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PubMed2001

Il-4 therapy prevents the development of proteinuria in active Heymann nephritis by inhibition of Tc1 cells.

The role of IL-4, a key Th2 cytokine, in promoting or inhibiting active Heymann nephritis (HN) was examined. HN is induced by immunization with Fx1A in CFA, and proteinuria in HN is associated with subepithelial IgG and C3 deposition and infiltration of CD8(+) T-cytotoxic 1 (Tc1) cells and macrophages into glomeruli, as well as induction of Abs to Crry. Treatment with rIL-4 from the time of Fx1A/CFA immunization stimulated an earlier IgG1 response to Fx1A, induced anti-Crry Abs, and up-regulated IL-4 mRNA in lymphoid tissue, but did not alter proteinuria. Treatment with MRCOx-81, an IL-4-blocking mAb, resulted in greater proteinuria, which suggests endogenous IL-4 regulated the autoimmune response. Delay of rIL-4 treatment until 4 wk post-Fx1A/CFA immunization and just before the onset of proteinuria prevented the development of proteinuria and reduced Tc1 cell infiltrate in glomeruli. Delayed treatment with IL-4 had no effect on titer or isotype of Abs to Fx1A or on Ig, C3, and C9 accumulation in glomeruli. Treatment with rIL-13, a cytokine that alters macrophage function such as rIL-4, but has no direct effect on T or B cell function, reduced glomerular macrophage infiltrate, but did not prevent proteinuria or CD8+ T cell infiltrate. Anti-Crry Abs were paradoxically only induced with rIL-4 therapy, not in HN controls with proteinuria. It was concluded that the rIL-4 effect was probably by inhibition of Tc1 cells, which normally mediate the glomerular injury that results in proteinuria.

Animals↗

PubMed2002

Endothelin-1 in the kidney and urine of patients with glomerular disease and proteinuria.

BACKGROUND: Endothelin-1 (ET-1) is a strong vasoconstrictive peptide that is involved in the pathogenesis of arterial hypertension. There is increasing evidence, based on studies in experimental animals, that endothelin-1 is produced by tubular epithelial cells in response to activation by filtered protein and is involved in the development of renal scarring. The aim of this study is to examine the distribution of ET-1 in the renal tissue of patients with heavy proteinuria and to estimate the changes in its urinary excretion after immunosuppressive therapy. PATIENTS AND METHODS: Twenty-four patients with severe proteinuria (7.5 +/- 6.5 g/24 h) due to different types of glomerular disease and normal renal function (creatinine clearance 91 +/- 14 ml/ min) were investigated. All patients underwent a renal biopsy and commenced on immunosuppressive therapy with corticosteroids and cyclosporin A. The localization of ET-1 in the renal tissue was examined by immunohistochemistry and compared to control renal tissue from 9 patients who underwent nephrectomies because of hypernephroma. In patients with proteinuria, endothelin-1 excretion in the urine at diagnosis was determined by radioimmunoassay and compared to that of 14 healthy subjects. A second measurement of urinary ET-1 excretion was performed after remission of proteinuria or 6 months after the initiation of treatment in patients with persistent nephrotic syndrome. RESULTS: ET-1 in renal tissue of patients and controls was localized within the cytoplasm of endothelial cells. In nephrotic patients, it was also localized within the cytoplasm of tubular epithelial cells. Urinary ET-1 levels were higher in nephrotic patients compared to healthy subjects (746 +/- 180 ng/24 h vs 410 +/- 112 ng/ml, p < 0.001). In 17 of 24 patients who showed remission of proteinuria with immunosuppressive therapy, the urinary ET-1 levels decreased (from 803 +/- 168 ng/24 h to 511 +/- 80 ng/24 h, p < 0.001) whereas in 7 patients with persistent proteinuria, urinary ET-1 excretion remained elevated. CONCLUSIONS: The increased urinary excretion of ET-1 in patients with severe proteinuria followed by a significant decrease after remission ofproteinuria with immunosuppressive treatment, along with its expression within tubular epithelial cells, suggests a possible relationship between proteinuria and renal ET-1 production.

Adult↗

PubMed2004

Prevalence of proteinuria and the development of chronic kidney disease in HIV-infected patients.

