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PubMed1999

The importance of proteinuria as a determinant of mortality following percutaneous coronary revascularization in diabetics.

OBJECTIVES: The aims of this study were to compare mortality and clinical events following percutaneous coronary intervention (PCI) between nondiabetics and diabetics with and without proteinuria. BACKGROUND: Diabetics have increased rates of late myocardial infarction, repeat revascularization and mortality when compared with nondiabetics following PCI. Proteinuria is a marker for diabetic nephropathy and potentially a surrogate marker for advanced atherosclerosis. It is unknown if proteinuria is a predictor of outcome in diabetics following PCI. METHODS: We performed an observational study of 2,784 patients who underwent PCI at the Cleveland Clinic between January 1993 and December 1995. There were 2,247 nondiabetics and 537 diabetics with urinalysis and follow-up data available (proteinuria n = 217, nonproteinuria n = 320). The diabetic proteinuria group was further prospectively stratified into low concentration (n = 182) and high concentration (n = 35). The end points were all-cause mortality and the composite end point of death, nonfatal myocardial infarction (MI) and need for revascularization. RESULTS: The mean follow-up time was 20.2 months. The two-year mortality rate was 7.3% and 13.5% for nondiabetics and diabetics, respectively (p < 0.001). The two-year mortality rate was 9.1% and 20.3% for the nonproteinuria and proteinuria groups, respectively (p < 0.001). There was a graded increase in mortality comparing the diabetic group. The two-year mortality rate was 9.1%, 16.2% and 43.1% for the nonproteinuria, low concentration and high concentration groups, respectively (p < 0.001). The difference in survival between the nondiabetic and nonproteinuric diabetics was not significant (p = 0.8). CONCLUSIONS: The presence of proteinuria is the key determinant of risk following PCI for diabetics. Diabetics without evidence of proteinuria have similar survival compared with nondiabetics.

Angioplasty, Balloon, Coronary↗
PubMed2004

Expression of alpha5beta1 and alpha6beta1 integrins in IgA nephropathy (IgAN) with mild and severe proteinuria. An immunohistochemical study.

Immunoperoxidase staining was carried out using monoclonal antibodies against integrin alpha5beta1 and integrin alpha6beta1 on renal biopsy specimens from patients with IgA nephropathy with mild proteinuria (n = 15) and with severe proteinuria (n = 10). Our study revealed increase in glomerular immunoexpression of alpha5beta1 in renal biopsies in IgA nephropathy with severe proteinuria. There were no statistical differences between interstitial alpha5beta1 immunostaining, as well as tubular alpha6beta1 immunoexpression in renal tissue between patients with mild and severe proteinuria. The intensity of interstitial alpha5beta1 integrin immunoexpression was positively correlated with the degree of interstitial fibrosis in both studied groups, meanwhile the intensity of tubular alpha6beta1 integrin immunoexpression was not related to the degree of renal interstitial fibrosis in patients with mild and severe proteinuria. Our results suggest that elevated immunoexpression of alpha5beta1 integrin on endothelial glomerular cells in the renal tissue in patients with severe proteinuria may point to the role of this integrin in the mechanism of glomerular injury in these cases of IgA nephropathy. The positive association between the interstitial expression of alpha5beta1 integrin and the relative interstitial cortical volume in renal biopsies in patients with mild and severe proteinuria suggests that alpha5beta1 integrin may play a role in the pathogenesis of chronic progressive renal disease in both studied group. Lack of positive correlation between tubular alpha6beta1 integrin immunoexpression and the relative interstitial cortical volumen may indicate that this molecule play no role in the pathomechanism of interstitial fibrosis in IgA nephropathy with mild and severe proteinuria.

Adolescent↗
PubMed1995

Low molecular weight proteinuria in Chinese herbs nephropathy.

