Published online before print August 9, 2004, doi: 10.1161/01.CIR.0000139860.33974.28
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(Circulation. 2004;110:921-927.)
© 2004 American Heart Association, Inc.
Original Articles |
Albuminuria, a Therapeutic Target for Cardiovascular Protection in Type 2 Diabetic Patients With Nephropathy
From the Department of Clinical Pharmacology, Groningen University Medical Center, the Netherlands (D.d.Z.); Mario Negri Institute for Pharmacological Research, Bergamo, Italy (G.R.); Steno Diabetes Center Gentofte and Faculty of Health Science, Aarhus University, Denmark (H.-H.P.); Merck Research Laboratories, Merck & Co, Inc, Whitehouse Station, NJ (W.F.K., Z.Z., S. Shahinfar, S. Snapinn); Baker Medical Research Institute, Melbourne, Australia (M.E.C.); Department of Medicine, University of Texas, Medical Branch, Galveston (W.E.M.); and Department of Medicine, Renal Division, Brigham and Women’s Hospital and Harvard School of Medicine, Boston, Mass (B.M.B.).
Correspondence to Prof Dr D. de Zeeuw, Department of Clinical Pharmacology, Groningen University Medical Center, Ant Deusinglaan 1, 9713 AV Groningen, Netherlands. E-mail d.de.zeeuw{at}med.rug.nl
Received July 22, 2003; de novo received November 17, 2003; revision received April 20, 2004; accepted April 22, 2004.
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Abstract |
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Background— Albuminuria is an established risk marker for both cardiovascular and renal outcomes. Albuminuria can be reduced with drugs that block the renin-angiotensin system (RAS). We questioned whether the short-term drug-induced change in albuminuria would predict the long-term cardioprotective efficacy of RAS intervention.
Methods and Results— We analyzed data from Reduction in Endpoints in Non-insulin dependent diabetes mellitus with the Angiotensin II Antagonist Losartan (RENAAL), a double-blind, randomized trial in 1513 type 2 diabetic patients with nephropathy, focusing on the relationship between the prespecified cardiovascular end point (composite) or hospitalization for heart failure and baseline or reduction in albuminuria. Patients with high baseline albuminuria (
3 g/g creatinine) had a 1.92-fold (95% CI, 1.54 to 2.38) higher risk for the cardiovascular end point and a 2.70-fold (95% CI, 1.94 to 3.75) higher risk for heart failure compared with patients with low albuminuria (<1.5 g/g). Among all available baseline risk markers, albuminuria was the strongest predictor of cardiovascular outcome. The association between albuminuria and cardiovascular outcome was driven by those patients who also had a renal event. Modeling of the initial 6-month change in risk parameters showed that albuminuria reduction was the only predictor for cardiovascular outcome: 18% reduction in cardiovascular risk for every 50% reduction in albuminuria and a 27% reduction in heart failure risk for every 50% reduction in albuminuria.
Conclusions— Albuminuria is an important factor predicting cardiovascular risk in patients with type 2 diabetic nephropathy. Reducing albuminuria in the first 6 months appears to afford cardiovascular protection in these patients.
Key Words: proteinuria • albuminuria • cardiovascular disease • angiotensin • diabetes
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Introduction |
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It is estimated that type 2 diabetes affects more than 150 million people worldwide, and the prevalence is projected to double in the next 25 years.1 Nephropathy, characterized by albuminuria, hypertension, and a progressive decline in glomerular filtration rate, develops in 10% to 40% of diabetic patients.2 An associated progressive loss of cardiovascular function leads to a predominantly cardiovascular mortality in this population.3 Treatment of type 2 diabetes has focused on attenuating hyperglycemia, hypertension, and dyslipidemia.4–6 Indeed, both blood pressure and hyperglycemia have not only proved to be important risk markers, but their control also serves as an indicator of the effectiveness of cardiovascular-protective therapy.7–9
Albuminuria in type 2 diabetic patients has been identified as another risk marker for both cardiovascular10 and renal outcome.11 Several antiproteinuric strategies are available, including interruption of the renin-angiotensin system (RAS) via either ACE inhibitor (ACEI) or angiotensin II antagonists (AIIA). Reduction in albuminuria using such drug strategies appears to be related to renal protection independent of blood pressure effects.12,13 This phenomenon was recently also documented in type 2 diabetes.14 Whether lowering albuminuria would reduce the subsequent risk for cardiovascular events has not been documented.