AIMS: HIV-related renal diseases are increasingly prevalent and are associated with proteinuria and rapid progression to end-stage renal failure. Early treatment with highly active antiretroviral therapy (HAART) and ACE inhibition may prevent the development of chronic kidney disease (CKD), but studies evaluating the epidemiology of proteinuria and early CKD in HIV-infected patients are lacking. METHODS: All consecutive patients at Wishard Memorial Hospital (Indiana University) whose initial HIV documentation occurred from 1990 to 1998, were retrospectively studied using a computerized medical record system. Clinical data were abstracted from time of first HIV documentation through 12/31/2000. The proportions of patients who developed CKD (doubling of serum creatinine from an initial level < or = 1.5 mg/dl) and who had proteinuria (> or = 1+ protein on the first urine dipstick after HIV documentation) were calculated. Case mix and laboratory variables at the time of HIV documentation were compared between those who did and did not develop CKD and between those who had and did not have initial proteinuria. RESULTS: Of 487 subjects with initially normal renal function, 10 (2% (95% CI, 1-4%)) developed CKD. In univariable analysis, black race, a diagnosis of diabetes or hypertension and proteinuria were all significantly associated with the development of CKD; 89 (29% (95% CI, 24-35%)) of 289 evaluable subjects had > or = 1+ proteinuria on urine analysis. Multivariable regression revealed only older age (OR 1.08 per year increase; 95% CI, 1.03-1.14) to be associated with proteinuria. CONCLUSIONS: A small, but potentially clinically meaningful proportion of HIV-infected patients develop CKD, and there appears to be a high prevalence of proteinuria on the first urine analysis obtained after HIV documentation.

Adult↗

PubMed2005

Adiponectin level is reduced and inversely correlated with the degree of proteinuria in type 2 diabetic patients.

AIMS: Adiponectin seems to be an important modulator for metabolic and vascular diseases. We aimed to measure plasma adiponectin levels in type 2 diabetic patients and investigate any association with the severity of proteinuria. METHODS: 80 patients (mean age, 46.9 +/- 5.1 years; body mass index (BMI), 25.8 +/- 1.98 kg/m2) and 47 healthy volunteers (mean age, 46.1 +/- 5.5 years; BMI 26.74 +/- 2.23 kg/m2) were included. Plasma adiponectin concentration, insulin levels, homeostasis model assessment (HOMA) indices, calculated glomerular filtration rate (GFR), high sensitive C reactive protein (hsCRP) and biochemistry panel were determined in all subjects. The association between adiponectin concentration and proteinuria was evaluated. Additionally, the relationship between adiponectin and hsCRP and calculated GFR were also investigated. RESULTS: Adiponectin levels in patients were significantly lower than those of controls (n = 80; 8.76 +/- 4.50 microg/ml for patients, n = 47; 24.27 +/- 5.59 microg/ml for controls, p < 0.001). Plasma adiponectin levels in patients with proteinuria were significantly lower than those without proteinuria (n = 43; 6.81 +/- 2.82 microg/ml for proteinuria, n = 37; 11.98 +/- 3.32 microg/ml for no proteinuria, p < 0.001). There was a significant negative correlation between plasma adiponectin concentrations and the degree of proteinuria (r = -0.433, p < 0.001). There were also significant negative correlations between adiponectin concentrations and insulin levels as well as HOMA index in the patient group (r = -0.322, p = 0.004; r = -0.301, p = 0.032). Additionally there was a significant negative correlation between adiponectin and hsCRP levels in the patient group (r = -0.872, p < 0.001). CONCLUSION: The results show that adiponectin is lower in patients with type 2 diabetes and the levels are negatively correlated with the severity of proteinuria.

Adiponectin↗

PubMed1999

Effect of proteinuria reduction on prevention of focal glomerulosclerosis by angiotensin-converting enzyme inhibition is modifiable.

