Studies on Brain Density in Hemodialysis and Peritoneal Dialysis

Greca, G. La; Biasioli, S; Chiaramonte, S; Dettori, P; Fabris, A; Feriani, M; Pinna, V.; Pisani, Elizabeth; Ronco, Claudio

doi:10.1159/000182634

Cited by 55 publications

(35 citation statements)

References 9 publications

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“…This has been confirmed both at autopsy and by computed tomography imaging of the brain in patients with renal failure who have undergone dialysis (21,22). Several animal models of DDS have been developed and brain swelling has been reported in hemodialyzed dogs (4,23) and rats (14).…”

Section: Discussionmentioning

confidence: 83%

Hemodialysis increases apparent diffusion coefficient of brain water in nephrectomized rats measured by isotropic diffusion-weighted magnetic resonance imaging.

Galons¹,

Trouard²,

Gmitro³

et al. 1996

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 83%

Hemodialysis increases apparent diffusion coefficient of brain water in nephrectomized rats measured by isotropic diffusion-weighted magnetic resonance imaging.

Galons¹,

Trouard²,

Gmitro³

et al. 1996

J. Clin. Invest.

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“…2), the list also includes cyclic changes in intradialytic hydration. Recent cerebral tono-densitometric studies have refuted a long-held belief and show that tissue density is greater before intermittent dialysis, returning rapidly to a normal level of hydration during dialysis [73]. These fluctuations in the state of hydration, resulting from RDT, are in turn triggered by marked osmotic variations.…”

Section: Brain Circulation and Changes In Brain Tissue Hydrationmentioning

confidence: 97%

Pathogenesis of Cerebral Atrophy in Uraemia

Savazzi

1988

Nephron

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This paper discusses the possible pathogenesis of the cerebral atrophy (CA) observed in a large percentage of uraemic patients, taking the form of prevalently cortical damage (cortical atrophy) and/or subcortical enlargement of ventricular cavities (subcortical atrophy). This central nervous system pathology seems to share very little either with the better known ‘dialysis encephalopathy’ or with the ‘acute encephalopathy syndrome’, even though sporadic cases of both these forms have shown concomitant CA. Histopathologically it offers the picture of loss of neurons and nerve fibres and can thus be compared with uraemic peripheral nervous system damage. CA is unquestionably important because of its implications in terms of impairment of superior cortical functions, just as in CA of non-uraemic aetiology. A first aetiopathogenic hypothesis might include endogenous uraemic intoxication to the nerve tissue, believed responsible for peripheral uraemic neuropathy, but other possibilities merit consideration: vascular calcification secondary to hyperparathyroidism, blood lipid disorders, and systemic hypertension – factors that contribute to impairing the brain vasculature, with cascade effects on brain tissue oxygenation, neuronal metabolism, and energy exchanges. Tissue oxygenation is already jeopardized in the uraemic patient by the concomitant chronic anaemia and by cardiac insufficiency in cases with hypertensive heart disease. In dialysis patients with volume-dependent hypertension the brain may be further damaged by abrupt pressure changes produced by dialytic ultrafiltration; these constitute a severe challenge to cerebral blood flow autoregulation. Cyclic variations of brain tissue hydration connected with regular dialysis treatment may have adverse effects on neurotransmitter functions, particularly those mediated by neuropeptidergic systems. Chronic intoxication may result from oral A1(OH)₃ of phosphorus-chelating agents: in animal studies and clinical observations in non-uraemic populations the neurotoxic potential of A1 is indicated by a significant correlation between histological neuronal damage, impaired function, and A1 concentration in brain tissues. In addition, a concausal role of malnutrition in central nervous system damage in the uraemic patient cannot be overlooked, since malnutrition is known to give rise to functional and structural alterations in non-uraemic human pathology. In the light of these clinical observations and experimental findings, it would appear that the prevention of CA in uraemia is today feasible.

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“…In addition, enlarged cortical sulci have been reported on cranial CT in up to 80% of pediatric cases with cystinosis (48). Widening of cerebrospinal fluid spaces secondary to brain atrophy (42), with lower cerebral density, has been typically associated with HD (43,49) in comparison with patients receiving continuous ambulatory PD (50). In general, the literature suggested that although brain atrophy was evident in patients with stable CKD and those receiving continuous ambulatory PD, it was definitely more frequent in HD patients.…”

Section: Findings In Pediatric Structural Neuroimaging Studiesmentioning

confidence: 99%

Systematic Review of Structural and Functional Neuroimaging Findings in Children and Adults with CKD

Moodalbail

Reiser

Detre³

et al. 2013

Clinical Journal of the American Society of Nephrology

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Summary CKD has been linked with cognitive deficits and affective disorders in multiple studies. Analysis of structural and functional neuroimaging in adults and children with kidney disease may provide additional important insights into the pathobiology of this relationship. This paper comprehensively reviews neuroimaging studies in both children and adults. Major databases (PsychLit, MEDLINE, WorldCat, ArticleFirst, PubMed, Ovid MEDLINE) were searched using consistent search terms, and studies published between 1975 and 2012 were included if their samples focused on CKD as the primary disease process. Exclusion criteria included case reports, chapters, and review articles. This systematic process yielded 43 studies for inclusion (30 in adults, 13 in children). Findings from this review identified several clear trends: (1) presence of cerebral atrophy and cerebral density changes in patients with CKD; (2) cerebral vascular disease, including deep white matter hyperintensities, white matter lesions, cerebral microbleeds, silent cerebral infarction, and cortical infarction, in patients with CKD; and (3) similarities in regional cerebral blood flow between patients with CKD and those with affective disorders. These findings document the importance of neuroimaging procedures in understanding the effect of CKD on brain structure, function, and associated behaviors. Results provide a developmental linkage between childhood and adulthood, with respect to the effect of CKD on brain functioning across the lifespan, with strong implications for a cerebrovascular mechanism contributing to this developmental linkage. Use of neuroimaging methods to corroborate manifest neuropsychological deficits or perhaps to indicate preventive actions may prove useful to individuals with CKD.

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Studies on Brain Density in Hemodialysis and Peritoneal Dialysis

Cited by 55 publications

References 9 publications

Hemodialysis increases apparent diffusion coefficient of brain water in nephrectomized rats measured by isotropic diffusion-weighted magnetic resonance imaging.

Hemodialysis increases apparent diffusion coefficient of brain water in nephrectomized rats measured by isotropic diffusion-weighted magnetic resonance imaging.

Pathogenesis of Cerebral Atrophy in Uraemia

Systematic Review of Structural and Functional Neuroimaging Findings in Children and Adults with CKD

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