Urinary excretion of five low molecular weight proteins (LMWP) [beta 2-microglobulin (beta 2m), cystatin C (cyst C), Clara cell protein (CC16), retinol-binding protein (RBP) and alpha 1-microglobulin (alpha 1m)], albumin and N-acetyl-beta-D-glucosaminidase (NAG) were quantified in 16 patients who followed a weight reduction program which included Chinese herbs, which have been incriminated in the genesis of Chinese herbs nephropathy (CHN). An additional group of four patients transplanted for CHN were investigated. Urinary data were obtained for comparison purpose in five groups of proteinuric patients: two groups with normal serum creatinine (SCr) and glomerular albuminura [12 patients with diabetes mellitus and microalbuminuria (DN), 10 patients with primary nephrotic syndrome (NS)]; two groups with normal SCr and toxic nephropathy [6 patients with analgesic (AN), 9 patients with cadmium nephropathy (CdN)]; and one group of seven patients with glomerular diseases and increased SCr (GN). Patients were classified according to serum level S beta 2m to take into account the possibility of overflow proteinuria at S beta 2m > or = 5 mg/liter. Three patients (CHN0) with a S beta 2m < 5 mg/liter, had a normal urinary protein pattern including NAG and a normal S beta 2m. Eight patients (CHN1) with a S beta 2m < 5 mg/liter had various abnormalities of their urinary protein pattern. In four of them (CHN1a) only beta 2m, RBP and CC16 were increased while total proteinuria and SCr were normal. In the other four (CHN1b and c) albumin, cyst C, alpha 1m and NAG were also elevated, while total proteinuria and SCr were moderately raised. Five patients (CHN2) with a S beta 2m > or = 5 mg/liter had a markedly increased excretion of all LMWP, albumin and NAG (CHN1 vs. CHN2, P < 0.05) as well as a further increase in total proteinuria and SCr. The urinary LMWP/albumin concentration ratio was strikingly higher in CHN patients than in patients with glomerular albuminuria (CHN1 vs. DN and NS, P < 0.01) or moderate renal failure with elevated S beta 2m level (CHN2 vs. GN, P < 0.01), confirming the existence of a tubular proteinuria independent of glomerular albuminuria or overflow proteinuria. A similar proteinuria pattern was present in the two toxic nephropathies (CdN and AN). This pattern was no longer recognizable after transplantation. In conclusion, CHN exhibits various profiles of tubular proteinuria which are the hallmarks of the disease. This pattern is still detectable in patients with renal failure and/or glomerular albuminuria. It is identical to that observed in cadmium and analgesic nephropathies. It does not recur after transplantation. Its most sensitive and reliable marker is a raised urinary level of CC16 or RBP.

Adult↗
PubMed2006

ADMA, proteinuria, and insulin resistance in non-diabetic stage I chronic kidney disease.

The rationale of this study is based on the fact that, both proteinuria and elevated asymmetric dimethyl arginine (ADMA) levels have been linked to the progression of vascular disease. Currently, there is not enough knowledge about any association between the levels of proteinuria and ADMA levels. Seventy-eight non-diabetic patients (42 men, 36 women, mean age of 26.1+/-5.2 years) with proteinuria having normal glomerular filtration rate were enrolled along with 38 healthy subjects (20 men, 18 women, mean age of 26.9+/-5.9 years). Proteinuria was below 3.5 g/day in 40 patients and above 3.5 g/day in 38 patients. Both groups had similar age, gender, and body mass index distributions. Serum ADMA, symmetric dimethyl arginine (SDMA), immunoreactive insulin, and high sensitivity C reactive protein (hsCRP) levels were measured. Insulin resistance was determined by homeostasis model assessment (HOMA). Serum ADMA, SDMA, insulin, hsCRP levels, and HOMA indexes were significantly higher in patients than in healthy control subjects. The above parameters were higher in the nephrotic range proteinuria group when compared to patients having protein levels below 3.5 g/day. There were significant correlations between the levels of proteinuria and the above parameters. According to the regression analysis, levels of proteinuria and hsCRP were significant determinants of serum ADMA levels. Our results indicate that, independent of other risk factors, ADMA is directly associated with proteinuria. Further studies are recommended to find out whether elevated ADMA levels are implicated in the high cardiovascular risk of proteinuric nephropathies.