We therefore sought to confirm that albuminuria is an independent cardiac risk marker in type 2 diabetes with nephropathy. We investigated whether albuminuria reduction is associated with a reduction in cardiovascular events and whether the degree of the short-term therapy-induced albuminuria reduction would be an indicator of the subsequent long-term cardiovascular protection. Finally, we questioned whether albuminuria-driven cardiovascular risk is associated with the renal risk in the same patient. If these issues are answered positively, it is predicted that albuminuria may become the target of a cardiovascular-protection treatment strategy beyond or in addition to blood pressure reduction. To this end, we performed a post hoc analysis of the Reduction in Endpoints in Non-insulin dependent diabetes mellitus with the Angiotensin II Antagonist Losartan (RENAAL) database. The overall RENAAL results have shown a beneficial effect of losartan on the "first hospitalization for heart failure" component of the secondary, cardiovascular end point, whereas the outcome of the cardiovascular composite end point was similar in the 2 treatment arms.15
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Methods |
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Patients and Study Design
RENAAL is a multinational, double-blind, randomized trial comparing losartan with placebo, each in addition to conventional antihypertensive therapy, excluding ACEIs and other AIIAs. The study was performed in 250 centers in 28 countries and involved 1513 patients. The study design, the inclusion/exclusion criteria, and the treatment protocol have been reported previously.16 In short, participants had to have had type 2 diabetes and nephropathy, evidenced by a urinary albumin:creatinine ratio >0.3 g/g in a first morning void or a 24-hour urine protein >0.5 g, and serum creatinine >1.5 mg/dL (1.3 mg/dL in women or in men <60 kg) to 3.0 mg/dL. We excluded patients who had sustained a myocardial infarction or had undergone coronary artery bypass graft surgery within the previous month, had a cerebrovascular accident or had undergone percutaneous transluminal coronary angioplasty within the previous 6 months, had a transient ischemic attack within the previous year, or had any history of heart failure before enrollment. All patients signed informed consent before enrollment, and the local Institutional Review Board of each participating center approved the study. Patients were followed up for an average of 3.4 years.
Data Analysis
Albuminuria was assessed using the albumin (g/L)-to-creatinine (g/L) ratio. For the initial albuminuria response, the month-6 change was chosen, expressed as 100%x(1–ratio of albuminuria month-6 over baseline).
The cardiovascular end point was defined as the composite of myocardial infarction, stroke, first hospitalization for heart failure or unstable angina, coronary or peripheral revascularization, or cardiovascular death. We analyzed the post hoc, non-heart failure cardiovascular end point, which consisted of all components of the cardiovascular end point, with the exception of hospitalization for heart failure. The renal end point is defined as the composite of the time to first doubling of serum creatinine, end-stage renal disease (ESRD), or death. For patients who had multiple end points of different types, the patients were counted once for the first event in each relevant analysis.
Statistical Analysis
All 1513 participants in the RENAAL study were included in the analysis from randomization through study termination. Independent baseline and month-6 predictors of the respective cardiovascular and heart failure end points were identified by the multivariate Cox model. For the baseline analysis, the Cox model included cardiovascular disease history (yes/no) and heart failure disease history (yes/no), age (y/10), sex, race, weight, smoking, sitting systolic blood pressure (SiSBP), sitting diastolic BP (SiDBP), mean arterial pressure, pulse pressure, total cholesterol, estimated glomerular filtration rate, hemoglobin, HBA1C, albuminuria, and treatment (losartan/placebo). For the baseline and month-6 change multivariate analysis, the multivariate Cox model included the baseline risk factors described above and month-6 changes and log-changes from baseline for the following risk factors: albuminuria, SiDBP, SiSBP, estimated glomerular filtration rate, weight, and HbA1C. For all multivariate analyses, a backward selection method was used with the significance level at P<0.01 for removing a covariate from the model. The strength of a risk factor as an independent predictor for each end point was determined by its magnitude of significance using 
2 statistics in the multivariate analysis.
The association between albuminuria and the cardiovascular and heart failure end points was estimated using the Kaplan-Meier procedure, with baseline albuminuria stratified into 3 subgroups: <1.5 g/g, 1.5<3.0 g/g, and 3.0 g/g. To estimate a risk increase between subgroups, a multivariate Cox regression model was performed with indicators of baseline albuminuria subgroups as a factor. For the adjusted analyses, the model includes other baseline covariates described above, with the exception of albuminuria and treatment group.
To estimate the effect of albuminuria change on the cardiovascular and heart failure end points, 3 groups of month-6 albuminuria reduction were generated: <0%, 0<30%, and 30%. For the adjusted analyses, the Cox model includes indicators of 3 subgroups for reduction of albuminuria, baseline covariates previously mentioned with exception of treatment group, and the month-6 and log-changes from baseline previously mentioned (excluding albuminuria).
To include all randomized patients into the analyses, imputed data were used in the analysis, using linear regression models with complete baseline covariates. All statistical analyses were performed using SAS version 8.
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Results |
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Baseline Albuminuria as Predictor of Cardiovascular Outcome
Table 1 shows baseline characteristics for all patients. Mean urine albumin was 1.8 g/g creatinine. The multivariate analysis (Table 2, top), shows that albuminuria is the strongest independent predictor of both the cardiovascular end point and heart failure.
