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PubMed1993

Divalency of the monoclonal antibody 5-1-6 is required for induction of proteinuria in rats.

A single i.v. injection of 3 mg of the F(ab')2 fragment of MoAb 5-1-6 into rats induced immediate proteinuria (128.1 +/- 80.7 mg/24 h on day 1) which lasted 1-2 days. In contrast, rats administered 10 mg of the corresponding Fab fragment did not develop abnormal proteinuria even though an equivalent dose of the intact MoAb 5-1-6 far exceeded the nephritogenic dose. The total kidney binding of 125I-Fab fragment was 209.5 +/- 34.3 micrograms/2 kidneys. This exceeded that obtained by injection of 3 mg MoAb 5-1-6 IgG1 (58.9 +/- 12.5 micrograms/2 kidneys at 1 h) and was similar to that obtained following injection of 3 mg F(ab')2 fragment (235.3 +/- 16.9 micrograms/2 kidneys). Immunofluorescence (IF) showed a linear pattern along the glomerular capillary wall at 1 h after the administration of MoAb 5-1-6 IgG1, F(ab')2 or Fab fragment. On day 5, fine to coarse granules were observed scattered in F(ab')2-injected rat glomeruli, whereas granules were densely localized in Fab-injected rat glomeruli. Complement-depleted rats injected with 3 mg of MoAb 5-1-6 IgG1 developed proteinuria with the same time course as non-depleted rats. This observation, together with the ability of F(ab')2 to induce proteinuria, indicates that proteinuria induced by MoAb 5-1-6 is complement-independent. This study suggests that MoAb 5-1-6-induced proteinuria is initiated by cross-linking of the epitopes by divalent MoAb 5-1-6 and is independent of complement activity.

Animals↗
PubMed1995

Strain variation in susceptibility to the development of monoclonal antibody 5-1-6-induced proteinuria in rats.

Susceptibility to the development of MoAb 5-1-6-induced proteinuria was investigated in four different rat strains, i.e. Brown-Norway (BN), Lewis (LEW), Sprague-Dawley (SD) and Wistar. An intravenous injection of 5 mg of MoAb 5-1-6 to female 7-week-old rats of a given strain induced massive proteinuria in BN, LEW and Wistar rats. However, SD rats developed almost no proteinuria. A similar tendency was observed in the second experiment, in which the injected dose of MoAb was adjusted according to the body weight of each rat (3 mg/100 g body weight). Immunofluorescence (IF) and immunoelectron microscopy (IEM) revealed no differences between the binding patterns of the MoAbs to normal rat kidneys derived from each strain. Quantitative study using 125I-labelled MoAb showed that there was no significant difference in the amount of antibody bound to the kidney 1 h and 5 days after injection between two rat strains, LEW and SD. Localization of 5-1-6 in vivo and its kinetics were investigated. In IF a linear-like pattern along capillary walls was observed 2 h after injection in both LEW and SD strains. This linear-like pattern was shifted to a granular pattern in proteinuric LEW rats 6 days after injection, whereas it remained linear-like in non-proteinuric SD rats. IEM confirmed this difference in the localization of injected MoAb 6 days after injection to LEW and SD rats also at the ultrastructural level. We conclude that there is a clear-cut strain difference in the development of proteinuria induced by MoAb 5-1-6. SD rats were less susceptible to MoAb-induced glomerular injury than BN, LEW and Wistar rats. Although the exact reason for strain variation in susceptibility to MoAb-induced proteinuria remains to be clarified, the movement of bound MoAb, presumably together with corresponding antigenic molecule along the glomerular epithelial cell surface followed by endocytosis into the epithelial cell, seems to be closely related to the induction of proteinuria.

Animals↗
PubMedDate not supplied

Proteinuria prevalence in insulin-treated patients: prediction of need for end-stage renal failure treatment.

In the Dundee Diabetic clinic area (population circa 250,000), a population-based survey of the prevalence of proteinuria in diabetic patients treated with insulin showed that 9.4% of such patients had persistent proteinuria. The percentage of males with proteinuria was 11.4%, against 7.2% of females. An additional 5.2% of patients had proteinuria observed once, but did not meet the criteria for persistent proteinuria. No result was available in 10% of patients for a variety of reasons. Not every patient with diabetes and persistent proteinuria will progress to end-stage renal failure, but consideration of the group as a whole allows predictions based on published reports, to be made of the likely future incidence of renal failure, and hence future need for renal replacement services. We estimate that over the next decade two patients per 125,000 total population will develop renal failure each year. If survival is unchanged, there could be two or three times that number on treatment at any time.

