Skip to main content
. Author manuscript; available in PMC: 2019 Jul 1.
Published in final edited form as: Adv Chronic Kidney Dis. 2018 Jul;25(4):334–350. doi: 10.1053/j.ackd.2018.05.005

Figure 2.

Figure 2.

(A) α-ketoglutarate production from glutamine in mitochondria. Each α-ketoglutarate molecule generates 2 HCO3− in gluconeogenesis (or the Kreb’s cycle) along with NH4+; (B) Schematic depiction of the consumption of 2 HCO3− and 2 NH4+ in ureagenesis; (C) Normal partitioning of ammonia produced in the kidney between the urine (~ 60%) and the renal vein (~40%). Of the total new HCO3− generated by the kidney, the portion remaining that is not consumed with NH4+ during ureagenesis is available for preventing the plasma HCO3− from decreasing as a resulting of dietary H+ production; (D) Titratable acid (TA) formation and excretion. Approximately 60% of TA is generated in the proximal tubule and ~ 40% is generated in the collecting duct.