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PubMed2002

Do severe systemic sequelae of proteinuria modulate the antiproteinuric response to chronic ACE inhibition?

BACKGROUND: ACE inhibition exerts an antiproteinuric and renoprotective effect. However, residual proteinuria is often present. As residual proteinuria is associated with a poor renal outcome, identification of its determinants is important. We found previously that the systemic sequelae of proteinuria enhance renal damage in untreated nephrotic rats. The impact of systemic nephrosis on renal therapy response, however, is unclear. In the present study we therefore investigated whether the severity of systemic nephrosis, estimated from plasma cholesterol, predicts residual proteinuria during ACE inhibition. METHODS: Sixty male Wistar rats with established adriamycin nephrosis were studied. Six weeks after the induction of nephrosis, rats were stratified for proteinuria and treated for 2 weeks with lisinopril (75 mg/l) or vehicle. RESULTS: At the start of treatment, median proteinuria was 744 mg/day (95% confidence interval (CI) 609-860) and plasma cholesterol was 10.4 mmol/l (95% CI 8.0-12.6), reflecting the state of systemic nephrosis. Lisinopril, but not vehicle, reduced blood pressure and proteinuria (-62%; range -70 to -48; P<0.001). Residual proteinuria was 275 mg/day, with a wide range (47-1119 mg/day). Pre-treatment proteinuria and pre-treatment cholesterol correlated positively with residual proteinuria. By multivariate analysis (r(2) of model =0.92), both pre-treatment cholesterol and pre-treatment proteinuria were independent predictors of residual proteinuria. The quantitative impact of this multivariate analysis is illustrated by the difference in residual proteinuria between rats with a cholesterol:proteinuria ratio less than, compared with greater than, the median (residual proteinuria 298 mg/day (CI 129-496) vs 439 mg/day (CI 158-670), respectively). Blood pressure response was not predicted by the tested predictor variables. CONCLUSIONS: In this model of proteinuria-induced renal damage, not only proteinuria as such, but also the concomitant nephrotic alterations predict residual proteinuria. Further studies, applying specific interventions, are needed to determine which components of the systemic derangements could play a causal role in the modulation of therapy response.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

The prognostic importance of severity and type of post-transplant proteinuria.

Proteinuria, developing after renal transplantation may influence allograft and patient outcomes. This study aimed to investigate the effect of proteinuria on patient and allograft survival. Among 514 patients, 56 (11%) patients with good allograft function and proteinuria were evaluated retrospectively. Patients with proteinuria were classified as group P (20 patients with permanent proteinuria, Male/Female: 16/4) and group T (36 patients with temporary proteinuria, M/F: 29/7) according to the type of proteinuria. Also, considering the amount of proteinuria, patients were classified as group M (32 patients with massive proteinuria, M/F: 29/3) and group NM (24 patients with non-massive proteinuria, M/F: 16/8). The mean time interval between transplantation and appearance of proteinuria was 23.7 months (range 0-121 months) and no difference was found between groups. Two- and 5-yr allograft survival rates were found to be 85 and 80% in group M, and 95 and 82% in group NM. respectively (p = 0.24). In terms of type of proteinuria, 2- and 5-yr allograft survival rates were found to be 70 and 58% in group P and 92 and 87% in group T, respectively. The difference between groups P and T was found to be statistically significant (p = 0.02). Most (85%) of the patients with permanent proteinuria also had massive proteinuria. In conclusion, we found a significant relation between type and severity of proteinuria. The type of post-transplant proteinuria had a stronger effect on allograft outcome than the severity of proteinuria.

Adult↗
PubMed2000

A modern approach to selectivity of proteinuria and tubulointerstitial damage in nephrotic syndrome.