Adolescent↗
PubMed2004

Podocyte foot process effacement is not correlated with the level of proteinuria in human glomerulopathies.

BACKGROUND: Nephrotic syndromes result from increased glomerular permeability to proteins and are structurally believed to be associated with podocyte foot process effacement. Despite increasing knowledge of the molecular composition of the glomerular filtration barrier, the relationship between proteinuria and foot process effacement is unclear. METHODS: We conducted a morphologic study on the relationship between podocyte foot process effacement and proteinuria. Electron microscope pictures of glomerular capillaries were randomly taken from 27 cases in various stages of minimal change nephrotic syndrome (MCNS), from six cases of IgA nephropathy (IgAN) with high proteinuria and from seven control kidneys. From each picture, the mean width of the foot processes (FPW) was quantitated. RESULTS: In normal kidney the mean FPW was 580 +/- 40 nm. In biopsies from patients with MCNS without treatment, foot processes were diffusely effaced, reflected by a FPW of 1600 +/- 440 nm. In biopsies from patients with MCNS relapsing under prednisolone treatment, foot processes were significantly less effaced than in untreated MCNS (FPW 920 +/- 200 nm). In biopsies displaying IgAN, effacement was significantly more segmental than in untreated MCNS (FPW 800 +/- 170 nm). Proteinuria did not differ significantly among the groups. Neither in MCNS nor in IgAN was the extent of foot process effacement correlated with the level of proteinuria. CONCLUSION: Podocyte foot process effacement is not correlated with proteinuria. The differences in podocyte effacement between MCNS, MCNS relapsing under prednisolone treatment, and IgAN may point to different mechanisms of podocyte injury in these diseases.

Basement Membrane↗
PubMed2004

Why is proteinuria an ominous biomarker of progressive kidney disease?

Progressive tubule injury and interstitial fibrosis frequently accompany glomerulopathies associated with proteinuria. Clinical experience indicates that higher levels of proteinuria prior to, as well as after initiation of treatment predict more rapid decline in renal function and more pronounced tubulointerstitial injury. It has been proposed that filtration of potentially tubulotoxic plasma proteins is responsible for the observed correlations between proteinuria and progression (i.e., proteinuria is a cause and not only a consequence of progressive renal injury). Numerous attempts have been made to identify the species of putative tubulotoxic proteins in this progressive injury process, but much uncertainty persists. These uncertainties stem from nonphysiologic exposure of apical cell surfaces to proteins in vitro, the extremely high concentrations of various proteins tested in vitro, and the nonuniformity of end points measured. Furthermore, there is often a lack of correlation between in vitro and in vivo findings, and a lack of uniformity of results even for seemingly similar in vitro experiments. Less controversy is evident in the potential pathways whereby injured tubules evoke a tubulointerstitial inflammatory and fibrotic response, with many in vivo models serving to incriminate excessive cytokine and chemokine production, infiltration of various inflammatory cells, and the balance between apoptosis and cell proliferation. Despite many years of concerted efforts, we believe it is still unclear whether proteinuria is a cause (and if so, which species of protein), or only a consequence of progressive renal injury. Nevertheless, pending the resolution of these uncertainties by more decisive and unambiguous experimentation, the strongly predictive inverse relationship between level of proteinuria and long-term renal survival currently justifies aggressive antiproteinuric treatment strategies, with a goal of reducing protein excretion rate to the lowest level possible without the induction of symptoms or undue risk.

Biomarkers↗
PubMed2005

Rapid resolution of proteinuria of native kidney origin following live donor renal transplantation.