BACKGROUND: Proteinuria is associated with a progressive loss of renal function; we recently found that both intrarenal effects of proteinuria and the state of systemic nephrosis play an independent role in proteinuria-induced renal damage. Reduction of proteinuria is an important mechanism underlying the renoprotective effect of angiotensin-converting enzyme inhibition (ACEi). Both the reduction of proteinuria and the attenuation of the systemic state of nephrosis may be involved in the renoprotection by ACEi. METHODS: This article entails a post hoc analysis of a previous study on the renoprotective effect of ACEi lisinopril in adriamycin nephrosis. It was attempted to modify therapeutic efficacy of ACEi by increasing lisinopril dose and by dietary sodium restriction, respectively. In this analysis, we aimed to delineate the contribution of proteinuria reduction and the reduction of other intermediate parameters such as hyperlipidemia and blood pressure on the protection against focal glomerulosclerosis (FGS). RESULTS: We found that in adriamycin nephrosis, ACEi significantly reduced proteinuria, lipids, and blood pressure and provided protection against FGS. Treatment modification by increasing the lisinopril dose resulted in a further reduction of FGS without significant effects on intermediate parameters (proteinuria, hyperlipidemia, and blood pressure), whereas surprisingly, treatment modification by sodium restriction resulted in a further attenuation of intermediate parameters, without additional protection against FGS. CONCLUSIONS: The renoprotective benefit of an obtained attenuation of intermediate parameters is modified by other factors. Further optimization of renoprotective therapy requires identification of such factors and explicit consideration of therapeutic efficacy on intermediate parameters as well as hard end points.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2001

Proteinuria: clinical signficance and basis for therapy.

Proteinuria is the hallmark of renal disease and proteinuria exceeding 1 gm a day in patients with renal disease augers a poorer prognosis. Proteinuria has been shown to be tubulotoxic and directly contributes to renal deterioration. Patients with non-selective proteinuria are more likely to have progressive renal disease. Diabetic patients with persistent microhaematuria have about 20 times the risk of developing diabetic nephropathy. In essential hypertension, the onset of de novo proteinuria after years of adequate BP control is a marker of subsequent decline in renal function. In glomerulonephritis, more severe proteinuria is associated with faster rate of progression. Even though the initial phase of proteinuria in patients with glomerulonephritis is usually of immunological origin, in the vast majority of patients with established disease, the latter progressive phase of proteinuric glomerulopathy is the result of glomerular hyperfiltration which shifts glomerular non-selective pores to larger dimensions resulting in excessive leakage of protein in the urine. Endothelial injury resulting from glomerular hyperfiltration causes increase in local generation of Angiotensin II in the kidney as part of the hemodynamic response. ACE inhibitors and angiotensin II receptor antagonists (ATRA) can improve glomerular pore-selectivity by remodelling the glomerular basement membrane. In addition, these agents also have beneficial effects by decreasing TGF-beta production therapy decreasing mesangial cell proliferation, hence ameliorating disease progression in patients with diabetic nephropathy and IgA nephropathy. A number of recent clinical trials have shown that ACEI and ATRA therapy can retard the progression of renal deterioration in patients with NIDDM and those with IgA nephropathy and even restore normal renal function in those with mild renal impairment. Treatment and control of proteinuria in patients with renal disease should be regarded as important as treatment of hypertension as it can prevent renal failure.

Angiotensin Receptor Antagonists↗

PubMed2000

[Re-evaluation of proteinuria and qualitive methods for diagnosis of diabetic nephropathy].

This study was aimed to re-evaluate the proteinuria quantitative and qualitative methods for diagnosis of diabetic nephropathy (DN). 136 cases were divided into two groups of proteinuria negativeness and postiveness by the results of urine routine examination. The clinical and biochemical indices and the frequencies of other diabetic complications of the two groups were compared. The results showed that the blood glucose and glycated Hb in the two groups were increased, especially in the proteinuria negative group (P < 0.01 and 0.05, respectively). There was a high prevalence of hypertension and other diabetic complications in the two groups, and it was higher in the positive group than in the negative group (P < 0.05 and 0.01, respectively). The frequencies of hyperlipoproteinemia in the two groups were over 40%, but no significant defference was observed between them (P > 0.05). There was correlation between hypertension and proteinuria (P < 0.01) but no correlation between diabetic retinopathy and proteinuria. The prevalence of azotemia in the proteinuria negative group was 17.07%. These suggest that the amount of proteinuria can not completely reflect the duration and severity of DN. Negative proteinuria in routine examination cannot rule out DN. For diagnosis of DN, it is necessary to think about all data on blood glucose, blood lipid, blood pressure and the change in fundus oculi.

