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PubMed2000

Enalapril prevents clinical proteinuria in diabetic patients with low ejection fraction.

OBJECTIVE: Clinical proteinuria is a risk factor for both end-stage renal disease and cardiovascular disease. The prevalence of clinical proteinuria, its correlates and predictive value, and the effect of ACE inhibitors in preventing clinical proteinuria in diabetic and nondiabetic patients with left ventricular (LV) dysfunction are unknown. RESEARCH DESIGN AND METHODS: The Studies of Left Ventricular Dysfunction (SOLVD) trials were analyzed to determine the baseline distribution of clinical proteinuria and related cardiovascular risk factors, the effect of baseline proteinuria on the risk of hospitalization for congestive heart failure (CHF) and mortality, and the effect of enalapril in preventing new clinical proteinuria. RESULTS: A total of 5,487 out of 6,797 SOLVD participants (81%) were assessed for proteinuria at baseline. A total of 177 patients (3.2%) had baseline proteinuria. These patients had significantly higher systolic (137 vs. 125 mmHg, P < or = 0.001) and diastolic (83 vs. 77 mmHg, P < or = 0.001) blood pressure levels, a higher prevalence of diabetes (41 vs. 18%, P < or = 0.001), a lower ejection fraction (26.2 vs. 27.3%, P < or = 0.05), and greater degree of CHF (New York Heart Association [NYHA] class III/IV in 22 vs. 10%, P < or = 0.001) than patients without baseline proteinuria. Patients with baseline proteinuria also had higher rates of hospitalization for CHF (relative risk 1.81 [95% CI 1.37-2.41], P = 0.0001) and mortality (1.73 [1.34-2.24], P = 0.0001). Enalapril prevented clinical proteinuria in diabetic patients (0.38 [0.17-0.81], P = 0.0123) but not in nondiabetic patients (1.43 [0.77-2.63], P = 0.2622) without baseline proteinuria. CONCLUSIONS: Clinical proteinuria is an independent predictor of hospitalization for CHF and mortality in diabetic and nondiabetic patients with LV dysfunction. Enalapril significantly reduces the risk of clinical proteinuria in diabetic patients with LV dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Proteinuria following conversion from azathioprine to sirolimus in renal transplant recipients.

Recent studies have reported a significant increase of proteinuria in kidney transplant recipients who were switched from a calcineurin inhibitor (CI) to sirolimus. This has (partly) been ascribed to the hemodynamic renal effects of CI withdrawal. We have evaluated the evolution of proteinuria in renal transplant recipients who underwent conversion from azathioprine to sirolimus. In a randomized, prospective, multicenter study called RESCUE (Recurrent cutanEous Squamous cell Carcinoma Under RapamunE) the efficacy and safety is investigated of conversion to sirolimus in stable renal transplant recipients with a cutaneus squamous cell carcinoma (SCC). In our center 25 patients have been included in this study of which 13 patients were randomized to continue their current immunosuppressive treatment and 12 to conversion to sirolimus. After a mean follow-up of 360 days mean proteinuria increased from 0.37+/-0.34 to 1.81+/-1.73 g/24 h after conversion to sirolimus (P<0.005). In the control group there was no change in proteinuria. A significant increase of proteinuria was observed in all seven patients with proteinuria before conversion, whereas proteinuria remained absent in all patients without previous proteinuria. Two of the patients with proteinuria were converted from cyclosporine and five were converted from azathioprine to sirolimus. Sirolimus was discontinued in five patients with proteinuria, and in all of them proteinuria declined to baseline values. Our study demonstrates that conversion from azathioprine to sirolimus after kidney transplantation may cause a reversible increase of proteinuria. Sirolimus-induced proteinuria therefore cannot be ascribed to the hemodynamic renal effects of withdrawal of CI.

Aged↗
PubMed1996

Proteinuria predicts stroke and other atherosclerotic vascular disease events in nondiabetic and non-insulin-dependent diabetic subjects.

