Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Proteinuria”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources

Association between heparan sulfate proteoglycan excretion and proteinuria after renal transplantation.

The aim of the study presented here was to investigate whether, in patients showing immediate graft function after renal transplantation, cold-ischemia and reperfusion lead to damage of the glomerular basement membrane and consequently to a loss of heparan sulfate proteoglycans. Loss of these heparan sulfate proteoglycans is a major cause of proteinuria. Time-dependent changes in urinary excretion rates of heparan sulfate proteoglycans but also of total protein, albumin, low- and high-molecular-weight proteins were analyzed quantitatively and by polyacrylamid-gel-electrophoresis in eight patients. Immediately after renal transplantation, severe proteinuria with an excretion rate of up to 251 +/- 108 mg/min was apparent and rapidly declined within 24 h to 4.11 +/- 2.80 mg/min. The gel-electrophoretic pattern showed a nonselective glomerular and tubular proteinuria. The excretion rate of heparan sulfate proteoglycan was increased in this initial reperfusion phase (up to 7 h), most probably because of ischemia- and reperfusion-induced damage of the glomerular basement membrane. The initial nonselective glomerular proteinuria disappeared within 48 h, changing to a mild selective glomerular proteinuria. In this second phase (7 to 48 h), lower levels of heparan sulfate proteoglycan excretion were observed (0.54 +/- 0.54 microgram/min versus 1.66 +/- 1.93 micrograms/min, P < 0.05). However, during the repair process of the glomerular basement membrane, heparan sulfate proteoglycan is synthesized de novo, leading to an increasing heparan sulfate proteoglycan content of the glomerular basement membrane. This second phase is paralleled by the change from a nonselective to a selective glomerular proteinuria. In the third phase, when the heparan sulfate proteoglycan content of the glomerular basement membrane normalizes, glomerular proteinuria was abolished in most of the patients.

Adult↗

Survival of cats with naturally occurring chronic renal failure is related to severity of proteinuria.

BACKGROUND: Tubulointerstitial kidney disease is a common cause of illness and death in pet cats and is typically not associated with overt proteinuria. HYPOTHESIS: Proteinuria would be independently related to survival in cats with renal failure, with or without hypertension. ANIMALS: The study included 136 client-owned cats; 28 apparently normal, 14 hypertensive but not azotemic, 66 azotemic but not hypertensive, and 28 both hypertensive and azotemic. METHODS: Cox's proportional hazards model was used to determine the influence of initial plasma creatinine concentration, proteinuria (urine protein-to-creatinine ratio or albumin-to-creatinine ratio), age, and systemic hypertension on the risk of death or euthanasia during the follow-up period. Multivariable linear regression was used to determine the relation between severity of proteinuria and predictive variables, including age, plasma creatinine concentration, systolic blood pressure, sex, and urine specific gravity. RESULTS: Plasma creatinine concentration and proteinuria were very highly related to survival. The hazard ratio (95% confidence intervals) for death or euthanasia was 2.9 (1.4-6.3) and 4.0 (2.0-8.0) for urine protein-to-creatinine ratio 0.2-0.4 and >0.4, respectively, compared with the baseline group with a urine protein-to-creatinine ratio of <0.2 and were 2.4 (1.2-4.8) and 4.9 (2.3-10.2) for an albumin-to-creatinine ratio of 30-82 mg/g and <82 mg/g, respectively, compared with a baseline group with albumin-to-creatinine ratio of <30 mg/g. Treated hypertensive cats did not have reduced survival, although systolic blood pressure, together with plasma creatinine concentration was positively related to the magnitude of proteinuria. CONCLUSIONS AND CLINICAL IMPORTANCE: Despite the relatively low concentrations of proteinuria typical of chronic renal disease in cats, this measurement is of prognostic significance.

Animals↗

Heterogeneity of prognosis in adult IgA nephropathy, especially with mild proteinuria or mild histological features.