BACKGROUND: The selectivity of proteinuria, introduced in clinical nephrology in 1960 and useful in predicting steroid responsiveness in nephrotic syndrome, found little place in clinical practice in subsequent decades, since its assessment did not appear to help predict histologic diagnosis or determine prognosis. The amount of proteinuria and the degree of tubulointerstitial damage appeared to be better predictors of functional outcome. A correlation between them has been found, referred to some toxicity of proteinuria on tubular cells, but so far no single feature or component of proteinuria has been identified as being responsible for this toxicity. METHODS: We evaluated 89 patients with nephrotic syndrome [9 with minimal change disease (MCD), 29 with primary focal segmental glomerulosclerosis (FSGS), and 51 with idiopathic membranous glomerulonephritis (MGN)] to determine if the selectivity of proteinuria was associated with tubulointerstitial damage. A semiquantitative grading of histologic lesions and qualitative evaluation of the "tubular" component of proteinuria expressed as a pattern of sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and as fractional excretion of the low molecular weight (LMW) protein alpha1-microglobulin (FE alpha1m) were used. A second aim of the study was to assess the predictive value on functional outcome [remission or progression to chronic renal failure (CRF)] and response to therapy of the selectivity of proteinuria, considered alone and in combination with FE alpha1m. RESULTS: Proteinuria was classified as highly selective [selectivity index (SI) < or = 0.10, N = 15], moderately selective (SI > or = 0.11 < or = 0.20, N = 34), or nonselective (SI > or = 0.21, N = 40). A significant relationship was found between the SI and the histologic degree of tubulointerstitial damage (score 0 to 1 vs. score > or =2, P = 0.000), severity of the tubular component of proteinuria (mixed SDS-PAGE pattern with LMW proteins not lower than 23 kD vs. mixed pattern with LMW proteins up to 20 to 10 kD, P = 0.000), and FE alpha1m (values below vs. above a defined cut-off, P = 0.000). The functional outcome was evaluated in 60 patients with baseline normal renal function (serum creatinine 0.97 +/- 0.19 mg/dL). The patients with high, moderate, or nonselective proteinuria had 100, 50, and 29% of complete or partial remission (P = 0.0001) and 0, 25, and 35% of progression to CRF, respectively (P = 0.050). In 45 patients with moderately selective (N = 28) and nonselective (N = 17) proteinuria, according to some arbitrary cutoffs for FE alpha1m (MGN, < or = vs. > 0. 240% of creatinine clearance; FSGS and MCD, < or = vs. > 0.350%), the remission rate was 62 versus 6% in patients with FE alpha1m below or above the cutoffs (P = 0.0001), and progression to CRF was 7 and 69%, respectively (P = 0.0001). The response to therapy (complete or partial remission at the last observation), evaluated retrospectively in 40 patients, was 100, 67, and 33% in high, moderate, and nonselective proteinuria (P = 0.0002); in 30 patients with moderate and nonselective proteinuria, according to an FE alpha1m value that was < or = or > the cutoffs, the response rate was 75 versus 10% (P = 0.001). CONCLUSIONS: There is a significant relationship between selectivity of proteinuria and tubulointerstitial damage. Moreover, the selectivity of proteinuria has a predictive value on functional outcome. When proteinuria is highly selective, the tubulointerstitial damage is rather infrequent, and 100% of patients develop clinical remission. When proteinuria is moderately selective or nonselective, increasing numbers of patients develop tubulointerstitial damage; in these patients, the functional outcome and response to therapy is partly dependent on tubulointerstitial involvement, and the best predictor of functional outcome is the combination of SI and FE alpha1m.

Adolescent↗
PubMed2002

[Changing profiles of proteinuria in renal transplantation. Predictive factors for its appearance].

Proteinuria is a risks factor that accelerates the progression of renal insufficiency by several mechanisms. In the renal transplant proteinuria is a predictor of progressive renal insufficiency and it is associated with poor patient and graft survival. We have performed a longitudinal observational case-control study to defect and quantify proteinuria in a group of 100 cadaveric renal transplant recipients and to evaluate the influence of several factors on its appearance. We have considered the variables age and sex of the donor and recipient, number of HLA-DR, A and B mismatches, cold ischemia time, basal renal disease, initial immunosuppression, immediate versus delayed graft function and acute rejection. Three patients who did with a functioning graft were excluded from the analysis of the data. All variables were analysed in a regression model of multivariate analysis. Proteinuria in the moths 1, 3, 6, 9 and 12 was: 0.38 +/- 0.27 g/day, 0.38 +/- 0.32 g/day, 0.44 +/- 0.99 g/day, 0.42 +/- 0.58 g/day and 0.37 +/- 0.54 g/day, respectively. We analysed the profile of the proteinuria in each patient individually. Fifty three patients (54.6%) did not develop proteinuria, 12 patients (12.4%) had transient initial proteinuria, 23 patients (23.7%) had persistent proteinuria and 9 patients (9.3%) had progressive proteinuria. The renal function differed between groups. Higher creatinine levels were found in the patients with persistent proteinuria and those with progressive proteinuria. We analysed the patients according to several variables. The age of the donor was higher in the group of patients with persistent proteinuria and the incidence of acute rejection was higher in the group of patients who developed progressive proteinuria, with differences statistically significant. There was no difference in the univariate analysis in the other variables considered. The multivariate analysis confirms that the age of the donor and the basal glomerular disease predict persistent proteinuria and acute rejection predicts progressive proteinuria. According to our study, proteinuria is frequent in the renal transplant recipient with different evolutionary profiles. Two types are associated with bad renal function and have different predictive factors. We encourage the use of drugs which reduce proteinuria.