BACKGROUND AND PURPOSE: Increased urinary albumin and protein excretion is associated with cardiovascular disease mortality independent of other cardiovascular risk factors in subjects with non-insulin-dependent diabetes mellitus (NIDDM). We assessed the relationship between the different degrees of proteinuria at baseline and the incidence of stroke, as well as other atherosclerotic vascular disease events, in a prospective study of nondiabetic and NIDDM subjects. METHODS: Our study was based on the 7-year follow-up of cohorts of nondiabetic (n = 1375) and NIDDM (n = 1056) subjects in Finland. The urinary protein concentration at baseline was stratified into three categories: no proteinuria (< 150 mg/L), borderline (150 to 300 mg/L), and clinical proteinuria (> 300 mg/L). RESULTS: The association between the different degrees of proteinuria and the atherosclerotic vascular events was similar in nondiabetic and NIDDM subjects. Cardiovascular disease mortality was higher both in nondiabetic and NIDDM subjects with clinical proteinuria than in those without proteinuria. The incidence of stroke was 1.6% in nondiabetic subjects without proteinuria, 3.2% in subjects with borderline proteinuria, and 8.5% in subjects with clinical proteinuria (P < .001 for trend). In NIDDM patients, the corresponding rates were 7.2%, 11.1%, and 23.0%, respectively (P < .001 for trend). The association between clinical proteinuria and the incidence of stroke remained significant both in nondiabetic and in NIDDM subjects after adjustment for other cardiovascular risk factors. Clinical proteinuria was also associated with the incidence of coronary heart disease events and that of lower-extremity amputation. NIDDM independently increased the risk of atherosclerotic vascular disease events regardless of the proteinuria status. CONCLUSIONS: Clinical proteinuria significantly predicted stroke and other atherosclerotic vascular disease events independent of other cardiovascular risk factors. This finding is compatible with the view that increased urinary protein excretion rate may be associated with widespread vascular damage.

Adult↗
PubMed1985

The effect of proteinuria on relative mortality in type 1 (insulin-dependent) diabetes mellitus.

We followed 1,134 patients with Type 1 (insulin-dependent) diabetes, diagnosed between 1933 and 1952, until 1982 or death or until their emigration. Their age at onset of diabetes was under 31 years. Information concerning the development of persistent proteinuria was sought in every case. In 104 cases, the data were either questionable or the patient could not be traced. Twenty-nine patients developed non-diabetic proteinuria. Among the remaining 1,001 patients, 406 developed persistent proteinuria (350 died) and 595 did not (166 died). The incidence of persistent proteinuria was highest among men; it decreased with increasing year of diabetes onset from 1933 to 1952, and decreased with increasing age at onset. The relative mortality was extremely high among patients with persistent proteinuria, increasing to a maximum of about 100 at age 35 years. Patients not developing proteinuria had a relatively constant low relative mortality of about 2. The decreasing incidence of persistent proteinuria and the decreasing mortality with increasing calendar year of diabetes onset resulted in a 50% increase in life-expectancy among patients diagnosed in 1950 compared with patients diagnosed in 1935. In patients who developed persistent proteinuria, relative mortality was higher in women than men at all ages. In patients who did not develop proteinuria, relative mortality was similar in men and women after the age of 35. Uraemia was the main cause of death in patients with persistent proteinuria, although cardiovascular deaths were more frequent than in patients without proteinuria. Thus, proteinuria is associated not only with death from uraemia but also from cardiovascular disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Denmark↗
PubMed1999

HBV and proteinuria in relatives and contacts of children with hepatitis B virus-associated membranous nephropathy.

