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PubMed1989

[Differentiation of renal and postrenal hematuria and proteinuria with SDS polyacrylamide gel electrophoresis and immunoblotting].

The pattern of serum proteins separated by SDS-PAGE is typified by the microprotein apolipoprotein A I which is split from high density lipoprotein by SDS. High density lipoprotein is generally retained by the glomerulus and does not appear in the urine even in glomerulopathies. Thus, apolipoprotein A I is generally absent in the SDS-PAGE protein pattern of renal proteinurias. However, in postrenal hematurias and proteinurias apolipoprotein A I can be found by SDS-PAGE, immunoblotting and Ouchterlony test. Using rabbit anti-human-apolipoprotein A I as primary antibody and alkaline phosphatase-conjugated anti-rabbit immunoglobulins as secondary antibody antibody apolipoprotein A I could be detected even at a 1:128,000 dilution of blood. This means a microhematuria of only 8 microliters blood/l urine theoretically can be identified as postrenal. Unfortunately, apolipoprotein A I is not only visible on the immunoblots of postrenal hematurias and proteinurias but could also be seen in renal proteinurias. Thus, only with reservation can apolipoprotein A I be called a marker of postrenal hematuria and proteinuria. On the other hand, most renal proteinurias can be identified reliably by SDS-PAGE and analysis of apolipoprotein A I is superfluous. Apolipoprotein A I, however, could become useful in the differentiation of microhematurias without proteinuria.

Apolipoprotein A-I↗
PubMed1989

Long-term outcome of patients with membranous nephropathy after complete remission of proteinuria.

To assess the prognostic significance of complete remission in patients with idiopathic membranous nephropathy, 33 patients were followed for a median of 96 months after remission of proteinuria. All patients had had a histological diagnosis of membranous nephropathy and a nephrotic syndrome. Only patients with a complete remission lasting for at least six months and with a follow-up of at least four years after remission were considered. No relapse of proteinuria developed in 17 patients (51%), 7 patients had relapse of non-nephrotic proteinuria (21%) and 9 (27%) relapse of nephrotic proteinuria. However proteinuria disappeared again in some patients so that at follow-up 73% of patients are in complete remission, 21% have non-nephrotic proteinuria and only 6% have nephrotic syndrome. All patients maintained a normal plasma creatinine over the years. It is concluded that complete remission of proteinuria is a strong predictor of long-term favourable outcome in patients with idiopathic membranous nephropathy.

Adolescent↗
PubMed1985

Plasma concentrations of the natural anticoagulants protein C and protein S in patients with proteinuria.

We measured the plasma concentrations of the natural anticoagulant protein C and its cofactor protein S in 17 patients with severe proteinuria. In addition, prothrombin and antithrombin III levels were measured in the same group of patients. These results were compared with results obtained in 26 healthy controls and a group of 14 patients with chronic renal insufficiency (CRI) but minimal proteinuria. Protein C, protein S, and prothrombin levels were not significantly different between healthy controls and patients with CRI. However, protein C, protein S, and prothrombin levels were significantly elevated in 71%, 82%, and 76%, respectively, of patients with proteinuria. Antithrombin III levels were decreased in three of these 17 patients with proteinuria. Plasma concentrations of protein C, protein S, and prothrombin correlated significantly with each other and were inversely correlated with serum albumin concentrations. In three patients, high protein C, protein S, and prothrombin levels returned to normal during remission of the proteinuric state. Proteins C and S were not detectable in the urine of two patients with high-grade proteinuria. Thus, the plasma levels of the vitamin K-dependent, natural anticoagulant protein C and its cofactor protein S are increased in patients with proteinuria. The elevated plasma levels of other vitamin K-dependent proteins, such as prothrombin, suggest a generalized elevation in vitamin K-dependent protein synthesis in patients with proteinuria.

Adolescent↗
PubMed1986

Glomerular epithelial cell structure and function in chronic proteinuria induced by homologous protein-load.