Adult↗
PubMed2001

Proteinuria after renal transplantation affects not only graft survival but also patient survival.

BACKGROUND: Proteinuria is associated with an increased risk of renal failure. Moreover, proteinuria is associated with an increased death risk in patients with diabetes mellitus or hypertension and even in the general population. METHODS: One year after renal transplantation, we studied the influence of the presence of proteinuria on the risk of either graft failure or death in all 722 recipients of a kidney graft in our center who survived at least 1 year with a functioning graft. Proteinuria was analyzed both as a categorical variable (presence versus absence) and as a continuous variable (quantification of 24 hr urine). Other variables included in this analysis were: donor/recipient age and gender, original disease, race, number of HLA-A and HLA-B mismatches, previous transplants, postmortal or living related transplantation, and transplantation year. At 1 year after transplantation, we included: proteinuria, serum cholesterol, serum creatinine, blood pressure, and the use of antihypertensive medication. RESULTS: In the Cox proportional hazards analysis, proteinuria at 1 year after transplantation (both as a categorical and continuous variable) was an important and independent variable influencing all endpoints. The influence of proteinuria as a categorical variable on graft failure censored for death showed no interaction with any of the other variables. There was an adverse effect of the presence of proteinuria on the graft failure rate (RR=2.03). The influence of proteinuria as a continuous variable showed interaction with original disease. The presence of glomerulonephritis, hypertension, and systemic diseases as the original disease significantly increased the risk of graft failure with an increasing amount of proteinuria at 1 year. The influence of proteinuria as a categorical variable on the rate ratio for patient failure was significant, and there was no interaction with any of the other significant variables (RR=1.98). The death risk was almost twice as high for patients with proteinuria at 1 year compared with patients without proteinuria. The influence of proteinuria as a continuous variable was also significant and also without interaction with other variables. The death risk increased with increasing amounts of proteinuria at 1 year. Both the risks for cardiovascular and for noncardiovascular death were increased. CONCLUSION: Proteinuria after renal transplantation increases both the risk for graft failure and the risk for death.

Adult↗
PubMed2005

[Influence of proteinuria on the lipoprotein (a) metabolism disorder].

BACKGROUND/AIM: Proteinuria causes lipid metabolism abnormalities. The aim of the present study was to examine the influence of proteinuria on the lipoprotein (a) metabolism disorder. METHODS: The study included 60 patients of the male-famele ratio (M: F = 32 : 28), mean age 37.15 +/- 9.85 years with, the average endogenous creatinine clearance 86.27 +/- 19.81 ml/min, and the average body mass index (BMI) 24.18 +/- 2.23 kg/m2. Regarding the level of glomerular proteinuria, the patients were divided into four groups. The first (control) group, with proteinuria levels less than 0.25 g/24h, included 15 patients (M: F = 6 : 9), mean age 34.66 +/- 4.82 years, the mean clearance of endogenous creatinine 99.70 +/- 12.94 ml/min, and mean BMI 23.28 +/- 3.50 kg/m2. The second group, with proteinuria between 0.25 and 1.0 g/24 h, includ 15 patients (M: F = 9 : 6) with primary glomerulonephritis, mean age 37.87 +/- 9.65 years, the mean clearance of endogenous creatinine 82.85 +/- 18.48 ml/min, and mean BMI 23.83 +/- 1.57 kg/m2. The third group includ 15 patients (M : F = 8 : 7) with primary glomerulonephritis, with proteinuria between 1.0 and 3.0 g/24 h, mean age 35.67 +/- 13.29 years, the mean clearance of endogenous creatinine 82.85 +/- 18.48 ml/min, and mean BMI 23.83 +/- 1.57 kg/m2. The fourth group, with proteinuria higher than 3.0 g/24 h, included 15 patients (M: F = 9 : 6) with primary glomerulonephritis, mean age 40.40 +/- 9.75 years, the mean clearance of endogenous creatinine 80.16 +/- 20.80 ml/min, and mean BMI 24.83 +/- 1.44 kg/m2. In order to assess the influence of proteinuria on the lipoprotein (a) metabolism abnormalities we investigated 24-hour proteinuria, the colloid osmotic pressure (COP) of plasma, and the serum concentration of lipoprotein (a). The results were statistically analyzed using ANOVA, Kruscal-Wallis test, Mann-Whitney U test, chi2 test and Spearman test. RESULTS: Statistically, the patients with proteinuria over 3.0 g/24 h had the significantly higher values of lipoprotein (a) in serum as compared to the control group, and the patients with proteinuria about 0.25-1.0 g/24 h. The patients with proteinuria between 1.0-3.0 g/24 h had the statistically significantly higher values of lipoprotein (a) in serum than the control group (proteinuria < 0.25 g/24 h). There was a highly statistically significant negative correlation between serum albumin concentration, COP and the concentration of lipoprotein (a) in serum. There was a highly statistically significant positive correlation between 24-hour proteinuria and the concentration of lipoprotein (a) in serum. CONCLUSION: Proteinuria leads to the deterioration of lipoprotein (a) abnormalities.

