Blood Sugar Control Reverses the Increase in Urinary Excretion of Prostaglandin D Synthase in Diabetic Patients

• Published in: Nephron Vol. 92; no. 1; pp. 77 - 85
• Main Authors: Hamano, Kumiko, Totsuka, Yasuo, Ajima, Miho, Gomi, Tomoko, Ikeda, Toshio, Hirawa, Nobuhito, Eguchi, Yutaka, Yamakado, Minoru, Takagi, Masao, Nakajima, Hiroshi, Oda, Hiroshi, Seiki, Kousuke, Eguchi, Naomi, Urade, Yoshihiro, Uehara, Yoshio
• Format: Journal Article
• Language: English
• Published: Basel, Switzerland S. Karger AG 01.09.2002
• Subjects: Adult; Aged; Albuminuria - blood; Albuminuria - urine; Blood Glucose - metabolism; Diabetes Mellitus, Type 2 - blood; Diabetes Mellitus, Type 2 - urine; Female; Humans; Hyperglycemia - blood; Hyperglycemia - urine; Immunohistochemistry; Intramolecular Oxidoreductases - blood; Intramolecular Oxidoreductases - urine; Kidney - enzymology; Lipocalins; Male; Middle Aged; Original Paper; Predictive Value of Tests; Prostaglandin D synthase; Diabetic nephropathy; Microalbuminuria; Proteinuria
• ISSN: 1660-8151; 2235-3186
• DOI: 10.1159/000064473

Background/Aims: We investigated basal levels of serum and urinary lipocalin-type prostaglandin D synthase/β-trace (L-PGDS) in type-2 diabetic patients and explored whether glycemic control affects L-PGDS status in another 55 diabetic inpatients with normoalbuminuria. Methods: Fifty-five type-2 diabetic outpatients (HbA1c, 9.14 ± 0.20%; creatinine (Cr), 85.1 ± 2.4 µmol/l), and 55 age-matched healthy control subjects were recruited. Serum and urinary levels of L-PGDS were determined with respect to the stage of diabetic nephropathy. The L-PGDS was localized by immunohistochemistry. Results: The urinary L-PGDS index increased in diabetic patients, compared with the controls (234.8 ± 27.4 vs. 73.8 ± 7.8 µg/mmol Cr, p < 0.001). Even in normoalbuminuric patients as well as in microalbuminuric patients, urinary L-PGDS indexes were higher than the controls (166.0 ± 21.1, p < 0.0001 and 338.6 ± 62.5 µg/mmol Cr, p < 0.0001, respectively), although the serum L-PGDS level was equal to that in the control subjects. Multiple regression analysis revealed that the urinary L-PGDS index was predicted solely by glucose levels and type-IV collagen index, whereas the serum L-PGDS was determined mainly by age and serum Cr. Glycemic control reduced the urinary L-PGDS index towards the normal range in diabetic patients with normoalbuminuria (172.3 ± 6.6 vs. 118.1 ± 2.6 (SE) µg/mmol Cr, p < 0.0001). Immunohistochemistry showed that L-PGDS was uniquely present in the renal tubules in diabetes while in nondiabetics, L-PGDS occurred solely in the peritubular interstitium, not in the tubular cells. Conclusion: Inadequate glycemic control is responsible for urinary L-PGDS excretion in the diabetic patients. Urinary L-PGDS is useful to predict subclinical renal injury associated with type-2 diabetes.