Adolescent↗

PubMed2004

[Relationship between podocyte molecule's distribution and expression, foot process morphology and proteinuria].

OBJECTIVE: To investigate the association between nephrin, podocin and alpha-actinin of the glomerular podocyte molecules, the morphometric change of podocyte foot process and the development of proteinuria. METHODS: Puromycin aminonucleoside (PAN) nephrosis was established. Immunofluorescence staining, image analysis and real time quantitative PCR were employed to study the distribution and quantitation of glomerular expression of nephrin, podocin and alpha-actinin. Morphometric methods were applied to evaluate the morphology change of podocyte foot processes under electron microscopy. RESULTS: (1) Before the onset of proteinuria, 2 days after PAN injection, the podocyte foot process became swollen nephrin and podocin staining were changed into discontinuous pattern accompanied by the decrease of podocin staining intensity. The foot process became more swollen on day 5,and podocin intensity continued to decrease. Meanwhile, nephrin decreased significantly both in protein intensity and at mRNA level. (2) When heavy proteinuria [(130.8+/-30.7) mg/d, P=0.02] occurred, complete effacement of podocyte foot processes was revealed; both podocin and nephrin staining intensity decreased dramatically(P<0.01), and no linear staining could be observed; nephrin and podocin mRNA gained back. (3) During the recovery of proteinuria, the foot process morphology recovered stepwise; both the intensity of nephrin and podocin increased. When proteinuria disappeared, the podocyte foot process reappeared; podocin immunofluorescence intensity recovered whereas nephrin did not; the intensity of alpha-actinin increased significantly and the distribution changed too. (4) Podocyte foot process volume density correlated negatively with nephrin(r(nephrin)=-0.78, P=0.000 1) and podocin immunofluorescence intensity(r(podocin)=-0.76, P=0.000 1), respectively. CONCLUSION: Before the onset of proteinuria, the first response of podocyte is the swollen foot process, the distribution change of nephrin and podocin and the decreased podocin intensity. There was close relationship between nephrin, podocin protein level and distribution pattern with the development of proteinuria and podocyte foot process effacement, whereas no major role was found for mRNA of nephrin and podocin. Our results suggest that proteinuria might occur after series of events of nephrin and podocin distribution change, their protein and mRNA expression level decrease, and morphology change of podocyte foot process.

Actinin↗

PubMed2004

[Differential diagnosis of proteinuria].

Normally, protein secretion in the urine is less than 150 mg/day or less than 100 mg/g creatinine. Orthostatic proteinuria, proteinuria in the presence of fever, and effort proteinuria are benign forms. In cases of persistent proteinuria, prerenal or overflow proteinuria are distinguished from renal and post-renal proteinuria. Renal forms can be differentiated into glomerular and tubular as well as mixed forms. The urine dipstick is of only low sensitivity, and is therefore unsuitable as a screening test for diabetic microalbuminuria. In addition, it cannot detect immunoglobulin light chains in Bence Jones proteinuria. For the differentiation between glomerular and tubular forms of proteinuria, the determination of marker proteins in the urine, for example, alpha1 microglobulin, albumin and IgG, has proven utility.

Albuminuria↗

PubMed2005

[Proteinuria and chronic renal failure in the coast of El Salvador: detection with low cost methods and associated factors].