The pathogenesis of glomerular scarring in proteinuric diseases is unknown, but glomerular epithelial cell (GEC) injury has been implied by the glomerular pathology seen in patients with focal segmental glomerular sclerosis and the nephrotic syndrome. We studied the effect of proteinuria on glomerular histology and GEC structure and function in rats made proteinuric for up to 8 weeks by the daily parenteral injection of homologous serum albumin. Proteinuria in the albumin-injected rats peaked at a mean level of 131 +/- 12 mg/24 hours (mean +/- SD) during the 1st week. It subsequently plateaued at 41 +/- 6 mg/24 hours but remained significantly greater than the saline-injected controls throughout the study. The albumin-injected rats developed slight but significant increases in blood pressure, serum albumin, plasma volume, and urine urea nitrogen compared to the saline injected controls. The serum creatinine was not different from controls. In the albumin-injected rats no glomerular scarring was observed after 8 weeks of proteinuria. The GEC developed albumin reabsorption droplets and signs of activity including increased numbers of organelles, vacuoles, and cytoplasmic hypertrophy, but there were no signs of irreversible GEC damage. The GEC foot processes were quantitated morphometrically, and there was no evidence of effacement after eight 4 or 8 weeks of proteinuria. GEC endocytic function, evaluated by the technique of protamine heparin aggregate disappearance, was not different from the saline injected controls. Proteinuria caused by the chronic administration of homologous serum albumin for 8 weeks is regularly associated with increased blood pressure, plasma volume, and serum albumin and ultrastructural changes in the GEC. These morphologic changes in the GEC apparently represent a normal response to proteinuria and are not evidence for irreversible cell damage. Despite their avid endocytosis of filtered plasma proteins, GEC endocytic function remains normal. These experimental results imply that glomerular sclerosis is not a consequence of proteinuria per se.

Animals↗
PubMed1982

The role of propranolol therapy and proteinuria in the etiology of post renal transplantation hyperlipidemia.

The effects of propranolol and proteinuria on the fasting lipoprotein profiles of 33 male renal allograft recipients have been studied. By isolating the two variables by division of the patients into four groups according to propranolol dose and proteinuria, i.e. 1. propranolol = 0 mg/24 hr, proteinuria; less than 0.5 g/24 hr; 2. propranolol less than 0 mg/24 hr, proteinuria; less than 0.5 g/24 hr; 3. propranolol = 0 mg/24 hr, proteinuria; less than 0.5 g/24 hr; and 4. propranolol greater than 0 mg/24 hr, proteinuria; greater than 0.5 g/24 hr, it has been shown that propranolol treatment elevates the very low density lipoprotein triglyceride and decreases the high density lipoprotein cholesterol and that proteinuria (greater than 0.5 g/24 hr) increases low density lipoprotein cholesterol. The possible significance of these results in terms of transplantee management is discussed.

Adolescent↗
PubMed1983

Significance of proteinuria on the outcome of renal function in patients with focal segmental glomerulosclerosis.

Kidney survival analysis was performed for 64 patients with focal segmental sclerosis to ascertain whether the degree of proteinuria and other factors determined at the time of renal biopsy might be associated with progression to end-stage renal failure. On the basis of urinary excretion of protein, which was measured in 63 of the 64 patients, three groups of patients were identified: 15 patients (group A) had asymptomatic proteinuria (less than 3.5 g/24 h), 38 patients (group B) had nephrotic proteinuria (3.5 to 14 g/24 h), and 10 patients (group C) had massive proteinuria (more than 14 g/24 h). Kidney survival curves showed that the median time from biopsy to end-stage renal failure was more than 11, 7, and 3 years for groups A, B, and C, respectively. Thus, patients with massive proteinuria had an accelerated course to renal failure as compared with other nephrotic patients who had a lesser degree of proteinuria (P = 0.014) and patients who had asymptomatic proteinuria (P less than 0.001). Higher initial serum creatinine levels and severe tubulointerstitial damage were associated with a shorter time to end-stage renal failure. Age at onset and at biopsy, systolic and diastolic blood pressure, serum albumin and cholesterol, percentage of sclerotic glomeruli, mesangial proliferation, hyalinosis, vascular sclerosis, and initial response to prednisone were not associated with the time to end-stage renal failure when each of these variables was considered separately.

