Houser M T, Milner L S
Department of Pediatrics, University of Nebraska Medical Center, Omaha.
Nephron. 1991;58(4):461-5. doi: 10.1159/000186480.
Competitive inhibition of renal tubular transport occurs between low- and high-molecular-weight proteins following intravenous infusion, but this relationship is less clear following de novo glomerular or renal tubular injury. The present study evaluated renal lysozyme and albumin handling following renal tubular injury induced by both low- and high-dose mercuric chloride (0.5 and 2.0 mg/kg) and maleic acid (50 and 400 mg/kg), and following glomerular injury induced by puromycin aminonucleoside (5 mg/100 g) or Adriamycin (5 mg/kg). Subtle renal tubular injury induced only mild isolated albuminuria, while severe tubular injury caused dramatic lysozymuria and moderate albuminuria. However, increased filtration of albumin in these models of glomerular injury did not inhibit lysozyme transport.
静脉输注后,低分子量和高分子量蛋白质之间会发生肾小管转运的竞争性抑制,但在原发性肾小球或肾小管损伤后,这种关系不太明确。本研究评估了低剂量和高剂量氯化汞(0.5和2.0mg/kg)及马来酸(50和400mg/kg)诱导肾小管损伤后,以及嘌呤霉素氨基核苷(5mg/100g)或阿霉素(5mg/kg)诱导肾小球损伤后肾脏溶菌酶和白蛋白的处理情况。轻微的肾小管损伤仅导致轻度孤立性蛋白尿,而严重的肾小管损伤则导致显著的溶菌酶尿和中度蛋白尿。然而,在这些肾小球损伤模型中白蛋白滤过增加并未抑制溶菌酶转运。