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Neutrophil Gelatinase‐Associated Lipocalin (NGAL) and Kidney Injury Molecule 1 (KIM1) in patients with diabetic nephropathy: a cross‐sectional study and the effects of lisinopril
Author(s) -
Nielsen S. E.,
Schjoedt K. J.,
Astrup A. S.,
Tarnow L.,
Lajer M.,
Hansen P. R.,
Parving H.H.,
Rossing P.
Publication year - 2010
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.2010.03083.x
Subject(s) - medicine , diabetic nephropathy , albuminuria , lipocalin , urine , lisinopril , microalbuminuria , nephropathy , urology , renal function , kidney disease , diabetes mellitus , endocrinology , gastroenterology , kidney , angiotensin converting enzyme , blood pressure
Diabet. Med. 27, 1144–1150 (2010) Abstract Aims Our aim was to evaluate the markers of tubulointerstitial damage, neutrophil gelatinase‐associated lipocalin (NGAL) and kidney injury molecule 1 (KIM1) in Type 1 diabetic patients with different levels of albuminuria and in control subjects. In addition, the effect of renoprotective treatment on urinary NGAL was evaluated in diabetic nephropathy. Methods This was a cross‐sectional study in 58 normoalbuminuric (u‐albumin < 30mg/24 h), 45 microalbuminuric (30–300 mg/24 h) and 45 macroalbuminuric (> 300 mg/24 h) Type 1 diabetic patients and 55 non‐diabetic control subjects. Furthermore, in a second study, urine‐NGAL was measured in a randomized cross‐over study of 56 Type 1 diabetic patients with diabetic nephropathy treated with lisinopril 20, 40 and 60 mg daily. Results Urine‐NGAL levels were [geometric mean (95% CI)]: control subjects 74 (52–104) (pg/mmol creatinine), normoalbuminuric 146 (97–221), microalbuminuric 222 (158–312) and macroalbuminuric group 261 (175–390). Urine‐NGAL increased significantly from the normo‐ to the micro‐ and further to the macroalbuminuric group ( P < 0.05). Urine‐NGAL was higher in normoalbuminuric vs. control subjects ( P < 0.01). Plasma‐NGAL was significantly higher in the normoalbuminuric and macroalbuminuric groups than in the control group. Urine‐KIM1 was higher in all diabetic groups than in the control group ( P < 0.001), with no difference between diabetic groups. During lisinopril treatment, urine‐NGAL was reduced (95% CI) 17% (11–50) (not significant). Conclusions Urine‐NGAL and urine‐KIM1 (u‐KIM1) are elevated in Type 1 diabetic patients, with or without albuminuria, indicating tubular damage at an early stage. Urine‐NGAL increases significantly with increasing albuminuria. The ACE inhibitor lisinopril reduced urine‐NGAL, but this was not statistically significant.