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PubMed2005

Blockade of the renin-angiotensin system increases plasma adiponectin levels in type-2 diabetic patients with proteinuria.

BACKGROUND/AIMS: Adiponectin seems to be an important modulator for metabolic and vascular diseases. A case study was designed to measure plasma adiponectin levels and to investigate the effects of angiotensin-converting enzyme inhibitors on adiponectin levels in type-2 diabetic patients with proteinuria. METHODS: Forty-nine patients (28 males, 21 females) and 23 healthy volunteers (13 males, 10 females) were included in the case study. Patients with proteinuria were treated with 5 mg/day ramipril (n = 21) for 4 weeks. RESULTS: Adiponectin levels of patients were significantly lower than those of healthy volunteers (p < 0.001). There were significant negative correlations between adiponectin concentrations and insulin levels as well as the homeostasis model assessment (HOMA) index in the patient group (r = -0.655, p < 0.001; r = -0.469, p = 0.001, respectively). There was also a significant negative correlation between plasma adiponectin concentrations and the degree of proteinuria (r = -0.912, p < 0.001). Plasma adiponectin levels in patients with proteinuria (n = 21; 4.81 +/- 3.17 microg/ml) were significantly lower than those without proteinuria (n = 28; 10.25 +/- 2.03 microg/ml; p < 0.001). After the treatment period, adiponectin levels significantly increased (p < 0.001) and proteinuria, plasma insulin, and HOMA indexes significantly decreased in the treatment group (p < 0.001, p < 0.001, p = 0.002, respectively). CONCLUSIONS: The results suggest that adiponectin is inversely correlated with proteinuria and treatment with ramipril both corrects proteinuria and increases the low adiponectin levels in diabetic patients.

Adiponectin↗
PubMed2006

Does the hyperfiltration of minoxidil result in increased proteinuria and loss of renoprotection conferred by angiotensin inhibition?

The objective of the present study was to retrospectively examine whether the addition of minoxidil to patients who were already treated with maximum doses of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers but who had not achieved target blood pressures, has any detrimental effect on proteinuria or renal function or whether its effect on blood pressure prove salutary. The clinical records of the patients seen at the Hypertension, Nephrology, Dialysis and Transplantation Clinic from June 1982 through May 2005 were reviewed to identify 54 patients (78% men, 82% African-American) who had taken minoxidil (with and without angiotensin inhibition and blockade) and who had documented 24-hour urines for creatinine clearance and quantification of proteinuria before the initiation of minoxidil and after the blood pressure had stabilized on its final dose. The study was done at the Hypertension, Nephrology, Dialysis and Transplantation Clinic, the regional referral center for renal problems in eastern Alabama, USA. Minoxidil, whether alone or in combination with maximum doses of ACEIs and ARBs, was very successful in reduction of mean arterial pressure, but there was a tendency towards an increase in proteinuria. When minoxidil was given alone, patients demonstrated a trend towards reduction of proteinuria associated with blood pressure reduction; however, when minoxidil was added after the maximal doses of ACEIs and ARBs had been reached there was a significant increase in proteinuria (p = 0.017) on paired comparison in the same patients whose proteinuria had already demonstrated a significant decrease (p = 0.02) on the ACEI and ARB alone despite further significant reduction of blood pressure with the minoxidil (p = 0.003). Renal function deterioration to end stage renal disease correlated with increase in proteinuria (p = 0.03). We conclude that minoxidil was very effective in lowering systemic blood pressure but when given to patients already on maximum doses of ACEI and ARBs, there was an increase in proteinuria which could be interpreted as a detrimental effect having in mind that the blood pressure was significantly lowered.

Angiotensin II Type 1 Receptor Blockers↗
PubMed1997

Hyperlipidemia is secondary to proteinuria and is completely normalized by angiotensin-converting enzyme inhibition in hypertensive fawn-hooded rats.