OBJECTIVE: The present study was undertaken to clarify the clinical course and prognosis of adult patients with primary IgA nephropathy (IgAN), especially with mild proteinuria or mild histological alternations. PATIENTS AND METHODS: A population of 735 IgAN patients whom we were able to observe for more than two years was examined. RESULTS: A total of 115 patients (15.6%) was on dialysis during the observation period. The overall 5-year renal survival rate was 92.0%. On the other hand, 166 patients (22.6%) were in clinical remission. A group with mild proteinuria included 197 patients (26.8%). Forty-seven patients of this group showed minor glomerular abnormalities, whereas 12 patients with mild proteinuria showed severe mesangial involvement. Three patients with mild proteinuria were on dialysis during the observation period, whose proteinuria was increased during the clinical course. A group with minor glomerular abnormalities included 82 patients (11.2%). Forty-seven patients of this group showed mild proteinuria, of whom 12 patients showed moderate proteinuria. However, three patients with minor glomerular abnormalities who were not on dialysis showed loss of renal function. CONCLUSION: These results indicated the heterogeneity of the course and prognosis in IgAN. Even if a patient's initial clinical or histological findings are comparatively mild, strict follow-up management is needed.

Adolescent↗

Spectrum of proteinuria in type I and type II diabetes.

We prospectively investigated the evolution of proteinuria in 52 type I diabetics over 7.8 +/- 0.3 (mean +/- SE) yr and in 61 type II diabetics over 6.4 +/- 0.3 yr. Measurements of renal protein clearance were performed serially, and the time course of proteinuria was classified in each subject based on a threshold albumin clearance of 11 nl/s, equivalent to a urinary albumin excretion rate of 30 micrograms/min. The classification based on this threshold yielded four distinct patterns of albuminuria: minimal, intermittent, progressing, and established. These patterns occurred in both type I and type II diabetics independently of the duration of follow-up. This study has identified a pattern of intermittent microalbuminuria that is also associated with transient elevations of transferrin and IgG clearances. The relationship of clinical and biochemical parameters to proteinuria patterns was evaluated. No relationship was detected between proteinuria patterns and glycemic control in either type I or type II diabetics. In type I but not type II diabetics, established proteinuria was associated with higher systolic blood pressure and decreased creatinine clearance. The phase of intermittent proteinuria detected in this study may represent a reversible stage in the development of diabetic nephropathy, but the factors that trigger the transition to progressing proteinuria remain obscure.

Adult↗

Dietary protein intake is not correlated with clinical proteinuria in NIDDM.

OBJECTIVE: To determine whether dietary protein intake is correlated with clinical proteinuria in subjects with non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: Cross-sectional analysis of data obtained from the San Antonio Heart Study, a population-based survey of diabetes and cardiovascular risk factors. Subjects were enrolled in two phases: phase 1 between 1979 and 1982 and phase 2 between 1984 and 1988. This study was based on 376 NIDDM subjects who had both urinalysis and complete dietary protein intake information available. Dietary protein intake was measured by 24-h dietary recall in phase 1 and by food-frequency questionnaire in phase 2. An early-morning spot urine was obtained from study subjects. Clinical proteinuria was defined as greater than or equal to 1 on Ames Albustix test. RESULTS: In phase 1, the subjects with negative or trace proteinuria had a mean protein intake of 79.9 g/day compared with 72.1 g/day for subjects with greater than or equal to 1 proteinuria. In phase 2, the mean protein intake was 72.2 g/day in the negative/trace group and 65.3 g/day in the greater than or equal to 1 proteinuria group. In multivariate analysis, adjusting for age, sex, ethnicity, systolic blood pressure, and 2-h blood glucose, we were again unable to detect a significant correlation between dietary protein intake and clinical proteinuria. CONCLUSIONS: These data do not support the hypothesis that high-protein intake is a risk factor for clinical proteinuria in NIDDM subjects. Therefore, any recommendation for protein restriction in the diets of NIDDM subjects, before the development of NIDDM-related nephropathy, must be made with caution.

Adult↗

Blood pressure, edema and proteinuria in pregnancy. 3. Study design, population and data characteristics.