Biopsy↗
PubMed1995

[Lifestyles and renal damage--association of smoking, drinking and physical activity with subsequent proteinuria].

To examine the role of lifestyles in the subsequent development of renal damage, the association of smoking, drinking and physical activity with subsequent proteinuria was investigated utilizing a longitudinal study. The subjects were 7,701 males aged 20-84 years, who participated in health examinations at Aichi Prefectural Center of Health Care, Nagoya, Japan, both in 1989-1990 and 1992-1993, and who showed no proteinuria at the first examination. Lifestyles at the first examination were compared between 140 men with, and 7,561 men without, newly developed proteinuria at the second examination. Age-adjusted odds ratios (ORs) of lifestyle factors for proteinuria were computed, and further the ORs were adjusted for age, systolic blood pressure, fasting plasma glucose level and other covariates obtained using multiple logistic regression analysis. Major significant findings which emerged from the present study were as follows. (a) The greater the consumption of alcohol per day, the higher the risk of subsequent proteinuria (trend p = 0.003). Heavy drinkers who consumed more than 58 g of alcohol per day experienced an increased risk (OR relative to non-drinker: 2.52). (b) Those who exercised less than once a week, and those who avoided walking even a short distance were at an increased risk (OR: 1.46, 1.55, respectively). Heavy drinking and low physical activity were found to be significantly associated with an increased risk of subsequent proteinuria even after adjusting for the covariates. An increasing risk of subsequent proteinuria with number of cigarette smoked per day was observed by univariate and multivariate analysis but without statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Value of fructosamine test in monitoring of diabetes complicated by proteinuria].

The aim of study was evaluation of fructosamine test in monitoring of diabetes mellitus complicated by proteinuria. Twenty patients with type 1 diabetes mellitus without proteinuria and 20 diabetic (type 1) patients with proteinuria were examined. Absent-present proteinuria was alone differential parameter between these groups. Correlations between past-glycaemia and other indices of diabetes balance as fructosamine, glycated haemoglobin and fructosamine: albumin molal ratio were examined. Results of study suggest that fructosamine test is useless in monitoring diabetes with proteinuria, but fructosamine: albumin molal ratio is a good parameter in monitoring of either: diabetes mellitus without proteinuria and with proteinuria.

Adult↗
PubMed1995

Screening proteinuria and hematuria in Malaysian children.

Screening for proteinuria and hematuria is important in the prevention of chronic renal disease. In Malaysia to date no such attempt has been made to establish the prevalence of proteinuria and hematuria. A total of 45,149 primary school children from three districts in Kelantan were screened for proteinuria and hematuria. They were 23,289 boys and 21,860 girls. The prevalence of abnormal urinary sediments after third screening was 0.17% ie 0.07% were in boys and 0.10% were in girls. The commonest abnormality was proteinuria (0.12%), followed by hematuria (0.03%) and combination of proteinuria and hematuria (0.02%). Hematuria was more commonly seen in girls compared to boys while proteinuria was seen in almost equal proportion in boys and girls. Despite screening large number of children the prevalence of asymptomatic proteinuria and hematuria was far lower than in an earlier reported study. Furthermore the majority had mild abnormalities.

Child↗
PubMed1997

Proteinuria predicts end-stage renal failure in non-diabetic chronic nephropathies. The "Gruppo Italiano di Studi Epidemiologici in Nefrologia" (GISEN).

