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At least 1,261 records · Page 70Linked to original sources
PubMed2005

Metformin lactic acidosis and anaesthesia: myth or reality?

AIMS: To determine whether a causal or coincidental relationship is indicated in the literature between metaformin and lactic acidosis and to recommend clinical guidelines for the withdrawal of metformin prior to surgery. METHOD: A broad review of the literature related to metformin associated acidosis was carried out. (There are few publications specifically related to metformin treatment and anaesthesiology). RESULTS: When metformin-associated lactic acidosis occurs, a concurrent pathology or contraindication to the use of metformin is often found. Anaesthesia and surgery can generate or aggravate concurrent pathologies. CONCLUSION: Although no association has been shown between metformin and lactic acidosis under usual conditions of use, vigilance is required when metformin is used prior to surgery. The following clinical guideline is proposed: to withdraw (when possible) metformin 48 hours prior to surgery and to wait until the patient's biological and clinical parameters return to normal before reintroducing it.

Acidosis, Lactic↗
PubMed1990

Glucose metabolism and the kidney.

Although the kidney both takes up and produces glucose, its net contribution to overall glucose homoeostasis is negligible since these two processes approximately counterbalance each other. Glucose uptake primarily occurs in the distal medullary segments of the nephron where the glycolytic enzymes are present in high concentration. The major metabolic fates of the glucose which is taken up by this region of the kidney are oxidation to carbon dioxide and conversion to lactate. In contrast, gluconeogenesis primarily occurs in the proximal tubular portion of the renal cortex where free fatty acids represent the major metabolic fuel which supplies the energy requirements of the cell. However, in certain conditions, including metabolic acidosis, prolonged fasting, and poorly controlled diabetes mellitus, renal gluconeogenesis can be enhanced markedly and a net output of glucose by the kidney is readily observed.

Animals↗
PubMedDate not supplied

Idiopathic Fanconi syndrome with progressive renal failure: a case report and discussion.

Fanconi syndrome is a complex of renal tubular dysfunctions defined by glycosuria without diabetes, aminoaciduria, phosphaturia, and renal tubular acidosis. It is often associated with hypokalemia, hypophosphatemia, and rickets or osteomalacia. Although it is usually found in the setting of other well-established non-renal diseases, Fanconi syndrome may present without identifiable etiology or association. Very infrequently a patient with idiopathic Fanconi syndrome will progress to chronic renal failure. This case report details the course of such a patient over the 20 years since his diagnosis and discusses the syndrome's genetic background, clinical features, putative pathophysiology, and therapeutic options, including transplantation.

Adult↗
PubMed1977

Lactic acidosis and ketoacidosis: biochemical and clinical implications.

A case of lactic acidosis presented the opportunity for review of the association between lactic acidosis and ketoacidosis. The diagnosis of lactic acidosis or the combination of lactic acidosis and ketoacidosis is established clinically by the detection of a metabolic acidosis of the "unmeasured anion gap" type in the absence of significant renal failure, poison intake or a strongly positive clinical test for ketones. Before treatment can be planned the biochemical basis of lactic acidosis and ketoacidosis must be understood -- especially the fact that lactic acidosis is not a single disease entity but has many possible causes. Among important considerations is the relation between the blood concentrations of bicarbonate and organic acid anions. After recovery from metabolic acidosis of the unmeasured anion gap type, metabolic alkalosis is common. Decreased bicarbonate excretion plays an important role in the pathogenesis of the latter and may be the result of potassium or chloride loss, or both. The deficits, if present, should be corrected with appropriate therapy.

Acidosis↗
PubMed1970

Hyperlactatemia.

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Acidosis↗