BACKGROUND: Hepatitis B virus (HBV)-associated membranous nephropathy (HBVMN) is an important cause of childhood nephrotic syndrome in regions endemic for the virus, but little is understood of the biosocial context in which the disease develops. We evaluated HBV status and proteinuria in family members and household contacts of index children with HBVMN to test the hypothesis that HBV carriage and asymptomatic proteinuria are closely linked and may be causally associated. METHODS: Thirty-one black children with biopsy-proven HBVMN were the index cases. One hundred and fifty-two family members and 43 black household contacts were the subjects of the study. We assessed HBV carrier status by testing for HBV antigens and antibodies using enzyme-linked immunosorbent assays (ELISA) and for HBV DNA by using slot-blot hybridization and the polymerase chain reaction. Sequencing of the precore region of HBV was done in a subset of both index cases and subjects. Proteinuria was assessed by measuring the urinary protein/creatinine ratio. RESULTS: Seventy-two (37%) of the 195 family members and household contacts were HBV carriers, and 53 (27%) had a protein/creatinine ratio greater than the physiological limit. The frequency of abnormal proteinuria was not significantly different in those with [22 out of 72 (30.5%)] or without [33 out of 104 (32%)] HBV carriage. This lack of association remained when carriers were classified into those who were HBsAg positive only and those with active viral replication (HBsAg and/or HBeAg and/or HBV DNA; P = 0.01). Family members were more predisposed to HBV carriage than household contacts, but abnormal proteinuria was present with equal frequency (P = 0.48). Age had a significant impact on proteinuria, with children less than five years being more likely to have abnormal proteinuria (P = 0.008). The prevalence of abnormal proteinuria in family members and household contacts of the index cases was more than that in community-based controls. The 10 index HBVMN cases and the 14 family members and household contacts who were tested all had HBV of genotype A. CONCLUSION: These results suggest that the family members and household contacts of children with HBVMN are at very high risk of HBV carriage; they also have asymptomatic proteinuria at a significantly higher rate than community-based controls. The HBV carrier status was not associated with proteinuria, a finding supported by peak prevalences of proteinuria in those under five years but no corresponding peak for HBV carriage. Proteinuria may indicate glomerular basement membrane dysfunction. Environmental and social factors may underpin development of these two covert disorders, but are insufficient to account for the index cases of HBVMN. The emergence of children with HBVMN from such households additionally depends on unidentified and possibly genetic factors.

Adolescent↗
PubMed2002

Influence of smoking and obesity on the development of proteinuria.

BACKGROUND: Proteinuria is a significant risk factor for end-stage renal disease. Previous evidence suggested that smoking and obesity increase the risk of proteinuria. However, it is unclear whether these risk factors predict the development of proteinuria independently of hypertension and diabetes mellitus. The aim of this study was to analyze the effects of obesity and smoking on the development of proteinuria in a screened cohort of subjects with normal kidney function. METHODS: A total of 5403 subjects (3403 men and 2000 women) who participated in the 1997 and 1999 health screening examinations in Okinawa Japan, and who were normal renal function (serum creatinine < or =1.2 mg/dL in men, < or =1.0 mg/dL in women) and negative proteinuria by dipstick examination in 1997 were eligible for study. Logistic analysis was used to examine the relation between the baseline state of smoking or obesity in 1997, and the development of proteinuria in 1999, adjusted for age, sex, and other confounding factors. RESULTS: Proteinuria developed in 5.8% of participants (6.7% in men, 4.4% in women; dipstick score, 1+ in 277, 2+ in 37, and > or =3+ in 4 participants). The incidence of proteinuria was positively associated with the number of cigarettes smoked per day (P = 0.04), and a body mass index (P < 0.0001) at baseline. Analysis showed that the relative risk (95% confidence interval) of developing proteinuria was 1.32 (1.00 to 1.74), P = 0.04 for cigarette smoking, 1.45 (1.13 to 1.86), P = 0.002 for obesity, 1.56 (1.19 to 2.06), P = 0.001 for hypertension, and 2.27 (1.55 to 3.32), P < 0.0001 for diabetes mellitus. Stratified with men and women, the relative risk was 1.28 (0.96 to 1.72), P = 0.09 for smoking, and 1.60 (1.19 to 2.14), P = 0.001 for obesity in men; the relative risk was 1.30 (0.44 to 3.80), P = 0.62 for smoking, and 1.04 (0.63 to 1.72), P = 0.87 for obesity in women. CONCLUSIONS: Hypertension and diabetes mellitus were superior to smoking and obesity in predicting the development of proteinuria in all subjects. Stratified with men and women, obesity was a significant risk factor for the development of proteinuria independently of both hypertension and diabetes mellitus in men. The risk of developing proteinuria also tended to be increased with cigarette smoking in men. Smoking and obesity in women were not significant in this data set.

Adult↗
PubMed2003

Perinatal outcomes in preeclampsia that is complicated by massive proteinuria.

