Objective：To explore the association of urine acidification function in patients with diabetic kidney disease（DKD）. Methods：A total of 42 DKD patients diagnosed by renal biopsy presenting to the first affiliated hospital of NMU from January 2015 to March 2017 were recruited. The prevalence of different kinds of renal tubular injury was analyzed by acidification function. In addition，urine acidification function of different stages，the correlation of urine pH levels and clinical parameters were compared. Results：Patients with DKD often had dysfunction in acidification of the tubules，of which the most common was dysfunction of the distal tubules in the secretion of ammonium，followed by dysfunction of the distal tubules in the secretion of hydrogen，and the least common was the reabsorption of bicarbonate dysfunction in the proximal tubules. The prevalence of the distal tubules dysfunction in the secretion of ammonium showed an increasing trend in different pathological stages（P=0.007）. Patients with re-absorption of bicarbonate dysfunction in DKD patients had higher parathormone levels（P < 0.05）. Differences in 24-hour urinary protein and hemoglobin levels between patients with and without distal tubules of hydrogenation dysfunction were observed（P < 0.05）. The levels of hemoglobin were significantly different between patients with or without ammonium secretion dysfunction in the distal tubules（P < 0.05）. Fasting urine pH was positively correlated with 24-h urinary protein level and negatively correlated with serum albumin. Especially when the urinary protein was higher than 3.5 g/d，there was a good linear correlation between urinary protein quantification and urine pH. Conclusion：The most common dysfunction of tubular acidification in patients with DKD was ammonium secretion in the distal tubules. Patients with titer acid anemia had lower hemoglobin levels and higher urinary protein levels than patients in the titer acid normal group. The increase of fasting urine pH in DKD patients may be related to 24-h urinary protein.