We correlated baseline parameters with glomerular filtration rate (GFR) decline and kidney survival in 274 patients with proteinuric non-diabetic chronic nephropathies (creatinine clearance 20 to 70 ml/min/1.73 m2 and proteinuria > 1 g/24 hr over the last three months) enrolled in the Ramipril Efficacy In Nephropathy (REIN) trial. The GFR, evaluated at baseline, one, three and six months after randomization then every six months, declined linearly by 0.52 +/- 0.83 ml/min/1.73 m2/month (mean +/- SD) over a follow-up (median: range) of 21:3 to 52 months, and kidney survival was 64%. In multivariate analysis, higher baseline proteinuria (P = 0.006), and lower GFR (P = 0.0001) and creatinine clearance (P = 0.0001) correlated with a faster GFR decline. Higher proteinuria was the only baseline predictor of a shorter kidney survival (P = 0.0007) and its predictive value was independent of the underlying renal disease, treatment randomization, and blood pressure control during the followup. Patients in the lowest tertile of baseline proteinuria (< 2.5 g/24 hr) had the slowest rate of GFR decline (-0.25 +/- 0.72 ml/min/1.73 m2/month) and the highest kidney survival (94%), compared with patients in the middle tertile (proteinuria 2.5 to 4.3 g/24 hr; delta GFR, -0.59 +/- 0.82 ml/min/1.73 m2/month, P = 0.008; kidney survival 57%, P = 0.0011) and in the highest tertile (proteinuria > 4.3 g/24 hr; delta GFR, -0.79 +/- 0.87 ml/min/1.73 m2/month, P = 0.0001, kidney survival 44%, P = 0.0001). Kidney survival significantly differed even between the middle and highest tertiles (P < 0.05). Thus, in non-diabetic chronic nephropathies proteinuria is an independent and accurate predictor of disease progression and ESRF.

Adolescent↗
PubMed1997

Proteinuria, other selected urinary abnormalities and hypertension among teenage secondary school students in Nairobi, Kenya.

Four hundred and three teenage secondary school students (50.6% males) from two girls' and two boys' Nairobi City Schools, selected by stratified sampling, were screened to determine the prevalence of proteinuria, haematuria, nitrituria and hypertension. Nine students (2.2%) had significant proteinuria while 14 (3.5%) had microscopic haematuria. Two students had combined proteinuria and haematuria. There was no statistically significant difference in the prevalence of proteinuria and/or haematuria between the sexes. Other urinary abnormalities detected were leucocyturia in 14(3.5%) and nitrites in four (1%). Leucocyturia was commonner in females (p = 0.001). Cloudy urinary appearance was significantly associated with the presence of leucocyturia (p = 0.0028) and proteinuria (p = 0.0276). Neither personal history of recurrent sore throat and skin infections nor family history of hypertension, diabetes mellitus or kidney disease was significantly associated with proteinuria or haematuria. Blood pressure tended to increase with age. Mean systolic and diastolic blood pressures were significantly higher in boys than girls in the age group 15-18 years (P < 0.001). Of the 397 students whose blood pressures were measured, four (1%) were found to be hypertensive. Weight and body mass index were strong positive correlates of blood pressure. The prevalence of proteinuria, haematuria, other urinary abnormalities and hypertension ranges between 1% and 3.5% among teenage secondary school children. The majority are asymptomatic and have no significant associations. It is recommended that routine urinalysis and blood pressure measurements should be part of the school health service so as to identify asymptomatic students who require close monitoring and/or intervention.

Adolescent↗
PubMed2001

Sequence of events in the glomerular capillary wall at the onset of proteinuria in passive Heymann nephritis.

Proteinuria in passive Heymann nephritis (PHN) results from complement-mediated glomerular injury, since complement depletion with cobra venom factor (CVF) prevents proteinuria. However, there are no comprehensive morphological studies identifying the sites of injury leading to onset of proteinuria. To address this issue, we attempted to locate sites of injury involved in the onset of proteinuria in PHN. PHN was induced in intact Munich-Wistar rats (PHN-rats, examined at days 3, 5, and 7) and in complement-depleted rats (CVF treated, PHN-CVF-rats, examined at days 3 and 5). The distribution of endogenous albumin in the glomerular basement membrane (GBM) was studied in in situ drip-fixed glomeruli using immunogold immunocytochemistry, and glomerular anionic sites were visualized by polyethyleneimine staining. In addition, the ultrastructural localization of an epitope recognized by a proteinuria-inducing monoclonal antibody (called 5-1-6) directed against the slit diaphragm was examined. Significant proteinuria was seen in intact PHN-rats, starting at day 5. The intensity of gold labeling for endogenous albumin was significantly increased at the outermost site of the GBM (GBM interfacing foot process and the filtration slit, designated area O) at day 3 in both PHN-rats and PHN-CVF-rats in comparison to untreated controls. At day 5, labeling for albumin in area O was decreased in PHN-rats, but not in PHN-CVF-rats, where it was then higher; in PHN-rats, some areas between epithelial cells and subepithelial deposits were almost free of albumin labeling at day 7. There was no evidence of epithelial cell detachment in any group at day 5, but on day 7 limited focal detachment was seen exclusively in PHN-rats. In proteinuric rats, amorphous material that stained for albumin could be seen in the urinary space, without any exocytosis of labeling by glomerular epithelial cells. A significant reduction of intensity of staining for anionic sites was seen in parallel in both groups, but only in the regions of the lamina rara externa adjacent to subepithelial deposits. This local loss of charge might contribute to enhanced permeability to albumin in both PHN- and PHN-CVF-rats. Changes in the appearance of the filtration slits and in the density and distribution of antigen recognised by monoclonal antibody 5-1-6 were similar in PHN- and PHN-CVF-rats at day 5. Complement depletion prevented neither the reduction in anionic sites of the GBM nor the changes in the slit diaphragm observed. These data suggest that albumin leakage between the epithelial cell and the GBM (area O) could occur in PHN-rats, perhaps as a result of epithelial foot-process changes. This may be the final link in the chain of events responsible for the onset of proteinuria in PHN.