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Figure 1 (top) shows the Kaplan-Meier curves for the cardiovascular and heart failure end points for albuminuria subgroups. Both the high (3.0 g/g) and middle (1.5<3.0 g/g) groups show significantly more cardiovascular events. Table 3 (top) summarizes the unadjusted and adjusted hazard ratios for the cardiovascular and heart failure end points. The risk for the cardiovascular end point was 1.92-fold (95% CI, 1.54 to 2.38) higher, and heart failure was 2.70-fold (95% CI, 1.94 to 3.75) higher in the high-albuminuria group compared with the low-albuminuria (<1.5 g/g) group. To confirm that the relationship between risk for the cardiovascular end point and level of albuminuria was not driven by heart failure, we excluded the heart failure component from the cardiovascular end point. Table 3 (top) shows that the risk for the non-heart failure cardiovascular end point was similar to that of the cardiovascular end point at different levels of albuminuria.
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Because of the potential for bias from arbitrary albuminuria categories, we also calculated hazard ratios for finer categories of albuminuria. Controlling for baseline risk markers, we found an almost linear positive relationship between degree of baseline albuminuria and risk for the cardiovascular end point or heart failure (Figure 1, bottom). An increase of 1 g/g albuminuria was associated with an increased risk of 17% (95% CI, 12% to 23%) for the cardiovascular end point and 26% (95% CI, 18% to 34%) for heart failure.
Albuminuria Reduction as Predictor of Cardiovascular Outcome
In the multivariate model (Table 2, bottom), when adding month-6 and log-changes from baseline for the different risk parameters, again, baseline albuminuria is the strongest independent predictor of the cardiovascular end point or heart failure. In addition, the albuminuria reduction (log-change) is shown to be a strong predictor of cardiovascular outcome.
In the whole study population, albuminuria was lowered by 14% (95% CI, 11% to 17%) in the first 6 months compared with baseline. In the placebo group, it did not change significantly (+4% [95% CI, +8 to –1%], but it decreased by 28% (95% CI, 25% to 36%) in the losartan group. Because 6-month albuminuria reduction was highly variable, we subdivided the total population into 3 subgroups according to their month-6 antiproteinuric response (<0%, 0<30%, 30%). The cardiovascular and heart failure end points occurred more frequently in the groups that had little (0<30%) to no (<0%) suppression of albuminuria (Figure 2, top). In contrast, the group that had the greatest reduction in albuminuria (30%) showed a significant reduction in risk for cardiac events. The unadjusted and adjusted hazard ratios for the cardiovascular and heart failure end points are summarized in Table 3 (bottom). The risk associated with the non-heart failure cardiovascular end point was similar to that of the cardiovascular and heart failure end points.
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Hazard ratios were calculated for finer categories of albuminuria reduction. Controlling for risk markers at baseline and month 6, we found an almost linear positive relationship between the degree of albuminuria reduction and risk for the cardiovascular end point or heart failure (Figure 2, bottom). Every 50% reduction in albuminuria reduces the risk for the cardiovascular end point by 18% (95% CI, 9% to 25%) and the heart failure end point by 27% (95% CI, 14% to 38%).
Baseline Albuminuria and the Relation Between Cardiovascular and Renal Risk
Figure 3 (left) shows that 28% of patients with albuminuria <1.5 g/g had a renal event, whereas more than 85% of patients with high albuminuria (3.0 g/g) had a renal event. The level of albuminuria was associated with an increase in cardiovascular events (29% versus 44%, respectively).
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Cardiovascular and renal events could have occurred in the same patient. To identify whether the relation between albuminuria and cardiovascular events is driven by renal events, we analyzed event rates in those patients who encountered only a cardiovascular event or only a renal event, stratified by baseline albuminuria. Albuminuria is clearly associated with renal events in those subjects who did not have a cardiovascular event, whereas albuminuria shows no association with cardiovascular events in those patients who did not have a renal event (Figure 3). To exclude the phenomenon that increased cardiovascular risk is driven by ESRD, the analysis was repeated with those patients who had renal events and cardiovascular events before ESRD. Figure 3 (far right) illustrates that a pre-ESRD cardiovascular event and a renal event in the same patient are driven by albuminuria. Overall, these results indicate that an increased level of baseline albuminuria is associated with increased risk for a cardiovascular event only in those patients who also had a renal event, regardless of whether the cardiovascular event occurred before or after ESRD.
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Discussion |
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Our results show that albuminuria is the strongest risk marker for cardiovascular events in type 2 diabetic subjects with nephropathy. We found that the relationship between albuminuria and the cardiovascular end point was not influenced by the effect of losartan on heart failure and was present predominantly in patients with renal events. Interestingly, suppression of albuminuria was the strongest predictor of long-term protection from cardiovascular events.
