Proteinuria Is a Determinant of Quality of Life in Diabetic Nephropathy: Modeling Lagged Effects with Path Analysis

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Abstract

Background: Diabetic nephropathy with overt proteinuria often progresses relentlessly to end-stage renal disease (ESRD). Material and Methods: To answer the question whether it is impaired glomerular filtration rate (GFR) or its precursor proteinuria which is more related with multiple domains of health-related quality of life (HRQOL), we measured GFR and proteinuria in 44 patients with type 2 diabetes and overt nephropathy and repeated the measurements after 4 months. 38 patients with ESRD due to diabetic nephropathy served as a control group. We used path analysis to examine the association of baseline proteinuria and GFR with baseline and subsequent HRQOL scales. Results: Compared to patients with ESRD, patients with non-dialysis CKD had Kidney Disease Burden (KDB) that was, on a scale from 0 to 100, 19.8 better (95% CI 6.9–32.8) (p = 0.003). Mental component score (MCS) did not differ and physical component score (PCS) was worse in non-dialysis CKD patients by 8.5 (p < 0.001). Proteinuria at baseline was a predictor of PCS, MCS and KDB score at 4 months, suggesting a lagged effect of proteinuria on HRQOL after controlling for the autoregressive effects. GFR was not shown to have a significant impact on HRQOL. One log unit increase in proteinuria was associated with 3.8 (p = 0.011) fall in PCS, 3.3 (p = 0.043) fall in MCS and 10.6 (p = 0.006) fall in KDB. Conclusion: In patients with advanced diabetic nephropathy, we found that proteinuria has a lagged and profound effect on multiple domains of HRQOL.

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Most cited references 13

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Prediction of Creatinine Clearance from Serum Creatinine

Donald W Cockcroft, Henry Gault (1976)

A formula has been developed to predict creatinine clearance (C cr ) from serum creatinine (S cr ) in adult males: Ccr = (140 – age) (wt kg)/72 × S cr (mg/100ml) (15% less in females). Derivation included the relationship found between age and 24-hour creatinine excretion/kg in 249 patients aged 18–92. Values for C cr were predicted by this formula and four other methods and the results compared with the means of two 24-hour C cr’s measured in 236 patients. The above formula gave a correlation coefficient between predicted and mean measured Ccr·s of 0.83; on average, the difference between predicted and mean measured values was no greater than that between paired clearances. Factors for age and body weight must be included for reasonable prediction.

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Proteinuria, a target for renoprotection in patients with type 2 diabetic nephropathy: lessons from RENAAL.

Dick de Zeeuw, Giuseppe Remuzzi, Hans-Henrik Parving … (2004)

Proteinuria or albuminuria is an established risk marker for progressive renal function loss. Albuminuria can be effectively lowered with antihypertensive drugs that interrupt the renin-angiotensin system (RAS). We investigated whether albuminuria could not only serve as a marker of renal disease, but also function as a monitor of the renoprotective efficacy of RAS intervention by the angiotensin II (Ang II) antagonist, losartan, in patients with diabetic nephropathy. The data from the RENAAL (Reduction in End Points in Noninsulin-Dependent Diabetes Mellitus with the Angiotensin II Antagonist Losartan) study, a double-blind, randomized trial, were used to examine the effects of losartan on the renal outcome [i.e., the primary composite end point of doubling of serum creatinine, end-stage renal disease (ESRD) or death] in 1513 type 2 diabetic patients with nephropathy. We examined the effect of the degree of albuminuria at baseline, initial antiproteinuric response to therapy, and the degree of remaining (residual) albuminuria on renal outcome (either the primary composite end point of RENAAL or ESRD). We also evaluated the contribution to renal protection of the antiproteinuric effect of losartan independently of changes in blood pressure. Baseline albuminuria is almost linearly related to renal outcome, and is the strongest predictor among all measured well-known baseline risk parameters. After adjusting for baseline risk markers of age, gender, race, weight, smoking, sitting diastolic blood pressure, sitting systolic blood pressure, total cholesterol, serum creatinine, albuminuria, hemoglobin, and hemoglobin A(1c) (HbA(1c)) patients with high baseline albuminuria (> or =3.0 g/g creatinine) showed a 5.2-fold (95% CI 4.3-6.3) increased risk for reaching a renal end point, and a 8.1-fold (95% CI 6.1-10.8) increased risk for progressing to ESRD, compared to the low albuminuria group (<1.5 g/g). The changes in albuminuria in the first 6 months of therapy are roughly linearly related to the degree of long-term renal protection: every 50% reduction in albuminuria in the first 6 months was associated with a reduction in risk of 36% for renal end point and 45% for ESRD during later follow-up. Albuminuria at month 6, designated residual albuminuria, showed a linear relationship with renal outcome, almost identical to the relationship between baseline albuminuria and renal risk. Losartan reduced albuminuria by 28% (95% CI -25% to -36%), while placebo increased albuminuria by 4% (95% CI +8% to -1%) in the first 6 months of therapy. The specific (beyond blood pressure lowering) renoprotective effect of the Ang II antagonist, losartan, in this study is for the major part explained by its antialbuminuric effect (approximately 100% for the renal end point, and 50% for ESRD end point). Albuminuria is the predominant renal risk marker in patients with type 2 diabetic nephropathy on conventional treatment; the higher the albuminuria, the greater the renal risk. Reduction in albuminuria is associated with a proportional effect on renal protection, the greater the reduction the greater the renal protection. The residual albuminuria on therapy (month 6) is as strong a marker of renal outcome as is baseline albuminuria. The antiproteinuric effect of losartan explains a major component of its specific renoprotective effect. In conclusion, albuminuria should be considered a risk marker for progressive loss of renal function in type 2 diabetes with nephropathy, as well as a target for therapy. Reduction of residual albuminuria to the lowest achievable level should be viewed as a goal for future renoprotective treatments.

