Clinical validation of a second-generation fructosamine assay

Abstract The serum fructosamine assay, used to monitor short-term clinical glycemic control, reportedly has several technical drawbacks. However, technical improvements have resulted in a new second-generation assay of fructosamine. We evaluated this second-generation assay (from Roche Diagnostics) in 529 nondiabetic and diabetic patients and found a highly significant correlation with results of the first-generation assay (r = 0.91, P less than 0.001). Use of the second-generation assay with samples from patients classified on the basis of glycemic control according to their glycohemoglobin (GHb) values, enabled us to discriminate between the nondiabetics, diabetics with "good/moderate" control (i.e., GHb less than 10%), and diabetics with "poor" control (GHb greater than or equal to 10%). We evaluated the validity of the second-generation assay to assess short-term glycemic control in 23 non-insulin-dependent diabetic patients who participated for 10 weeks in an intensive intervention program designed to rapidly normalize the clinical glycemic profile. Results correlated significantly with the one-week average capillary blood glucose concentration (CBG) and with the three-week average CBG in all 23 patients. In addition, the second-generation fructosamine assay results demonstrated a significant decrease at each week of study, as did the average CBG. Results of the first- and second-generation assays correlated significantly at each week of study. GHb correlated significantly with both the second- (r = 0.78, P less than 0.001) and first-generation fructosamine assay results (r = 0.77, P less than 0.001) for the baseline blood samples of the intervention study, but this correlation decreased (to r = 0.35, P = 0.09 and r = 0.34, P = 0.09, respectively) by the conclusion of the study.

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Short-term Effect of Insulin and 5(3-Piridyl) Tetrazole on Serum Triglycerides in Insulin-dependent Diabetic Patients

Diabetes ◽

10.2337/diab.26.7.615 ◽

1977 ◽

Vol 26 (7) ◽

pp. 615-618

Author(s):

M. Alvarez-Reynolds ◽

J. M. Dominguez

Keyword(s):

Term Effect ◽

Diabetic Patients ◽

Short Term ◽

Serum Triglycerides ◽

Short Term Effect ◽

Insulin Dependent ◽

Insulin Dependent Diabetic

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Effect of Posture and Acute Glycaemic Control on the Excretion of Retinol-Binding Protein in Normoalbuminuric Insulin-Dependent Diabetic Patients

Clinical Science ◽

10.1042/cs0840461 ◽

1993 ◽

Vol 84 (4) ◽

pp. 461-467 ◽

Cited By ~ 14

Author(s):

Carlo Catalano ◽

Peter H. Winocour ◽

Susan Gillespie ◽

Ian Gibb ◽

K. George M. M. Alberti

Keyword(s):

Blood Glucose Concentration ◽

Excretion Rate ◽

Binding Protein ◽

Insulin Dependent Diabetes ◽

Retinol Binding Protein ◽

Diabetic Patients ◽

Control Subjects ◽

Protein Excretion ◽

Insulin Dependent ◽

Insulin Dependent Diabetic

1. It has been suggested that tubular damage may precede gomerular damage at the onset of diabetic nephropathy. This may be reflected by increased urinary excretion of low-molecular-mass proteins, such as retinol-binding protein. 2. We have measured the urinary excretion rate of retinol-binding protein overnight, during orthostasis and during a hyperinsulinaemic euglycaemic clamp (blood glucose concentration 7.0 mmol/l) with stable diuresis in 34 normotensive, normoalbuminuric insulin-dependent diabetic patients and in 10 normal control subjects. Normal control subjects were not clamped. A further four normoalbuminuric insulin-dependent diabetic patients were rendered euglycaemic without a water load. 3. Overnight retinol-binding protein excretion rate was 58 (16-157) [median(range)] ng/min in patients with insulin-dependent diabetes and 32 (15-72) ng/min in control subjects (P < 0.01). The excretion rate did not change during orthostasis [patients with insulin-dependent diabetes, 67 (3-173) ng/min; control subjects, 23 (5-78) ng/min]. During the euglycaemic clamp retinol-binding protein excretion rate increased to 383 (78-4897) ng/min in patients with insulin-dependent diabetes (P < 0.01). An average increment in retinol-binding protein excretion rate of greater than 4000% was noted after acute euglycaemia in those patients with insulin-dependent diabetes who were not water-loaded. 4. In insulin-dependent diabetes, both overnight and orthostatic retinal-binding protein excretion was not correlated with fasting blood glucose concentration, HbA1, fructosamine or duration of diabetes. The absolute and incremental excretion rates of retinol-binding protein during the clamp were, however, correlated with both fasting blood glucose concentration and glucose excretion rate (rs = 0.41-0.48, P < 0.01). 5. The study demonstrates that retinol-binding protein excretion is increased in insulin-dependent diabetes in the absence of microalbuminuria and that this increase in retinol-binding protein excretion is particularly pronounced after acute euglycaemia. Acute tubular dysfunction related to acute changes in glucose control appears to be the most likely explanation, but established tubular damage could also be implicated. Postural variation in retinol-binding protein excretion was not detected.

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