Albumins↗
PubMed2005

Change in serum creatinine levels between 6 and 12 months and kidney graft survival: influence of proteinuria.

Renal function within the first year after transplantation has been shown to be an important parameter influencing long-term survival. In this study, we examined the relationship between long-term outcome in 365 renal transplants and renal function in the first year, expressed as serum creatinine (SCr) level at 6 months and at 1 year as well as namely deltaCr, the change in SCr between 6 months and 1 year. In addition, we examined the influence of the presence of proteinuria as a predictive factor for a worse evolution. Graft survival was worse among patients with higher deltaCr, especially among those who developed proteinuria. In a Cox regression analysis of long-term graft survival, both deltaCr and proteinuria were important predictors of half-life. The risk of graft loss when deltaCr >0.3 was 2.65 (1.8-3.8; P < .000), whereas the risk increased to 5.67 (3.3-9.4; P < .00) when proteinuria was present. In conclusion, deltaCr values predict long-term graft survival. Patients who developed proteinuria were at higher risk for graft loss compared with those without proteinuria. By using a combination of SCr and deltaCr with proteinuria, it is possible to identify a subset of transplant recipients with a predictably shortened half-life.

Adult↗
PubMed1997

Characterization of proteinuria in primary glomerulonephritides: urinary polymers of albumin.