Adult↗
PubMed2001

Proteinuria and tubulointerstitial lesions in lupus nephritis.

BACKGROUND: Response of the renal tubules to proteinuria is implicated in progression of renal disease. Experimentally, proteinuria causes increased tubular synthesis of macrophagic and other chemokines, with increased tubular cellular proliferation and apoptosis, leading to interstitial inflammation and fibrosis. Clinically, diminution of proteinuria leads to the slowing of progression, but whether this leads to reduction in tubular lesions has not been directly demonstrated in humans. METHODS: Initial (Bx1) and systematic six-month biopsies (Bx2) from 71 patients with lupus nephritis were studied, with a subset of 34 biopsies also stained for proliferating cell nuclear antigen (PCNA), the macrophage marker PGM1, and cytokeratins (AE1/AE3), and morphometric cell and tubular profile counts performed. RESULTS: Positive correlations were found between increasing levels of proteinuria and the following light microscopic parameters: tubular epithelial pyknosis, tubular epithelial nuclear "activation," tubular lumenal macrophages, interstitial inflammation and fibrosis, but not with tubulointerstitial immunofluorescence. Significant positive correlations also were found with the following immunohistochemical parameters: PCNA in epithelial cells (r = 0.74) and tubular luminal cells (r = 0.47); tubular lumenal macrophages (r = 0.63) and tubular epithelial cells with acquired PGM1 staining (r = 0.36); and pyknotic tubular epithelial cells (r = 0.47). All showed strong correlations with serum creatinine (S(Cr)) as well. All were reduced at Bx2, generally in parallel to the reduction in proteinuria. Tubulointerstitial immune deposits appear to play only a minor role in the development of tubular epithelial lesions and the progression of renal disease in lupus. They show only limited correlation with SCr and no correlation with proteinuria. By multiple regression, they are not associated with tubular epithelial lesions, interstitial inflammation or interstitial fibrosis at either biopsy, whereas tubular epithelial lesions are strongly associated with interstitial inflammation at Bx1 and with interstitial fibrosis at Bx2. Cytokeratin correlated strongly with S(Cr) (r = 0.53, P = 0.002) but not with proteinuria (r = 0.27, NS), and was the sole immunohistochemical parameter to increase at Bx2. It appears to be a sensitive marker for tubular atrophy. CONCLUSIONS: In this study both proteinuria and SCr showed a hierarchy of correlations with morphologic variables: Tubular epithelial cell changes> tubular macrophages> interstitial inflammation> interstitial fibrosis, corresponding to current experimental models, but not previously demonstrated in humans.

Creatinine↗
PubMed2002

Triglyceride, but not total cholesterol or low-density lipoprotein cholesterol levels, predict development of proteinuria.

BACKGROUND: Epidemiological data about the relationship between dyslipidemia and proteinuria are sparse. We conducted a retrospective and longitudinal study in a large screened cohort to evaluate whether triglyceride, high-density lipoprotein (HDL) cholesterol, total cholesterol, and low-density lipoprotein (LDL) cholesterol levels increase the risk of development of proteinuria and loss of renal function. METHODS: Post hoc analysis was performed for 4326 subjects who were free from proteinuria (dipstick 1+ or higher) at baseline (1997) with a follow-up period through 2000. Outcome measures were the development of proteinuria (1+ or higher) and change in glomerular filtration rate (GFR). Multiple logistic analysis and multiple regression analysis were used to analyze baseline characteristics related to the outcome measures. RESULTS: During the observational period, 505 (11.7%) of subjects had one or more episodes of proteinuria (>/=1+). Adjusted relative risk of triglycerides for one or more incidences of proteinuria was 1.007 (95% CI 1.000 to 1.105, P = 0.04) in men and 1.032 (95% CI 1.004 to 1.061, P = 0.02) in women. Total cholesterol, HDL cholesterol, and LDL cholesterol were not significant predictors of proteinuria. The mean change in GFR between 1997 and 2000 was -6.3 (SD = 9.0) mL/min/1.73 m2 in men, and -7.8 (SD = 10.7) mL/min/1.73 m2 in women. HDL cholesterol (beta = 0.04, t = 3.7, P = 0.0002) in men and triglycerides (per 10 mg/dL, beta = -0.09, t = -2.2, P = 0.02) in women were correlated with the change in GFR. CONCLUSIONS: High triglyceride levels predicted a risk of developing proteinuria in both men and women, but not total cholesterol nor LDL cholesterol. High triglyceride in women and low HDL cholesterol in men predicted the decline of renal function. It remains to be determined whether prospective treatment of dyslipidemia will protect against renal injury.

