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R Lubrano

Publications and source records attributed to R Lubrano.

41 records · Page 3Linked to original sources
PubMedDate not supplied

Renal tubular damage in fetuses with intrauterine growth retardation.

Fetal hypoxemia is one of the most frequent causes of intrauterine growth retardation (IUGR). In chronic fetal hypoxia, peripheral blood flow and blood flow to the kidneys is reduced to maintain heart, brain and adrenal perfusion, the 'brain-sparing effect'. In kidneys the cells of the proximal tubules seem to be most sensitive to hypoxia caused by reduced blood flow. Damage to the cells of the proximal tubules can be easily diagnosed by urinary levels of N-acetyl-beta-D-glucosaminidase (NAG), an enzyme present in high concentrations in these cells. The aim of the present study was to define the levels of NAG in the amniotic fluid, to diagnose damage to the cells of the proximal renal tubules in fetuses, and to correlate them with a detectable brain-sparing effect. The study was conducted on a total of 55 pregnancies: 9 pregnancies were complicated by IUGR, and the remaining 46 normal pregnancies formed the control group. Higher levels of NAG were detected in the amniotic fluid from the IUGR-complicated pregnancies (p < 0.025). In particular, fetuses with IUGR had high levels of NAG in the amniotic fluid in 8 of 9 cases (+ 2 SD compared with controls), while 1 had normal concentrations. In the 8 cases with high concentrations of NAG in the amniotic fluid, velocimetric Doppler study documented a brain-sparing effect, which was not present in the 1 fetus with normal NAG levels. In conclusion, high levels of NAG in the amniotic fluid may identify in uterus fetuses with renal damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMedDate not supplied

Administration of GSH has no influence on the RBC membrane: oxidative damage to patients on hemodialysis.

In patients on hemodialysis, a metabolic block of the pentose phosphate shunt has been described that impairs the reduction of oxidized glutathione. The block results in lack of detoxication of the free hydroxyl radicals produced inside the red blood cell (RBC) and causes oxidative damage to the polyunsaturated fatty acids of the RBC membrane that results in formation of aldehydes. Malonyldialdehyde has been used as an index of the oxidative damage. In a study group of 13 patients on hemodialysis, the authors have tested whether administering reduced glutathione (GSH) at 1200 mg/day for 1 month could minimize oxidative damage to the RBC membranes and improve the hematologic parameters. Treatment with GSH was followed by significant improvement of hematocrit (P = 0.008), hemoglobin (P = 0.03), and RBC count (P = 0.0037); however, oxidative damage to the membranes was increased (P = 0.0004), which suggests that improvement of the hematologic parameters is not related to reduction of the oxidative damage. This is because oxidized glutathione, formed in the oxidative process, cannot be reduced back to GSH because of alteration of the pentose phosphate shunt.

Adult↗
PubMedDate not supplied

Vitamin E supplementation and oxidative status of peripheral blood mononuclear cells and lymphocyte subsets in hemodialysis patients.

Increased oxidative damage to cell membrane constituents causes profound changes in the membrane cytoarchitecture and modifications of the membrane physiological properties, e.g., the ability to respond to hormonal stimuli. In uremic patients receiving intermittent hemodialysis, a metabolic block of the phosphate pentose shunt has been described. This leads to insufficient detoxication of the hydroxyl radicals formed within the cells and therefore to increased oxidative damage to the polyunsaturated fatty acid constituents of the cell membranes. Vitamin E is known to reduce this oxidative damage and its harmful effects. We studied vitamin E (alpha-tocopherol acetate) administration in 10 chronically uremic patients receiving intermittent hemodialysis for positive effects on cell membrane-receptor response. The patients were studied before and after treatment for the extent of oxidative damage in peripheral mononuclear cells and for response to monoclonal antibodies to specific markers of T-lymphocyte subsets. After vitamin E treatment, oxidative damage decreased, and the membranes of peripheral mononuclear cells contained greater amounts of some unsaturated fatty acids. This is in agreement with a modification of the membrane phenotype markers of T-lymphocyte subsets and seems to confirm in vivo that changes in membrane structure first induced by increased oxidative damage due to the blockage of the phosphate pentose shunt can be reduced by the antioxidant action of vitamin E, which significantly influences the expression of membrane determinants.

Adult↗
PubMedDate not supplied

[Reye's syndrome: pathogenetic problems (author's transl)].

The authors describe six subjects with Reye's syndrome. All subjects died nevertheless the treatment (exchange-transfusions infusions of citrulline and ornithine). The autoptical studies showed cerebral oedema and fatty degeneration of the liver. Hepatic and seric OTC activity was measured in three patients: enzyme activity was virtually absent in one patient and normal in the other two. Instead in one patient was found partial CPS deficiency. However, Reye's syndrome is not only correlated with enzymatic deficiency of urea's cycle but sometimes also with toxic and metabolic causes.

Child↗