OBJECTIVE: Current treatment of preeclampsia no longer mandates delivery for proteinuria of >5 g per 24 hours. We sought to determine whether delayed delivery of preeclampsia with massive proteinuria (>10 g/24 h) increased maternal or neonatal morbidity. STUDY DESIGN: Records of all women with preeclampsia who were delivered at <37 weeks of gestation between January 1, 1997, and June 30, 2001, were reviewed. Patients with underlying renal disease or multiple gestation were excluded. Patients were characterized as having mild (<5 g/24 h), severe (5-9.9 g/24 h), or massive (>10 g/24 h) proteinuria. Outcomes were compared using the chi(2) test, one-way analysis of variance, or Fisher exact test. RESULTS: Two hundred nine patients met the inclusion criteria: 125 patients had mild proteinuria, 43 patients had severe proteinuria, and 41 patients had massive proteinuria. No significant differences in maternal morbidity were seen. Massive proteinuria was associated with earlier onset of preeclampsia, earlier gestational age at delivery, and higher rates of prematurity complications. After correction for prematurity, massive proteinuria has no significant effect on neonatal outcomes. CONCLUSION: Women with preeclampsia and massive proteinuria did not have increased maternal morbidity compared with women with severe or mild proteinuria. Massive proteinuria appears to be a marker for early-onset disease and progression to severe preeclampsia. Neonatal morbidity appears to be a function of prematurity rather than of massive proteinuria itself.

Abruptio Placentae↗
PubMed2002

Proteinuria in renal artery occlusion is related to active renin concentration and contralateral kidney size.

OBJECTIVES: Angiotensin II, in addition to having vasopressor effects, induces proteinuria in experimental models. Proteinuria has been reported, sometimes in the nephrotic range, in patients with chronic complete renal artery occlusion. We aimed to identify the factors associated with proteinuria in such cases. DESIGN AND MAIN OUTCOME MEASURE: Complete renal artery occlusion was detected by intra-arterial angiography in 96 patients referred for hypertension. We analysed patient characteristics at presentation to identify the factors associated with proteinuria. SETTING: A referral hypertension unit. RESULTS: Median protein excretion was 0.25 g/day (range 0-11). Nine patients had nephrotic syndrome (proteinuria >/= 3.5 g/day per 1.73 m2). Patients in the upper tertile for proteinuria differed from those with lower proteinuria in terms of total cholesterol levels (P < 0.01), the proportion of diabetics (P < 0.01) and supine active renin concentration (P = 0.02). They tended to have higher systolic blood pressure levels (P = 0.07), a lower frequency of contralateral renal artery stenosis (P = 0.09) and a longer contralateral kidney (P = 0.09). In multivariate logistic regression, the factors independently linked to proteinuria in the upper tertile were active renin concentration (P = 0.05) and contralateral kidney length (P = 0.02). Proteinuria significantly decreased in nephrotic patients (P < 0.01) treated with revascularization or nephrectomy and/or angiotensin converting enzyme inhibition. CONCLUSIONS: Proteinuria in renal artery occlusion is positively related to active renin concentration, which reflects plasma angiotensin II concentration. Therapy aimed at lowering angiotensin II levels decreased proteinuria in nephrotic patients. The positive relationship between proteinuria and contralateral kidney length may reflect compensatory hypertrophy in response to nephron function loss.

Adult↗
PubMed1997

Influence of proteinuria on long-term transplant survival in kidney transplant recipients.

Long-term prognosis in kidney transplant recipients depends on multiple factors. To investigate whether mild proteinuria within the first 6 months following transplantation is a determinant of the long-term function and survival of kidney transplants, 357 patients transplanted between 1980 and 1990 were retrospectively examined over a period of 5 years. 25.5% of the patients developed an early proteinuria between 0.25 and 1.0 g/day over 6 or more months. This group was well matched concerning gender, age of recipient, underlying disease, time on hemodialysis, donor age, cold ischemia time and HLA mismatches with the group without proteinuria (n = 266). Five-year transplant survival in the group with proteinuria was 58.9% in contrast to 85.6% in recipients without proteinuria. Intermittent proteinuria did not worsen long-term prognosis. Proteinuria of 12 months or longer further reduced 5-year transplant survival to 42.6%. Over the whole observation period, serum creatinine in recipients with proteinuria was about 0.5 mg/dl higher as compared with patients without proteinuria. No correlation between proteinuria and gender, age of recipient, duration of hemodialysis, age of donor, cold ischemia time and mismatches could be detected. In conclusion, early proteinuria apparently is not due to established donor or recipient factors. However, there is a strong correlation of proteinuria with worse transplant function and survival.

