Urine electrolytes and the urine anion and osmolar gaps

Kirschbaum, Barry B.; Sica, Domenic A.; Anderson, F.Phillip

doi:10.1016/s0022-2143(99)90190-7

Cited by 50 publications

(52 citation statements)

References 13 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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“…Both severe hypokalemia (despite hyperchloremic metabolic acidosis with normal anion gap present) and alkaline urine with increased urinary anion gap were crucial to make the diagnosis. 3,4 Recurrent nephrolithiasis and fatigue and muscle weakness were points of attention in medical history. We ruled out gastrointestinal bicarbonate loss and urinary infection with urease positive microorganisms.…”

Section: Discussionmentioning

confidence: 99%

A distal (type 1) renal tubular acidosis case that mimic coronary ischemia

2013

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Introduction: Type 1 (distal) renal tubular acidosis (RTA) is a rare clinical condition characterized with defect of urinary acidification in distal tubulus. If diagnosis delays, RTA may cause metabolic and clinical complications and comorbidities. We describe here a type 1 distal RTA case with symptoms mimicking coronary ischemia. Case report: A 46-year-old woman admitted with complaints of chest pain, palpitation, walking disability, fatigue and nausea. On physical examination muscles were weaken 3/5 in four extremities. An electrocardiogram revealed supraventricular tachycardia and ST depression on precordial V2-6 derivations. An acute coronary syndrome diagnosis made based on anginal symptoms, supraventricular tachycardia, ST depression on V2-6 derivations and elevated cardiac enzymes. Urgent coronary angiography was normal except a 30% narrowing in LAD. She had recurrent nephrolithiasis and had operated because of hydronephrosis. She had two episodes of fatigue and walking disability previously. Hyperchloremic metabolic acidosis with normal anion gap determined in blood gas analyze. Patient diagnosed with type I RTA with the signs and symptoms of recurrent nephrolithiasis, fatigue, severe hypokalemia (1.8 mmol/L), hyperchloremic metabolic acidosis with normal anionic gap, alkaline urine (pH 8) and positive urinary anionic gap (13.7 mmol/L). Sodium bicarbonate infusion and potassium replacement therapy administered. Clinical and laboratory signs of the patient dissolved during treatment. Conclusion: Type 1 RTA should be considered in acidotic patients admitted with hypokalemia and coronary symptoms. Urinary and blood gas analyses should be done beside cardiac tests initially. Therefore, a precise diagnosis may be possible without the possible complications of unnecessary coronary interventions.

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“…4 However, the urinary anion gap has been shown to be poorly correlated with urine ammonium concentration. 5,6 While the urine osmolar gap has shown a statistical correlation with ammonium concentration, 5,6 the agreement is poor in many individual cases, 5 making this method of estimating urinary ammonium unreliable in the clinical setting.…”

Section: Introductionmentioning

confidence: 99%

Direct urine ammonium measurement: time to discard urine anion and osmolar gaps

Chiu

Davidson

2012

Ann Clin Biochem

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Background: A failure of urine ammonium to increase during acidosis indicates impaired renal acidification, and the urinary ammonium concentration is therefore a useful investigation in determining the cause of a metabolic acidosis. However, urine ammonium measurements are not widely available in routine diagnostic laboratories. This has led to the use of urine anion or osmolar gaps, which are unsatisfactory as surrogates for urine ammonium measurement. Methods: We evaluated the adaptation of two widely available automated plasma ammonium assays for measurement of urinary ammonium. Results: Both assays showed good recovery and linearity in urine samples spiked with ammonium chloride, and acceptable precision. Urine ammonium concentrations estimated from urinary anion and osmolar gaps showed poor agreement with measured urine ammonium concentrations. Conclusions: Direct urine ammonium measurements are easily performed with modern autoanalysers by simple adaptation of routine plasma ammonium assays. The use of urine anion and osmolar gaps should be abandoned where direct measurement is available.

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Urine electrolytes and the urine anion and osmolar gaps

Cited by 50 publications

References 13 publications

Drug-induced acid-base disorders

Drug-induced acid-base disorders

A distal (type 1) renal tubular acidosis case that mimic coronary ischemia

Direct urine ammonium measurement: time to discard urine anion and osmolar gaps

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