Zlotat O. The mechanism of the development of the hepatorenal syndrome in to the polyuric stage of sublimate nephropathy.

Українська версія

Thesis for the degree of Candidate of Sciences (CSc)

State registration number

0412U004187

Applicant for

Specialization

  • 14.03.04 - Патологічна фізіологія

12-09-2012

Specialized Academic Board

К 76.600.02

Essay

Object - early mechanisms the pathogenesis of the hepatorenal a syndrome; the purpose - to find out early mechanisms of development of the hepatorenal a syndrome into the polyuric a stage of sublimate nephropathy with development of ways of correction of this disease; methods - experimental; physiological; biochemical; statistical; results - the dissertation has investigated the pathogenesis of the hepatorenal syndrome as a basis of a deterioration of the course of renal and hepatic failure under the conditions of the polyuric stage of sublimate nephropathy . Et has been established that the pathogenesis of the development of secondary oliguria into the polyuric stage of sublimate nephropathy is due to a reperfusion injury of the proximal portion of the nephron in particular the S3- segments with an abatemend of the enzymatic fibrinolytic activity of the renal papilla due to the development of urothrombosis of the tubular lumen of the nephron . Secondary damage of the proximal and distat tubules at the expense of realizing the reperfusion "no-reflow" syndrome causes the establishment of positive correlations of relative water reabsorption with the proximal and distal reabsorptions of sodium ions . The polyuric stage of sublimate nephropathy is characherized by damage of the 3d functional site , of the hepatic lobule with phenomena of vacuolar degeneration , an inhibition of the activity of succinate dehydrogenase and a dilatation of the lumen of the central vein . The GA-40 medication under the conditions of the development of the hepatorenal syndrome in case of the polyuric stage of sublimate nephropathy exerts a protective effect that is manifested in the restoration of the activity of succinate dehydrogenase in Cortex I , Cortex II - the subcapsular and juxtamedullary areas of the cortical substance of the kidneys the 3d functional site of the hepatic lobule a decrease of the degree of the hydropic degeneration of nephrocytes and hepatocytes .

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