Adult↗
PubMed2005

Angiotensin inhibition or blockade for the treatment of patients with quiescent lupus nephritis and persistent proteinuria.

Angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor blocker (ARB) reduces proteinuria and the rate of renal function deterioration in diabetic nephropathy and other glomerular diseases, but its role in quiescent lupus nephritis has not been established. We conducted a retrospective study to investigate the effects of ACEI/ARB on proteinuria and renal function in patients with persistent proteinuria (>1 g/day) despite resolution of acute lupus nephritis following immunosuppressive treatment. Fourteen out of 92 patients were included. The duration of treatment with ACEI/ARB was 52.1 +/- 35.7 months. The levels of proteinuria, serum albumin, serum creatinine, systolic and diastolic blood pressure were 1.10 to 6.90 g/day, 35.8 +/- 3.6 g/L, 102.54 +/- 34.48 micromol/L, 137.6 +/- 10.9 and 81.9 +/- 9.2 mmHg at baseline. Proteinuria and serum albumin showed significant sustained improvements after 6 and 24 months of treatment. Comparison of slopes for serial proteinuria, albumin and reciprocal of serum creatinine before and after treatment showed significant improvements in six (43%), eight (57%) and two patients, respectively. At last follow-up proteinuria remained significantly lower (0.36 g/day, P = 0.043) and albumin higher (41.3 +/- 2.2 g/L, P = 0.023). Eleven (78.6%) patients had proteinuria improved by >50%, and five had insignificant proteinuria at last follow-up. Systolic blood pressure was significantly reduced from 6 months onwards, but this did not correlate with proteinuria reduction. Diastolic blood pressure, serum creatinine, creatinine clearance, anti-dsDNA, C3 and haemoglobin were not altered. We conclude that ACEI/ARB effectively reduces proteinuria and improves serum albumin in patients with persistent proteinuria despite quiescent lupus nephritis.

Adult↗
PubMed1975

[Proteinuria in mature diabetic patients. Quantitative and qualitative analysis].

Proteinuria has been analysed in 334 maturity-onset diabetics and 80 matched controls. Proteinuria measured in the recumbent position exceeded 100 mug/min in 53% of the diabetic population. The percentage of excessive proteinuria increased with duration of the disease. Sex and age had no influence. Out of 55 first year diabetics, 49% had abnormal quantitative proteinuria; this is in contrast to 76 longterm diabetics (over 12 years) of whom 38% had proteinuria under 100 mug/min. Electrophoresis and immuno-electrophoresis showed a glomerular pattern in 40%, a tubular pattern in 15% and a mixed pattern in 8% of all the diabetics. 32% of the diabetics with quantitatively normal proteinuria were abnormal qualitatively, and this may be the first manifestation of diabetic nephropathy. Thirty-eight other patients had a normal electrophoretic pattern in spite of increased proteinuria. Proteinuria levels were significantly associated with hematuria, bacteriuria and reduced GFR, but not with leukocyturia, insulin dependence and hypertension. Upright position increased the proteinuria to a greater degree amongst the patients with normal proteinuria. We discuss the role of increased filtration pressure and glomerular permeability in modifying proteinuria in diabetes. Sensitive quantitative and qualitative proteinuria determinations are important tools both in early diagnosis of diabetic nephropathy in clinical practice and in epidemiological studies.

Adult↗
PubMed1991

Proteinuria in essential hypertension.

Proteinuria was estimated using modified biuret method in 100 consecutive essential hypertensives of both sexes with mean age of 40 +/- 0.9 (18-50 yr) attending hypertension clinic. Proteinuria (mg/1.73 M2/24 h) in 60 mild hypertensives ranged from 45.4 to 493.0 with 9 (15%) patients having abnormal proteinuria (greater than 250 mg). In 26 moderate hypertensives proteinuria ranged from 96-1010; 7 (27%) had abnormal proteinuria. The proteinuria in 14 severe accelerated, malignant hypertensives ranged from 146.5-6132.6 with 10 (71%) having abnormal proteinuria. Duration of hypertension had no correlation with the amount of proteinuria. The amount of proteinuria was much higher (P less than 0.001) in patients with renal insufficiency (1322.5 +/- 586.4) and in patients with grades III and IV hypertensive retinopathy. LVH on ECG also correlated positively with proteinuria. The group with abnormal proteinuria had more patients with LVH (42.3% vs 12.2%), severe hypertensive retinopathy (30.8% vs 4.1%) and renal insufficiency (34.6% vs 0%) as compared to patients without elevated proteinuria.