1. The mean blood pressure runs a curvilinear pattern during the course of pregnancy, with the lowest reading between 20 and 27 weeks of gestation, a continuous rise from 28 to 36 weeks, followed by a plateau. 2. the mean blood pressure in pregnancies without edema and proteinuria are lowest throughout pregnancy. However, the mean blood pressures in pregnancies complicated by edema, proteinuria, or both, are less than 5 mm. Hg higher after 28 weeks of gestation. 3. The mean blood pressures are lower in black gravidas than in white gravidas throughout pregnancy, independent of the presence or absence of edema, proteinuria, or their combinations. 4. The mean blood pressure is related to age and parity. Median-age gravidas (20-34 years) of parity 1-5 have the lowest mean blood pressures overall at any time during gestation. The mean blood pressure of nulliparas, independent of age, is elevated over the mean blood pressure of comparable multiparas. Independent of parity, maternal age systematically affects the mean blood pressure. 5. The standard deviations for the mean diastolic and systolic blood pressures are approximately 9 and 11 mm. Hg, respectively, independent of the weeks of gestation. They are affected very little by the absence or presence of edema or proteinuria, or both. 6. Edema of hands and/or face occurs more often in black gravidas. 7. The overall perinatal mortality rates in pregnancies complicated by edema are not higher than in pregnancies without edema. Perinatal mortality rates in pregnancies with proteinuria, or edema and proteinuria, on the other hand, are approximately double the rates for pregnancies without edema and proteinuria.

Adolescent↗

[Significance of proteinuria in patients with acute ischemic brain disease].

Brain vascular diseases are ranked the third as the cause of morbidity and mortality in majority of the countries of the world. In about 80% of the cases of vascular brain diseases, it is ischemic brain disease (IBD). Atherosclerosis of main cerebral arteries is most frequently responsible for the occurrence and development of IBD. In recent years it was reported for the first time of the association of atherosclerosis and/or its complications and proteinuria. Assuming that there exists the significant association between the degree of proteinuria and clinical parameters of IBD, the aim of this study was to investigate the frequency and patterns of the association of proteinuria and clinical IBD parameters. The study was performed in 180 patients with IBD of atherothrombotic origin and 60 patients with the diseases of non-vascular origin, as the control group. In all patients quantitative determination of proteinuria was performed, and in the patients with IBD was determined the degree of IBD and afterwards the degree of functional and neurologic impairment prior to and at the end of treatment in acute phase using the standardized scales. The results of the study revealed the existence of significant frequency of proteinuria in the patients with IBD, as well as the significant association between the degree of proteinuria and severity of IBD. It was concluded that proteinuria in patients with IBD was probably associated with the atherogenic processes and physiopathologic processes of IBD, respectively, which could have predictive value for the outcome of the disease in the early stage.

Acute Disease↗

Do patients with obstructive sleep apnea have clinically significant proteinuria?

AIM: Previous studies report a high prevalence of proteinuria in patients with obstructive sleep apnea syndrome (OSAS). This common syndrome may therefore be an important cause ofproteinuria and renal failure in the general population. This study was undertaken to assess the prevalence of proteinuria among OSAS patients, and to identify the factors associated with urine protein excretion in these patients. METHODS: Overnight polysomnography, urine protein to creatinine ratio (PTCR), body mass index (BMI), mean arterial pressure (MAP), and hematocrit were assessed prospectively in 224 patients referred for evaluation of suspected OSAS. Sleep apnea was defined as apnea-hypopnea score (AHS) > or = 5 events/hour. Proteinuria was defined as PTCR > 0.2 mg/mg. RESULTS: Sleep apnea was present in 143 subjects (63.8%), and proteinuria in 10 (4.5%). The highest PTCR was 0.677 mg/mg. PTCR and AHS were weakly correlated (r = 0.12, p = 0.08). PTCR correlated (alpha = 0.05) with lowest oxygen saturation (r = -0.18, p = < 0.01), time spent with oxygen saturation below 90% (r = 0.19, p = < 0.01), and BMI (r= 0. 17, p = < 0.01). The mean PTCR was similar in subjects with and without sleep apnea. Proteinuria was present in 7 of 143 (4.9%) subjects with AHS > or = 5 and 3 of 81 (3.7%) subjects with AHS < 5, a relative risk of 1.34, 95% CI (0.34, 5.32). Predictors of LogPTCR in multiple linear regression (model R2 - 0.104) were: AHS (< 5 or > or = 5), baseline oxygen saturation, sex, and MAP. CONCLUSIONS: Clinically significant proteinuria is uncommon in OSAS. The prevalence and severity of proteinuria are similar in both OSAS patients and patients without sleep-disordered breathing. Sleep apnea severity is weakly associated with urine protein excretion, related more to hypoxemia than to frequency of apneic events.

