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      Urinary Alpha- and Pi-Glutathione S-Transferases in Adult Patients with Type 1 Diabetes

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          Abstract

          Background/Aims: Glutathione S-transferases (GSTs) are cytosolic enzymes excreted from renal tubules following tubular damage. α-GST primarily originates from proximal tubules, while π-GST from distal tubules and collecting ducts. We investigated if GST levels are associated with renal function in patients with type 1 diabetes. Methods: We conducted a cross-sectional study including 189 Caucasian patients with type 1 diabetes and 16 nondiabetic controls. α- and π-GST were measured by ELISA and reported as GST/urinary creatinine excretion (μg/mmol). Results: The subjects were 53 ± 14 years old, 66 (35%) were female and the estimated glomerular filtration rate was 85 ± 29 ml/min/1.73 m<sup>2</sup>. Normo- (<30 mg/24 h), micro- (30-299 mg/24 h) and macroalbuminuria (≥300 mg/24 h) was present in 57, 61 and 71 patients, respectively. α- and π-GST/creatinine ratios in controls versus all patients were 0.07 (0-0.3) and 0.11 (0-0.8) μg/mmol versus 0.05 (0-2.3) and 0.16 (0-4.9) μg/mmol (p ≥ 0.16; adjusted for age and gender, p ≥ 0.18). The α-GST/creatinine ratio positively correlated with female gender (p = 0.04), while the π-GST/creatinine ratio was associated with age and female gender (p ≤ 0.016). Comparing normo-, micro- and macroalbuminuric patients, α- and π-GST levels were similar (p = 0.10; adjusted p = 0.11). Neither α- nor π-GST levels were significantly associated with renal function (p ≥ 0.34). Conclusion: α- and π-GST/creatinine ratios were similar among controls and patients with type 1 diabetes. In addition, we did not find associations with albuminuria degree or level of renal function. The significance of increased or decreased excretion of α- and π-GST among patients with diabetes needs to be clarified.

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          Most cited references 23

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          Diabetic nephropathy: diagnosis, prevention, and treatment.

          Diabetic nephropathy is the leading cause of kidney disease in patients starting renal replacement therapy and affects approximately 40% of type 1 and type 2 diabetic patients. It increases the risk of death, mainly from cardiovascular causes, and is defined by increased urinary albumin excretion (UAE) in the absence of other renal diseases. Diabetic nephropathy is categorized into stages: microalbuminuria (UAE >20 microg/min and or =200 microg/min). Hyperglycemia, increased blood pressure levels, and genetic predisposition are the main risk factors for the development of diabetic nephropathy. Elevated serum lipids, smoking habits, and the amount and origin of dietary protein also seem to play a role as risk factors. Screening for microalbuminuria should be performed yearly, starting 5 years after diagnosis in type 1 diabetes or earlier in the presence of puberty or poor metabolic control. In patients with type 2 diabetes, screening should be performed at diagnosis and yearly thereafter. Patients with micro- and macroalbuminuria should undergo an evaluation regarding the presence of comorbid associations, especially retinopathy and macrovascular disease. Achieving the best metabolic control (A1c 1.0 g/24 h and increased serum creatinine), using drugs with blockade effect on the renin-angiotensin-aldosterone system, and treating dyslipidemia (LDL cholesterol <100 mg/dl) are effective strategies for preventing the development of microalbuminuria, in delaying the progression to more advanced stages of nephropathy and in reducing cardiovascular mortality in patients with type 1 and type 2 diabetes.
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            Urinary biomarkers in the clinical prognosis and early detection of acute kidney injury.

            Several novel urinary biomarkers have shown promise in the early detection and diagnostic evaluation of acute kidney injury (AKI). Clinicians have limited tools to determine which patients will progress to more severe forms of AKI at the time of serum creatinine increase. The diagnostic and prognostic utility of novel and traditional AKI biomarkers was evaluated during a prospective study of 123 adults undergoing cardiac surgery. Urinary neutrophil gelatinase-associated lipocalin (NGAL), cystatin C (CyC), kidney injury molecule-1 (KIM-1), hepatocyte growth factor (HGF), π-glutathione-S-transferase (π-GST), α-GST, and fractional excretions of sodium and urea were all measured at preoperative baseline, postoperatively, and at the time of the initial clinical diagnosis of AKI. Receiver operator characteristic curves were generated and the areas under the curve (AUCs) were compared. Forty-six (37.4%) subjects developed AKI Network stage 1 AKI; 9 (7.3%) of whom progressed to stage 3. Preoperative KIM-1 and α-GST were able to predict the future development of stage 1 and stage 3 AKI. Urine CyC at intensive care unit (ICU) arrival best detected early stage 1 AKI (AUC = 0.70, P < 0.001); the 6-hour ICU NGAL (AUC = 0.88; P < 0.001) best detected early stage 3 AKI. π-GST best predicted the progression to stage 3 AKI at the time of creatinine increase (AUC = 0.86; P = 0.002). Urinary biomarkers may improve the ability to detect early AKI and determine the clinical prognosis of AKI at the time of diagnosis.
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              Development and Progression of Renal Insufficiency With and Without Albuminuria in Adults With Type 1 Diabetes in the Diabetes Control and Complications Trial and the Epidemiology of Diabetes Interventions and Complications Study

              OBJECTIVE This multicenter study examined the impact of albumin excretion rate (AER) on the course of estimated glomerular filtration rate (eGFR) and the incidence of sustained eGFR 300 mg/24 h) before they reached stage 3 chronic kidney disease. Macroalbuminuria is associated with a markedly increased rate of fall in eGFR (5.7%/year vs. 1.2%/year with AER <30 mg/24 h, P < 0.0001) and risk of eGFR <60 ml/min/1.73 m2 (adjusted hazard ratio 15.3, P < 0.0001), whereas microalbuminuria had weaker and less consistent effects on eGFR. CONCLUSIONS Macroalbuminuria was a strong predictor of eGFR loss and risk of developing sustained eGFR <60 ml/min/1.73 m2. However, screening with AER alone would have missed 24% of cases of sustained impaired eGFR.
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                Author and article information

                Journal
                NNE
                NNE
                10.1159/issn.1664-5529
                Nephron Extra
                S. Karger AG
                1664-5529
                2014
                May – August 2014
                31 July 2014
                : 4
                : 2
                : 127-133
                Affiliations
                aSteno Diabetes Center, Gentofte, bAarhus University, Aarhus, and cUniversity of Copenhagen, Copenhagen, Denmark
                Author notes
                *Bernt Johan von Scholten, MD, Niels Steensens Vej 1, DK-2820 Gentofte (Denmark), E-Mail bjos@steno.dk
                Article
                365481 PMC4164068 Nephron Extra 2014;4:127-133
                10.1159/000365481
                PMC4164068
                25337081
                © 2014 S. Karger AG, Basel

                Open Access License: This is an Open Access article licensed under the terms of the Creative Commons Attribution-NonCommercial 3.0 Unported license (CC BY-NC) ( http://www.karger.com/OA-license), applicable to the online version of the article only. Distribution permitted for non-commercial purposes only. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Tables: 1, Pages: 7
                Categories
                Original Paper

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