There is an increasing body of evidence that albuminuria is a strong risk marker for cardiovascular disease. Results from the Framingham study demonstrated that proteinuria is associated with cardiovascular risk in the general population.17 The Steno hypothesis suggests that albuminuria is an independent risk marker of diabetic microangiopathy and macroangiopathy.18 Interestingly, Samuelsson et al19 showed that proteinuria remains a strong predictor for cardiovascular morbidity despite effective blood pressure lowering by non-RAS-blocking conventional therapies. Large clinical trials have shown that subgroups with albuminuria have a greater cardiovascular risk than those without albuminuria.20,21 Our results show that albuminuria as a risk factor for cardiovascular outcomes parallels that of renal outcomes in patients with type 2 diabetes and that this risk factor is present irrespective of conventional cardiovascular risk markers.
Since the discovery that blood pressure and serum cholesterol are independent modifiable risk markers for cardiovascular events, therapeutic strategies have been tested to lower blood pressure and serum cholesterol to reduce cardiovascular risks.22,23 Different therapeutic strategies can reduce albuminuria, including a low-protein diet,24 indomethacin,25 and antihypertensive agents such as ACEIs26 and AIIAs.27 It is of interest to determine whether these or other interventions for the reduction of albuminuria also afford cardiac protection. The presented data are the first, to the best of our knowledge, to show that lowering albuminuria is in fact related to decreased risk for cardiovascular events.
The mechanism for the relationship between albuminuria and cardiovascular risk or between the albuminuria reduction and cardiovascular protection remains unclear. Nevertheless, our results are potentially clinically important, because albuminuria is relatively easy to measure and quantify and is relatively inexpensive compared with the other strategies for measuring risks of cardiac disease and monitoring success of cardioprotective therapy effectiveness. At present, there is no parameter for monitoring the short-term therapeutic efficacy and adjusting the dose of cardioprotective therapy with RAS intervention, but if prospectively validated, albuminuria could potentially serve these purposes.
Assessing the effect of treatment on reduction of albuminuria was a secondary end point in this trial; however, evaluating the relationship between albuminuria and the cardiovascular or heart failure end points was not prespecified. The arbitrary choice of cut points for baseline and reduction in albuminuria could have influenced the results; however, the outcome of the analyses was similar for the cardiovascular end points using tertile and quintile cut points (data not shown). Although these analyses indicate a strong association between albuminuria and cardiovascular outcome, this association does not imply causality. Because the effect of treatment on reduction of albuminuria per se was not the primary aim of the RENAAL study, the findings presented in this article cannot be considered definitive evidence that treatment with the goal of reducing albuminuria will reduce the risk for cardiovascular events.
These results extend the concept that suppressing albuminuria should be evaluated further as a goal of therapy to achieve optimal cardiovascular protection in the individual patient with type 2 diabetes. Because the dose-response curves for blood pressure and albuminuria appear to be different,28,29 it is possible that therapy aimed at reducing albuminuria could result in additional benefit beyond that achieved with blood pressure lowering alone. These results emphasize the need for new studies in which the primary target of therapy is reduction of albuminuria in other diseases affecting the kidney.
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Acknowledgments |
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Disclosure
Dr de Zeeuw has served as a consultant to Merck, Bristol-Myers Squibb, Sanofi, Pfizer, Actelion, and Solvay. Dr Remuzzi has received research grants from Aventis Pharma, Abbott, and Novartis. He has been a member of speakers’ bureaus sponsored by Merck, AstraZeneca, Novartis, and Aventis Pharma. Dr Parving has served as a consultant to Merck, Bristol-Meyers Squibb, Sanofi, Pfizer, and BioStratum; has received research grants from Merck, Bristol-Meyers Squibb, Sanofi, and AstraZeneca; and has been a member of speakers’ bureaus sponsored by Merck, Bristol-Meyers Squibb, Sanofi, Pfizer, and AstraZeneca. Dr Cooper has served as consultant to Pfizer, Sanofi, and Alteon. He has received research grants from AstraZeneca, Merck, Bristol-Myers Squibb, and Servier. He has been a member of speakers’ bureaus sponsored by AstraZeneca and Solvay. Dr Mitch has served as a consultant to Merck. Drs Keane, Zhang, Shahinfar, and Snapinn are employees of Merck & Co, Inc, and potentially own stock and/or hold stock options in the Company.
