Effects of ureteral obstruction on the renal metabolism of alpha-ketoglutarate and other substrates in vivo.
The renal metabolims of alpha-ketoglutarate, glutamate, oxygen, carbon dioxide, and citrate during the infusion of beta-hydroxybutyrate and/or alpha-ketoglutarate was evaluated in vivo in the awake, resting dog after varying periods of unilateral ureteral obstruction. The induction of reversible renal damage by 2 weeks of obstruction was associated with (i) decreased utilization of alpha-ketoglutarate and oxygen; (ii) decreased production of carbon dioxide; (iii) elevated respiratory quotient; and (iv) nearly complete lack of citrate production. The induction of irreversible renal damage by 6 weeks of obstruction was associated with (i) a nearly total absence of alpha-ketoglutarate utilization; (ii) a markedly decreased amount of oxygen utilization and carbon dioxide production; (iii) a normal respiratory quotient; and (iv) a nearly total absence of citrate production. The metabolic changes observed after obstruction indicate that aerobic metabolism is inhibited by either reversible or irreversible renal damage. However, certain anaerobic reactions continued in the reversibly damaged kidney. Differences in the extent and character of metabolic changes may make it possible to predict the degree of renal damage.
D000693:Anaerobiosis; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D004285:Dogs; D005260:Female; D005971:Glutamates / Q000378:metabolism; D006869:Hydronephrosis / Q000209:etiology / Q000378:metabolism; D006885:Hydroxybutyrates; D007656:Ketoglutaric Acids / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism*; D010101:Oxygen Consumption; D014517:Ureteral Obstruction / Q000150:complications / Q000378:metabolism*
D005971:Glutamates; D006885:Hydroxybutyrates; D007656:Ketoglutaric Acids; D002245:Carbon Dioxide