Adult↗
PubMed2003

Ethnic differences and determinants of proteinuria among South Asian subgroups in Pakistan.

BACKGROUND: Hypertension, diabetes, increasing age, and smoking are known risk factors for proteinuria. Prevalence of proteinuria is high in South Asians. However, ethnic subgroup differences and determinants of proteinuria within the South Asian population have not been explored. METHODS: The National Health Survey of Pakistan conducted between 1990 and 1994 was used to explore ethnic subgroup variation in proteinuria. Distinct ethnic subgroups, the Muhajir, the Punjabi, the Sindhi, the Pashtun, and the Baluchi, were defined by mother tongue. We report results in individuals aged >or=15 years (N = 9442). Proteinuria was defined as dipstick positive for protein on random urine sample. RESULTS: Increasing age, high consumption of meat, and presence of hypertension and diabetes were each independently associated with proteinuria. The age-standardized prevalence of proteinuria was 4.6% (4.2% to 5.1%) and varied among ethnic subgroups (P < 0.001). The highest was among the Sindhi (men 9.5%, women 10.3%), then the Muhajir (men 8.2%, women 4.7%), the Punjabi (men 3.2% women 3.5%), and lowest among the Baluchi (men 2.4%, women 4.2%) and the Pashtun (men 2.7%, women 1.2%). The ethnic differences persisted after adjusting for the above-mentioned sociodemographic, dietary, and clinical risk factors [adjusted odds ratio (OR) (95% CI)] were 6.42 (3.97 to 10.38) for the Sindhis, 3.58 (2.22 to 5.79) for the Muhajirs, 2.03 (1.25 to 3.29) for the Punjabis, and 1.75 (0.79 to 3.88) for the Baluchis compared to the Pashtuns). CONCLUSION: We conclude that unmeasured environmental or genetic factors account for ethnic variations in proteinuria, and deserve further study.

Adult↗
PubMed2003

Proteinuria and the risk of developing end-stage renal disease.

BACKGROUND: Dipstick urinalysis for proteinuria and hematuria has been used to screen renal disease, but evidence of the clinical impact of this test on development of end-stage renal disease (ESRD) is lacking. METHODS: We assessed development of ESRD through 2000 in 106,177 screened patients (50,584 men and 55,593 women), 20 to 98 years old, in Okinawa, Japan, who participated in community-based mass screening between April 1983 and March 1984. We used data from the Okinawa Dialysis Study Registry to identify ESRD patients. Multivariate logistic analyses were performed to calculate adjusted odds ratio and 95% confidence interval (95% CI) for the significance of proteinuria and hematuria on the risk of developing ESRD with confounding variables such as age, gender, blood pressure, and body mass index. A similar analysis was repeated in a subgroup of screened patients in whom serum creatinine data existed. RESULTS: During 17 years of follow-up, 420 screened persons (246 men and 174 women) entered the ESRD program. We identified a strong, graded relationship between ESRD and dipstick urinalysis positive for proteinuria; adjusted odds ratio (95% CI) was 2.71 (2.51 to 2.92, P < 0.001). Similar trends were observed after adding serum creatinine data. Compared with dipstick-negative proteinuria, adjusted odds ratio (95% CI) of proteinuria (1+) was 1.93 (1.53 to 2.41, P < 0.001) in men and 2.42 (1.91 to 3.06, P < 0.001) in women. CONCLUSION: Proteinuria was a strong, independent predictor of ESRD in a mass screening setting. Even a slight increase in proteinuria was an independent risk factor for ESRD. Therefore, asymptomatic proteinuria warrants further work-up and intervention.

