Urinary prostaglandin D synthase (beta-trace) excretion increases in the early stage of diabetes mellitus.
OBJECTIVE
Circulating levels of lipocalin-type prostaglandin D synthase (L-PGDS)/beta-trace reportedly increase in renal failure as well as in cardiovascular injuries. We investigated the alterations of L-PGDS in urine and plasma in the early stage of type-2 diabetic patients.


METHODS
Thirty-six type-2 diabetic patients and 29 normal subjects were studied. Overnight spot urine and plasma samples were obtained in the morning. L-PGDS was measured by ELISA method using anti-L-PGDS antibody. Variables indicating renal function were determined.


RESULTS
Plasma L-PGDS concentration was slightly higher in the patients with diabetes mellitus than in the control subjects, whereas the urinary L-PGDS excretion almost doubled in the diabetic patients as compared with that in the control subjects. Plasma L-PGDS was determined by plasma creatinine (Cr) concentration while urinary L-PGDS excretion was correlated solely with urinary protein excretion. There was no relationship between plasma L-PGDS concentration and urinary L-PGDS excretion. The averaged plasma concentration of L-PGDS in the diabetics with a normal Cr level in plasma, corresponding to that in the controls, was determined by the plasma Cr concentration. On the other hand, the urinary L-PGDS excretion was determined by the amount of proteinuria and greater in the diabetics with a normal Cr level in plasma than in the controls even when the patients exhibited urinary protein excretion equal to that in the control subjects.


CONCLUSIONS
Urinary L-PGDS excretion increased in the early stage of kidney injury in patients with type-2 diabetes mellitus. The urinary excretion was correlated independently with urinary protein excretion even when there was no difference in urinary protein or albumin excretions, thereby suggesting that urinary L-PGDS excretion is possibly a more sensitive indicator of renal injuries than proteinuria. Urinary L-PGDS may thus predict the progression of renal injuries in diabetic patients.
Hirawa
N
N
Health Service Center and Department of Medicine, University of Tokyo, Tokyo, Japan.
Uehara
Y
Y
Ikeda
T
T
Gomi
T
T
Hamano
K
K
Totsuka
Y
Y
Yamakado
M
M
Takagi
M
M
Eguchi
N
N
Oda
H
H
Seiki
K
K
Nakajima
H
H
Urade
Y
Y
D000704:Analysis of Variance; D015415:Biomarkers / Q000652:urine; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D003404:Creatinine / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000201:enzymology / Q000503:physiopathology / Q000652:urine*; D003928:Diabetic Nephropathies / Q000175:diagnosis / Q000503:physiopathology / Q000652:urine*; D004797:Enzyme-Linked Immunosorbent Assay; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D019746:Intramolecular Oxidoreductases / Q000097:blood / Q000652:urine*; D007677:Kidney Function Tests; D054834:Lipocalins; D008875:Middle Aged; D012016:Reference Values; D012044:Regression Analysis; D012680:Sensitivity and Specificity; D014280:Triglycerides / Q000097:blood
D015415:Biomarkers; D001786:Blood Glucose; D002784:Cholesterol; D003404:Creatinine; D006442:Glycated Hemoglobin; D019746:Intramolecular Oxidoreductases; D054834:Lipocalins; D014280:Triglycerides; C022466:prostaglandin R2 D-isomerase