The Urine Anion Gap: A Clinically Useful Index of Ammonium Excretion

Goldstein, Marc B.; Bear, Robert A.; Richardson, Robert; Marsden, Philip A.; Halperin, Mitchell L.

doi:10.1097/00000441-198610000-00003

Cited by 116 publications

(83 citation statements)

References 17 publications

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“…A negative UAG indicates increased NH 4 + excretion (e.g., diarrhea) of the kidney. In metabolic acidosis without elevated AG, positive UAG is associated with low urinary NH 4 + (e.g., RTA) [18][19][20].…”

Section: Introductionmentioning

confidence: 99%

Drug-induced acid-base disorders

et al. 2014

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The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal antiinflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g

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Section: Introductionmentioning

confidence: 99%

Drug-induced acid-base disorders

et al. 2014

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“…+ Excretion Because direct measurements of urinary NH 4 + excretion are not available in most clinical laboratories, investigators have made use of the effect of changes in urinary NH 4 + and its accompanying anions on urinary charge (urine anion gap) or osmolality (urine osmolal gap) to indirectly estimate urinary NH 4 + concentration (25,(36)(37)(38)(39).…”

Section: Indirect Estimates Of Urinary Nhmentioning

confidence: 99%

“…Under most circumstances, any increment in urine NH 4 + is accompanied by an increment in urine Cl 2 . Assuming that the urinary concentrations of the cations and anions other than Na + , K + , and Cl 2 and NH 4 + do not change appreciably with an acid load (an assumption that is not completely correct), the urinary NH 4 + concentration can be estimated by subtracting the Cl 2 concentration from the sum of the concentrations of Na + + K + (36,37), using a calculation termed the urine anion gap, which is as follows:…”

Section: Indirect Estimates Of Urinary Nhmentioning

confidence: 99%

“…In studies examining the relationship between urine NH 4 + concentration and the urine anion gap, a linear relationship was detected (37), with the urine anion gap becoming more negative as urinary NH 4 + excretion rose. The following mathematical formula was derived from these studies: NH 4 + = 20.8 (urine anion gap) + 82, which allowed for an estimate of urinary NH 4 + excretion (37).…”

Section: Indirect Estimates Of Urinary Nhmentioning

confidence: 99%

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Differential Diagnosis of Nongap Metabolic Acidosis

Kraut

Madias

2012

Clinical Journal of the American Society of Nephrology

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SummaryNongap metabolic acidosis is a common form of both acute and chronic metabolic acidosis. Because derangements in renal acid-base regulation are a common cause of nongap metabolic acidosis, studies to evaluate renal acidification often serve as the mainstay of differential diagnosis. However, in many cases, information obtained from the history and physical examination, evaluation of the electrolyte pattern (to determine if a nongap acidosis alone or a combined nongap and high anion gap metabolic acidosis is present), and examination of the serum potassium concentration (to characterize the disorder as hyperkalemic or hypokalemic in nature) is sufficient to make a presumptive diagnosis without more sophisticated studies. If this information proves insufficient, indirect estimates or direct measurement of urinary NH 4 + concentration, measurement of urine pH, and assessment of urinary HCO 3 2 excretion can help in establishing the diagnosis. This review summarizes current information concerning the pathophysiology of this electrolyte pattern and the value and limitations of all of the diagnostic studies available. It also provides a systematic and cost-effective approach to the differential diagnosis of nongap metabolic acidosis.

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“…New anions may be detected in the urine by calculating the urine anion gap (Na ϩ ϩ K ϩ ϩ NH 4 ϩ Ϫ Cl Ϫ in mEq/L). 16 The second issue is the 1:1 ratio between the rise in P anion gap and the fall in P HCO3 in patients with metabolic acidosis as a result of added acids. Although it is useful to compare the change in the P anion gap with that of the P HCO3 to detect mixed metabolic acid-base disorders, this will also lead to underestimation of the magnitude of the HCO 3 Ϫ deficit-the added H ϩ load-if the ECFV is contracted, because these calculations are based on concentration terms and hence do not reflect the change in content of HCO 3 Ϫ (Table 1).…”

Section: Detection Of Added Acids By Finding New Anionsmentioning

confidence: 99%

Some Observations on the Clinical Approach to Metabolic Acidosis

Halperin¹,

Kamel²

2010

Journal of the American Society of Nephrology

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The first step in the clinical approach to patients with metabolic acidosis is to deal with emergencies and to anticipate and prevent dangers associated with therapy. The traditional clinical analysis for the presence of metabolic acidosis suffers from a number of limitations that at times hinders one's ability to reach a proper diagnosis. Our aim here is to raise awareness of some of the nuanced difficulties and illustrate why other considerations add value.In patients with metabolic acidosis, analyses based on the anion gap in plasma (P anion gap ) 1 or the strong ion difference 2 have major deficiencies. For example, the diagnosis of metabolic acidosis may be missed if one relies solely on pH and the concentration of bicarbonate (HCO 3 Ϫ ) in plasma (P HCO3 ) without considering changes in the content of HCO 3 Ϫ in the extracellular fluid (ECF) compartment. In addition, the rules of respiratory compensation, which are based solely on the arterial PCO 2 rather than the more valuable PCO 2 in capillary blood-draining skeletal muscle (as reflected by the venous PCO 2 ), fail to assess the effectiveness of the bulk of the bicarbonate buffer system to remove H ϩ and, hence, whether more H ϩ will bind to intracellular proteins in vital organs, such as the brain or the heart. 3 DIAGNOSIS OF METABOLIC ACIDOSISThe traditional definition of metabolic acidosis is based on a low pH in plasma, a low P HCO3 , and a high value for the P anion gap if its basis is added acids. A major decrease in ECF volume (ECFV), however, will raise the P HCO3 because this parameter is the ratio of the content of HCO 3 Ϫ in the ECF compartment to the ECFV. This explains why the diagnosis of metabolic acidosis was missed in a patient with diabetic ketoacidosis and a very low ECFV, for whom the provisional diagnosis was hyperglycemic hyperosmolar nonketotic coma. 4 In fact, a severe degree of metabolic acidosis was clearly evident after calculation of the content of HCO 3 Ϫ in the ECF compartment. Similarly, the presence of a severe degree of metabolic acidosis was missed in patients with massive diarrhea as a result of cholera, because the P HCO3 was in the near-normal range. 5 Again, this error was revealed by calculation of the content of HCO 3 Ϫ in the ECF compartment. 6 Failure to recognize the presence of metabolic acidosis led to a severe degree of acidemia when the ECFV was re-expanded with a solution that did not contain HCO 3 Ϫ 7 or one of its precursors, organic anions that undergo metabolism to neutral end products. Moreover, pulmonary edema developed in this patient before his intravascular volume was reexpanded completely. Perhaps the development of acidemia led to constriction of the venous capacitance vessels and hence a significant increase in central blood volume. 8 We suggest that one must calculate the content of HCO 3 Ϫ in the ECF compartment to deduce whether metabolic acidosis is present when there is a significantly contracted ECFV. A quantitative assessment of the ECFV is required for this purpose. Because the physica...

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The Urine Anion Gap: A Clinically Useful Index of Ammonium Excretion

Cited by 116 publications

References 17 publications

Drug-induced acid-base disorders

Drug-induced acid-base disorders

Differential Diagnosis of Nongap Metabolic Acidosis

Some Observations on the Clinical Approach to Metabolic Acidosis

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