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W. A. K. M. Windt, R. H. Henning, A. C. A. Kluppel, Y. Xu, D. de Zeeuw, and R. P. E. van Dokkum Myocardial infarction does not further impair renal damage in 5/6 nephrectomized rats Nephrol. Dial. Transplant., October 1, 2008; 23(10): 3103 - 3110. [Abstract] [Full Text] [PDF]
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X. Yang, W. Y. So, R. Ma, G. Ko, A. Kong, C. Lam, C. S. Ho, C. Cockram, C.-C. Chow, P. Tong, et al. Effects of albuminuria and renal dysfunction on development of dyslipidaemia in type 2 diabetes--the Hong Kong Diabetes Registry Nephrol. Dial. Transplant., September 1, 2008; 23(9): 2834 - 2840. [Abstract] [Full Text] [PDF]
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A. H. Brantsma, S. J.L. Bakker, D. de Zeeuw, P. E. de Jong, R. T. Gansevoort, and for the PREVEND Study Group Extended Prognostic Value of Urinary Albumin Excretion for Cardiovascular Events J. Am. Soc. Nephrol., September 1, 2008; 19(9): 1785 - 1791. [Abstract] [Full Text] [PDF]
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 C. Abaterusso, A. Lupo, V. Ortalda, V. De Biase, A. Pani, M. Muggeo, and G. Gambaro Treating Elderly People with Diabetes and Stages 3 and 4 Chronic Kidney Disease Clin. J. Am. Soc. Nephrol., July 1, 2008; 3(4): 1185 - 1194. [Abstract] [Full Text] [PDF]
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 H.-H. Parving, F. Persson, J. B. Lewis, E. J. Lewis, N. K. Hollenberg, and the AVOID Study Investigators Aliskiren Combined with Losartan in Type 2 Diabetes and Nephropathy N. Engl. J. Med., June 5, 2008; 358(23): 2433 - 2446. [Abstract] [Full Text] [PDF]
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P. Ruggenenti, E. Perticucci, P. Cravedi, V. Gambara, M. Costantini, S. K. Sharma, A. Perna, and G. Remuzzi Role of Remission Clinics in the Longitudinal Treatment of CKD J. Am. Soc. Nephrol., June 1, 2008; 19(6): 1213 - 1224. [Full Text] [PDF]
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A. Nikzamir, M. Nakhjavani, A. Esteghamati, and A. Rashidi Correlates of ACE activity in macroalbuminuric type 2 diabetic patients treated with chronic ACE inhibition Nephrol. Dial. Transplant., April 1, 2008; 23(4): 1274 - 1277. [Abstract] [Full Text] [PDF]
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D. de Zeeuw and I. Raz Albuminuria: A Great Risk Marker, but an Underestimated Target in Diabetes Diabetes Care, February 1, 2008; 31(Supplement_2): S190 - S193. [Full Text] [PDF]
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S. Basi, P. Fesler, A. Mimran, and J. B. Lewis Microalbuminuria in Type 2 Diabetes and Hypertension: A marker, treatment target, or innocent bystander? Diabetes Care, February 1, 2008; 31(Supplement_2): S194 - S201. [Full Text] [PDF]
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B. K. Mahmoodi, M. K. ten Kate, F. Waanders, N. J.G.M. Veeger, J.-L. P. Brouwer, L. Vogt, G. Navis, and J. van der Meer High Absolute Risks and Predictors of Venous and Arterial Thromboembolic Events in Patients With Nephrotic Syndrome: Results From a Large Retrospective Cohort Study Circulation, January 15, 2008; 117(2): 224 - 230. [Abstract] [Full Text] [PDF]
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 S. Nguyen, C. McCulloch, P. Brakeman, A. Portale, and C.-y. Hsu Being Overweight Modifies the Association Between Cardiovascular Risk Factors and Microalbuminuria in Adolescents Pediatrics, January 1, 2008; 121(1): 37 - 45. [Abstract] [Full Text] [PDF]
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G. L. Bakris Slowing Nephropathy Progression: Focus on Proteinuria Reduction Clin. J. Am. Soc. Nephrol., January 1, 2008; 3(Supplement_1): S3 - S10. [Abstract] [Full Text] [PDF]
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S. D. Solomon, J. Lin, C. G. Solomon, K. A. Jablonski, M. M. Rice, M. Steffes, M. Domanski, J. Hsia, B. J. Gersh, J. M. O. Arnold, et al. Influence of Albuminuria on Cardiovascular Risk in Patients With Stable Coronary Artery Disease Circulation, December 4, 2007; 116(23): 2687 - 2693. [Abstract] [Full Text] [PDF]
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A. A.M. Zandbergen, L. Vogt, D. de Zeeuw, S. W.J. Lamberts, R. J.T.H. Ouwendijk, M. G.A. Baggen, and A. H. Bootsma Change in Albuminuria Is Predictive of Cardiovascular Outcome in Normotensive Patients With Type 2 Diabetes and Microalbuminuria Diabetes Care, December 1, 2007; 30(12): 3119 - 3121. [Full Text] [PDF]
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E. L. Schiffrin, M. L. Lipman, and J. F.E. Mann Chronic Kidney Disease: Effects on the Cardiovascular System Circulation, July 3, 2007; 116(1): 85 - 97. [Abstract] [Full Text] [PDF]