Adult↗
PubMed2001

Low body weight is a risk factor for proteinuria in multiracial Southeast Asian pediatric population.

We examined the impact of low birth weight and low current body weight on proteinuria in a cohort of children participating in the pilot study of a nationwide screening program. Two thousand eighty-three children underwent screening examinations, including birth history, anthropometric measures, blood pressure measurements, and urinalysis. On this study, children with proteinuria were found to have significantly lower mean body weights compared with children without proteinuria (38.7 +/- 7.6 versus 42.8 +/- 11.0 kg; P < 0.001). Progressively decreasing body weights were associated with increasing degrees of proteinuria (42.8 +/- 11.0, 38.9 +/- 7.6, and 37.2 +/- 8.5 kg for 0, 30, and 100 mg/dL of protein, respectively; P = 0.05). When examined by multiple logistic regression, low body weight was associated with a 1.8-fold greater risk (95% confidence interval, 1.27 to 2.64; P = 0.0019) for proteinuria after adjusting for potential confounders. There were trends for lower birth weights in children with proteinuria (3,047.6 +/- 445.2 versus 3,175.0 +/- 608.6 g for proteinuric and nonproteinuric groups, respectively; P = 0.275) and a greater prevalence of children with birth weights less than the 25th percentile (31.3% versus 25.0%; P = 0.786). The relationship between low current body weight and proteinuria was not explained by differences in blood pressure. In conclusion, low current body weight had a stronger relationship with proteinuria than low birth weight in this pediatric population. We hypothesize that the effect of low birth weight on renal disease may be significantly enhanced by environmental factors that result in a low current body weight.

Asia↗
PubMed1984

Proteinuria in Sudanese children.

One thousand, eight hundred and forty-six apparently healthy nursery and school children living in the Khartoum area and belonging to different socio-economic classes were studied. Nine hundred and thirty-seven were boys, 909 girls. Their ages ranged from three to 16 years. N-multistix strips were used to test for proteinuria and haematuria, the former being also checked by the sulphosalicylic acid test. Children with proteinuria of 1+ or more were further investigated by examining their urinary sediment for abnormal deposits and by testing for orthostatic proteinuria using day and night specimens of urine with specific gravity of 1.018 or more. Children who had no proteins on orthostatic testing were rescreened for proteinuria 10-14 days after the initial screening. The prevalence rate for proteinuria was 7.2% with no significant difference between boys and girls. In both sexes the prevalence rate increased significantly with age but was not influenced by the socio-economic status. Of the children with proteinuria, haematuria occurred in 27% and abnormal urinary deposits in 14.8%. Orthostatic testing showed a negative result for proteins in 44%, orthostatic proteinuria in 40%, of whom a third had either abnormal urinary sediments or haematuria, and continuous proteinuria in 15.6% of whom the majority had abnormal deposits.

Adolescent↗
PubMed2004

Random urinary protein-to-creatinine ratio for prediction of significant proteinuria in women with preeclampsia.

OBJECTIVE: To evaluate the accuracy of random urinary protein-to-creatinine ratio for prediction of significant proteinuria in women with suspected preeclampsia. METHODS: A prospective study was conducted in hospitalized pregnant women with a suspicion of preeclampsia. Random mid-stream urine specimens were obtained for protein-to-creatinine ratio determination, and then participants were instructed to collect 24-h urine samples for protein measurement. With the criterion of 24-h proteinuria of at least 300 mg as a significant proteinuria, the sensitivity and specificity of a random urinary protein-to-creatinine ratio of > or = 0.19 for prediction of significant proteinuria were analyzed and a receiver operating characteristic curve was constructed to determine the optimal cutoff value. RESULTS: Forty-two patients completed the study. Sixty-nine percent of the study population had significant proteinuria. A cutoff of 0.19 demonstrated a sensitivity of 100% and a specificity of 53.8%. A ratio below 0.22 could rule out a significant proteinuria. The optimal cutoff value is 0.25 which yielded sensitivity, specificity and accuracy of 96.6%, 92.3% and 95.2% respectively. CONCLUSION: In hospitalized preeclamptic patients, the random urinary protein-to-creatinine ratio at a cutoff of > or = 0.25 revealed a highly accurate prediction of significant proteinuria and could be a more practical alternative for assessment of proteinuria.