Two substrains of the fawn-hooded (FH) rat have been developed, one of which develops progressive hypertension and proteinuria, the FHH, and one which shows little increase in blood pressure and no renal damage, the FHL. Other hypertensive rodent models show primary metabolic disturbances before the development of renal damage, notably hypertriglyceridemia, which may also contribute to progression of renal disease. In this study we evaluated whether hyperlipidemia is a primary disturbance in FHH, or only occurs secondary to proteinuria. Lipid levels were determined before and after development of proteinuria, and compared to those found in age-matched FHL. We also determined whether reducing proteinuria with lisinopril would normalize lipid levels in aging FHH. At 4 weeks of age, proteinuria was very low (2-3 mg/day) in both FHH and FHL. While proteinuria increased steadily in aging FHH, reaching 350 +/- 62 mg/day at 40 weeks, much less increase was observed in FHL over the same period (32 +/- 5 mg/day at 40 weeks). Blood pressure was markedly higher in adult FHH than in FHL (158 +/- 2 vs. 129 +/- 2 mm Hg, p < 0.01). In 4-week-old FHL and FHH, plasma cholesterol levels were similar. Subsequently, cholesterol increased in FHH, reaching 3.4 +/- 0.9 mmol/l at 40 weeks, whereas cholesterol was barely affected by aging in FHL (2.1 +/- 0.2 mmol/l at 40 weeks). At 4 weeks, triglyceride levels were lowest in FHH. Subsequently, triglycerides increased in FHH, reaching 3.5 +/- 1.5 mmol/l at 40 weeks, as compared to 1.3 +/- 0.2 mmol/l in FHL. Besides a transient increase in triglyerides in lisinopril-treated FHH at 11 weeks, increments in blood pressure, proteinuria, cholesterol, triglycerides and apolipoproteins A-I, B and E aging FHH were effectively prevented by lisinopril. These data strongly suggest that there is no primary difference in lipid metabolism between FHH and FHL and that changes in plasma lipids in FHH as compared to FHL are all secondary to proteinuria.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2005

Uric acid is as important as proteinuria in identifying fetal risk in women with gestational hypertension.

Gestational hypertension is differentiated into higher and lower risk by the presence or absence of proteinuria. We asked if hyperuricemia, a common finding in pregnancy hypertension, might also be an indicator of increased risk. We examined fetal outcome data from 972 pregnancies collected from 1997 to 2002 in a nested case-control study. Participants were nulliparous with no known medical complications. The frequency of preterm birth, the duration of pregnancy, frequency of small-for-gestational-age infants, and birth weight centile were determined for pregnancies assigned to 8 categories by the presence or absence of combinations of hypertension, hyperuricemia, and proteinuria. In women with gestational hypertension, hyperuricemia was associated with shorter gestations and smaller birth weight centiles and increased risk of preterm birth and small-for-gestational-age infants. Hyperuricemia increased the risk of these outcomes in the presence or absence of proteinuria. Risk was also increased in a small group of women with hyperuricemia and proteinuria without hypertension. Women with only hypertension and hyperuricemia have similar or greater risk as women with only hypertension and proteinuria. Those with hypertension, proteinuria, and hyperuricemia have greater risk than those with hypertension and proteinuria alone. The risk of these outcomes increased with increasing uric acid. Hyperuricemia is at least as effective as proteinuria at identifying gestational hypertensive pregnancies at increased risk. Uric acid should be reexamined for clinical and research utility.

Adult↗
PubMed1998

Proteinuria precedes cerebral edema in stroke-prone rats: a magnetic resonance imaging study.

