Renal tubular function modulates urinary levels of interleukin-6.
This study was designed to determine whether urinary excretion of IL-6 can be modified as a consequence of deterioration in renal tubular function. In patients with Kawasaki disease, IgA nephropathy and renal hypoplasia, IL-6 and beta 2-microglobulin were measured in the plasma and urine, and the excreted fractions of filtered IL-6 (FEIL-6) and beta 2-microglobulin (FE beta 2-microglobulin were calculated. Patients with renal hypoplasia had elevated FE beta 2-microglobulin which was associated with increased FEIL-6, and there was a significant relationship between these variables as the severity of renal hypoplasia increased. It was concluded that IL-6 in renal tubular fluid may be reabsorbed, catabolized as well as excreted by the renal tubule and that the level of urinary IL-6 excretion could be influenced not only by mesangial proliferation but also renal tubular dysfunction.
D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D002648:Child; D002675:Child, Preschool; D003404:Creatinine / Q000097:blood; D005922:Glomerulonephritis, IGA / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D015850:Interleukin-6 / Q000097:blood / Q000652:urine*; D007684:Kidney Tubules / Q000503:physiopathology*; D009080:Mucocutaneous Lymph Node Syndrome / Q000378:metabolism / Q000503:physiopathology; D012141:Respiratory Tract Infections / Q000378:metabolism / Q000503:physiopathology; D001613:beta 2-Microglobulin / Q000378:metabolism* / Q000652:urine
D015850:Interleukin-6; D001613:beta 2-Microglobulin; D003404:Creatinine