Adolescent↗
PubMed1999

Glomerular and tubular proteinuria as markers of nephropathy in rheumatoid arthritis.

OBJECTIVE: We examined the prevalence of nephropathy in unselected patients with rheumatoid arthritis (RA) by measurement of marker proteins for glomerular and tubular damage in urine. METHODS: A highly sensitive immunoluminometric assay was used to measure albumin, immunoglobulin G and alpha1-microglobulin in 24 h urines of 44 RA patients and a control group of 46 patients with generalized osteoarthritis (OA). RESULTS: Fifty-five per cent of RA patients were found to have proteinuria as a symptom of renal disease. Drug therapy or vasculitis were identified as possible reasons for proteinuria in only 25% of these patients; in most patients (75%), no reason for proteinuria was found. Tubular and mixed proteinuria were more frequent than glomerular proteinuria. Only 15% of the control group exhibited mild proteinuria, which was attributable to nephrotoxic factors. The renal function of RA patients and the control group did not differ significantly. CONCLUSIONS: Proteinuria is a frequent symptom of nephropathy in RA. Screening for renal disease in RA should not only include creatinine measurement and dipstick examination of urine, but also more sensitive methods to detect tubular and glomerular proteinuria as a marker of tubular and early stages of glomerular damage.

Adult↗
PubMed2006

Viral hepatitis and proteinuria in an area endemic for hepatitis B and C infections: another chain of link?

BACKGROUND AND OBJECTIVES: Virus hepatitis may lead to nephropathy as one of its multiple extrahepatic manifestations. Proteinuria by dipstick, a simple test in practice, is a useful and cardinal sign of underlying renal abnormalities. The aim of this study was to elucidate the impact of hepatitis B virus (HBV) and/or hepatitis C virus (HCV) infections on the occurrence of proteinuria amongst adults. DESIGN AND SETTING: A prospective, cross-sectional, community-based study was conducted in an HBV/HCV endemic area of southern Taiwan. Eligible subjects aged 40-65 years (n=9934) underwent testing of hepatitis B surface antigen (HBsAg), HCV antibody (anti-HCV) and other related biochemical profiles. Urinalysis with repeated dipstick for proteinuria detection was performed. RESULTS: Anti-HCV-positive rate amongst proteinuria subjects was significantly higher than nonproteinuria subjects (9.6% vs. 6.2%, P<0.001). By contrast, HBsAg-positive rate did not differ between subjects with and without proteinuria (13.0% vs. 13.8%, P=0.57). Prevalence of proteinuria amongst anti-HCV-positive subjects (10.2%) was significantly higher than that in HBsAg-positive subjects (6.4%, P=0.004) and in HBsAg-negative or anti-HCV-negative subjects (7.0%, P=0.004). The difference persisted even after excluding diabetics. Multivariate logistic regression analyses showed that diabetes was the most important significant factor associated with proteinuria, followed by hypertension, anti-HCV seropositivity, body mass index, age and triglyceride levels. CONCLUSION: We demonstrated the significant association between proteinuria and HCV, but not HBV, infection in this HBV/HCV-endemic area.

Adult↗
PubMed2006

Proteinuria on dipstick urine analysis after sexual intercourse.

