Impact of glucose load in an oral glucose tolerance test on urinary albumin excretion varies with 2‐h glucose levels

Abstract Background The aim of the present study was to investigate whether an oral glucose load can induce an increase in urinary albumin excretion ( UAE ). Methods One hundred and thirty subjects without macroalbuminuria or increased fasting serum glucose (≥7.0 mmol/L) were included in the study. At 0600 hours, subjects were asked to empty their bladder and drink 300 mL water. At 0800 hours, venous blood and 2‐h urine were collected for fasting examination. Subjects were then asked to drink 300 mL solution containing 75 g glucose and, at 1000 hours, samples were collected again for post‐challenge examination. Concentrations of serum glucose, urinary glucose, albumin, N ‐acetyl‐ β ‐ D ‐glucosaminidase and retinol‐binding protein were measured. Results Based on the results of the oral glucose tolerance test, subjects were divided into three groups: (i) normal glucose tolerance ( NGT ; n  = 55); (ii) impaired glucose tolerance ( IGT ; n  = 39); and (iii) newly diagnosed diabetes mellitus ( NDM ; n  = 36). In the NDM group, post‐challenge urinary excretion of glucose and albumin was 14‐ and 1.6‐fold greater than fasting values, respectively. In the IGT and NGT groups, although post‐challenge urinary glucose excretion was 2.6‐ and 1.6‐fold greater than fasting values, UAE did not increase. There was a positive correlation between post‐challenge serum glucose and the UAE rate ( UAER ; r  = 0.24, P <  0.01) and the UAER increment (Δ UAER ; r  = 0.19, P <  0.05), as well as between the serum glucose increment and post‐challenge UAER ( r  = 0.23, P <  0.01) and Δ UAER ( r  = 0.18, P <  0.05). Post‐challenge serum glucose levels were independently correlated with logarithmically converted post‐challenge UAER ( β  = 0.322, P  = 0.008). Conclusions Oral glucose load can induce a significant increase in UAE in NDM subjects. The main mechanism may be glomerular hyperfiltration.