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Urine anion and osmolal gaps in metabolic acidosis

INTRODUCTION

Measurement of the urine anion gap and urine osmolal gap may be helpful in the evaluation of patients with a normal anion gap (hyperchloremic) metabolic acidosis by providing an estimate of urinary ammonium (NH4) excretion (table 1) [1-5]. The normal renal response to metabolic acidosis is to increase urinary NH4 excretion. (See "Approach to the adult with metabolic acidosis".)

The clinical use of the urine anion and osmolal gaps will be reviewed here. Issues related to use of the serum anion and osmolal gaps are discussed separately. (See "The Δanion gap/ΔHCO3 ratio in patients with a high anion gap metabolic acidosis" and "Serum osmolal gap".)

BRIEF OVERVIEW OF RENAL ACID EXCRETION

Ingestion of a typical Western diet generates approximately 50 to 100 meq of hydrogen ions (nonvolatile acid: ie, acids other than CO2) per day. To maintain acid balance, these hydrogen ions must be excreted in the urine in a process that includes the following (see "Chapter 11A: Renal hydrogen excretion"):

  • Reabsorption of filtered bicarbonate, since bicarbonate loss is equivalent to the generation of hydrogen ions.
  • Excretion of the daily nonvolatile acid load. Only trivial amounts of free hydrogen can be excreted since, at a urine pH of 4.5, the free hydrogen ion concentration is less than 0.04 meq/L. Thus, free hydrogen ions are either bound to buffers (such as phosphate) or to ammonia (NH3) to form ammonium (NH4).
  • The main adaptive renal response to metabolic acidosis is to increase hydrogen ion excretion in the form of NH4. In patients with severe metabolic acidosis and normal renal function, NH4 excretion can increase from the normal value of 30 to 40 meq/day to as much as 200 to 300 meq/day [6,7]. NH4 is usually excreted with Cl but is sometimes excreted with other anions such as ketoacid anions, hippurate, or HCO3.

URINE ANION GAP

Calculation of the difference between the urine sodium (Na) plus potassium (K) concentration and the urine chloride (Cl) concentration can be helpful in patients with various acid-base disorders. This calculation has been called the urine anion gap (UAG):

     

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Literature review current through: Apr 2013. | This topic last updated: Jan 22, 2013.
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References
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  1. Batlle DC, Hizon M, Cohen E, et al. The use of the urinary anion gap in the diagnosis of hyperchloremic metabolic acidosis. N Engl J Med 1988; 318:594.
  2. Halperin ML, Vasuvattakul S, Bayoumi A. A modified classification of metabolic acidosis: a pathophysiologic approach. Nephron 1992; 60:129.
  3. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, McGraw-Hill, New York 2001. p.590.
  4. Inase N, Ozawa K, Sasaki S, Marumo F. Is the urine anion gap a reliable index of urine ammonium excretion in most situations? Nephron 1990; 54:180.
  5. Oh M, Carroll HJ. Value and determinants of urine anion gap. Nephron 2002; 90:252.
  6. Owen OE, Licht JH, Sapir DG. Renal function and effects of partial rehydration during diabetic ketoacidosis. Diabetes 1981; 30:510.
  7. CLARKE E, EVANS BM, MACINTYRE I, MILNE MD. Acidosis in experimental electrolyte depletion. Clin Sci (Lond) 1955; 14:421.
  8. Kim GH, Han JS, Kim YS, et al. Evaluation of urine acidification by urine anion gap and urine osmolal gap in chronic metabolic acidosis. Am J Kidney Dis 1996; 27:42.
  9. Dyck RF, Asthana S, Kalra J, et al. A modification of the urine osmolal gap: an improved method for estimating urine ammonium. Am J Nephrol 1990; 10:359.
  10. Tizianello A, Garibotto G, Robaudo C, et al. Renal ammoniagenesis in humans with chronic potassium depletion. Kidney Int 1991; 40:772.
  11. Han KH, Lee HW, Handlogten ME, et al. Effect of hypokalemia on renal expression of the ammonia transporter family members, Rh B Glycoprotein and Rh C Glycoprotein, in the rat kidney. Am J Physiol Renal Physiol 2011; 301:F823.
  12. Carlisle EJ, Donnelly SM, Vasuvattakul S, et al. Glue-sniffing and distal renal tubular acidosis: sticking to the facts. J Am Soc Nephrol 1991; 1:1019.
  13. Sulyok E, Guignard JP. Relationship of urinary anion gap to urinary ammonium excretion in the neonate. Biol Neonate 1990; 57:98.
  14. Kamel KS, Halperin ML. An improved approach to the patient with metabolic acidosis: a need for four amendments. J Nephrol 2006; 19 Suppl 9:S76.
  15. Meregalli P, Lüthy C, Oetliker OH, Bianchetti MG. Modified urine osmolal gap: an accurate method for estimating the urinary ammonium concentration? Nephron 1995; 69:98.