OBJECTIVE: To examine the role of sexual intercourse as a cause of proteinuria, and establishes its duration, as a knowledge of benign causes of proteinuria is required to avoid unnecessary testing. SUBJECTS AND METHODS: Twenty-four married couples were instructed to produce a urine sample before and after sexual intercourse; their urine was tested for proteinuria by dipstick analysis. RESULTS: Samples were assayed from 22 men and 11 women. Whereas none of the 24 men originally assessed for the study had proteinuria before sexual intercourse, six of the 22 who were eventually enrolled had proteinuria after intercourse (27.3%, 95% confidence interval, 10-50%; P = 0.008). None of the women had proteinuria after sexual intercourse (95% confidence interval, 70-100%). The time to disappearance of proteinuria was <12 h. CONCLUSION: Sexual intercourse is confirmed as a benign cause of proteinuria in men. Whenever possible, it is wise to avoid sexual intercourse at least 12 h before urinary dipstick testing.

Coitus↗
PubMed1995

Proteinuria and mortality in diabetes: the WHO Multinational Study of Vascular Disease in Diabetes.

The relation between proteinuria and mortality was investigated in 1188 patients with Type 1 diabetes and 3234 patients with Type 2 diabetes, aged 35-55 at baseline and followed up for a mean of 9.4 +/- 3.1 years in the WHO Multinational Study of Vascular Disease in Diabetes. Baseline prevalence of light or heavy proteinuria was the same (25%) in both types of diabetes after adjustment for differences in diabetes duration. Compared with patients with no proteinuria, all cause mortality ratios were 1.5 (95% confidence interval 1.1-2.0) and 2.9 (2.2-3.8) for Type 1 patients with light and heavy proteinuria, respectively, and 1.5 (1.2-1.8) and 2.8 (2.3-3.4) for Type 2 patients, after adjustment for age, duration of diabetes, blood pressure, cholesterol, and smoking. Proteinuria was associated with significantly increased mortality from renal failure, cardiovascular disease, and all other causes of death. In both types of diabetes, the association was strongest for renal deaths, and of similar magnitude for cardiovascular and all other causes of death. In conclusion, proteinuria is a common, important, and rather non-specific risk factor for increased morbidity and mortality in diabetes. The relation of proteinuria to mortality is similar for both types of diabetes. The benefits and risks of proteinuria reduction should be examined in large randomized trials with clinical endpoints.

Adult↗
PubMed1997

Improved methods of assessing proteinuria in hypertensive pregnancy.

OBJECTIVE: To determine whether use of an automated urinalysis device will improve the accuracy of detecting proteinuria, and whether spot urine protein to creatinine ratio will provide accurate quantitation of proteinuria in hypertensive pregnant women. DESIGN: Prospective studies assessing the accuracy of both detection and quantitation of proteinuria. SETTING: Antenatal ward and pregnancy day assessment unit of St George Hospital, a teaching hospital in Sydney, Australia. POPULATION: Hypertensive pregnant women admitted to hospital or day assessment unit for management of their hypertensive disorders. METHODS: 1. Routine dipstick urinalysis and 2. urinalysis by an automated device (Clinitek 100 Ames) on a midstream urine sample were compared with measurement of protein concentration on that sample (n = 103). In a third study, the protein:creatinine ratio on a midstream (spot) urine sample was compared with protein excretion over the subsequent 24 hours (n = 100). MAIN OUTCOME MEASURES: Relations between urine protein concentrations and 1. dipstick urinalysis and 2. automated urinalysis; 3. Positive and negative predictive values of spot protein:creatinine ratio for true proteinuria (> or = 300 mg/day). RESULTS: Automated urinalysis improved the percentage of true positive urinalyses from 48% with visual urinalysis to 74% (P = 0.02). True negatives were 98% to 100% for both methods. Spot urine protein:creatinine ratio correlated well with subsequent 24-hour urine proteinuria (r = 0.93, P < 0.001). A protein:creatinine ratio > 30 mg protein/mmol creatinine was the optimum discriminant value for true proteinuria, with sensitivity 93%, specificity 92%, positive predictive value 95% and negative predictive value 90%. CONCLUSIONS: Use of an automated urinalysis device improved accurate detection of proteinuria, particularly reducing false positive tests. A random urine protein:creatinine ratio provides an accurate and rapid quantitation of proteinuria in hypertensive pregnant women. This should improve clinical care, especially when managing hypertensive pregnant women as outpatients.