OBJECTIVES: El Salvador has high mortality rates from chronic kidney disease (CKD). The actual prevalence and causes remain unknown and local resources are scarce. Previous studies have suggested very high prevalence in specific populations: adult male farmers living in the coastlands, with high frequency of pesticides exposure and alcohol consumption. This population has low incomes and poor healthcare accessibility. Our aim was to detect CKD cases in this population using proteinuria as an inexpensive initial screening, investigating associations with those characteristics and comparing them with another population from the midlands. METHODS: We performed a transversal study on volunteer men from both regions, taking into consideration the variables: age, farmer living, pesticides, exposure, alcohol consumption, medical past history, blood pressure level, glycemia and proteinuria in a random urine sample. Coastland men with proteinuria were additionally screened for CKD measuring hemoglobin and serum creatinine levels. Finally, we employed a logistic regression model, and Perason's Chi2 to investigate associations between those variables and the presence of proteinuria or CKD. RESULTS: We included 291 men from the coastlands and 62 from the midlands: 35 and 16% off the total male population from their respective communities. Proteinuria (table I) was found in 133 (45.7%) and 8 cases (12.9%). CKD was diagnosed in 37 (12.7%) coastland men (table III), with mean creatinine 2.64 +/- 2.5 mg/dl, hemoglobin 12.32 +/- 1.9 g/dl and 81.1% with proteinuria 15-30 mg/l. Only 14 (37.8%) out of those 37 CKD patients featured diabetes or hypertension, while the remaining (62.2%) did not appear to have a clear-cut cause for CKD. Only one of them was formerly diagnosed with CKD. Farmer living, pesticides exposure and alcohol consumption were found to be very common characteristics in both populations, and were not associated to the presence of proteinuria or CKD (table II and III) DISCUSSION: The prevalence of CKD within the adult male farmers from the Salvadoran coastlands is remarkably high: at least 12.7%. There is a large number of undiagnosed cases, but they can be easily detected with inexpensive methods. This high prevalence is not completely explained by usual CKD causes like diabetes or hypertension. In addition, pesticides exposure and alcohol consumption may not be related, too. The disease is moderate, non symptomatic and has fairly mild proteinuria, possibly from interstitial origin. Further research is required to investigate environmental, occupational and hereditary factors, and to determine the real extent of the problem.

Adult↗

PubMed2005

[A case control study on the risk factors of proteinuria in patients with type 2 diabetes].

OBJECTIVE: To assess factors predisposing to proteinuria in patients with type 2 diabetes mellitus (DM). METHODS: A case-control study was conducted on two groups of patients with type 2 diabetes without proteinuria (urine protein < 300 mg/24 h, n = 106) and with proteinuria (urine protein >or= 500 mg/24 h, n = 106). The two groups were matched by age (+/- 3 years), sex, race and place of residence. Information on these subjects including demography, history of disease, family history of diseases, lifestyle and behavioral variables, were obtained through questionnaire. Variables including blood pressure, fasting blood glucose (FBG), quantity of protein in 24-h urine were measured. Cox's proportional hazards regression analysis was then performed. RESULTS: Factors that were independently associated with the development of proteinuria, would include occupation, diabetic duration, glycemic control, hypertension, duration of hypertension and daily intake of vegetable after diagnosis of DM. Their corresponding odds ratios (OR) with 95% confidence intervals (CI) were 2.429 (1.299 - 4.542), 1.078 (1.029 - 1.131), 2.316 (1.341 - 3.998), 1.810 (1.059 - 3.092), 1.043 (1.012 - 1.074) and 0.551 (0.334 - 0.907), respectively, while the presence of proteinuria was not associated with family history of DM, family history of hypertension, certain dietary habits and smoking habit. Multivariate logistic regression model was then fitted with three variables, including diabetic duration, glycemic control and hypertension. CONCLUSION: The prevalence of proteinuria in labor workers was higher than that in intellectuals. Longer history of diabetic duration, poor glycemic control, hypertension and longer duration of hypertension all independently contributed to the development of proteinuria. The risk of proteinuria decreased with increasing daily intake of vegetables after the patients being diagnosed as having DM.

Adult↗

PubMed1985

Origin of proteinuria in human malaria.

The prevalence and pathogenesis of renal involvement was investigated in 74 patients with malarial infections. A rise in proteinuria of 150 to 5,000 mg per day was seen in 12 out of 27 patients with Plasmodium falciparum infections. SDS-polyacrylamide gel electrophoresis revealed either an increase in albumin and high molecular weight proteins alone or an increase in low and high molecular weight proteins. Serum creatinine and urea were increased in 5 patients. In P. vivax infections, 8 out of 46 patients developed a proteinuria level of up to 462 mg per day. Low and, to a lesser degree, high molecular weight proteins were increased. In one patient with quartan malaria infection, proteinuria rose as far as 432 mg per day. There was a correlation between the appearance of proteinuria and fever; however, there was no correlation between the amount of proteinuria and the height of fever. It is therefore unlikely that a rise in temperature is the only cause of proteinuria in malarial infections. The electrophoretic analyses of proteinuria indicate that in malarial infections, glomerular as well as tubular lesions may cause reversible proteinuria.