To assess the contribution of the protein content of urine from the native kidneys to post-transplant proteinuria, we prospectively studied 14 live donor transplant recipients with a pre-transplant random urine protein to creatinine ratio (UPr:Cr) >0.5. Seven patients received preemptive transplants, and seven patients were on dialysis pre-transplant (with residual urine output). Resolution of proteinuria was defined as UPr:Cr < 0.2. Immunosuppression consisted of tacrolimus, mycophenolate mofetil and corticosteroids. Anti-hypertensive drugs that might reduce proteinuria were avoided during the study. The serum creatinine was 8.7 +/- 0.7 mg/dL pre-transplant, and the nadir post-transplant serum creatinine was 1.4 +/- 0.1 mg/dL. The pre-transplant UPr:Cr ranged between 0.5 and 9.2 (mean = 2.9 +/- 0.6). The UPr:Cr decreased to <0.2 in all 14 patients at a mean of 4.5 weeks post-transplant (range 1-10 weeks). In conclusion, in live donor renal transplant recipients with immediate graft function, proteinuria of native kidney origin resolves in the early post-transplant period. After the immediate post-transplant period, proteinuria cannot be attributed to the native kidneys, and work up for proteinuria should focus on the allograft.

Adult↗
PubMed1982

Renal biopsy findings in orthostatic proteinuria.

Percutaneous renal biopsy was performed on 15 patients with orthostatic proteinuria and 6 control subjects without proteinuria in order to investigate possible renal alterations. The light-microscopic findings were either normal or showed slight mesangial proliferation in the orthostatic group but were normal in the control subjects, while the immunofluorescence-microscopic study revealed mesangial, capillary or arteriolar deposits of complement C3 and/or immunoglobulins in 10 out of 12 cases with orthostatic proteinuria; complement C3 was seen in only one control subject. The electron-microscopic findings were similar in the two groups, showing slight subepithelial, intramembranous and mesangial alterations. Focal loss of the epithelial foot processes was seen in only one case with orthostatic proteinuria. It is concluded that there are no histological, electron microscopical or immunohistochemical alterations specific for orthostatic proteinuria. A finding of complement in the glomeruli in about half and of immunoglobulin in some of the patients with orthostatic proteinuria is in favour of an association to present or previous glomerulonephritis.

Adult↗
PubMed2003

Effect of nitric oxide on exercise-induced proteinuria in rats.

Temporary proteinuria occurring after exercise is a common finding, and it is explained predominantly by alterations in renal hemodynamics. In this study, we investigated whether nitric oxide (NO), which is known to have an effect on renal hemodynamics and to increase during exercise, has a role in postexercise proteinuria. In the first step of this study, the effect of acute NO synthase blockage on exercise proteinuria was evaluated. The urinary protein levels in animals that performed acute exhaustive treadmill running exercise were considerably elevated compared with the control animals. Significantly elevated urinary protein levels were also detected in animals that received Nomega-nitro-L-arginine methyl ester before exhaustion, compared with both control and exhausted groups, and mixed-type proteinuria was detected in electrophoresis, as in all exhausted animals. In the second step of the study, a NO donor (isosorbide mononitrate) was given to rats 1 h before exhaustive exercise. Mixed-type proteinuria and the elevation in urinary protein levels that occur as a consequence of exhaustive exercise were prevented by NO donor treatment. Finally, in the third step of our study, a calcium channel blocker (diltiazem), another vasodilator, was applied to the rats 1 h before exhaustive exercise. Urinary protein levels were not different in exhausted rats with or without calcium channel blocker treatment. On the other hand, in both groups, urinary protein levels were higher than in the control group. The tail-cuff blood pressure alterations caused by vasodilator drug applications before exercise were not different for NO donor and calcium channel blocker groups. These results suggest that endogenous NO might prevent the postexercise proteinuria from becoming more severe by affecting hemodynamic changes that occur during exercise.

Animals↗
PubMed1999

Poor renal accumulation of 99mTc-DMSA in idiopathic tubular proteinuria.

In Japanese patients idiopathic tubular proteinuria presents mainly as asymptomatic tubular low molecular weight proteinuria. This disease has recently been shown to resemble Dent's disease which is characterized by tubular proteinuria, hypercalciuria, rickets and eventual renal failure. We report on 4 children with idiopathic tubular proteinuria. Although they had normal renal function, as evidenced by serum creatinine or creatinine clearance, they had very poor renal accumulation of 99mTc-DMSA and the presence of large amounts of tracer in the bladder. Additionally, the patient with the largest amounts of tubular proteinuria had the poorest renal accumulation of the 4 patients. The renal accumulation of tracer decreased with time from a maximum at 10 min after injection. These findings demonstrate that the tracer, once taken to be confined to the proximal tubular cells, is immediately excreted to the tubular lumen. We suggest that poor renal accumulation of 99mTc-DMSA is very important in elucidating the mechanism of idiopathic tubular proteinuria, and that 99mTc-DMSA renoscintigraphy is useful in the evaluation of the patient's renal function over time.

