Reversible microproteinuria induced by L-aspartate infusion.
Infusion of an acidic amino acid, L-aspartate, to 10 volunteers resulted in transient, significant increases in urinary excretion of the major urinary trypsin inhibitor (p less than 0.002) and beta 2-microglobulin (p less than 0.02). Simultaneously with the proteinuria, urinary pH rose significantly (p less than 0.02). These changes appeared following the infusion and after the excretion of L-aspartate had reached the preinfusion level. Albumin excretion was unchanged indicating that the proteinuria was due to a decreased tubular reabsorption. The mechanism for the reversible tubular proteinuria is unknown. A simple pH effect due to alkalization of the urine was excluded, as NaHCO3 infusion was not followed by an increase in the excretion of the major urinary trypsin inhibitor and beta 2-microglobulin.
Odum
L
L
Department of Clinical Chemistry, Rigshospitalet, Copenhagen, Denmark.
Hansen-Nord
G
G
Nielsen
C A
CA
D000328:Adult; D000419:Albuminuria / Q000652:urine; D001120:Arginine / Q000652:urine; D001224:Aspartic Acid / Q000008:administration & dosage / Q000009:adverse effects*; D001639:Bicarbonates / Q000494:pharmacology; D005260:Female; D006023:Glycoproteins / Q000652:urine; D006801:Humans; D007262:Infusions, Intravenous; D007687:Kidney Tubules, Proximal / Q000378:metabolism; D008297:Male; D011507:Proteinuria / Q000139:chemically induced*; D012964:Sodium / Q000494:pharmacology; D017693:Sodium Bicarbonate; D001613:beta 2-Microglobulin / Q000652:urine
D001639:Bicarbonates; D006023:Glycoproteins; D001613:beta 2-Microglobulin; D001224:Aspartic Acid; D017693:Sodium Bicarbonate; D001120:Arginine; D012964:Sodium; C028665:urinastatin