Adolescent↗

PubMedDate not supplied

Clinical usefulness of cellulose acetate electrophoresis as a screening of proteinuria in childhood.

Urine samples from 110 patients with different proteinuric diseases in childhood were analysed by Cellulose Acetate Electrophoresis (CAE) and several samples were also analysed by Sodium Dodecyl Sulphate Polyacrylamide Gel Electrophoresis (SDS-PAGE). CAE allowed the classification of proteinurias into 4 patterns; Tubular, Glomerular I, Glomerular II and Glomerular III, by albumin/globulin ratio, value of % gamma globulin fraction (% gamma) and alpha 1/alpha 2 globulin ratio. Proteinurias of the Tubular pattern included various diseases with tubular proteinuria, while proteinurias of the Glomerular I, II and III patterns included mainly postural proteinuria, proteinuria of nephrotic syndrome and proteinuria of various nephropathies, respectively. SDS-PAGE confirmed the tubular and the glomerular origins of the proteins. In the present study we described the clinical usefulness of CAE in the screening of proteinuric children for the following reasons. This method could be performed easily and immediately. This is one of the necessities for mass screening of proteinuric children. CAE can be helpful as one of indications of renal biopsy, since patients with the Glomerular III pattern often showed glomerular alterations and should be diagnosed histologically. Good correlation between % gamma and clinical data was found in follow-up study, so CAE is also helpful in understanding the disease course. Thus. CAE is recommended as a routine screening method of proteinuria as well as SDS-PAGE.

Child↗

PubMed1994

[Selectivity of glomerular proteinuria and liver function in gestosis].

Proteinuria in preeclamptic women was qualitatively differentiated and in cases of pure glomerular proteinuria three groups according to the low-, medium- or high selectivity of glomerular proteinuria were formed. In these patients the incidence of liver dysfunction and severe proteinuria together with an increase in mean arterial blood pressure was investigated. The aim of this study was to find out if there is any connection between glomerular proteinuria of different selectivity and disturbed liver function. In patients with EPH-gestosis a pure glomerular proteinuria in SDS-PAA-disc electrophoresis of the urine was found. Together with the increase in glomerular selectivity an increase in quantitative urinary protein loss was found. In patients with high selective glomerular proteinuria the extent of proteinuria was about three times higher than in patients with low selectivity. In all patients a moderate elevation of the liver enzymes was found. In all patients disturbed liver function returned to normal within a few days after delivery. We conclude from these data that glomerular functional lesions pregnancy in patients with preexisting glomerulopathies or pregnancy induced renal dysfunction are accompanied in a high rate by moderate disorders of liver function.

Alanine Transaminase↗

PubMed1993

Early-pregnancy proteinuria in diabetes related to preeclampsia.

OBJECTIVE: To test the hypothesis that the risk of preeclampsia in diabetic mothers is increased with incipient diabetic nephropathy as well as with overt nephropathy. METHODS: Pregnancy outcome was studied in 311 women with class B-RF diabetes from two institutions. Using 104 women without chronic hypertension followed at the University of California, San Francisco, we constructed a receiver-operating characteristic curve relating 24-hour urinary total protein before 20 weeks' gestation to the subsequent development of preeclampsia. From the curve, a predictive cutoff level of proteinuria was selected and tested in two validation groups not used to construct the curve: 158 women without chronic hypertension followed at the University of Cincinnati and 49 women with chronic hypertension from both institutions. RESULTS: The receiver-operating characteristic curve showed an increased risk of preeclampsia with early-pregnancy proteinuria of 190 mg/day or more. In the Cincinnati validation group, the rate of preeclampsia was 7% in women with early-pregnancy proteinuria of less than 190 mg/day, 31% with proteinuria of 190-499 mg/day, and 38% with proteinuria of 500 mg/day or more. In the chronic-hypertension validation group, the rates were 0, 50, and 58%, respectively. By multiple logistic regression, the increased risk of preeclampsia with proteinuria above 190 mg/day persisted after controlling for the effects of parity, chronic hypertension, retinopathy, and glycemic control. CONCLUSIONS: Diabetic gravidas with early-pregnancy proteinuria of 190-499 mg/day are at increased risk for preeclampsia. The risk is comparable to that in women with overt diabetic nephropathy and is independent of chronic hypertension. We speculate that diabetic women with proteinuria in this range have incipient or subclinical diabetic nephropathy.