Creatinine↗
PubMed2002

Proteinuria and glomerulosclerosis in the Sabra genetic rat model of salt susceptibility.

In search of an experimental model that would simulate the association between proteinuria and salt sensitivity in humans, we studied protein excretion in the Sabra rat model of salt susceptibility. Monthly measurements of urinary protein excretion in animals fed standard rat chow revealed that normotensive salt-sensitive SBH/y developed proteinuria that averaged 65 +/- 7 mg/day (n = 10) at 9 mo, whereas proteinuria in normotensive salt-resistant SBN/y was 39 +/- 4 mg/day (n = 10) (P < 0.01). Histopathological evaluation revealed focal and segmental glomerulosclerosis (FSGS) lesions grade 2 in SBH/y and normal histology in SBN/y. To amplify the differences between the strains, uninephrectomy was performed. At 9 mo, proteinuria in SBH/y with one kidney (SBH/y-1K) was 195 +/- 12 mg/day (n = 10) and in SBN/y was 128 +/- 10 mg/day (n = 10) (P < 0.001); histopathology revealed FSGS grade 3 in SBH/y-1K and grade 1-2 in SBN/y-1K. To determine the effect of salt loading, animals were provided with 8% NaCl in chow, causing hypertension in SBH/y but not in SBN/y. Proteinuria markedly increased in both SBH/y with two kidneys (SBH/y-2K) and SBH/y-1K, but not in SBN/y; histopathology revealed FSGS grade 1-2 in SBH/y-2K, grade 2 in SBH/y-1K, no lesions in SBN/y-2K, and grade 0-1 in SBN/y-1K. We concluded that the SBH/y strain is more susceptible to develop proteinuria and glomerulosclerosis than SBN/y. In search for the genetic basis of this phenomenon, we investigated the role of candidate proteinuric gene loci. Consomic strains were constructed by introgressing chromosome 1 (which harbors the rf-1 and rf-2 proteinuric loci) or chromosome 17 (which harbors rf-5) from SBH/y onto the SBN/y genomic background. The resulting consomic strains developed marked proteinuria that was severalfold higher than in SBN/y-1K; histopathological evaluation, however, revealed FSGS lesions grade 1-2, similar to those found in SBN/y-1K and less severe than in SBH/y-1K. These results suggest a functional role of gene systems located on chromosomes 1 and 17 in inducing proteinuria in the salt-susceptible Sabra rat strain. These genetic loci do not appear to harbor major genes for glomerulosclerosis.

Age Factors↗
PubMed2006

Genetic dissection of proteinuria in the Sabra rat.

The pathophysiology underlying proteinuria remains incompletely understood and warrants further research. We currently initiated the investigation of the genetic basis of proteinuria in the Sabra rat, a model of salt susceptibility that we showed previously to be also a model of spontaneous proteinuria that is unrelated to salt loading or development of hypertension. We applied the total genome scan strategy in 75 F2 male animals derived from a cross between SBH/y, which are prone to develop proteinuria, and SBN/y, which are relatively resistant to the development of proteinuria. Animals were subjected to uninephrectomy (UNx) to accelerate the development of proteinuria and were provided chow with a low salt content, thus avoiding the development of hypertension. Urinary protein excretion was monitored before UNx and monthly thereafter for 8 mo. The genotype of F2 was determined with microsatellite markers. The data were analyzed for cosegregation by ANOVA and for genetic linkage with a novel multifaceted statistical genetic paradigm. We detected three proteinuria-related quantitative trait loci (QTL) that were associated with the salt sensitivity (H) alleles from SBH/y: SUP2, SUP17, and SUP20 on rat chromosomes (Chr) 2, 17, and 20. We detected an additional QTL on Chr 3, SUP3, that was associated with the salt resistance (N) alleles from SBN/y. A temporal effect was noted: QTL SUP2 and SUP17 surfaced at months 7-8, QTL SUP20 at months 6-8, and QTL SUP3 at months 5-6. The QTL emerging from this study lead us a step closer to identifying the genes associated with and elucidating the pathophysiology of proteinuria.

Animals↗