Adult↗
PubMed1991

Pattern of proteinuria in IgA nephritis by SDS-PAGE: clinical significance.

Of sixty patients with IgA nephritis, none had CRF at first examination, 13 developed CRF with creatinine above 1.6 mg/dl within 6 years. Among these patients who had analysis of proteinuria by sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE), 31 patients had middle molecular weight (MMW) proteinuria alone (pattern 1), 10 had MMW and Low MW (LMW) or tubular proteinuria (pattern 2), 10 had high MW (HMW) and MMW proteinuria (Pattern 3) and 9 had HMW, MMW and LMW proteinuria (Pattern 4). At the end of a follow up period of 6 years (1983-1989) patients with mixed proteinuria had a higher incidence of chronic renal failure (CRF), 11/29 (38%) compared to those with pattern 1 proteinuria, 2/31 (6%) (chi 2 = 8.7, p less than 0.005). Based on the glomerular selectivity index (GSI), 19 patients had nonselective proteinuria but they did not have a higher incidence of CRF. By the selectivity index (SI), 18 patients had nonselective proteinuria and they showed a significantly higher incidence of CRF. Compared to the 41 patients who did not have LMW proteinuria, 19 patients with LMW proteinuria had more severe proteinuria. After a follow-up period of 6 years, patients with LMW proteinuria had a higher incidence of CRF (10% versus 47%, p less than 0.001). The presence of LMW proteinuria indicates a less favourable outcome and the pattern of proteinuria as assessed by the SDS-PAGE appears to be a better prognostic index in IgA nephritis than the SI and the GSI.

Adult↗
PubMed2006

Proteinuria and risk for stroke and coronary heart disease during 27 years of follow-up: the Honolulu Heart Program.

BACKGROUND: Urinary protein excretion has been linked to coronary heart disease (CHD); the relationship to stroke is less clear. We assessed whether urine dipstick screening for protein predicted stroke and CHD in the Honolulu Heart Program cohort. METHODS: Prospective, observational study of 6252 Japanese American men in Honolulu aged 45 to 68 years. Proteinuria was detected by means of urine dipstick screening during the first and third examinations. Subjects were classified as having no proteinuria if results were negative at both examinations, transient proteinuria if results were positive at 1 examination, and persistent proteinuria if results were positive at both examinations. Relative risk was derived using those subjects with no proteinuria as the reference. Outcomes were assessed through 27 years. RESULTS: No proteinuria was found in 92.8% of subjects, transient proteinuria in 6.1%, and persistent proteinuria in 1.1%. The age-adjusted incident stroke rates were 3.7, 7.3, and 11.8 per 1000 person-years in subjects with no, transient, or persistent proteinuria, respectively (P<.001). Age-adjusted rates of incident CHD were 9.4, 15.8, and 35.2 events per 1000 person-years, respectively (P<.001). Using Cox proportional hazards models, adjusting for age, body mass index, physical activity, smoking status, cholesterol level, presence of hypertension or diabetes mellitus, and alcohol consumption, the relative risk for 27-year incident stroke was 1.66 (95% confidence interval, 1.21-2.30; P = .002) with transient proteinuria and 2.84 (95% confidence interval, 1.51-5.34; P = .001) with persistent proteinuria, and relative risk for 27-year incident CHD was 1.48 (95% confidence interval, 1.19-1.83; P<.001) with transient proteinuria and 3.72 (95% confidence interval, 2.62-5.27; P<.001) with persistent proteinuria. CONCLUSION: Proteinuria detected at urine dipstick screening independently predicted increased risk for incident stroke and incident CHD over 27 years in this cohort.