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Predictors of the progression of renal disease in the Modification of Diet in Renal Disease Study.

Lawrence G Hunsicker, Sharon G. Adler, Arlene Caggiula … (1997)

The Modification of Diet in Renal Disease (MDRD) Study examined the effects of dietary protein restriction and strict blood pressure control on the decline in glomerular filtration rate (GFR) in 840 patients with diverse renal diseases. We describe a systematic analysis to determine baseline factors that predict the decline in GFR, or which alter the efficacy of the diet or blood pressure interventions. Univariate analysis identified 18 of 41 investigated baseline factors as significant (P < 0.05) predictors of GFR decline. In multivariate analysis, six factors--greater urine protein excretion, diagnosis of polycystic kidney disease (PKD), lower serum transferrin, higher mean arterial pressure, black race, and lower serum HDL cholesterol--independently predicted a faster decline in GFR. Together with the study interventions, these six factors accounted for 34.5% and 33.9% of the variance between patients in GFR slopes in Studies A and B, respectively, with proteinuria and PKD playing the predominant role. The mean rate of GFR decline was not significantly related to baseline GFR, suggesting an approximately linear mean GFR decline as renal disease progresses. The 41 baseline predictors were also assessed for their interactions with the diet and blood pressure interventions. A greater benefit of the low blood pressure intervention was found in patients with higher baseline urine protein. None of the 41 baseline factors were shown to predict a greater or lesser effect of dietary protein restriction.

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Author and article information

Journal

Journal ID (publisher-id): AJN

Journal ID (nlm-ta): Am J Nephrol

Journal ID (doi): 10.1159/issn.0250-8095

Title: American Journal of Nephrology

Publisher: S. Karger AG

ISSN (Print): 0250-8095

ISSN (Electronic): 1421-9670

Publication date Subscription-year: 2007

Publication date (Print): September 2007

Publication date (Electronic): 27 July 2007

Volume: 27

Issue: 5

Pages: 488-494

Affiliations

^aInquiry Methodology Program and ^bEducational Psychology, Indiana University, Bloomington, Ind., ^cDivision of Nephrology, Department of Medicine, Indiana University School of Medicine, and ^dRichard L. Roudebush VA Medical Center, Indianapolis, Ind., USA

Article

Publisher ID: 106672 Other ID: Am J Nephrol 2007;27:488–494

DOI: 10.1159/000106672

PubMed ID: 17664865

SO-VID: cc434f38-437e-4333-8ad9-c8b495046311

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. 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.

History

Date received : 26 March 2007

Date accepted : 26 June 2007

Page count

Figures: 3, Tables: 3, References: 25, Pages: 7

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Proteinuria Is a Determinant of Quality of Life in Diabetic Nephropathy: Modeling Lagged Effects with Path Analysis

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Karger: Nephrology

Most cited references 13

Prediction of Creatinine Clearance from Serum Creatinine

Proteinuria, a target for renoprotection in patients with type 2 diabetic nephropathy: lessons from RENAAL.

Predictors of the progression of renal disease in the Modification of Diet in Renal Disease Study.

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