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There is a need for prediction scores that identify individuals at increased risk for developing progressive chronic kidney disease (CKD). Therefore, this study was performed to develop and validate a "renal risk score" for the general population. Design, setting, participants,measurements For this study we used data from the PREVEND (Prevention of Renal and Vascular ENdstage Disease) study, a prospective population-based cohort study with a median follow-up of 6.4 years. Participants with two or three consecutive estimated GFR (eGFR) measurements during follow-up were included. Participants within the group who had the most renal function decline (top 20% of the total population) and had an eGFR value60 ml/min per 1.73 m² during follow-up were defined as having progressive CKD. Possible predictors for progressive CKD were selected on the basis of univariable logistic regression analyses.A final prediction model was built using backward logistic regression analysis. Besides baseline eGFR, the model contained age, urinary albumin excretion, systolic BP, C-reactive protein, and known hypertension. The area under the receiver operating characteristic (ROC) curve was 0.84. We performed internal validation by using a bootstrapping procedure. As expected, after the regression coefficients were corrected for optimism, the area under the ROC curve was still 0.84. For clinical use we divided all predictors in meaningful clinical categories to develop a score chart. The area under the ROC curve was 0.83, indicating the high discriminative value of this model.Given the high internal validity of this renal risk score, this score can be helpful to identify individuals at increased risk for progressive CKD.

Item does not contain fulltext In 2006, the Dutch Nierstichting (Kidney Foundation) provided people with urinary dipsticks to determine whether they suffered from urinary protein loss. It was suspected that 0.5% of adult inhabitants would have hidden renal disease. Within two weeks, more than one million people had applied to receive the dipsticks. They were advised to contact their general practitioner if they tested positive. Blockade of the renin-angiotensin-aldosterone system (RAAS) in subjects with known renal disease and proteinuria improves renal and cardiac survival. However, many patients currently develop end-stage renal disease without prior knowledge ofhaving chronic kidney disease. These patients can be detected by screening for proteinuria or albuminuria. Japanese studies showed that about 5% of the general population have positive dipstick tests. It is to be expected that about 1% will be truly macroalbuminuric and another 2-3% will be microalbuminuric. Macroalbuminuria is the consequence of manifest glomerular damage, while microalbuminuria is in most cases related to underlying diabetes or hypertension (which frequently are not yet diagnosed). In both conditions, treatment with RAAS blockade is indicated and is aimed at both cardiac and renal protection. There are arguments indicating that screening of the general population for urinary protein loss is cost-effective.

Background: As yet little is known about the effect of delayed separation of whole blood stored at room temperature on the stability of the kidney function markers creatinine and cystatin C.Methods: We used plasma samples of 45 patients with a wide range of creatinine and cystatin C concentration. Samples were sent by post as whole blood, and differences in creatinine and cystatin C concentrations when measured (by enzymatic assay and PETIA, respectively) in plasma separated shortly after blood withdrawal or in plasma obtained after delayed separation at 24, 48 and 72 h. Intra- and inter-assay variability was assessed and total change limit was calculated to assess analyte stability.Results: Total change limit was 3.3% for creatinine and 3.9% for cystatin C. In whole blood creatinine and cystatin C remained stable up to 48 h. Delayed separation of whole blood did not induce more variability in measured concentrations of both analytes. Glomerular filtration rate estimated with the CKD-EPI equations showed less than 3 mL/min/1.73 m(2) difference when using creatinine or cystatin C concentration measured in plasma separated up to 48 h after blood withdrawal compared to plasma separated shortly after blood withdrawal. The new CKD-EPI equation that uses creatinine as well as cystatin C to estimate GFR showed even at 72 h less than 3 mL/min/1.73 m(2) difference.Conclusions: Creatinine and cystatin C remain stable in whole blood stored at room temperature up to 48 h before separation, and changes in these analytes during this time period do not affect variability and eGFR. (C) 2013 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.

Background. Chronic kidney disease is a growing public health problem worldwide. Previous studies have identified several predictors for renal function decline. However, these studies used a single measurement of these risk factors. Therefore, the aim of this study was to investigate whether besides the baseline values of these risk factors, changes in risk factors are associated with subsequent rate of renal function loss.Methods. Five thousand, six hundred and fifty-one participants in the Prevention of Renal and Vascular ENd-stage Disease (PREVEND) Study, a prospective, community-based cohort study, completed three screening visits during a follow-up of 6.5 years for detailed clinical and biochemical measurements. Change in renal function between the second and third screening rounds was chosen as the study parameter of interest. Changes in risk factors between the first and second screening rounds were incorporated as potential predictors for renal function loss in multivariable linear regression analyses. Based on the results of a previous study, gender-specific analyses were performed.Results. In males, an increase in urinary albumin excretion (UAE), systolic blood pressure (SBP) and cholesterol was associated with a subsequent higher rate of renal function loss, whereas in females, increases in glucose levels were associated with an increase in renal function. For males, the analyses showed that both the baseline values and the change in UAE and cholesterol were significant predictors for increased rate of renal function loss during subsequent follow-up. With respect to SBP, when taking also the change in this variable into account, the baseline value was no longer a significant predictor for renal function loss.Conclusions. The results of the present study show the value of screening programs including repeated measurements of risk factors. Furthermore, these data indicate that, besides baseline values of risk factors, the changes over time in these factors should also be taken into account when developing 'Renal Risk Scores' to identify subjects in the general population who are at risk for accelerated renal function deterioration.

The gradual onset of the antiproteinuric effects of ACE inhibition suggests that structural effects on the glomerular basement membrane (GBM) may be involved in their renoprotective action. To test this hypothesis, we studied the effects of lisinopril (5 mg/kg/24 h) on proteinuria, focal glomerulosclerosis (FGS) and glomerular heparan sulfate (HS) proteoglycan (HSPG) GEM staining in rats with established Adriamycin nephrosis, Treatment was started 6 weeks after disease induction. As expected, lisinopril reduced blood pressure, proteinuria and the FGS score. In control rats, Adriamycin nephrosis was associated with significantly impaired GEM staining for both HSPG core protein (assessed from BL-31 staining) and HS staining (assessed from JM-403 staining) 12 weeks after disease induction. In rats treated with lisinopril (5 mg/kg/24 h) GEM stianing was significantly better preserved for HS as well as for HSPG core protein. These data suggest that structural effects on the GEM, improving glomerular permselectivity, may be involved in the renoprotective effects of ACE inhibition in proetinuria-induced renal damage. Copyright (C) 2000 S. Karger AG, Basel.