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 E. Ingelsson, J. Sundstrom, L. Lind, U. Riserus, A. Larsson, S. Basu, and J. Arnlov Low-grade albuminuria and the incidence of heart failure in a community-based cohort of elderly men Eur. Heart J., July 2, 2007; 28(14): 1739 - 1745. [Abstract] [Full Text] [PDF]
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Authors/Task Force Members:, G. Mancia, G. De Backer, A. Dominiczak, R. Cifkova, R. Fagard, G. Germano, G. Grassi, A. M. Heagerty, S. E. Kjeldsen, et al. 2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) Eur. Heart J., June 11, 2007; (2007) ehm236v1. [Full Text] [PDF]
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A. K. Bello, D. de Zeeuw, M. E. Nahas, A. H. Brantsma, S. J. L. Bakker, P. E. de Jong, and R. T. Gansevoort Impact of weight change on albuminuria in the general population Nephrol. Dial. Transplant., June 1, 2007; 22(6): 1619 - 1627. [Abstract] [Full Text] [PDF]
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R. E. Schmieder, C. Delles, A. Mimran, J. P. Fauvel, and L. M. Ruilope Impact of Telmisartan Versus Ramipril on Renal Endothelial Function in Patients With Hypertension and Type 2 Diabetes Diabetes Care, June 1, 2007; 30(6): 1351 - 1356. [Abstract] [Full Text] [PDF]
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 S. Laurent and P. Boutouyrie Recent Advances in Arterial Stiffness and Wave Reflection in Human Hypertension Hypertension, June 1, 2007; 49(6): 1202 - 1206. [Full Text] [PDF]
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W. B.A. Eijkelkamp, Z. Zhang, G. Remuzzi, H.-H. Parving, M. E. Cooper, W. F. Keane, S. Shahinfar, G. W. Gleim, M. R. Weir, B. M. Brenner, et al. Albuminuria Is a Target for Renoprotective Therapy Independent from Blood Pressure in Patients with Type 2 Diabetic Nephropathy: Post Hoc Analysis from the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) Trial J. Am. Soc. Nephrol., May 1, 2007; 18(5): 1540 - 1546. [Abstract] [Full Text] [PDF]
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 M. Banikazemi, J. Bultas, S. Waldek, W. R. Wilcox, C. B. Whitley, M. McDonald, R. Finkel, S. Packman, D. G. Bichet, D. G. Warnock, et al. Agalsidase-Beta Therapy for Advanced Fabry Disease: A Randomized Trial Ann Intern Med, January 16, 2007; 146(2): 77 - 86. [Abstract] [Full Text] [PDF]
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 K C Tse, M F Lam, S C. Tang, C S. Tang, and T M Chan A pilot study on tacrolimus treatment in membranous or quiescent lupus nephritis with proteinuria resistant to angiotensin inhibition or blockade Lupus, January 1, 2007; 16(1): 46 - 51. [Abstract] [PDF]
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J. Tian, Y. Liu, L. A. Williams, and D. de Zeeuw Potential role of active vitamin D in retarding the progression of chronic kidney disease Nephrol. Dial. Transplant., November 22, 2006; (2006) gfl595v1. [Full Text] [PDF]
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S. Laurent, J. Cockcroft, L. Van Bortel, P. Boutouyrie, C. Giannattasio, D. Hayoz, B. Pannier, C. Vlachopoulos, I. Wilkinson, H. Struijker-Boudier, et al. Expert consensus document on arterial stiffness: methodological issues and clinical applications Eur. Heart J., November 1, 2006; 27(21): 2588 - 2605. [Abstract] [Full Text] [PDF]
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W. A.K.M. Windt, W. B.A. Eijkelkamp, R. H. Henning, A. C.A. Kluppel, P. A. de Graeff, H. L. Hillege, S. Schafer, D. de Zeeuw, and R. P.E. van Dokkum Renal Damage after Myocardial Infarction Is Prevented by Renin-Angiotensin-Aldosterone-System Intervention J. Am. Soc. Nephrol., November 1, 2006; 17(11): 3059 - 3066. [Abstract] [Full Text] [PDF]
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R. M.A. van de Wal, R. T. Gansevoort, P. van der Harst, F. Boomsma, H.W. Thijs Plokker, D. J. van Veldhuisen, P. E. de Jong, W. H. van Gilst, and A. A. Voors Predictors of Angiotensin-Converting Enzyme Inhibitor-Induced Reduction of Urinary Albumin Excretion in Nondiabetic Patients Hypertension, November 1, 2006; 48(5): 870 - 876. [Abstract] [Full Text] [PDF]
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L. M. Ruilope and J. Segura Predictors of the Evolution of Microalbuminuria Hypertension, November 1, 2006; 48(5): 832 - 833. [Full Text] [PDF]
