Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Diabetes Care |
| Vol/bind | 32 |
| Udgave nummer | 9 |
| Sider (fra-til) | 1684-1688 |
| Antal sider | 4 |
| ISSN | 0149-5992 |
| DOI | |
| Status | Udgivet - 2009 |
Bibliografisk note
Keywords: Adult; Albuminuria; Angiotensin-Converting Enzyme Inhibitors; Case-Control Studies; Creatinine; Cross-Sectional Studies; Diabetes Mellitus, Type 1; Diabetic Nephropathies; Fatty Acid-Binding Proteins; Female; Humans; Lisinopril; Male; Middle AgedAdgang til dokumentet
Citationsformater
- APA
- Standard
- Harvard
- Vancouver
- Author
- BIBTEX
- RIS
Tubular and glomerular injury in diabetes and the impact of ACE inhibition. / Nielsen, Stine E; Sugaya, Takeshi; Tarnow, Lise; Lajer, Maria; Schjoedt, Katrine J; Astrup, Anne Sofie; Baba, Tsuneharu; Parving, Hans-Henrik; Rossing, Peter.
I: Diabetes Care, Bind 32, Nr. 9, 2009, s. 1684-1688.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
}
TY - JOUR
T1 - Tubular and glomerular injury in diabetes and the impact of ACE inhibition
AU - Nielsen, Stine E
AU - Sugaya, Takeshi
AU - Tarnow, Lise
AU - Lajer, Maria
AU - Schjoedt, Katrine J
AU - Astrup, Anne Sofie
AU - Baba, Tsuneharu
AU - Parving, Hans-Henrik
AU - Rossing, Peter
N1 - Keywords: Adult; Albuminuria; Angiotensin-Converting Enzyme Inhibitors; Case-Control Studies; Creatinine; Cross-Sectional Studies; Diabetes Mellitus, Type 1; Diabetic Nephropathies; Fatty Acid-Binding Proteins; Female; Humans; Lisinopril; Male; Middle Aged
PY - 2009
Y1 - 2009
N2 - OBJECTIVE: We studied tubular and glomerular damage in type 1 diabetic patients by measuring urinary-liver fatty acid binding protein (U-LFABP) and albuminuria. Subsequently, we evaluated the effect of ACE inhibition on U-LFABP in patients with diabetic nephropathy. RESEARCH DESIGN AND METHODS: We studied Caucasians with type 1 diabetes: 58 with normoalbuminuria (urinary albumin <30 mg/24 h), 45 with persistent microalbuminuria (30-300 mg/24 h), and 45 with persistent macroalbuminuria (> or =300 mg/24 h). A control group consisted of 57 healthy individuals. The groups were matched by sex and duration of diabetes. In addition, U-LFABP was measured in 48 type 1 diabetic patients with diabetic nephropathy in a randomized crossover trial consisting of 2 months of treatment with 20, 40, and 60 mg lisinopril once daily in random order. RESULTS: In the cross-sectional study, levels of U-LFABP were significantly higher in normoalbuminuric patients versus those in the control group (median 2.6 [interquartile range 1.3-4.1] vs. 19 [0.8-3.0] microg/g creatinine, P = 0.02) and increased with increasing levels of albuminuria (microalbuminuric group 4.2 [1.8-8.3] microg/g creatinine and nephropathy group 71.2 [8.1-123.4], P < 0.05 for all comparisons). U-LFABP correlates with the urinary albumin-to-creatinine ratio (R(2) = 0.54, P < 0.001). In the intervention study, all doses of lisinopril significantly reduced urinary albumin excretion rate and U-LFABP from baseline. The reductions in U-LFABP were 43, 46, and 40% with increasing doses of lisinopril (NS). CONCLUSIONS: An early and progressive increase in tubulointerstitial damage as reflected by increased U-LFABP levels occurs in type 1 diabetic patients and is associated with albuminuria. Furthermore, ACE inhibition reduces the tubular and glomerular damage and dysfunction.
AB - OBJECTIVE: We studied tubular and glomerular damage in type 1 diabetic patients by measuring urinary-liver fatty acid binding protein (U-LFABP) and albuminuria. Subsequently, we evaluated the effect of ACE inhibition on U-LFABP in patients with diabetic nephropathy. RESEARCH DESIGN AND METHODS: We studied Caucasians with type 1 diabetes: 58 with normoalbuminuria (urinary albumin <30 mg/24 h), 45 with persistent microalbuminuria (30-300 mg/24 h), and 45 with persistent macroalbuminuria (> or =300 mg/24 h). A control group consisted of 57 healthy individuals. The groups were matched by sex and duration of diabetes. In addition, U-LFABP was measured in 48 type 1 diabetic patients with diabetic nephropathy in a randomized crossover trial consisting of 2 months of treatment with 20, 40, and 60 mg lisinopril once daily in random order. RESULTS: In the cross-sectional study, levels of U-LFABP were significantly higher in normoalbuminuric patients versus those in the control group (median 2.6 [interquartile range 1.3-4.1] vs. 19 [0.8-3.0] microg/g creatinine, P = 0.02) and increased with increasing levels of albuminuria (microalbuminuric group 4.2 [1.8-8.3] microg/g creatinine and nephropathy group 71.2 [8.1-123.4], P < 0.05 for all comparisons). U-LFABP correlates with the urinary albumin-to-creatinine ratio (R(2) = 0.54, P < 0.001). In the intervention study, all doses of lisinopril significantly reduced urinary albumin excretion rate and U-LFABP from baseline. The reductions in U-LFABP were 43, 46, and 40% with increasing doses of lisinopril (NS). CONCLUSIONS: An early and progressive increase in tubulointerstitial damage as reflected by increased U-LFABP levels occurs in type 1 diabetic patients and is associated with albuminuria. Furthermore, ACE inhibition reduces the tubular and glomerular damage and dysfunction.
U2 - 10.2337/dc09-0429
DO - 10.2337/dc09-0429
M3 - Journal article
C2 - 19502542
VL - 32
SP - 1684
EP - 1688
JO - Diabetes Care
JF - Diabetes Care
SN - 0149-5992
IS - 9
ER -