title: Renal tubular dysfunction in chronic alcohol abuse--effects of abstinence.
abstract: BACKGROUND
  Alcohol abuse may be accompanied by a variety of disorders of electrolyte and acid-base metabolism. The role of the kidney in the pathogenesis of these disturbances is obscure. We sought to evaluate the alcohol-induced abnormalities of renal function and improvement during abstinence and to assess the relation between renal dysfunction and electrolyte and acid-base disorders.
  
  
  METHODS
  We measured biochemical constituents of blood and renal function before and after four weeks of abstinence in 61 patients with chronic alcoholism who had little or no liver disease.
  
  
  RESULTS
  On admission, 18 patients (30 percent) had hypophosphatemia and hypomagnesemia, 13 patients (21 percent) had hypocalcemia, and 8 patients (13 percent) had hypokalemia. Twenty-two patients (36 percent) had a variety of simple and mixed acid-base disorders. Twenty of these patients had metabolic acidosis, and among them, 80 percent had alcoholic acidosis. A wide range of defects in renal tubular function, with normal glomerular filtration rate, were detected in these patients. The defects included decreases in the threshold and maximal reabsorptive ability for glucose (38 percent of patients) and in the renal threshold for phosphate excretion (36 percent); increases in the fractional excretion of beta 2-microglobulin (38 percent), uric acid (12 percent), calcium (23 percent), and magnesium (21 percent); and aminoaciduria (38 percent). Seventeen patients (28 percent) had a defect in tubular acidification, and five an impairment in urinary concentrating ability. Urinary excretion of N-acetyl-beta-D-glucosaminidase and alanine aminopeptidase were increased in 41 and 34 percent of patients, respectively. The abnormalities of blood chemistry and renal tubular function disappeared after four weeks of abstinence.
  
  
  CONCLUSIONS
  Transient defects in renal tubular function are common in patients with chronic alcoholism and may contribute to their abnormalities of serum electrolyte and blood acid-base profiles.
authors.affiliation: Department of Internal Medicine, University of Udine Medical School, Italy.
authors.forename: S
authors.initials: S
authors.lastname: De Marchi
authors.forename: E
authors.initials: E
authors.lastname: Cecchin
authors.forename: A
authors.initials: A
authors.lastname: Basile
authors.forename: A
authors.initials: A
authors.lastname: Bertotti
authors.forename: R
authors.initials: R
authors.lastname: Nardini
authors.forename: E
authors.initials: E
authors.lastname: Bartoli
mesh_terms: D000137:Acid-Base Imbalance / Q000209:etiology; D000328:Adult; D000428:Alcohol Drinking; D000437:Alcoholism / Q000150:complications*; D005260:Female; D005919:Glomerular Filtration Rate; D006728:Hormones / Q000097:blood; D006801:Humans; D017674:Hypophosphatemia / Q000209:etiology; D007684:Kidney Tubules / Q000503:physiopathology*; D008274:Magnesium / Q000097:blood; D008297:Male; D008875:Middle Aged; D009752:Nutritional Status; D012044:Regression Analysis; D013695:Temperance; D014883:Water-Electrolyte Imbalance / Q000097:blood / Q000209:etiology* / Q000503:physiopathology
chemical_list: D006728:Hormones; D008274:Magnesium