BACKGROUND AND PURPOSE: Stroke-prone spontaneously hypertensive rats (SHRSP) subjected to high sodium intake develop severe hypertension, cerebral edema, and proteinuria, culminating in organ damage and early death. MRI, which can be applied serially, provides the unique opportunity to study temporal and quantitative relations between these changes and whether diminution of sodium intake can attenuate established cerebral edema. METHODS: SHRSP were subjected to 1% NaCl in drinking water. Cerebral MRI, proteinuria and systolic blood pressure (SBP) were measured serially. After detection of cerebral edema (T2-weighted MRI), 6 rats were killed for histology, to confirm the diagnosis of cerebral edema. The others were followed up for 7 more days while salt loading was continued (n = 10, group 1) or after sodium intake was normalized (n = 7, group 2). RESULTS: SHRSP invariably developed cerebral edema in 30 days (range, 8 to 54 days). At this point neurological signs were absent in 16 of 23 rats. SBP rose until 1 week before detection of cerebral edema, and then stabilized at approximately 265 mm Hg. Proteinuria invariably preceded cerebral edema, with a concentration exceeding 40 mg/d predicting development of cerebral edema in 9 days (range, 3 to 15 days). There was linear correlation (R=.62, P<.0001) between proteinuria and cerebral edema (pixels with an intensity above a defined threshold). Rats in group 1 showed an increase in cerebral edema (from 5.8+/-1.1% to 12.5+/-2.8%; P<.05), and proteinuria remained high (from 305+/-44 to 338+/-29 mg/d); and 2 died spontaneously. Rats in group 2 showed no significant change in edema (from 4.9+/-0.5% to 6.9+/-1.3%) but a marked fall in proteinuria (from 294+/-24 to 119+/-10 mg/d; P<.05), both significantly different from group 1 (P<.05); all survived. SBP remained unaltered in both groups. CONCLUSIONS: Our data establish MRI as a sensitive method for detection of cerebral edema, often prior to neurological signs, in SHRSP. Proteinuria predicts cerebral edema, and these two variables, both obtained noninvasively, are quantitatively related. Moreover, in SHRSP normalizing sodium intake after salt loading attenuates development of cerebral edema and reduces proteinuria.

Animals↗
PubMed1999

Proteinuria is an independent risk factor for ischemic stroke in non-insulin-dependent diabetes mellitus.

BACKGROUND AND PURPOSE: Proteinuria is an independent risk factor for cardiovascular disease in patients with NIDDM. The aim of this study was to assess the relationship between proteinuria and ischemic stroke in subjects with NIDDM, and to determine whether proteinuria is an independent risk factor for stroke. METHODS: We performed a case-control study of 59 diabetic patients with first-ever ischemic stroke due to thrombotic arterial occlusion, who were considered cases, and 180 diabetic patients without stroke, matched by gender, age, and diabetes duration, as a control group. WHO criteria for verified definite or possible stroke were used to ascertain the diagnosis of stroke. For the purpose of this study proteinuria was defined as a 24-hour urinary protein excretion rate of >/=20 and <200 microg/min. Risk factors included were smoking, blood pressure, body mass index, serum total cholesterol, hyperglycemia, and proteinuria. RESULTS: Subjects with stroke had higher proteinuria proportion and systolic and diastolic blood pressures. Both frequency of antihypertensive treatment and antihypertensive drugs used were similar among subjects with and without stroke. In multivariate logistic regression analysis, the ORs and 95% CIs for the variables identified as risk factors for stroke were as follows: systolic pressure (OR 3.10; 95% CI 3.01 to 4.21; P=0.03); diastolic pressure (OR 3.30; 95% CI 1.04 to 4.48; P<0.0001); fasting glucose >/=11.1 mmol (OR 1.82; 905% CI 1.4 to 3.8; P=0.04), HbA1c >/=9.5% (OR 1.7; 95% CI 1.3 to 5.1; P<0.01), and proteinuria (OR 3.23; 95% CI 1.06 to 4.36; P<0.0001). CONCLUSIONS: Our case-control study gives evidence that proteinuria is an independent risk factor for ischemic stroke in patients with NIDDM.

Aged↗
PubMed2004

Peroxisome proliferator-activated receptor gamma (PPAR-gamma) agonist increases plasma adiponectin levels in type 2 diabetic patients with proteinuria.