Age Factors↗
PubMed2005

Evolution of proteinuria after conversion from calcineurin inhibitors (CNI) to sirolimus (SRL) in renal transplant patients: a multicenter study.

Conversion from calcineurin inhibitors (CNI) to sirolimus (SRL) has become an option in patients with chronic allograft nephropathy or other conditions. However, in some cases an increase of proteinuria has been reported after such therapeutic intervention. The aim of this study was to characterize the clinical course of this so far unexplained proteinuria after conversion. We performed a retrospective analysis evaluating 94 renal transplant patients from various Spanish centers. Proteinuria (629 determinations) and clinical developments were analyzed between 6 months before and 6 months after conversion. Patients were divided into three groups according to mean proteinuria before conversion (group A: <300 mg/d; group B: 300 to 2000 mg/d; and group C: >2 g/d). The mean proteinuria level was 1.69 g/24 h (n = 312 determinations) before and 2.36 g/24 h after conversion (n = 317 determinations; P = .006), which corresponds to an overall increase of 25% (1.55 to 1.69 g/24 h considering only determinations of 1 month before and 1 month after conversion; P = NS). We could not detect any clear correlation between proteinuria and serum creatinine nor between changes of proteinuria and changes of serum creatinine. A variance analysis for repeated measures showed an increase in proteinuria compared to the preconversion values (P = .003), and when the three groups of preconversion proteinuria were evaluated separately it could be observed that this change in the evolution of proteinuria was almost completely dependent of an increase in the group C (preconversion proteinuria greater than 2 g/d; P = .03), whereas in the other two groups changes were almost irrelevant. Finally, the switch to SRL in renal transplant recipients is followed by an increase in the level of proteinuria predominantly dependent of an increase in patients with high levels of preconversion proteinuria, whereas it seems to be irrelevant in patients without or with light or moderate proteinuria. These results suggest that this might not be a direct effect of SRL.

Calcineurin Inhibitors↗
PubMed2003

Retarding progression of chronic renal disease: the neglected issue of residual proteinuria.

BACKGROUND: Findings that early changes in proteinuria independently predict long-term glomular filtration rate (GFR) decline (Delta GFR) would highlight proteinuria as a major determinant of progression in chronic renal disease. METHODS: We investigated whether percent changes (3 months vs. baseline) in proteinuria (adjusted for concomitant changes in GFR) and residual proteinuria at 3 months, predicted Delta GFR [over a median (IQ range) follow up of 31.3 (24.5 to 50.3) months] in 273 patients with proteinuric chronic nephropathies enrolled in the Ramipril Efficacy In Nephropathy (REIN) study. RESULTS: Short-term changes and residual proteinuria (r = -0.23, P = 0.0001 for both) significantly correlated with Delta GFR and, at multivariate analyses, independently predicted Delta GFR (beta = -0.23, P = 0.0002; beta = -0.21, P = 0.0004, respectively). For comparable levels of residual proteinuria, patients with greater short-term reduction had slower Delta GFR (-0.28 +/- 0.04 mL/min/1.73 m2/ vs. -0.53 +/- 0.07 mL/min/1.73 m2/month, P = 0.04). On ramipril and conventional treatment, specular short-term changes in proteinuria (-18.2 +/- 3.5% vs. 24.2 +/- 6.7%, P < 0.0001, respectively) were associated with significantly different Delta GFRs. However, similar changes in proteinuria resulted in a difference in Delta GFR (ramipril, 0.39 +/- 0.07 mL/min/1.73 m2/month; conventional therapy, 0.74 +/- 0.11 mL/min/1.73 m2/month; P < 0.01) that was sevenfold higher (0.35 vs. 0.05 mL/min/1.73 m2/month) in patients with basal proteinuria > or =3 g/24 hours as compared to those with basal proteinuria 1 to 3 g/24 hours (ramipril, 0.25 +/- 0.06 mL/min/1.73 m2/month; conventional therapy, 0.30 +/- 0.07 mL/min/1.73 m2/month; P = NS). CONCLUSION: Regardless of blood pressure control and treatment randomization, short-term changes in proteinuria and residual proteinuria reliably predict long-term disease progression. Reducing proteinuria is renoprotective, particularly in nephrotic patients. As for arterial hypertension, proteinuria should be a specific target for renoprotective treatment.