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 M. Rodriguez-Yanez, M. Castellanos, M. Blanco, M. Millan, F. Nombela, T. Sobrino, I. Lizasoain, R. Leira, J. Serena, A. Davalos, et al. Micro- and macroalbuminuria predict hemorrhagic transformation in acute ischemic stroke. Neurology, October 10, 2006; 67(7): 1172 - 1177. [Abstract] [Full Text] [PDF]
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W. Y. So, A. P.S. Kong, R. C.W. Ma, R. Ozaki, C. C. Szeto, N. N. Chan, V. Ng, C. S. Ho, C. W.K. Lam, C. C. Chow, et al. Glomerular filtration rate, cardiorenal end points, and all-cause mortality in type 2 diabetic patients. Diabetes Care, September 1, 2006; 29(9): 2046 - 2052. [Abstract] [Full Text] [PDF]
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C. D.A. Stehouwer and Y. M. Smulders Microalbuminuria and Risk for Cardiovascular Disease: Analysis of Potential Mechanisms J. Am. Soc. Nephrol., August 1, 2006; 17(8): 2106 - 2111. [Abstract] [Full Text] [PDF]
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P. E. de Jong and G. C. Curhan Screening, Monitoring, and Treatment of Albuminuria: Public Health Perspectives J. Am. Soc. Nephrol., August 1, 2006; 17(8): 2120 - 2126. [Abstract] [Full Text] [PDF]
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 J. J. Wang, S. X. Zhang, R. Mott, R. R. Knapp, W. Cao, K. Lau, and J.-x. Ma Salutary Effect of Pigment Epithelium-Derived Factor in Diabetic Nephropathy: Evidence for Antifibrogenic Activities Diabetes, June 1, 2006; 55(6): 1678 - 1685. [Abstract] [Full Text] [PDF]
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T. Miyata and C. van Ypersele de Strihou Renoprotection of angiotensin receptor blockers: beyond blood pressure lowering Nephrol. Dial. Transplant., April 1, 2006; 21(4): 846 - 849. [Full Text] [PDF]
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G. Remuzzi, M. Macia, and P. Ruggenenti Prevention and Treatment of Diabetic Renal Disease in Type 2 Diabetes: The BENEDICT Study J. Am. Soc. Nephrol., April 1, 2006; 17(4_suppl_2): S90 - S97. [Abstract] [Full Text] [PDF]
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S. Ogawa, T. Mori, K. Nako, T. Kato, K. Takeuchi, and S. Ito Angiotensin II Type 1 Receptor Blockers Reduce Urinary Oxidative Stress Markers in Hypertensive Diabetic Nephropathy Hypertension, April 1, 2006; 47(4): 699 - 705. [Abstract] [Full Text] [PDF]
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 J. Vora and C. Weston BENEDICT: primary prevention of microalbuminuria in hypertensive type 2 diabetes: Bergamo NEphrologic Diabetes Complication Trial (BENEDICT) The British Journal of Diabetes & Vascular Disease, March 1, 2006; 6(2): 84 - 88. [PDF]
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H. Ibsen, M. H. Olsen, K. Wachtell, K. Borch-Johnsen, L. H. Lindholm, C. E. Mogensen, B. Dahlof, S. M. Snapinn, Y. Wan, and P. A. Lyle Does Albuminuria Predict Cardiovascular Outcomes on Treatment With Losartan Versus Atenolol in Patients With Diabetes, Hypertension, and Left Ventricular Hypertrophy?: The LIFE study. Diabetes Care, March 1, 2006; 29(3): 595 - 600. [Abstract] [Full Text] [PDF]
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R. E. Gilbert, K. Connelly, D. J. Kelly, C. A. Pollock, and H. Krum Heart Failure and Nephropathy: Catastrophic and Interrelated Complications of Diabetes Clin. J. Am. Soc. Nephrol., March 1, 2006; 1(2): 193 - 208. [Abstract] [Full Text] [PDF]
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T. Berl and W. Henrich Kidney-Heart Interactions: Epidemiology, Pathogenesis, and Treatment Clin. J. Am. Soc. Nephrol., January 1, 2006; 1(1): 8 - 18. [Full Text] [PDF]
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 B. Westendorp, R. G. Schoemaker, H. Buikema, D. de Zeeuw, F. Boomsma, W. H. van Gilst, and D. J. van Veldhuisen Beneficial effects of add-on hydrochlorothiazide in rats with myocardial infarction optimally treated with quinapril Eur J Heart Fail, December 1, 2005; 7(7): 1085 - 1094. [Abstract] [Full Text] [PDF]
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M. Shlipak and C. Stehman-Breen Observational Research Databases in Renal Disease J. Am. Soc. Nephrol., December 1, 2005; 16(12): 3477 - 3484. [Abstract] [Full Text] [PDF]
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G. Mancia and G. Grassi Efficacy of antihypertensive treatment: which endpoints should be considered? Nephrol. Dial. Transplant., November 1, 2005; 20(11): 2301 - 2303. [Full Text] [PDF]
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K. R. Tuttle, G. L. Bakris, R. D. Toto, J. B. McGill, K. Hu, and P. W. Anderson The Effect of Ruboxistaurin on Nephropathy in Type 2 Diabetes Diabetes Care, November 1, 2005; 28(11): 2686 - 2690. [Abstract] [Full Text] [PDF]