Adolescent↗
PubMed1985

Marked proteinuria in hypertensive nephrosclerosis.

Heavy proteinuria in patients with essential hypertension raises the question of underlying primary renal disease. While malignant hypertension may be associated with proteinuria in the nephrotic range, it is generally held that protein excretion in benign nephrosclerosis is almost invariably less than 0.5-1.0 g/24 h. We report 18 patients with biopsy-proven hypertensive nephropathy and heavy proteinuria, of which only 6 had malignant hypertension. In the remaining 12 patients with benign nephrosclerosis, protein excretion reached up to 6.5 g/24 h, and nephrotic range proteinuria was present in 3 patients. All patients with heavy proteinuria suffered from long-standing moderate or severe, poorly controlled hypertension and were azotemic. We suggest that hypertensive nephrosclerosis be included in the differential diagnosis of massive proteinuria accompanying azotemia in poorly controlled hypertensives.

Adult↗
PubMed1980

Clinicopathological correlations of persistent asymptomatic proteinuria in children.

36 patients with persistent asymptomatic proteinuria were studied over an average period of 2.9 years. All fulfilled the following criteria:persistent proteinuria, normal blood pressure, renal function and pyelogram, no previous nor family history of renal disease. Renal biopsy showed minimal change or diffuse proliferation of glomeruli. The disappearance of proteinuria correlated inversely with the degree of glomerular sclerosis. 12 of 14 children with minimal or no sclerosis lost their proteinuria. In contrast, in 8 of 11 patients with moderate sclerosis and in all 7 patients with marked sclerosis proteinuria persisted. Age over 16 years or heavy proteinuria with or without haematuria were indicative of marked glomerular sclerosis. The thickness of the glomerular basement increased with age. Impairment of renal function occurred in only 1 patient.

Adolescent↗
PubMed2002

Effect of pravastatin on proteinuria in patients with well-controlled hypertension.

Proteinuria is an important risk factor for cardiovascular and renal morbidity and mortality. The effects of 3-hydroxy-3-methyglutaryl coenzyme A reductase inhibitor (statin) therapy on proteinuria in normolipidemic patients with well-controlled hypertension have not been studied. A total of 63 normolipidemic (total cholesterol <240 mg/dL) and proteinuric (300 to 3000 mg/d) patients with well-controlled blood pressure (<140/90 mm Hg) were randomized to receive either placebo (n=32) or pravastatin (10 mg/d; n=31) after a 3-month placebo period. Pravastatin lowered proteinuria after 6 months by 54% (P<0.0001). Creatinine clearance was stable throughout the study in the 2 groups. Despite unchanged plasma endothelin-1 levels throughout the study, urinary excretion of the peptide was decreased and significantly correlated with improvement in urinary protein excretion in pravastatin-treated patients (r=0.64, P=0.001). The urinary excretion of retinol-binding protein decreased after pravastatin administration, probably reflecting an improvement in tubular function. In contrast, the urinary excretion of IgG did not change significantly throughout the study in either group. Multivariate analysis revealed that proteinuria was only significantly correlated with statin use (P<0.0001, R2= 0.66). Linear regression analysis in the statin-treated group did not show any correlation between changes in lipid profiles and proteinuria regression. Thus, in addition to their primary function of antilipidemia, the addition of pravastatin to treatment for well-controlled hypertension may have an additive effect on reducing proteinuria independent of hemodynamics and lipid-lowering effects, possibly through inhibiting renal endothelin-1 synthesis and improving tubular function.

Adult↗
PubMed1994

Isolated proteinuria in children. Natural history and indications for renal biopsy.

