Electrolyte Blood Press.  2009 Jun;7(1):9-13. 10.5049/EBP.2009.7.1.9.

Renal Handling of Ammonium and Acid Base Regulation

Affiliations
  • 1Department of Internal Medicine, Chungbuk National University College of Medicine, Cheongju, Korea. hyekim@chungbuk.ac.kr

Abstract

Renal ammonium metabolism is the primary component of net acid excretion and thereby is critical for acid - base homeostasis. Briefly, ammonium is produced from glutamine in the proximal tubule in a series of biochemical reactions that result in equimolar bicarbonate. Ammonium is predominantly secreted into the luminal fluid via the apical Na++xchanger, NHE3. The thick ascending limb of the loop of Henle reabsorbs luminal ammonium, predominantly by transport of NH4+y the apical Na++Cl - cotransporter, BSC1/NKCC2. This process results in renal interstitial ammonium accumulation. Finally, the collecting duct secretes ammonium from the renal interstitium into the luminal fluid. Although in past ammonium was believed to move across epithelia entirely by passive diffusion, an increasing number of studies demonstrated that specific proteins contribute to renal ammonium transport. Recent studies have yielded important new insights into the mechanisms of renal ammonium transport. In this review, we will discuss renal handling of ammonium, with particular emphasis on the transporters involved in this process.

Keyword

ammonia; kidney; kidney tubules, collecting; acidosis

MeSH Terms

Ammonia
Diffusion
Extremities
Glutamine
Handling (Psychology)
Homeostasis
Kidney
Kidney Tubules, Collecting
Loop of Henle
Phenobarbital
Proteins
Quaternary Ammonium Compounds
Ammonia
Glutamine
Phenobarbital
Proteins
Quaternary Ammonium Compounds

Figure

  • Fig. 1 Schematic representation of the ammonium transport mechanisms in the kidney. Ammonium is predominantly secreted into the luminal fluid via the apical Na+/H+ exchanger, NHE3. The thick ascending limb of the loop of Henle reabsorbs luminal ammonium, predominantly by transport of NH4+ by the apical Na+/K+/2Cl-cotransporter, BSC1/NKCC2. The renal countercurrent mechanism results in renal interstitial ammonium accumulation. Finally, the collecting duct secretes ammonium from the renal interstitium into the luminal fluid. NH3 is transported across the basolateral membrane, predominantly by Rhcg, but also by lipid diffusion (dashed line) and possibly by Rhbg. Intracellular NH3 is secreted across the apical membrane by apical Rhcg. In inner medullary collecting duct, basolateral Na+,K+-ATPase transports NH4+. There is also likely to be a component of diffusive apical NH3 transport (dashed line). H+-ATPase secretes H+, which combines with luminal NH3 to form NH4+. Modified from Kim et al.42).


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