Adolescent↗
PubMed1996

Effect of ACE inhibition by benazepril, enalapril and captopril on chronic and post exercise proteinuria.

Although post exercise proteinuria has long been known, its exact pathophysiology is unclear. Our objective was to determine whether long-term angiotensin converting enzyme (ACE) inhibition by different ACE inhibitors had an influence on post exercise proteinuria. We studied 14 patients who also had mild, chronic proteinuria caused by diabetes mellitus or chronic glomerulonephritis. We compared changes both in chronic (baseline) and post exercise proteinuria, during and after treatment with three different ACE inhibitors, with appropriate washout periods for the three drugs to all 14 patients. Proteinuria (mg/24 hours +/- SD), prior to the treatment was 682 +/- 92. Proteinuria after treatment for 30 days with benazepril was 464.4 +/- 82.6 (p < 0.001), with enalapril: 477.1 +/- 105.5 (p < 0.001), and captopril: 504.7 +/- 100.1 (p < 0.001). Proteinuria three days after discontinuing the treatment with benazepril was 532.4 +/- 113.5, (p < 0.01), with enalapril: 561.3 +/- 128.5, (p < 0.01), and with captopril: 620.8 +/- 101.8, p = n.s. Post exercise proteinuria prior to treatment (mg/min. +/- SD) was: 1.38 +/- 0.32, vs. after a 30-day treatment period with benazepril: 0.81 +/- 0.19 (p < 0.001), enalapril: 0.95 +/- 0.24, (p < 0.001), captopril: 1.09 +/- 0.27 (p < 0.02). Post exercise proteinuria three days after discontinuing the treatment was (blood pressure already back to baseline): in case of benazepril: 1.26 +/- 0.36 (p = n.s.), of enalapril: 1.17 +/- 0.46 (p = n.s.), and of captopril: 1.34 +/- 0.41 (p = n.s.). We conclude that the renin-angiotensin system plays a significant role in the pathogenesis of post exercise proteinuria; the antiproteinuric effect of ACE inhibition in exercise-induced proteinuria seems to be associated chiefly with the hemodynamic changes due to these drugs, whereas in chronic proteinuria the antiproteinuric and antihypertensive effects are, at least partially, dissociated.

Adult↗
PubMed2005

Proteinuria in children after renal transplantation.

Proteinuria is associated with poor long-term allograft as well as patient survival among adults after renal transplantation. In children, there are no studies focusing primarily on posttransplant proteinuria. The aim of this cross-sectional study was to investigate the prevalence of and possible risk factors associated with proteinuria. Thirty-three children (mean age of 13.7 +/- 4.3 years; mean time after renal transplantation = 2.3 +/- 2.2 years) were eligible for the study. There was an 82% prevalence of proteinuria (> or =96 mg/m2/d) with nephrotic range proteinuria (> or =960 mg/m2/d) in 12% of children. The mean urinary protein excretion was 256 +/- 299 mg/m2/d (range = 47 to 1264). Children with hypertension, as defined by ambulatory blood pressure monitoring, showed significantly higher proteinuria than normotensive children (382 +/- 435 vs 163 +/- 79 mg/m2/d, P < .05). Children with a history of a previous acute rejection episode showed significantly higher proteinuria than children who never had an episode (416 +/- 445 vs 165 +/- 91 mg/m2/d, P < .05). Children with proteinuria did not show statistically different graft function than children without proteinuria. No statistically significant correlation was observed between proteinuria and ambulatory blood pressure values or graft function. In conclusion, proteinuria is a frequent finding also in children after renal transplantation; it is associated with hypertension and a history of rejection episodes.