In 142 patients with primary glomerulonephritis (GN), there were polymers of albumin (PAs) in the urine samples of 87% of 15 minimal-change disease (MCD) patients, 52% of 27 focal segmental glomerulosclerosis (FSGS) patients, 51% of 47 membranous glomerulonephritis (MGN) patients, 55% of 20 membranoproliferative glomerulonephritis (MPGN) patients, and 9% of 33 immunoglobulin A nephropathy (IgAN) patients (P = 0.000). In IgAN, only three patients with nephrotic syndrome were PA positive. The PAs were significantly correlated with nephrotic syndrome (NS) (P = 0.000) and with the degree of proteinuria, ranging from 8% in patients with proteinuria less than 0.5 g/d to 58% in patients with proteinuria > or = 15.0 g/d (P = 0.001), but 40% of the nephrotic syndrome patients were PA-negative despite values of proteinuria comparable to those of PA-positive patients, suggesting that the presence of PAs is not simply related to protein loss, but probably to some other unidentified factor or lesion. For 72 patients (43 with NS) (22 FSGS, 36 MGN, and 14 MPGN patients) with normal renal function at entry (serum creatinine, 1.02 +/- 0.23 mg/dL) and a mean follow-up duration of 52 +/- 27 months, for whom PAs were determined and urinary protein characterized by sodium-dodecyl-sulphate polyacrylamide gel electrophoresis (SDS-PAGE) at the beginning of the follow-up period, the functional outcome was correlated with the patterns of proteinuria. Chronic renal failure (CRF) developed in 24% of all 72 patients, in 36% of the PA-positive patients, in 9% of the PA-negative patients (P = 0.007), in 44% of the SDS-PAGE 10-kd mixed glomerulotubular pattern patients, and in 17% of the SDS-PAGE 23-kd mixed-pattern patients (P = 0.001). The association of PAs with the 10-kd pattern enhanced the predictive value for CRF outcome: CRF developed in 62% of the PA-positive patients with the 10-kd pattern compared with 11% of the PA-negative patients with the 23-kd pattern (P = 0.0001). CRF developed in 32% of 43 patients with the nephrotic syndrome, in 48% of the PA-positive patients, and in 11% of the PA-negative patients (P = 0.037); in 50% of the 10-kd patients and in 24% of the 23-kd patients (P = 0.007); and in 70% of the PA-positive patients with the 10-kd pattern and 14% of the PA-negative patients with the 23-kd pattern (P = 0.001). In a retrospective study of 21 treated patients (11 FSGS, nine MGN, and one MPGN patient), a response to therapy with complete or partial remission was observed in 57% of all 21 patients; in 58% of patients with the nephrotic syndrome; in 88% of the PA-negative patients versus 38% of the PA-positive patients (P = 0.027); in 90% of the 23-kd patients versus 27% of the 10-kd patients (P = 0.004); and in 100% of the PA-negative patients with the 23-kd pattern versus 12% of the PA-positive patients with the 10-kd pattern (P = 0.001). In conclusion, urinary PAs are associated with GN characterized by lesions mainly localized in the glomerular capillary wall, with the presence of the nephrotic syndrome, and with the degree of proteinuria. In patients with FSGS, MGN, MPGN, and normal renal function at entry, the presence of polymers has a predictive value for CRF outcome; this value is enhanced by the contemporaneous presence of an SDS-PAGE proteinuric pattern with low molecular weight proteins up to 10-kd, which is known to be associated with diffuse tubulointerstitial lesions. Therefore, the best predictive value for either CRF outcome or for response to therapy was provided by a combination between a marker associated with the degree of proteinuria and the types of GN characterized by lesions mainly localized in the glomerular capillary wall and a marker associated with tubulointerstitial damage (SDS-PAGE mixed glomerulotubular pattern with low molecular weight proteins between 20 and 10 kd).

Adolescent↗
PubMed2003

Time course of proteinuria after living-donor kidney transplantation.

BACKGROUND: After cadaveric kidney transplantation, preservation-reperfusion damage results in glomerular and tubular proteinuria. There are no data on the time course of proteinuria after living-donor (LD) transplantation. METHODS: In 10 patients receiving a kidney graft from an LD, the excretion of high molecular weight proteins (albumin, transferrin, and immunoglobulin G) and low molecular weight proteins (beta2-microglobulin and alpha1-microglobulin) was measured at various time points during the first 5 days after transplantation. RESULTS: Immediately after restoration of the circulation, we observed a massive nonselective high molecular weight proteinuria, indicative of glomerular damage. This proteinuria rapidly decreased to slightly elevated values beyond 24 hr after transplantation. Low molecular weight proteinuria, reflecting tubular damage, was also prominent and remained grossly abnormal even at day 5. CONCLUSION: After LD transplantation, preservation-reperfusion injury causes massive proteinuria during the first 24 hr. Thereafter proteinuria rarely exceeds 1 g per day.

Adult↗
PubMedDate not supplied

[Protein/creatinine ratio in single urine samples for the semiquantitation of proteinuria in children with nephrosis]

