular disease

Correspondence to: R.T. Krediet, Division of Nephrology, Department of Medicine, Academic Medical Center, P.O. Box 22700, 1100 DE Amsterdam, The Netherlands. Various mathematical models have been used for the assessment of the peritoneum as a dialysis membrane, for example, membrane models and distributed models. These have been discussed by Lysaght and Farrel (1) and by Waniewski (2). The present review is based on the three-pore model (3–5). The peritoneal membrane, as used for peritoneal dialysis (PD), can be divided into three parts for the purpose of simplicity. These are the mesothelium, the interstitial tissue, and the microvessels present in the interstitial tissue. It is unlikely that the mesothelium is an important barrier to solute transport because no osmotic pressure gradient across it was found during PD in rats (6). The barrier function of interstitial tissue is not very well known. Using in vivo microscopy of the rat mesentery, a size-selective restriction in the transport of macromolecules was detected and has been reported (7). More recent studies comparing the transport properties of liver peritoneum (almost no interstitial tissue) with that of parietal peritoneum were unable to show differences (8,9). The capillary wall is probably the most important structure. Solute transport across it is generally considered to occur through a system of pores (10,11). This process occurs mainly through a large number of small pores (radius 40 – 50 A), probably represented by paracellular clefts in the endothelium, together with a very low number of large pores (radius approximately 250 A), allowing transport of macromolecules from blood to peritoneum. In addition, an abundance of water-conductive “ultrasmall pores” (radius approximately 3 – 5 A) in the plasmalemma has been assumed, allowing water transport but rejecting the transfer of solutes (3–5). It has been made plausible that aquaporins, and especially aquaporin–1, are the proteins constituting these transendothelial water channels (12–14). For high glucose concentrations (3.86%/4.25%) in dialysis fluid, the three-pore model predicted approximately one half of transperitoneal ultrafiltration (UF) would occur through aquaporins, with the other half through small pores.

Pathophysiology of Peritoneal Membrane Failure

In the present review, we summarize the principles governing the transport of fluid and electrolytes across the peritoneum during continuous ambulatory peritoneal dialysis (CAPD) in "average" patients and during ultrafiltration failure (UFF), according to the three-pore model of peritoneal transport. The UF volume curves as a function of dwell time [V(t)] are determined in their early phase by the glucose osmotic conductance [product of the UF coefficient (LpS) and the glucose reflection coefficient (sigmag)] of the peritoneum; in their middle portion by intraperitoneal volume and glucose diffusivity; and in their late portion by the LpS, Starling forces, and lymph flow. The most common cause of UFF is increased transport of small solutes (glucose) across the peritoneum, whereas the LpS is only moderately affected. Concerning peritoneal ion transport, ions that are already more or less fully equilibrated across the membrane at the start of the dwell, such as Na+ (Cl-), Ca2+, and Mg2+, have a convection-dominated transport. The removal of these ions is proportional to UF volume (approximately 10 mmol/L Na+ and 0.12 mmol/L Ca2+ removed per deciliter UF in 4 hours). The present article examines the impact on fluid and solute transport of varying concentrations of Ca2+ and Na+ in peritoneal dialysis solutions. Particularly, the effect of "ultralow" sodium solutions on transport and UF is simulated and discussed. Ions with high initial concentration gradients across the peritoneum, such as K+, phosphate, and bicarbonate, display a diffusion-dominated transport. The transport of these ions can be adequately described by non-electrolyte equations. However, for ions that are in (or near) their diffusion equilibrium over the peritoneum (Na+, Ca2+, Mg2+), more complex ion transport equations need to be used. Due to the complexity of these equations, however, non-electrolyte transport formalism is commonly employed, which leads to a marked underestimation of mass transfer area coefficients (PS). This can be avoided by determining the PS when transperitoneal ion concentration gradients are steep.

Fluid and electrolyte transport across the peritoneal membrane during CAPD according to the three-pore model.

https://www.kidney-international.org/article/S0085-2538(15)59269-7/pdf

Ultrafiltration and solute kinetics using low sodium peritoneal dialysate

Atherosclerotic cardiovascular disease is a significant cause of morbidity and mortality in patients with chronic renal failure. It is unclear, however, if atherosclerosis in fact occurs at a higher incidence compared with the nonuremic population matched for age, hypertension, and diabetes mellitus or if it occurs at an accelerated rate following the onset of end-stage renal disease. The extent of true atherosclerotic lesions, versus clinically diagnosed "atherosclerosis," in patients with chronic renal failure is equally unclear. Potentially, the uremic state per se, the dialysis treatment, and factors unrelated to renal failure may participate in atherogenesis. The relative contribution of each of these factors is unknown. In this review, we discuss the pathology of "atherosclerotic" lesions in patients with chronic renal failure and the putative factors involved in atherogenesis in this population and describe the results of available studies examining the issue of accelerated atherosclerosis in uremia.

Atherosclerosis in chronic renal failure

In 1919, Ernest Goodpasture described the case of a young man with a fatal illness characterized by hemoptysis, alveolar hemorrhage and necrosis, and proliferative glomerulonephritis (1). Stanton and Tange, in 1958, were the first to use the eponym Goodpasture’s syndrome to describe cases of pulmonary hemorrhage and necrotizing glomerulonephritis (2), although a large number of similar cases have been reported in the literature since the original description by Goodpasture. The original diagnosis of this syndrome was based on the clinical presence of pulmonary and renal involvement, and the underlying pathology described in literature reports varied. As we have come to understand, such pulmonary-renal syndromes have more than one etiology (Table 1).

Goodpasture’s Syndrome

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Ultrafiltration and solute kinetics using low sodium peritoneal dialysate

Atherosclerosis in chronic renal failure

Goodpasture’s Syndrome