Adolescent↗
PubMed2003

Long-term antiproteinuric and renoprotective efficacy and safety of losartan in children with proteinuria.

BACKGROUND: Angiotensin receptor antagonists are effective in reducing proteinuria by an action independent of blood pressure. As a consequence, such agents retard progressive renal dysfunction in adults with chronic proteinuria. Long-term efficacy and tolerability data in children are unavailable. METHODS: Efficacy of losartan in reducing proteinuria and in preserving renal function was prospectively assessed in 52 consecutive children under 18 years of age with chronic proteinuric renal disorders, an initial creatinine clearance > or =25 mL/min/1.73 m(2), and a minimum of two or more follow-up visits. Thirty had proteinuria (P), and 22 had proteinuria combined with hypertension (P+H). Adverse effects were also evaluated. RESULTS: Proteinuria had persisted or increased during a mean interval of 8.5 months before initiation of losartan at a mean dosage of 0.8 mg/kg/d. Mean protein excretion before starting losartan was 2453 mg/m(2)/d and fell by 34% at a mean follow-up time of six weeks (visit I, P<.05), and between 64% and 67% at mean follow-up periods of 0.38, 0.71, and 2.48 years corresponding to visits II, III, and IV (all P<.001 compared with baseline). The proportion of children with protein excretion exceeding 40 mg/m(2)/h (nephrotic range proteinuria) or nephrotic syndrome (>3500 mg/1.73 m(2)/d) fell from 42% and 40% at the start, to 24% and 8%, respectively, at visit IV (P<.01). Mean creatinine clearance as well as serum potassium and total CO(2) levels remained unchanged during the time of follow-up. Reduction in proteinuria in the P subgroup alone correlated with lowering in diastolic blood pressure at visit II and with both diastolic and systolic blood pressure at visits III and IV (all P<.05); it was largely independent of reduction in blood pressure in the P+H subgroup. The concomitant use of immunosuppressive agents in 28 of the 52 children had an influence on proteinuria only at baseline and at visit I (P<.05). There was no significant change in height or body mass index Z scores. Thirteen children had adverse effects potentially ascribed to losartan; most of these either improved or resolved with dosage adjustment or resulted in its discontinuation in 9 of the 52 children (17%). CONCLUSION: Losartan therapy was associated with a marked and sustained reduction in proteinuria and in preservation of GFR in children with chronic proteinuric disorders. The association between proteinuria and systemic blood pressure reduction was complex: it was largely limited to the first year of losartan therapy and was more pronounced in the normotensive subgroup. Losartan was generally well tolerated.

Adolescent↗
PubMed2000

ACEI/ATRA therapy decreases proteinuria by improving glomerular permselectivity in IgA nephritis.

BACKGROUND: It has been postulated that angiotensin-converting enzyme inhibitor/angiotensin receptor antagonist (ACEI/ATRA) may decrease proteinuria in patients with glomerulonephritis by its action on the glomerular basement membrane. We therefore studied the relationship between the response of patients with IgA nephritis (IgAN) to ACEI/ATRA therapy by decreasing proteinuria and its effect on the selectivity index (SI) in these patients. METHODS: Forty-one patients with biopsy-proven IgAN entered a control trial, with 21 in the treatment group and 20 in the control group. The entry criteria included proteinuria of 1 g or more and/or renal impairment. Patients in the treatment group received ACEI/ATRA or both with three monthly increases in dosage. In the control group, hypertension was treated with atenolol, hydrallazine, or methyldopa. The following tests were performed at three monthly intervals: serum creatinine, total urinary protein, SI, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and low molecular weight (LMW) proteinuria. RESULTS: After a mean duration of therapy of 13 +/- 5 months, in the treatment group, there was no significant change in serum creatinine, proteinuria, or SI, but in the control group, serum creatinine deteriorated from 1.8 +/- 0.8 to 2.3 +/- 1.1 mg/dL (P < 0.05). Among the 21 patients in the treatment group, 10 responded to ACEI/ATRA therapy determined as a decrease in proteinuria by 30% (responders), and the other 11 did not respond (nonresponders). Among the responders, SI improved from a mean of 0.26 +/- 0.07 to 0.18 +/- 0. 07 (P < 0.001), indicating a tendency toward selective proteinuria. This was associated with an improvement in serum creatinine from mean 1.7 +/- 0.6 to 1.5 +/- 0.6 mg/dL (P < 0.02) and a decrease in proteinuria from a mean of 2.3 +/- 1.1 to 0.7 +/- 0.5 g/day (P < 0. 001). After treatment, proteinuria in the treatment group (1.8 +/- 1. 6 g/day) was significantly less than in the control group (2.9 +/- 1. 8 g/day, P < 0.05). The post-treatment SI in the responder group (0. 18 +/- 0.07) was better than that of the nonresponder group (0.33 +/- 0.11, P < 0.002). Eight out of 21 patients in the treatment group who had documented renal impairment had improved renal function compared with two in the control group (chi2 = 4.4, P < 0. 05). Of the eight patients in the treatment group who improved their renal function, three normalized their renal function compared with one from the control group. CONCLUSION: Our data suggest that ACEI/ATRA therapy may be beneficial in patients with IgAN with renal impairment and nonselective proteinuria, as such patients may respond to therapy with improvement in protein selectivity, decrease in proteinuria, and improvement in renal function. ACEI/ATRA therapy probably modifies pore size distribution by reducing the radius of large unselective pores, causing the shunt pathway to become less pronounced, resulting in less leakage of protein into the urine.

