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	<title>Kidney Function &#187; Elizabeth F.O. Kern, Penny Erhard, Wanjie Sun, Saul Genuth, Miriam F. Weiss</title>
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	<description>Renal Information</description>
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		<title>Early Urinary Markers of Diabetic Kidney Disease: A Nested Case-Control Study From the Diabetes Control and Complications Trial (DCCT) &#8211; Corrected Proof</title>
		<link>http://kidneyfunction.org/early-urinary-markers-of-diabetic-kidney-disease-a-nested-case-control-study-from-the-diabetes-control-and-complications-trial-dcct-corrected-proof/</link>
		<comments>http://kidneyfunction.org/early-urinary-markers-of-diabetic-kidney-disease-a-nested-case-control-study-from-the-diabetes-control-and-complications-trial-dcct-corrected-proof/#comments</comments>
		<pubDate>Mon, 08 Feb 2010 10:00:00 +0000</pubDate>
		<dc:creator>Elizabeth F.O. Kern, Penny Erhard, Wanjie Sun, Saul Genuth, Miriam F. Weiss</dc:creator>
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		<guid isPermaLink="false">10.1053/j.ajkd.2009.11.009</guid>
		<description><![CDATA[Background: Urinary markers were tested as predictors of macroalbuminuria or microalbuminuria in patients with type 1 diabetes.Study Design: Nested case-control of participants in the Diabetes Control and Complications Trial (DCCT).Setting &#38; Participants: 87 cases of microalbuminuria were matched to 174 controls in a 1:2 ratio, while 4 cases were matched to 4 controls in a 1:1 ratio, resulting in 91 cases and 178 controls for microalbuminuria. 55 cases of macroalbuminuria were matched to 110 controls in a 1:2 ratio. Controls were free of micro-/macroalbuminuria when their matching case first developed micro-/macroalbuminuria.Predictors: Urinary N-acetyl-β-d-glucosaminidase (NAG), pentosidine, advanced glycation end product (AGE) fluorescence, and albumin excretion rate (AER).Outcomes: Incident microalbuminuria (2 consecutive annual AERs &#62; 40 but ≤ 300 mg/d) or macroalbuminuria (AER &#62; 300 mg/d).Measurements: Stored urine samples from DCCT entry and 1-9 years later when macro- or microalbuminuria occurred were measured for the lysosomal enzyme NAG and the AGE pentosidine and AGE fluorescence. AER and adjustor variables were obtained from the DCCT.Results: Submicroalbuminuric AER levels at baseline independently predicted microalbuminuria (adjusted OR, 1.83; P &#60; 0.001) and macroalbuminuria (adjusted OR, 1.82; P &#60; 0.001). Baseline NAG excretion independently predicted macroalbuminuria (adjusted OR, 2.26; P &#60; 0.001) and microalbuminuria (adjusted OR, 1.86; P &#60; 0.001). Baseline pentosidine excretion predicted macroalbuminuria (adjusted OR, 6.89; P = 0.002). Baseline AGE fluorescence predicted microalbuminuria (adjusted OR, 1.68; P = 0.02). However, adjusted for NAG excretion, pentosidine excretion and AGE fluorescence lost the predictive association with macroalbuminuria and microalbuminuria, respectively.Limitations: Use of angiotensin-converting enzyme inhibitors was not directly ascertained, although their use was proscribed during the DCCT.Conclusions: Early in type 1 diabetes, repeated measurements of AER and urinary NAG excretion may identify individuals susceptible to future diabetic nephropathy. Combining the 2 markers may yield a better predictive model than either one alone. Renal tubule stress may be more severe, reflecting abnormal renal tubule processing of AGE-modified proteins, in individuals susceptible to diabetic nephropathy.]]></description>
			<content:encoded><![CDATA[Background: Urinary markers were tested as predictors of macroalbuminuria or microalbuminuria in patients with type 1 diabetes.Study Design: Nested case-control of participants in the Diabetes Control and Complications Trial (DCCT).Setting & Participants: 87 cases of microalbuminuria were matched to 174 controls in a 1:2 ratio, while 4 cases were matched to 4 controls in a 1:1 ratio, resulting in 91 cases and 178 controls for microalbuminuria. 55 cases of macroalbuminuria were matched to 110 controls in a 1:2 ratio. Controls were free of micro-/macroalbuminuria when their matching case first developed micro-/macroalbuminuria.Predictors: Urinary N-acetyl-β-d-glucosaminidase (NAG), pentosidine, advanced glycation end product (AGE) fluorescence, and albumin excretion rate (AER).Outcomes: Incident microalbuminuria (2 consecutive annual AERs > 40 but ≤ 300 mg/d) or macroalbuminuria (AER > 300 mg/d).Measurements: Stored urine samples from DCCT entry and 1-9 years later when macro- or microalbuminuria occurred were measured for the lysosomal enzyme NAG and the AGE pentosidine and AGE fluorescence. AER and adjustor variables were obtained from the DCCT.Results: Submicroalbuminuric AER levels at baseline independently predicted microalbuminuria (adjusted OR, 1.83; P < 0.001) and macroalbuminuria (adjusted OR, 1.82; P < 0.001). Baseline NAG excretion independently predicted macroalbuminuria (adjusted OR, 2.26; P < 0.001) and microalbuminuria (adjusted OR, 1.86; P < 0.001). Baseline pentosidine excretion predicted macroalbuminuria (adjusted OR, 6.89; P = 0.002). Baseline AGE fluorescence predicted microalbuminuria (adjusted OR, 1.68; P = 0.02). However, adjusted for NAG excretion, pentosidine excretion and AGE fluorescence lost the predictive association with macroalbuminuria and microalbuminuria, respectively.Limitations: Use of angiotensin-converting enzyme inhibitors was not directly ascertained, although their use was proscribed during the DCCT.Conclusions: Early in type 1 diabetes, repeated measurements of AER and urinary NAG excretion may identify individuals susceptible to future diabetic nephropathy. Combining the 2 markers may yield a better predictive model than either one alone. Renal tubule stress may be more severe, reflecting abnormal renal tubule processing of AGE-modified proteins, in individuals susceptible to diabetic nephropathy.]]></content:encoded>
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