Analysis of Variance↗

Cost-benefit analysis and prediction of 24-hour proteinuria from the spot urine protein-creatinine ratio.

AIM: A prospective cross-sectional study was performed on 170 patients with various glomerular diseases to study the accuracy of predicting 24-hour proteinuria from the spot urine protein-creatinine ratio (Up/Uc). A cost-benefit analysis was performed for the New Zealand health economic system to obtain the best cut-off values for proteinuria. SUBJECTS, METHODS AND RESULTS: Two spot urine samples (Up/Uc1 and Up/Uc2) were collected on the same day as the collection of a 24-hour urine. A randomly chosen subsample of 50 patients provided a second set of urine samples. The correlation and precision of agreement between the two methods were examined. The predictive intervals were calculated for derived 24-hour proteinuria. The level of agreement was evaluated by the Bland-Altman method and concordance analysis. The limits of agreement were evaluated against the clinical limits of agreement. A cost-benefit analysis (CBA) was performed to obtain the optimum operating points on receiver operating characteristic (ROC) curves for the best decision threshold. Correlations of r = 0.97 and 0.99 were observed between Up/Uc1, Up/Uc2 and 24-hour proteinuria, respectively. The 95% predictive intervals were wide. A high concordance correlation coefficient was obtained. The most of the differences between the two methods fell within the clinical limits of agreement. The Up/Uc1 of 0.26 and 3.20 represent the best thresholds to detect normal and nephrotic proteinuria, respectively. CONCLUSIONS: Despite wide confidence intervals, a good correlation and precision of agreement were demonstrated between the two methods across the whole range of proteinuria, regardless of the level of renal function. The difference between the two methods was less than the biological variability in the protein excretion and its measurement, enabling the methods to be used interchangeably. The optimum thresholds for abnormal and nephrotic range proteinuria were obtained.

Adult↗

[Correlation between the onset of early proteinuria and the outcome of renal transplantation. Experience of a single centre].

BACKGROUND: Proteinuria is associated with an increased risk of renal failure. In chronic kidney transplant failure it is associated with poorer graft outcome. MATERIALS AND METHODS: In our Unit 405 renal transplants were performed between April 1992 and December 2001. We analysed 1) the main causes of post-transplant proteinuria and 2) the prognostic significance for graft outcome in patients with a minimum follow-up of 6 months. RESULTS: Early proteinuria was associated with a higher incidence of chronic allograft nephropathy (CAN) and de novo/recurrent nephropathies. Graft outcome was poorer in patients with early persistent proteinuria. CONCLUSIONS: Proteinuria after renal transplantation increases the risk of graft failure. We can, therefore, hypothesize that a graft biopsy is the best way to reveal the causes of proteinuria so that therapeutic interventions, which have been shown to reduce proteinuria, can be applied immediately.

Adult↗

Autologous immune complex nephropathy. I. Sequential study of immune complex deposition, ultrastructural changes, proteinuria, and alterations in glomerular sialoprotein.

Experimental evidence suggests that barriers to glomerular filtration of macromolecules exist at the glomerular basement membrane itself and at the level of the epithelial cell and epithelial slit pores. The distribution of negatively charged glomerular sialoprotein (GSP) at the latter site and the reduction in histochemical staining for GSP reported in several clinical and experimental glomerular diseases suggest a role for this material in the regulation of glomerular permeability. Alternatively, reductions in GSP associated with proteinuria may reflect only epithelial cell swelling consequent to the proteinuria. The sequence of subepithelial immune complex deposition, epithelial cell swelling and foot process fusion, alterations in histochemical staining for GSP, and development of proteinuria was studied in 12 Lewis rats biopsied weekly during development of autologous immune complex (Heymann) nephropathy. Deposition of IgG was detectable 3 weeks after antigen injection by immunofluorescence. Electron-dense deposits were first seen by electron microscopy coincident with the appearance of complement at week 4. Proteinuria began at 6 to 8 weeks, 3 to 5 weeks after detectable immune complex deposition. Proteinuric animals had marked subepithelial immune complex deposition and extensive epithelial cell swelling and foot process fusion. Despite these changes, there was no detectable reduction in staining for GSP until week 14, 6 to 8 weeks after onset of proteinuria. Reductions in GSP apparently do not play a role in altering glomerular permeability early in autologous immune complex (Heymann) nephropathy, and proteinuria and epithelial cell swelling can be present in this model without detectable changes in GSP. These findings suggest that early alterations in GSP reported in some other proteinuric disorders may be of pathogenetic significance rather than simply a reflection of changes in epithelial cell morphology secondary to proteinuria. In this experimental model of membranous nephropathy, immunofluorescence was more sensitive than electron microscopy in the early detection of immune deposits.

