Abstract
Creatinine (Cr) is the end product of guanidinoacetic acid (GAA) -creatine metabolism, an essential energy source for muscle and nerve tissue. GAA is produced mainly by the kidney. Previously, we reported that the serum concentration and urinary excretion of GAA were decreased in patients with chronic renal failure, especially in diabetic nephropathy.
In this study, we evaluated the urinary excretion of Cr (U-Cr) during the progression of renal failure in 48 noninsulin dependent diabetic patients. Hemodialysis therapy was required for only about 2 years from the early stage of renal impairment (serum Cr=2mg/dl). In this study, body weight (BW) and U-Cr were significantly decreased (57.3±10.6→51.0±11.2kg and 664±208→551±201mg/day). U-Cr of diabetic patients was also significantly lower than that (739±311mg/day) of patients with chronic glomerulonephritis (CGN) at the initiation of hemodialysis therapy. U-Cr/BW of diabetic patients (10.8mg/kg) was significantly lower than that of CGN patients (14.0mg/kg).
These data showed that the lean body mass rapidly decreased in the short course of renal failure and suggested that the deterioration of GAA production in addition to lean body mass might cause the decrease in urinary Cr excretion in diabetic patients.
