Man S. Oh

The anion gap.

The anion gap can be readily calculated from routine laboratory data, and although it has its widest application in the diagnosis of various forms of metabolic acidosis,1 , 2 it may sometimes provide an important clue to the diagnosis of disorders such as multiple myeloma3 4 5 or bromide intoxication.6 However, the concept of the anion gap is often misunderstood and misapplied. The purpose of this communication is to discuss in some detail the concept of the anion gap, the implications of abnormalities of the anion gap and, finally, its application to the differential diagnosis of metabolic acidosis. Concept of the Anion Gap The .xa0.xa0.

D-Lactic Acidosis: A Review of Clinical Presentation, Biochemical Features, and Pathophysiologic Mechanisms

This report describes a case of d-lactic acidosis observed by the authors and then reviews all case reports of d-lactic acidosis in the literature in order to define its clinical and biochemical features and pathogenetic mechanisms. The report also reviews the literature on metabolism of d-lactic acid in humans. The clinical presentation of d-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis. The diagnosis should be considered in a patient who presents with metabolic acidosis and high serum anion gap, normal lactate level, negative Acetest, short bowel syndrome or other forms of malabsorption, and characteristic neurologic findings. Development of the syndrome requires the following conditions 1) carbohydrate malabsorption with increased delivery of nutrients to the colon, 2) colonic bacterial flora of a type that produces d-lactic acid, 3) ingestion of large amounts of carbohydrate, 4) diminished colonic motility, allowing time for nutrients in the colon to undergo bacterial fermentation, and 5) impaired d-lactate metabolism. In contrast to the initial assumption that d-lactic acid is not metabolized by humans, analysis of published data shows a substantial rate of metabolism of d-lactate by normal humans. Estimates based on these data suggest that impaired metabolism of d-lactate is almost a prerequisite for the development of the syndrome.

The First Kidney Stone

The proper approach to diagnosis and management in patients with a first episode of a calcium-containing kidney stone is controversial, and we have reviewed the literature in a search for objective information. Six large retrospective studies show the natural cumulative recurrence rate of renal stones to be 14% at 1 year, 35% at 5 years, and 52% at 10 years. Randomized studies of the use of either thiazides or allopurinol suggest a modest beneficial effect of about 35% over placebo. Considering that the risk of this specific therapy is about 5%, the morbidity associated with renal stones is limited, and relatively less invasive procedures can often replace nephrolithotomy, we conclude that use of specific drug therapy, namely thiazides or allopurinol, is not warranted in patients with a first kidney stone and, therefore, that extensive metabolic evaluation is unnecessary.

D-lactic acidosis in a man with the short-bowel syndrome.

WE have recently studied a patient who had short-bowel syndrome that presented with peculiar neurologic manifestations and severe metabolic acidosis. The anion gap was increased, but the identity o...

A mechanism for hyporeninemic hypoaldosteronism in chronic renal disease

Abstract Selective aldosterone deficiency in chronic renal disease has been attributed to damage to the renin-producing mechanism. Four patients with selective aldosterone deficiency and chronic renal diseases were studied. These patients had hypertension, increased extracellular fluid volume, and increased total exchangeable sodium, unlikely concomitants of a clinical syndrome in which primary reduction in angiotensin generation led to deficient aldosterone secretion. In two patients who were treated with furosemide to produce sustained diminution in extracellular fluid volume, the gradual increase in plasma renin activity and plasma aldosterone indicated that physiologic suppression, not disease-induced damage, had been preventing elaboration of renin by juxtaglomerular apparatus. Salt and water retention associated with renal disease is proposed as the initial physiologic aberration.

Hyperchloremic Acidosis During the Recovery Phase of Diabetic Ketosis

We have studied 35 patients to find the occurrence of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. At admission the patients had typical normochloremic acidosis, with increased anion gap exactly balancing decreased serum bicarbonate. In contrast, in 18 patients with phenformin-induced lactic acidosis, the increase in anion gap at admission was much greater than the decrease in bicarbonate. The difference between lactic acidosis and ketoacidosis may be explained by a slower rate of excretion of lactate than of ketone anions. After the patients with ketoacidosis were treated, the acidosis became predominantly hyperchloremic with normal anion gap. Failure to normalize serum bicarbonate is attributed to excretion of ketone anions in the urine.

Disorders of sodium metabolism: hypernatremia and hyponatremia.

ObjectiveDiscussion of abnormal plasma sodium concentrations with an emphasis on the pathogenesis, diagnosis, and treatment. Data SourcesRelevant literature in the English language and the authors clinical experience. Study SelectionNo special study has been carried out for the present discussion. Data ExtractionThe information from the literature and the data from the authors clinical experience have been used to illustrate important points in the discussion. Data SynthesisA most important aspect in the approach to hypernatremia is determination of the mechanism responsible for impaired water intake. Various mechanisms of abnormal water loss can be determined from measurement of urine osmolality. Hypernatremia is treated by water replacement and measures to reduce abnormal water loss. In most instances, hyponatremia is caused by inappropriate concentration of urine because of either appropriate or inappropriate antidiuretic hormone secretion. The determination of appropriateness of antidiuretic hormone secretion requires the assessment of effective arterial volume. Treatment depends on the pathogenetic mechanism. ConclusionsAbnormal plasma sodium concentration results from abnormal water intake or water output. Treatment is guided by determining the pathogenetic mechanism. (Crit Care Med 1992; 20:94)

The Mechanism of Hyperchloremic Acidosis During the Recovery Phase of Diabetic Ketoacidosis

To determine the mechanism of hyperchloremic acidosis during recovery from diabetic ketoacidosis (DKA), serial measurements were made in eight patients of serum and urinary electrolytes and organic acids, and of urinary net acid. On admission, the average decrease in serum total CO2 was 17.5 mmol/L, corresponding to the excess anion gap, 18.5 meq/L, and the serum organic acids, 17.1 meq/L. With the treatment, the anion gap and organic acids decreased by 16.1 and 14.7 meq/L, respectively, but the serum CO2 increased only by 8.4 mmol/L; serum electrolyte balance was maintained by increase in chloride concentration. Fluid retention was insufficient to explain the disparity between the increase in CO2 and the decrease in organic acids. Renal loss of bicarbonate precursors during treatment was modest and was exceeded by renal bicarbonate production. The disparity between the increase in serum CO2 and the decrease in organic acids during treatment of DKA may be explained to a large extent by a difference in volume of distribution between bicarbonate and organic anions The renal loss of ketone anions before admission, however, is ultimately responsible for the persistence of substantial metabolic acidosis.

Opinion: What Unique Acid-Base Considerations Exist in Dialysis Patients?: Acid-Base Considerations

Address correspondence to: Man S. Oh, MD, Department of Medicine, SUNY, Downstate Medical Center, Brooklyn, NY 11203, or e-mail: man.oh@downstate.edu. Because a typical modern diet results in net production of acid, and the kidney is normally the main organ responsible for generating alkali to maintain acid-base homeostasis, chronic metabolic acidosis is commonly observed in patients with chronic renal insufficiency. In this article we will deal with the clinical characteristics, pathophysiology, and therapeutic approach to this condition.