Adult↗

PubMed1996

Proteinuria in recipients of liver transplants.

We investigated the incidence and significance of proteinuria in recipients of liver transplants. The overall incidence of proteinuria was 59.72%. The peak incidence of proteinuria was at 3 months and at the end of 1 yr posttransplant. Proteinuria was higher in those patients who developed posttransplant diabetes mellitus, and those who developed both posttransplant diabetes and posttransplant hyperlipidemia. Patients who received higher total dosage of steroids and CsA had significantly greater proteinuria. Patients who had a Cr Cl greater than 50 ml/min had greater proteinuria posttransplant for the first 6 months, but the trend was reversed later. We did not find any association of proteinuria with age, weight, rejection episodes, or with the etiology of liver failure. Hypertension was a common occurrence in our patients, and therefore its significance in the causation of proteinuria could not be defined.

Adolescent↗

PubMed1994

Remission of nephrotic range proteinuria in type I diabetes. Collaborative Study Group.

The present study assessed the extent to which remission of nephrotic-range proteinuria occurred in patients with Type I diabetes enrolled in the Captopril Study, a placebo controlled multicenter clinical trial of captopril therapy in diabetic nephropathy. Of the 409 patients recruited into the Captopril Study, 108 had nephrotic-range proteinuria (> 3.5 g/24 hr) at entry in the Study (baseline). This group was the subject of the present study. Remission of nephrotic-range proteinuria was defined as follows: (1) Onset of the remission was taken as the date when proteinuria was first noted to be < or = 1.0 g/24 hr. (2) The reduction in proteinuria had to be sustained for a minimum of six months and until the end of the Captopril Study. (3) During the remission, the average of all 24 hour proteinuria measurements could not exceed 1.5 g. (4) Decline in renal function could not explain the reduced proteinuria. That is, the patient's serum creatinine during the entire period of observation in the Captopril Study had to remain at less than a doubling of the baseline serum creatinine. Remission of nephrotic-range proteinuria occurred in 7 of 42 patients assigned to captopril (16.7%, mean follow-up 3.4 +/- 0.8 years) and in 1 of 66 patients assigned to placebo (1.5%, mean follow-up 2.3 +/- 1.1 years; P = 0.005, comparing remission rate in captopril vs. placebo-treated patients).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2005

The relationship between magnitude of proteinuria reduction and risk of end-stage renal disease: results of the African American study of kidney disease and hypertension.

BACKGROUND: The magnitude of proteinuria is associated with a graded increase in the risk of progression to end-stage renal disease and cardiovascular events. The objective of this study was to relate baseline and early changes in proteinuria and glomerular filtration rate (GFR) to long-term progression of hypertensive nondiabetic kidney disease. METHODS: Post hoc analysis of a randomized 3 x 2 factorial trial. A total of 1094 African Americans with hypertensive renal disease (GFR, 20-65 mL/min per 1.73 m(2)) were followed up for a median of 3.8 years. Participants were randomized to a mean arterial pressure goal of 102 to 107 mm Hg (usual) or 92 mm Hg or less (lower) and to initial treatment with a beta-blocker (metoprolol), an angiotensin-converting enzyme inhibitor (ramipril), or a dihydropyridine calcium channel blocker (amlodipine) RESULTS: Baseline proteinuria and GFR predicted the rgate of GFR decline. For each 10-mL/min per 1.73 m(2) lower baseline GFR, an associated mean +/- SE 0.38 +/- 0.08-mL/min per 1.73 m(2) per year greater mean GFR decline occurred, and for each 2-fold higher proteinuria level, a mean +/- SE 0.54 +/- 0.05-mL/min per 1.73 m(2) per year faster GFR decline was observed (P < .001 for both). In multivariate analysis, the effect of baseline proteinuria GFR decline persisted. Initial change in proteinuria from baseline to 6 months predicted subsequent progression, with this relationship extending to participants with baseline urinary protein levels less than 300 mg/d. CONCLUSIONS: The change in the level of proteinuria is a predictor of subsequent progression of hypertensive kidney disease at a given GFR. A prospective trial is needed to confirm this observation.

Adolescent↗