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Amadori‐albumin correlates with microvascular complications and precedes nephropathy in type 1 diabetic patients
Author(s) -
Schalkwijk C. G.,
Chaturvedi N.,
Twaafhoven H.,
Van Hinsbergh V. W. M.,
Stehouwer C. D. A.
Publication year - 2002
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2002.01011.x
Subject(s) - albumin , medicine , fibrinogen , diabetic nephropathy , nephropathy , microalbuminuria , endocrinology , amadori rearrangement , albuminuria , retinopathy , c reactive protein , excretion , diabetic retinopathy , renal function , diabetes mellitus , gastroenterology , glycation , inflammation
Background Amadori‐albumin, a major glycated protein, is involved in experimental hyperglycaemia‐induced microvascular complications, and is associated with advanced nephropathy in Type I diabetic patients in humans. Our aim was to assess the association of Amadori‐albumin with early nephropathy and with retinopathy in Type I diabetic patients and the involvement of chronic low‐degree inflammation therein. Design and Methods Amadori‐albumin, the Amadori product of haemoglobin (HbA1c), C‐reactive protein, and fibrinogen levels were measured in the EUCLID study, a 2‐year randomised, double‐blind, placebo‐controlled trial of lisinopril in 447 Type I diabetic patients. Retinal photographs were taken in 341 patients at baseline and 294 at follow up. Results Amadori‐albumin was positively associated with albumin the excretion rate and retinopathy status ( P =  0·0001 and P =  0·02 for trend, respectively) and with the progression from normoalbuminuria to (micro)albuminuria (38·6 U mL −1 in nonprogressors, 44·3 U mL −1 in progressors; P =  0·02), but not with the development or progression of retinopathy during a 2‐year follow up. Amadori‐albumin levels at baseline were associated with C‐reactive protein and fibrinogen ( P =  0·0007 and P =  0·0001, respectively). C‐reactive protein and fibrinogen were also associated with albumin excretion rates ( P =  0·03 and P =  0·01, respectively) and retinopathy status ( P =  0·02 and P =  0·0006, respectively). Adjustment for these inflammatory markers did not markedly attenuate the association between Amadori‐albumin and the albumin excretion rate, while adjustment for fibrinogen, but not C‐reactive protein, abolished the association between Amadori‐albumin and retinopathy. Lisinopril had no impact on the association between the levels of Amadori‐albumin and albumin excretion rates or retinopathy. Conclusions Amadori‐albumin was associated with early nephropathy and with retinopathy in Type I diabetic patients and preceded an increase in albumin excretion rate, but not retinopathy. A chronic low‐degree inflammation does not appear to be involved in Amadori‐albumin‐associated microvascular complications in Type I diabetes.

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