American journal of kidney diseases : the official journal of the National Kidney Foundation
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To investigate the clinical significance of urine anion gap and urine osmolal gap as indirect markers of urine acidification in chronic metabolic acidosis, we evaluated urine ammonium (NH4+), net acid excretion (NAE), urine anion gap (Na(+) + K(+) - Cl-), and urine osmolal gap (urine osmolality - [2(Na(+) + K(+)) + urea]) in 24 patients with chronic renal failure (CRF), eight patients with classic distal renal tubular acidosis (dRTA), and eight NH4Cl-loaded normal controls (NCs). Urine NH4+ excretion was lower (P < 0.001) in the CRF (5.4 +/- 0.6 mmol/d) and dRTA (19.2 +/- 2.7 mmol/d) patients than in the NCs (52.6 +/- 3.7 mmol/d); NAE was also lower (P < 0.001) in the CRF (9.8 +/- 1.6 mmol/d) and dRTA (16.7 +/- 4.7 mmol/d) patients than in the NCs (79.4 +/- 4.7 mmol/d). ⋯ When the data from all subjects were pooled, urine anion gap correlated inversely with urine NH4+ (r = -0.70, P < 0.001) and with NAE (r = -0.83, P < 0.001), and urine osmolal gap correlated positively with urine NH4+ (r = 0.69, P < 0.01) and with NAE (r = 0.71, P < 0.05). We conclude that impaired urine acidification in CRF and dRTA patients is associated with an increase in urine anion gap and a decrease in urine osmolal gap, and that both urine anion gap and urine osmolal gap correlate well with NAE as well as with urine NH4+.
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Case Reports
Acute renal failure associated with the retinoic acid syndrome in acute promyelocytic leukemia.
All-trans-retinoic acid is an effective agent to induce remission in patients with acute promyelocytic leukemia (APL). Unlike conventional chemotherapy, this drug exerts its effect by inducing differentiation of immature leukemic cells. ⋯ We describe a patient with APL in whom acute renal failure developed during treatment with all-trans-retinoic acid. Transient renal enlargement during a period of leukocytosis and a beneficial response to treatment with dexamethasone suggest that renal failure in this patient was probably related to the retinoic acid syndrome.
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Ethylene glycol poisoning classically presents as a metabolic acidosis with an increased anion gap. Metabolism of ethylene glycol to organic acids, and increased production of lactate, are responsible for the increased gap. We report the case of an alcohol user who consumed ethanol and ethylene glycol concurrently, and presented without acidosis, with a normal anion gap. ⋯ An increased osmolal gap, not accounted for by the serum ethanol level, proved to be an important clue to the diagnosis. In this patient, ingestion of ethanol inhibited the hepatic metabolism of ethylene glycol to organic acids, obscuring the diagnosis. In intoxicated alcohol users, even in the absence of metabolic acidosis, serum osmolality measurements and calculation of the osmolal gap may facilitate the rapid diagnosis of ethylene glycol poisoning.