Evaluation of brain and kidney energy metabolism in an animal model of contrast-induced nephropathy

• Published in: Metabolic brain disease 2011-06, Vol.26 (2), p.115-122
• Main Authors: Roza, Clarissa A., Scaini, Giselli, Jeremias, Isabela C., Ferreira, Gabriela K., Rochi, Natalia, Benedet, Joana, Rezin, Gislaine T., Vuolo, Francieli, Constantino, Larissa S., Petronilho, Fabricia C., Dal-Pizzol, Felipe, Streck, Emilio L.
• Format: Article
• Language: English
• Subjects: Animal models; Animals; Biochemistry; Biomedical and Life Sciences; Biomedicine; Brain; Brain - enzymology; Brain Diseases, Metabolic - etiology; Brain Diseases, Metabolic - pathology; Coma; Contrast media; Contrast Media - administration & dosage; Contrast Media - adverse effects; Cortex; Cortex (prefrontal); Creatine kinase; Creatine Kinase - metabolism; Creatinine - blood; Cytochrome-c oxidase; Disease Models, Animal; Electron transport; Electron Transport Chain Complex Proteins - metabolism; Encephalopathy; Energy metabolism; Energy Metabolism - physiology; Hippocampus; Humans; Kidney; Kidney - metabolism; Kidney Diseases - chemically induced; Kidney Diseases - complications; Metabolic Diseases; Metabolic disorders; Mitochondria; Mitochondria - metabolism; Neostriatum; Nephropathy; Neurological complications; Neurology; Neurosciences; Oncology; Original Article; Oxidative Stress; Rats; Rats, Wistar; Renal failure; Sodium; Veins
• ISSN: 0885-7490; 1573-7365
• DOI: 10.1007/s11011-011-9240-3

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.