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      Hypertension as an Etiopathological Factor in the Development of Cerebral Atrophy in Hemodialyzed Patients

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          Abstract

          Twenty-five patients on long-term regular hemodialysis treatment (RDT) at our dialysis unit who underwent diagnostic cerebral computed tomography (CCT) participated in a study aimed at clarifying the pathogenesis of cerebral atrophy occasionally found at their original scan. The upper age limit was 55 years to exclude the physiological involutive brain changes occurring with age. Cerebral atrophy (CA), as defined morphologically (enlargement of cerebral sulci or an increased Evan’s Index), was detected in all cases. Seventeen patients underwent magnetic resonance imaging (MRI) to define possible white matter changes more accurately. No significant correlation was found between the degree of atrophy and the following uremia-altered hematoseric parameters: creatinine, hematocrit, cholesterol, triglyceridemia, albumin, PTH, calcium, inorganic phosphate. There was no correlation between degree of atrophy and number of months the patients had been on RDT or time that passed between the finding of a creatinine clearance <30 ml/min and the start of RDT. Very high correlations were found between the degree of CA and predialytic blood pressure values, and between CA and the duration of hypertension (n = 13, r = 0.66, p < 0.013). Thus, hypertension seems to be an early cause of cerebral parenchymal damage in RDT patients, and should be promptly corrected.

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          Author and article information

          Journal
          NEF
          Nephron
          10.1159/issn.1660-8151
          Nephron
          S. Karger AG
          1660-8151
          2235-3186
          1999
          1999
          13 January 1999
          : 81
          : 1
          : 17-24
          Affiliations
          aDepartment of Clinical Medicine and Nephrology, bDepartment of Radiological Sciences, and cLaboratory of Industrial Toxicology, University of Parma, Italy
          Article
          45240 Nephron 1999;81:17–24
          10.1159/000045240
          9884414
          © 1999 S. Karger AG, Basel

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          Page count
          Tables: 3, References: 32, Pages: 8
          Product
          Self URI (application/pdf): https://www.karger.com/Article/Pdf/45240
          Categories
          Original Paper

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