OBJECTIVE: To estimate, semiquantitatively, the proteinuria of nephrotic patients by the use of the value of protein/creatinine ratio in single urine samples and determine its correlation with 24-hour proteinuria.METHODS: Analysis of 30 single urine samples and thirty 24-hour urine samples from 20 children with nephrosis followed up at the Division of Pediatric Nephrology of the University Hospital, Faculty of Medicine of Ribeirão Preto, University of São Paulo. Proteinuria in single urine samples and 24-hour urine samples was measured by the turbidimetric method with 3% sulfosalicylic acid. Urinary creatinine concentration was measured by the method of Hare, modified by Haugen and Blegen, adapted to the microtechnique.RESULTS: An excellent correlation was observed between 24-hour proteinuria and the protein/creatinine ratio in single urine samples, by linear regression analysis before (r = 0.82; p < 0.001) and after logarithmic transformation (r = 0.93; p < 0.001). All patients with 24-hour proteinuria at physiological levels (less than 0.1 g/m(2)/day) had a protein/creatinine ratio of less than 0.1 (mg/mg) in single urine samples. All patients with nephrotic 24-hour proteinuria (more than 1.0 g/m(2)/day) had a protein/creatinine ratio of more than 1.0 (mg/mg). The patients with intermediate proteinuria (between 0.1 and 1.0 g/m(2)/day) had a protein/creatinine ratio distributed on the three levels.CONCLUSIONS: The protein/creatinine ratio in a single urine sample is a simple and reliable method for the evaluation of proteinuria and eliminates the errors due to inadequate 24-hour urine collection.

Journal Article↗
PubMed1964

STUDIES ON THE MECHANISM OF EXPERIMENTAL PROTEINURIA INDUCED BY RENIN.

Renin-induced proteinuria in the rat was investigated, with special emphasis on the relationship between the enzymatic activity and the proteinuric effect of renin. The dependence of the proteinuric effect on the enzymatic activity was shown by using (a) renin preparations of widely varying purity and (b) chemically modified "active" and "inactive" renin derivatives. Angiotensin II, the pressor product of the enzymatic action of renin, also produced significant proteinuria. Adrenalectomy abolished the proteinuria induced by renin. Proteinuria, however, occurred as a result of pretreatment with DOCA, or aldosterone, or without treatment, 7 to 8 weeks after adrenalectomy. Electron microscopic studies of the kidney at the time of maximal proteinuria showed focal flattening and fusion of epithelial foot processes, as well as swelling and vesicle formation in endothelial and epithelial cells of the glomeruli. Studies with intravenously injected saccharated iron oxide showed increased permeability of the glomerular capillary basement membrane to these particles. These changes were transient and were not seen 24 hours after renin injection. Adrenalectomy prevented these changes. It is concluded that renin, acting through angiotensin, causes glomerular capillary damage with increased permeability of these structures to protein and resultant proteinuria. The adrenal glands participate in a permissive role in this phenomenon.

Adrenalectomy↗
PubMed2005

Reversal of ongoing proteinuria in autoimmune mice by treatment with C-reactive protein.

OBJECTIVE: To examine the ability of injection of C-reactive protein (CRP) to treat systemic lupus erythematosus (SLE) in the (NZB x NZW)F(1) (NZB/NZW) mouse and to use a nephrotoxic nephritis (NTN) model to further examine the mechanism of this activity. METHODS: NZB/NZW mice were given a single injection of 200 mug of CRP prior to disease onset or after the onset of high-grade proteinuria. Mice were monitored weekly for proteinuria and monthly for anti-double-stranded DNA (anti-dsDNA) antibodies. NTN was induced by immunization with rabbit IgG followed by rabbit anti-mouse glomerular basement membrane. Proteinuria was measured daily, and renal pathology was scored. CRP was injected at the time of disease induction or 9 days later. RESULTS: Treatment of NZB/NZW mice with CRP prior to disease onset delayed the onset of high-grade proteinuria by 16 weeks (P < 0.0001) and prolonged survival by 13 weeks (P < 0.002). CRP treatment of NZB/NZW mice during acute disease rapidly decreased proteinuria, and the treated mice remained aproteinuric for at least 10 weeks. Control and CRP-treated mice developed similar levels of anti-dsDNA. In C57BL/6 mice, injection of CRP either before or after induction of NTN suppressed proteinuria and glomerular pathology. CRP was completely ineffective in treating NTN in interleukin-10 (IL-10)-deficient mice. CONCLUSION: CRP injection suppresses inflammation in the kidney in SLE and NTN. The requirement for IL-10 in this protection suggests that CRP must rapidly initiate an IL-10-dependent antiinflammatory process. These findings suggest that a major function of CRP during the acute-phase response is to limit tissue damage and modulate acute inflammation.

Animals↗