Adult↗
PubMed2004

Proteinuria: a new marker of long-term graft and patient survival in kidney transplantation.

BACKGROUND: Proteinuria developing after renal transplantation is associated with increased renal failure. Moreover, proteinuria in the general population has been shown to be associated with morbidity and mortality due to cardiovascular disease, which is the main cause of death in renal transplant patients. The purpose of the present study was to investigate whether persistent proteinuria following renal transplantation was associated with a worse patient and graft survival. METHODS: We analysed kidney recipients included in the Spanish Chronic Allograft Nephropathy Study (n = 3365). Proteinuria at 1 year post-transplantation was analysed as a categorical variable (< 0.5, 0.5-1, > 1 g/day). RESULTS: Post-transplant proteinuria at 1 year was detected in 15.3% of patients. Graft survival in proteinuric patients was significantly lower as compared with patients without proteinuria and the survival was worse with increasing amounts of proteinuria. In the groups with proteinuria, renal graft function at the time of the analysis was worse than in the group without proteinuria. Patient survival was lower in patients with proteinuria although there was no difference between the two groups of proteinuric patients. The main cause of death was vascular disease in all groups of patients but especially in proteinuric patients. The relative risk of graft failure and patient death was higher in proteinuric patients: graft failure [0.5-1 g/day: 2.33 (1.79-3.01, P<0.0001); > 1 g/day: 3.46 (2.73-4.39, P<0.0001)], patient death [0.5-1 g/day: 2.05 (1.39-3.01, P = 0.0002); > 1 g/day: 2.3 (1.55-3.39, P<0.0001)]. CONCLUSIONS: Proteinuria, as in native kidney disease, is an excellent marker of poor long-term allograft prognosis and is an independent risk factor for total and cardiovascular mortality in the renal transplant population.

Adult↗
PubMed1983

Proteinuria with gold therapy: when should gold be permanently stopped?

The treatment records of patients on gold therapy have been studied with particular respect to the development of proteinuria. This was classified as mild (up to 0.3 g/l), moderate (0.4-2 g/l), or heavy (more than 2.0 g/l). Particular attention was paid to the mode of onset and prognosis of the proteinuria and to subsequent gold administration. Twenty-seven patients with moderate or heavy proteinuria were identified. Two were suffering from psoriatic arthropathy, the rest were diagnosed as having rheumatoid arthritis, although three were persistently sero-negative. There was a direct correlation between the degree of proteinuria and its duration. Heavy proteinuria persisted for at least three months, whereas moderate proteinuria cleared within this period. No patient developed permanent renal impairment. Nine of 10 patients with heavy proteinuria had preceding mild or moderate proteinuria during which period gold administration had been continued. Fourteen of 17 patients with moderate proteinuria had their gold injections continued or re-started and none of these subsequently developed heavy proteinuria. It is suggested that moderate proteinuria should lead to cessation of gold therapy until the urine is clear but that subsequently treatment may be safely re-started.

Adult↗