Adolescent↗
PubMed2005

Importance of baseline distribution of proteinuria in renal outcomes trials: lessons from the reduction of endpoints in NIDDM with the angiotensin II antagonist losartan (RENAAL) study.

A key issue in the analysis of outcome trials is the adjustment for baseline covariates that influence the primary outcome. Imbalance of an important covariate between treatment groups at baseline is of considerable concern if one treatment group is favored over another with respect to the hypothesis testing outcome. With the use of the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) study database as an example, the influence of baseline proteinuria on the primary composite endpoint, ESRD, and ESRD or death after adjusting for baseline proteinuria as a continuous covariate was examined. Increasing baseline proteinuria was associated with increased risk for renal events, confirming that proteinuria is an important covariate for renal outcomes. When the randomization was stratified according proteinuria <2000 mg/g or >/=2000 mg/g, within the higher proteinuria stratum (>/=2000 mg/g), patients in the losartan group had a higher baseline mean proteinuria value. When the imbalance was adjusted, an increase in the magnitude and the significance of the risk reduction with losartan for each outcome was observed. No apparent interaction between treatment effect and baseline proteinuria was found, and there was no heterogeneity in the treatment response in patients with different baseline proteinuria levels. After proteinuria was adjusted as a continuous variable, greater treatment effects were observed in the RENAAL study. This effect was due solely to the imbalance in baseline proteinuria. Considering the importance of proteinuria as a risk factor, adjustment for baseline proteinuria as a continuous covariate should be prespecified in the design and analysis of clinical trials involving renal outcomes, even when patients are stratified on the basis of level of proteinuria.

Adult↗
PubMed2000

Trends in persistent proteinuria in adult-onset diabetes: a population-based study.

OBJECTIVE: This study investigates temporal trends in the prevalence and incidence of persistent proteinuria among people with adult-onset diabetes (age > or =40 years). RESEARCH DESIGN AND METHODS: The complete community-based medical records of all Rochester, Minnesota, residents with a diagnosis of diabetes or diabetes-like condition from 1945 through 1989 were reviewed to determine whether they met National Diabetes Data Group (NDDG) criteria. All confirmed diabetes cases residing in Rochester on 1 January 1970 (n = 446), 1980 (n = 647), and/or 1990 (n = 940) were identified. The medical records of these prevalence cases were reviewed from the time of the first laboratory urinalysis value to the last visit, death, or 1 April 1992 (whichever came first) for evidence of persistent proteinuria (two consecutive urinalyses positive for protein, with no subsequent negative values). Similarly, the medical records of all 1970-1989 diabetes incidence cases (n = 1,252) were reviewed to investigate temporal changes in 1) the likelihood of having persistent proteinuria before the date NDDG criteria was met, i.e., baseline; 2) the risk of persistent proteinuria after baseline; and 3) the relative risk of mortality associated with persistent proteinuria. RESULTS: The proportion of diabetes prevalence cases with persistent proteinuria on or before the prevalence date declined from 20% in 1970 to 11% in 1980 and 8% in 1990. Among the 1970-1989 diabetes incidence cases, 77 (6%) had persistent proteinuria on or before baseline; the adjusted odds declined by 50% with each 10-year increase in baseline calendar year (P<0.001). Among individuals free of persistent proteinuria at baseline, 136 subsequently developed persistent proteinuria; the estimated 20-year cumulative incidence was 41% (95% CI 31-59); the adjusted risk did not differ as a function of baseline calendar year. Survival of individuals with persistent proteinuria relative to those without was reduced but did not differ by baseline calendar year. CONCLUSIONS: The prevalence of persistent proteinuria among people with adult-onset diabetes in Rochester, Minnesota, declined 60% between 1970 and 1990. The decline appears because of a decrease in the proportion of diabetes incidence cases with persistent proteinuria before baseline rather than secular declines in the risk of persistent proteinuria after baseline or secular increases in the risk of mortality associated with persistent proteinuria. Similarity over time in age and fasting glucose at baseline, and at prevalence dates, is evidence that earlier detection of diabetes is not the sole explanation for the decline.

Blood Glucose↗