The significance of isolated proteinuria in pediatric patients is uncertain. Therefore, we retrospectively studied all children evaluated for this urinary abnormality during the 6-year period from 1986 to 1992. Thirty-one patients (19 males), age 2 to 20 years, were identified as having isolated proteinuria that had persisted for a mean interval of 9.6 +/- 1.9 (SEM) months. The diagnosis was based upon the presence of a urine protein:creatinine ratio > 0.2 in an early-morning specimen. None of the patients had hematuria, edema, or azotemia. Seventeen children underwent a renal biopsy. There was no difference between the patients who were biopsied and those who were not with respect to age, magnitude of proteinuria, glomerular filtration rate (GFR), or serum albumin and cholesterol concentrations. The renal histopathology revealed focal segmental glomerulosclerosis (FSGS) (n = 8), membranous nephropathy (n = 1), postinfectious nephritis (n = 2), focal global glomerulosclerosis (FGGS) (n = 1), and normal kidney tissue (n = 5). Twelve of the patients who did not undergo a kidney biopsy and four of the five children with a normal renal biopsy were followed for at least 12 months; there was complete resolution of the proteinuria in 11 (69%) of these patients. The level of proteinuria did not predict the presence or absence of important kidney disease. However, if isolated proteinuria persists for more than 1 year, it is then unlikely to spontaneously remit and a renal biopsy is indicated to clarify the nature of any underlying glomerulopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2005

Use of protein:creatinine ratio measurements on random urine samples for prediction of significant proteinuria: a systematic review.

BACKGROUND: Proteinuria is recognized as an independent risk factor for cardiovascular and renal disease and as a predictor of end organ damage. The reference test, a 24-h urine protein estimation, is known to be unreliable. A random urine protein:creatinine ratio has been shown to correlate with a 24-h estimation, but it is not clear whether it can be used to reliably predict the presence of significant proteinuria. METHODS: We performed a systematic review of the literature on measurement of the protein:creatinine ratio on a random urine compared with the respective 24-h protein excretion. Likelihood ratios were used to determine the ability of a random urine protein:creatinine ratio to predict the presence or absence of proteinuria. RESULTS: Data were extracted from 16 studies investigating proteinuria in several settings; patient groups studied were primarily those with preeclampsia or renal disease. Sensitivities and specificities for the tests ranged between 69% and 96% and 41% and 97%, respectively, whereas the positive and negative predictive values ranged between 46% and 95% and 45% and 98%, respectively. The positive likelihood ratios ranged between 1.8 and 16.5, and the negative likelihood ratios between 0.06 and 0.35. The cumulative negative likelihood ratio for 10 studies on proteinuria in preeclampsia was 0.14 (95% confidence interval, 0.09-0.24). CONCLUSION: The protein:creatinine ratio on a random urine specimen provides evidence to "rule out" the presence of significant proteinuria as defined by a 24-h urine excretion measurement.

Creatinine↗
PubMed1998

Physiopathology of proteinuria and laboratory diagnostic strategy based on single protein analysis.

A quantification of proteins of different molecular size has been shown to be useful in characterizing the mechanism and medical causes of proteinuria. By analyzing urine albumin, alpha1-microglobulin, immunoglobulin G and alpha2-macroglobulin together with total protein, prerenal, glomerular, tubular and postrenal causes of proteinuria can be detected and differentiated by their specific urine protein patterns. Using automated turbidimetric procedures, prerenal proteinurias are characterized by an albumin/total protein ratio below 0.4. Tubulo-interstitial diseases which are negative in the protein test strip procedure are detected and clearly differentiated from other causes of proteinuria by their high alpha1-microglobulin/albumin ratios. In post-renal proteinuria, alpha2-macroglobulin proved to be a useful marker, when albumin excretion exceeds 100 mg/l urine. This protein exhibits plasma-like ratios to albumin in postrenal causes, whereas it is much lower in renal proteinurias. The new strategy, which has been evaluated in more than 500 clinically and partly histologically proven cases of renal diseases, more sensitively detects glomerular and tubulo-interstitial diseases when applied in urine screening and allows us to distinguish all clinically important causes from analysis of a morning spot urine sample.

Clinical Laboratory Techniques↗
PubMed2005

Autoimmune thyroiditis with associated proteinuria: report of two patients.