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M. R. Weir Blood pressure salt sensitivity: a biomeasure of kidney disease susceptibility in diabetics? Nephrol. Dial. Transplant., October 1, 2005; 20(10): 2022 - 2024. [Full Text] [PDF]
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R. E. Schmieder, A. U. Klingbeil, E. H. Fleischmann, R. Veelken, and C. Delles Additional Antiproteinuric Effect of Ultrahigh Dose Candesartan: A Double-Blind, Randomized, Prospective Study J. Am. Soc. Nephrol., October 1, 2005; 16(10): 3038 - 3045. [Abstract] [Full Text] [PDF]
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K. Rossing, K. J. Schjoedt, U. M. Smidt, F. Boomsma, and H.-H. Parving Beneficial Effects of Adding Spironolactone to Recommended Antihypertensive Treatment in Diabetic Nephropathy: A randomized, double-masked, cross-over study Diabetes Care, September 1, 2005; 28(9): 2106 - 2112. [Abstract] [Full Text] [PDF]
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X. J, L. G, W. P, V. H, Y. X, L. Y, W. Y, P. A, C. S, D. GV, et al. Kidney and Blood Pressure--The Story Unfolds: Renalase Is a Novel, Soluble Monoamine Oxidase That Regulates Cardiac Function and Blood Pressure. J Clin Invest J. Am. Soc. Nephrol., September 1, 2005; 16(9): 2521 - 2527. [Full Text] [PDF]
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R. Agarwal and M. J. Andersen Correlates of Systolic Hypertension in Patients With Chronic Kidney Disease Hypertension, September 1, 2005; 46(3): 514 - 520. [Abstract] [Full Text] [PDF]
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J. Arnlov, J. C. Evans, J. B. Meigs, T. J. Wang, C. S. Fox, D. Levy, E. J. Benjamin, R. B. D'Agostino, and R. S. Vasan Low-Grade Albuminuria and Incidence of Cardiovascular Disease Events in Nonhypertensive and Nondiabetic Individuals: The Framingham Heart Study Circulation, August 16, 2005; 112(7): 969 - 975. [Abstract] [Full Text] [PDF]
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C. W, Y. PX, L. BM, C. RD, M. DL, M. RH, I. H, O. MH, W. K, B.-J. K, et al. Anorexia and Cachexia in Renal Failure--Is Leptin the Culprit?: Role of Leptin and Melanocortin Signaling in Uremia-Associated Cachexia. J Clin Invest 115: 1659-1665, 2005 J. Am. Soc. Nephrol., August 1, 2005; 16(8): 2245 - 2250. [Full Text] [PDF]
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D. de Zeeuw Albuminuria, Just a Marker for Cardiovascular Disease, Or Is It More? J. Am. Soc. Nephrol., July 1, 2005; 16(7): 1883 - 1885. [Full Text] [PDF]
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J. Redon Urinary Albumin Excretion: Lowering the Threshold of Risk in Hypertension Hypertension, July 1, 2005; 46(1): 19 - 20. [Full Text] [PDF]
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F. Togel, Z. Hu, K. Weiss, J. Isaac, C. Lange, C. Westenfelder, T. Stasko, M.D. Brown, J.A. Carucci, S. Euvrard, et al. Amelioration of Acute Renal Failure by Stem Cell Therapy--Paracrine Secretion Versus Transdifferentiation into Resident Cells: Administered Mesenchymal Stem Cells Protect against Ischemic Acute Renal Failure through Differentiation-Independent Mechanisms. Am J Physiol Renal Physiol E-pub February 15, 2005 J. Am. Soc. Nephrol., May 1, 2005; 16(5): 1153 - 1163. [Full Text] [PDF]
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 Other articles noted Evid. Based Med., April 1, 2005; 10(2): 63 - 64. [Full Text] [PDF]
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A. Smith, J. Karalliedde, L. De Angelis, D. Goldsmith, and G. Viberti Aortic Pulse Wave Velocity and Albuminuria in Patients with Type 2 Diabetes J. Am. Soc. Nephrol., April 1, 2005; 16(4): 1069 - 1075. [Abstract] [Full Text] [PDF]
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M. R. Weir Reduction in Microalbuminuria: A Biomeasure of Therapeutic Success? Hypertension, February 1, 2005; 45(2): 181 - 182. [Full Text] [PDF]
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H. Ibsen, M. H. Olsen, K. Wachtell, K. Borch-Johnsen, L. H. Lindholm, C. E. Mogensen, B. Dahlof, R. B. Devereux, U. de Faire, F. Fyhrquist, et al. Reduction in Albuminuria Translates to Reduction in Cardiovascular Events in Hypertensive Patients: Losartan Intervention for Endpoint Reduction in Hypertension Study Hypertension, February 1, 2005; 45(2): 198 - 202. [Abstract] [Full Text] [PDF]
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W. E. Mitch Treating Diabetic Nephropathy -- Are There Only Economic Issues? N. Engl. J. Med., November 4, 2004; 351(19): 1934 - 1936. [Full Text] [PDF]
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