Normal Anion Gap Acidosis Research Articles

Ethylene glycol poisoning with a normal anion gap due to occult bromide intoxication

Ethylene glycol poisoning causes metabolic acidosis with an increased anion gap, due to production of organic acid anions during its metabolism. Bromide poisoning may cause a spuriously decreased anion gap when chloride determination is performed with a colorimetric technique. A 39-year-old woman with ethylene glycol poisoning presented in coma, with a hyperchloremic normal anion gap acidosis. The serum bromide level was found to be in the toxic range, confirming the diagnosis of bromide poisoning. Hemodialytic therapy resulted in resolution of electrolyte and acid-base abnormalities, and restoration of a normal state of consciousness. In this patient, clinically occult bromide intoxication caused a spurious lowering of the anion gap, normalizing what was in reality an increased anion gap due to ethylene glycol poisoning.

Effects of extreme hyperinsulinaemia on serum levels of trace metals, trace metal binding proteins, and electrolytes in normal females.

In order to assess the possible effects of insulin on serum concentrations of trace metals (iron, copper, zinc) and trace metal binding proteins (ferritin, transferrin, coeruloplasmin), five normal females were studied with the hyperinsulinaemic-euglycaemic clamp technique. A 0.1 U/kg insulin bolus was administered, followed by an insulin infusion at a rate of 10 mU/kg/min for 12-16 h. Insulin levels of 1500-2000 microU/ml (9.21-12.28 nmol/l) were attained. When iron levels in serum were assayed colorimetrically, there appeared to be a progressive rise in the mean concentration during the course of the insulin infusion. Direct analysis of serum samples by atomic absorption spectrophotometry also showed that the level of non-haeme iron increased 3-fold in the serum of the subject with the lowest concentration of this metal at the start of the study. In contrast with the results for serum iron, the levels of ferritin, total iron binding capacity (transferrin), zinc, copper and coeruloplasmin were not altered in any subject during the insulin infusion or at 24 h following discontinuation of the infusion. Within 4 h of institution of the hyperinsulinaemic clamp significant reductions in serum levels of potassium, phosphorus, cholesterol, total protein and albumin were noted. As the insulin infusion progressed, the urea nitrogen, uric acid and bicarbonate levels fell as well. These observations suggest that supraphysiologic hyperinsulinaemia of 12-16 h duration may alter serum levels of iron, but not serum levels of zinc, copper or trace metal binding proteins in some individuals.(ABSTRACT TRUNCATED AT 250 WORDS)

Severe Hyperkalemia During Piroxicam Therapy

Severe hyperkalemia developed in an 85-year-old man after he had been receiving piroxicam treatment for several months. At admission his serum potassium level was 9.3 mEq/L; total CO2 level, 11 mmole/L; chloride level, 122 mEq/L; serum urea nitrogen level, 54 mg/dL; and creatinine level, 2.5 mg/dL. Hyperkalemia resolved after withdrawal of the drug and polystyrene sodium sulfonate therapy and the nonanion gap acidosis subsided concomitantly. His serum urea nitrogen and creatinine levels remained unchanged. He had abnormally low plasma renin activity, which gradually returned to normal, and aldosterone concentration, which remained low. The nonsteroidal drug may have impaired renin secretion, adrenal responsiveness to angiotensin, or the action of aldosterone on the renal tubule.

Hyporeninemic Hypoaldosteronism in a Patient With Multiple Myeloma

A patient with progressive renal failure due to multiple myeloma presented with a mixed acid-base disorder (non-anion gap acidosis and respiratory alkalosis) with persistent severe hyperkalemia. Studies revealed an intact ability to lower urine pH during acid loading, markedly decreased plasma renin and aldosterone concentrations despite volume depletion, and an inappropriately low fractional excretion of potassium. Renal biopsy demonstrated plasma cell infiltration of the renal interstitium and typical proteinaceous intratubular casts. Both proximal and distal renal tubular acidification defects have been described previously in patients with multiple myeloma, but this is the first report of hyporeninemic hypoaldosteronism, hyperkalemia, and hyperchloremic metabolic acidosis in association with renal involvement in multiple myeloma.

8Drug and chemical-induced metabolic acidosis

Metabolic acidosis produced by drugs and/or chemicals can be conveniently divided into those with an increase in the anion gap (anion gap = Na- (Cl + HCO3)) and those with a normal anion gap. The increase in the anion gap is due to the accumulation of unmeasured organic anions, such as lactate or acetoacetate and beta-hydroxybutyrate, as occurs in ketoacidosis and lactic acidosis, or the accumulation of toxic anions such as formate or glycolate, as occurs with the ingestion of methanol or ethylene glycol. Increased concentrations of lactic acid may also be present in the toxic forms of metabolic acidosis. The most common drugs and chemicals that induce the anion gap type of acidosis are biguanides, alcohols, polyhydric sugars, salicylates, cyanide and carbon monoxide. In normal anion gap acidosis the reduction in bicarbonate is balanced by a reciprocal increase in the chloride concentration so that the sum of the two remains unchanged. Normal anion gap acidosis is caused by carbonic anhydrase inhibitors, hydrochloride salts of amino acids, toluene, amphotericin, spironolactone and non-steroidal anti-inflammatory drugs. The mechanism by which these substances produce metabolic acidosis and the therapy are discussed.