Animals↗

Effects of angiotensin II receptor blocker on proteinuria in renal transplant recipients.

INTRODUCTION: Therapeutic approaches directed at reducing proteinuria are under development. The aim of the present study was to prospectively elucidate the impact of losartan treatment in renal transplant recipients with persistent proteinuria. PATIENTS AND METHODS: Twenty-eight patients with persistent proteinuria or mild hypertension were assigned to receive losartan. Proteinuria was defined as a ratio of urinary protein to urinary creatinine (U(P)/U(Cr)) >0.5 in continual urinary tests in the outpatient setting. RESULTS: All patients with mild hypertension reached target blood pressure (BP) with losartan treatment, but the change was not significant. In twelve patients with proteinuria before initiation of the study, urinary protein excretion was significantly reduced with treatment. No correlation was observed between reductions in proteinuria and mean BP. A significant decrease was identified in the hemoglobin concentration of patients with serum creatinine concentrations >2.0 mg/dl before the study. DISCUSSION: Losartan efficiently reduces proteinuria in renal transplant recipients with adequate tolerance. Multicentric prospective studies are required to confirm its clinical effectiveness.

Adult↗

[Localized expressing tendency of nuclear transcription factor kappa-B, pro-fibrosis genetic factors and fibronectin mRNA in renal tissues in proteinuria overload nephrotic young rats].

OBJECTIVE: Terminal stage renal failure is the final common fate of chronic nephropathies independent of the type of initial insult. Abnormally filtered proteins have an intrinsic renal toxicity linked to their over-reabsorption by proximal tubular cells and activation of tubular-dependent pathways of interstitial inflammation and fibrosis. The functional importance of tubulointerstitial events in progressive renal disease is supported by evidence that the severity of tubular interstitial damage strongly correlates with the risk of renal failure. The present study aimed to investigate the expressive tendency of some pro-fibrosis genetic factors mRNA, including thrombospondin-1 (TSP-1), transforming growth factor-beta1 (TGF-beta1), connective tissue growth factor (CTGF) and the major component of extracellular matrix-fibronectin (FN) in renal tissues at different time points during early stage of renal lesions caused by proteinuria in bovine serum albumin (BSA) injection-induced proteinuria overload nephrotic young rats and the significance of these factors on tubulointerstitial fibrosis development. METHODS: Female young Wistar rats aged 3-4 weeks with proteinuria overload nephrosis induced by BSA (1.0 g/d) injected intraperitoneally were used as experimental models. The 80 young rats were divided into control group (n = 40) and BSA injected group (n = 40). At different time points (weeks 1, 2, 3 and 4), the urinary protein was measured by Coomassie brilliant blue colorimetric assay; the renal tissues morphologic changes were evaluated after HE staining; the P(65)/Rel-A, TSP-1, TGF-beta1 and CTGF mRNA expression in renal tissues was determined by in situ hybridization method and the FN mRNA expression was detected by Northern blot. The experimental data were evaluated by statistics software SPSS10.0. RESULTS: (1) Three to four weeks after BSA injection, heavy proteinuria was observed in the rats of BSA group (week 3: 104.3 +/- 21.8 mg/24 h; week 4: 131.1 +/- 18.3 mg/24 h). The proteinuria deteriorated progressively afterwards. Histopathological examination revealed that inflammatory cells infiltrated into tubulointerstitial areas extensively, protein casts were seen in tubules and edema occurred in tubulointerstitial areas. (2) In situ hybridization showed that NF-kappaB (P(65)/Rel-A) mRNA expression was up-regulated progressively in nuclei of tubular epithelial cells, the semi-quantitative scores (at 1, 2, 3 and 4 weeks) were 2.33 +/- 0.20, 2.76 +/- 0.12, 2.96 +/- 0.19, and 3.76 +/- 0.18, respectively (F = 37.34, P < 0.01). (3) At 1 week after BSA injection, the TSP-1 mRNA expression appeared in glomeruli and increased, but was light in tubulointerstitial areas, its expressive peak was observed at week 2, and declined to mild after weeks 3 and 4. The semi-quantitative scores at different time points suggested that TSP-1 mRNA was expressed mainly in early stage of lesion in this model, then, this tendency turned to a flat roof smoothly. (4) TGF-beta1 and CTGF mRNA was up-regulated simultaneously in tubular epithelial cells (F = 8.80, P < 0.01 F = 19.41, P < 0.01). (5) Northern blotting showed that FN mRNA was considerably up-regulated at second week in the kidneys of rats in BSA group, 2.7-fold higher at week 4 than that at week 1 in BSA group rats, and was 3.6-fold higher than that of control group. CONCLUSION: The present study suggested that NF-kappaB (P(65)/Rel-A) mRNA expression and its activity was enhanced significantly by proteinuria-loading and synchronized with high expression of TSP-1, TGF-beta1, and CTGF mRNA in the kidney, at the same time, FN mRNA was up-regulated in renal tissues and an aggravating tendency in tubulointerstitial lesions was observed in nephrotic young rats with heavy proteinuria.

