title: Evaluation of brain and kidney energy metabolism in an animal model of contrast-induced nephropathy.
abstract: Contrast-induced nephropathy is a common cause of acute renal failure in hospitalized patients, occurring from 24 to 48 h and up to 5 days after the administration of iodinated contrast media. Encephalopathy may accompany acute renal failure and presents with a complex of symptoms progressing from mild sensorial clouding to delirium and coma. The mechanisms responsible for neurological complications in patients with acute renal failure are still poorly known, but several studies suggest that mitochondrial dysfunction plays a crucial role in the pathogenesis of uremic encephalopathy. Thus, we measured mitochondrial respiratory chain complexes and creatine kinase activities in rat brain and kidney after administration of contrast media. Wistar rats were submitted to 6.0 ml/kg meglumine/sodium diatrizoate administration via the tail vein (acute renal failure induced by contrast media) and saline in an equal volume with the radiocontrast material (control group); 6 days after, the animals were killed and kidney and brain were obtained. The results showed that contrast media administration decreased complexes I and IV activities in cerebral cortex; in prefrontal cortex, complex I activity was inhibited. On the other hand, contrast media administration increased complexes I and II-III activities in hippocampus and striatum and complex IV activity in hippocampus. Moreover, that administration of contrast media also decreased creatine kinase activity in the cerebral cortex. The present findings suggest that the inhibition of mitochondrial respiratory chain complexes and creatine kinase caused by the acute renal failure induced by contrast media administration may be involved in the neurological complications reported in patients and might play a role in the pathogenesis of the encephalopathy caused by acute renal failure.
authors: Laboratório de Fisiopatologia Experimental and Instituto Nacional de Ciência e Tecnologia Translacional em Medicina, Programa de Pós-graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, Santa Catarina, Brazil.
authors: Clarissa A
authors: CA
authors: Roza
authors: Giselli
authors: G
authors: Scaini
authors: Isabela C
authors: IC
authors: Jeremias
authors: Gabriela K
authors: GK
authors: Ferreira
authors: Natalia
authors: N
authors: Rochi
authors: Joana
authors: J
authors: Benedet
authors: Gislaine T
authors: GT
authors: Rezin
authors: Francieli
authors: F
authors: Vuolo
authors: Larissa S
authors: LS
authors: Constantino
authors: Fabricia C
authors: FC
authors: Petronilho
authors: Felipe
authors: F
authors: Dal-Pizzol
authors: Emilio L
authors: EL
authors: Streck
mesh_terms: D000818:Animals; D001921:Brain / Q000201:enzymology; D001928:Brain Diseases, Metabolic / Q000209:etiology / Q000473:pathology; D003287:Contrast Media / Q000008:administration & dosage / Q000009:adverse effects; D003402:Creatine Kinase / Q000378:metabolism*; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D045222:Electron Transport Chain Complex Proteins / Q000378:metabolism*; D004734:Energy Metabolism / Q000502:physiology*; D006801:Humans; D007668:Kidney / Q000378:metabolism; D007674:Kidney Diseases / Q000139:chemically induced / Q000150:complications; D008928:Mitochondria / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar
chemical_list: D003287:Contrast Media; D045222:Electron Transport Chain Complex Proteins; D003404:Creatinine; D003402:Creatine Kinase