The association of renal disease and autoimmune thyroid disorders has been reported previously. Renal findings associated with autoimmune thyroiditis present more commonly as proteinuria ranging from mild to nephrotic levels. We report here two adolescent girls with hyperthyroidism associated with transient proteinuria correlated with thyroid hormone levels. They had positive antithyroid peroxidase and antithyroglobulin antibodies. Ultrasonographic and scintigraphic findings of the thyroid gland were consistent with Graves' disease in both. Their renal functions were normal except proteinuria (daily protein excretion of 13.5 mg/m2/h in patient 1 and 11 mg/m2/h in patient 2). When they became euthyroid on antithyroid treatment, proteinuria decreased without associated hematuria and/or hypertension. In conclusion, patients with autoimmune thyroid disease should be assessed for the possibility of proteinuria and the etiological investigation of proteinuria should include evaluation of thyroid functions.

Adolescent↗
PubMed2004

Association between cigarette consumption and proteinuria in healthy Japanese men and women from an occupational population.

The association between cigarette consumption and prevalence of mild proteinuria (30-99 mg/dl of albumin) was analyzed in 11,569 male and 4,715 female workers aged 18-67 yr recruited from an occupational population. Proteinuria was found in 274 (2.4%) of the total male workers and in 50 (1.1%) of the total females. Stepwise logistic regression analyses showed that sex, suspected diabetes mellitus, blood pressure (BP) and Brinkman Index (BI) levels (0, 1-199, 200-499, 500-799, 800-) were significantly related to proteinuria, and that the odds ratio of each BI level for proteinuria was 1.11 (C.I.: 1.01-1.67). In the subjects aged 50 yr or older, after excluding those suspected of having hypertension and/or diabetes mellitus, the odds ratio reached 1.37 (C.I.: 1.15-1.63), with the gender difference then no longer significant. The odds ratio for proteinuria was calculated as 5.44 (C.I.: 2.27-13.0) in male and female smokers having a BI of 500 or above and normal-high BP (130-139/85-89 mmHg) in comparison with nonsmokers having normal BP (<130/85 mmHg). These results suggest that heavy cigarette consumption represented by a BI of 500 or above is a risk factor of proteinuria even in healthy Japanese workers, particularly in those aged 50 yr or older and having normal-high BP.

Adolescent↗
PubMed2006

Association of single measurements of dipstick proteinuria, estimated glomerular filtration rate, and hematocrit with 25-year incidence of end-stage renal disease in the multiple risk factor intervention trial.

The incidence of ESRD is increasing rapidly. Limited information exists regarding early markers for the development of ESRD. This study aimed to determine over 25 yr the risk for ESRD associated with proteinuria, estimated GFR (eGFR), and hematocrit in men who did not have identified kidney disease and were randomly assigned into the Multiple Risk Factor Intervention Study (MRFIT). A total of 12,866 men who were at high risk for heart disease were enrolled (1973 to 1975) and followed through 1999. Renal replacement therapy was ascertained by matching identifiers with the United States Renal Data System's data; vital status was from the National Death Index. Men who initiated renal replacement therapy or died as a result of kidney disease were deemed to have developed ESRD. Dipstick urine for proteinuria, eGFR, and hematocrit were related to development of ESRD. During 25 yr, 213 (1.7%) men developed ESRD. Predictors of ESRD were dipstick proteinuria of 1+ or > or =2+ (hazard ratio [HR] 3.1 [95% confidence interval (CI) 1.8 to 5.4] and 15.7 [95% CI 10.3 to 23.9] respectively) and an eGFR of <60 ml/min per 1.73 m(2) (HR 2.4; 95% CI 1.5 to 3.8). Correlation between eGFR and serum creatinine was 0.9; the risk for ESRD with a 1-SD difference of each was identical (HR 1.21). Bivariate analysis demonstrated a 41-fold increase in ESRD risk in those with an eGFR <60 ml/min per 1.73 m(2) and > or =2+ proteinuria (95% CI 15.2 to 71.1). There was no association between hematocrit and ESRD. Other baseline measures that independently predicted ESRD included age, cigarette smoking, BP, low HDL cholesterol, and fasting glucose. Among middle-aged men who were at high risk for cardiovascular disease but had no clinical evidence of cardiovascular disease or significant kidney disease, dipstick proteinuria and an eGFR value <60 ml/min per 1.73 m(2) were strong predictors of long-term development of ESRD. It remains unknown whether intervention for proteinuria or early identification of those with chronic kidney disease reduces the risk for ESRD.

Adult↗