Animals↗

Prevalence of proteinuria in rural adult population in Tamil Nadu.

BACKGROUND & OBJECTIVES: Presence of proteinuria is considered as an early marker of an increased risk of progressive kidney disease. Angiotensin converting enzyme (ACE) inhibitors (ACEi) and angiotensin II receptor blockers (ARB) treatment to persons with proteinuria and chronic kidney disease has been shown to decrease the progression to endstage renal disease. As the exact prevalence of proteinuria is not known in the general population, we undertook this study to estimate the same in a rural adult population in Vellore district, Tamil Nadu. METHODS: A convenient sample of 5,043 adults was included. All individuals were tested for albuminuria by albumin dipstick examination in an untimed urine sample. Individuals who tested positive for albuminuria underwent a second dipstick examination after a gap of one week. Individuals with persistent albuminuria on the second dipstick examination underwent further evaluation which included medical history, physical examination, 24 h urine protein estimation, total serum protein and albumin estimation. Ultrasound of the abdomen was done in patients with renal failure and renal biopsy was performed in selected patients. RESULTS: Of the total 5,043 individuals screened, 63.1 per cent were females. Mean age of the study population was 50.94 +/- 11.2 yr. First dipstick test identified 594 individuals positive for albuminuria. Repeat dipstick could be done in only 576, of whom 212 showed persistent albuminuria. Significant proteinuria was detected in 24 individuals of the 208 who had 24 h urine protein measured. Of these 24 patients, 3 were found to have chronic renal failure, 12 were presumed to have diabetic nephropathy clinically, one each had focal segmental glomerulosclerosis and biopsy proven diabetic nephropathy, and 7 patients had proteinuria of unknown aetiology. INTERPRETATION & CONCLUSION: The prevalence of proteinuria in this adult rural population was 0.47 per cent (0.30-0.67%). The detection and treatment of chronic kidney disease in 24 individuals is bound to reduce the rate of decline of renal functions. Screening programme for proteinuria in different parts of country may be an effective measure to bring a decline in rate of progression of chronic kidney disease in general population.

Adult↗

[Proteinuria in dermal vasculitis (incidence, degree and possible mechanisms of onset)].

The paper comprises 63 patients with diagnosed vasculitis of the skin who had abnormal findings in the urine. Thirteen of these patients had positive skin findings and abnormal findings in the urine, with concomitant attacks of dyspnea as seen in bronchial asthma. These patients account for 20% of the entire group, while there was an incidence of 37% of systemic manifestations. Skin findings: 45% had a maculopapular rash, 36% had urticarial findings, 13% had urticaria and angioedema and 6% had angioedema alone. Nonspecific biologic syndrome of evolution was statistically significant while no significant changes were found in the number of white blood cells and eosinophils. The degree of proteinuria ranged from 0.1 g/L to 1.16 g/L. Most patients with proteinuria above 0.25 g/L had microhematuria. Slightly over 50% of the patients had signs of complement activation by the alternative pathway, along with the presence of cryoglobulins. Increased histamine in the serum was found in over 50% of the patients although the values of histamine did not correlate with the degree of proteinuria. Proteinuria was not detected in patients with very high values of histamine (and without signs of vasculitis), which indicates that histamine itself responsible for changes in the glomeruli. There is a possibility that local tissue hyperhistaminemia is responsible for the increased permeability of the basal membrane of the glomeruli. According to the obtained results, the etiology of proteinuria and microhematuria should be pursued in the pathogenesis of vasculitis as signs of complement activation indicate. Other possible causes for proteinuria were excluded. The proteinuria was selective, benign according to its course and degree, occurred concomitantly with skin findings and was absent during remission of the disease.

Adult↗

The incidence of gross proteinuria in people with insulin-dependent diabetes mellitus.

Epidemiologic data on the incidence of gross proteinuria in people with diabetes are important in medical counseling, in projecting estimates of needs and costs of health care, and for developing approaches to prevent renal complications. We performed a population-based incidence study in southern Wisconsin of insulin-taking diabetic persons diagnosed before 30 years of age. The presence of gross proteinuria (greater than or equal to 0.30 g/L) was determined by means of a reagent strip. The incidence of proteinuria in a 4-year interval was 14.4% (95% confidence interval, 11.7% to 17.0%). The relative risk of developing proteinuria after 4 years for those with glycosylated hemoglobin levels in the highest quartile compared with those in the lowest quartile was 3.0 (95% confidence interval, 1.6 to 5.3). The incidence of proteinuria was also associated with higher diastolic blood pressure, being male, taking more insulin, and having more severe retinopathy at the baseline examination. The relationship between glycosylated hemoglobin level and the incidence of proteinuria was significant even after controlling for these other risk variables. These data suggest that hyperglycemia, as measured by glycosylated hemoglobin level, is a significant risk factor for the development of gross proteinuria.

Adolescent↗

The pattern of proteinuria in congestive cardiac failure due to common heart diseases.

The association between proteinuria and congestive cardiac failure was investigated in patients with hypertensive heart disease, cardiomyopathy, rheumatic heart disease and cor pulmonale. In 33 such patients, proteinuria occurred before and after successful treatment of the cardiac failure. Overall there was a wide variation in the degree of proteinuria amongst the various groups and statistical analysis showed that the distribution of levels of proteinuria and the mean levels of proteinuria were statistically different between any two groups of patients, P = 0.05. Biopsy proven hypertensive nephrosclerosis was found to be a cause of heavy proteinuria which was in the nephrotic range in two such patients. Congestive cardiac failure due to hypertensive heart disease should be included in the differential diagnosis of massive proteinuria even in the absence of renal insufficiency.

Adult↗

[Mechanism of reduction in proteinuria by cyclosporine A: effects on the glomerular anionic sites].

To consider the mechanism of reduction of proteinuria by cyclosporine A (CYA) in the patient with intractable nephrotic syndrome, the effect of CYA on proteinuria and anionic sites (AS) of the glomerular basement membrane (GBM) was studied in puromycin aminonucleoside (PA) nephrotic rats. In addition the rats exogenously given human recombinant interleukin-2 (hrIL-2) every day repeated the same proteinuria were used. The PA nephrotic rats were made by single injection of PA 150 mg/kg excrete of urinary protein as compared 10 mg/day of urinary protein in the controls. The increase of urinary protein in the PA rats was inhibited by CYA10-20 mg/kg administrated orally from the day of PA injection for 15 days. To evaluate AS, the kidney were treated with a polyethyleneimine (PEI) staining method and the deposits in the lamina rara externa (LRE) of the GBM were counted on the electron micrographs. On the 15th day, in the PA rats, AS decreased greatly but were normal in the CYA-treated rats. On one hand, rats injected of hr IL-2 2.5 X 10(5)U/rat intraperitoneally for 14 days showed slight proteinuria on the 14th day, and the proteinuria was also inhibited by oral administration of CYA 25 mg/kg. As reduced in the rats treated with hrIL-2 as well as PA. The findings indicate that the proteinuria in the PA nephrotic rats and rats treated with hrIL-2 might result from reduction of AS and that the improvement of proteinuria in these rats by CYA might be due to the recovery of AS in the GBM.

Animals↗