Adiponectin appears to be an important modulator for metabolic and vascular diseases. A case-controlled study was designed to measure plasma adiponectin levels and investigate the effects of rosiglitazone on adiponectin levels in type 2 diabetic patients with proteinuria. Sixty-four patients (mean age, 46.1+/-4.6 yr; 30 male, 34 female) and 26 healthy volunteers (mean age, 45.3+/-4.8 yr; 14 male, 12 female) were included. Patients with proteinuria were treated with 4-mg/d rosiglitazone (n=21, 10 males, 11 females) for 4 wk. Adiponectin levels in patients were significantly lower than those of controls (p<0.001). There were significant negative correlations between adiponectin concentrations and insulin levels as well as homeostasis model assessment (HOMA) index in patient's group (r=- 0.538, p<0.001; r=- 0.393, p=0.001, respectively). There was also a significant negative correlation between plasma adiponectin concentrations and the degree of proteinuria (r=- 0.526, p=0.002). Plasma adiponectin levels in patients with proteinuria (n=31; 3.91+/-2.57 microg/mL) were significantly lower than those without proteinuria (n=33; 10.15+/-1.97 microg/mL) (p<0.001). After the treatment period, adiponectin levels significantly increased (p<0.001) and proteinuria, plasma insulin, and HOMA indexes significantly decreased in treatment group (p<0.001, p<0.001, p<0.001, respectively). The results suggest that adiponectin is inversely correlated with proteinuria and treatment with peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist rosiglitazone both corrects proteinuria and increases the low adiponectin levels in diabetic patients.

Adipocytes↗
PubMed1985

Proteinuria in autoimmune thyroid disease.

We have investigated the prevalence of proteinuria in patients with Graves' disease and chronic autoimmune thyroiditis attending a routine thyroid clinic. Using the urine protein creatinine index, proteinuria was found in 29.8% of patients with autoimmune thyroid disease and in 9.5% of patients attending the same clinic but without these conditions. When patients with Graves' disease were treated with 131I, proteinuria measured by 24 h collections developed in 9 of 14 patients without pre-existing proteinuria and appeared to diminish in 4 patients in whom proteinuria had been present before treatment. The prevalence and fluctuation of proteinuria was independent of thyroglobulin and microsomal antibody levels. We were unable to confirm previous reports of a high prevalence of circulating immune complexes in autoimmune thyroid disease; complexes were detected in only 7.9% of patients and did not correlate with proteinuria. The causes of mild proteinuria in autoimmune thyroid disease are not apparent, but previous case reports suggesting that membranous glomerulonephritis is associated with Graves' disease, albeit rarely, indicate that immunological mechanisms may be implicated.

Adult↗
PubMed2004

[Proteinuria in hypertensive syndrome of pregnancy: maternal and perinatal outcome].

AIM: The purpose of this study was to determine the role of proteinuria on pregnancy outcome in hypertensive syndrome with singleon pregnancies. METHODS: Transversal study with retrospective data of 334 pregnancies complicated by hypertensive syndromes who were delivered in the Department of Obstetrics of UNIFESP/EPM from January 1, 1999 to December 31, 2002. RESULTS: The patients were divided into four groups: (I) without proteinuria (n-203); (II) with proteinuria of 0.3 to 1.0g (n-39); (III) 1.0 to 2.0g (n-45); and (IV) 2.0g or more. Without proteinuria there was one case of placental abruption. The presence of proteinuria predicted adverse maternal outcome with increase of complications proportional to his elevation; among them, HELLP syndrome was the most frequent with 30.5% (40/131) followed by eclampsia with 3.8% (5/131), DPP 3.1% (4/131) and renal insufficiency with 0.7% (1/131). It was confirmed one maternal death in that group, when Maternal Mortality of 763/100.000nv was added up. As to the perinatal effects there was not increase of adverse effects without proteinuria. In the presence of proteinuria and its levels was observed the worst perinatal outcome with the elevation of the following indicatives: increase prematurely (62.2% vs 11.5%), newborn with weight < 2500g (6.5% vs 1.5%), newborn with Apgar < 7 in the 5th minute (30.4% vs 3.5%), concepts with growing restriction of intrauterine (41.9% vs 6.5%), newborn interned in the neonatal undid, (59.8% vs 15.5%) stillborn (14.4% vs 1.4%), neonatal deaths (6.1% vs 0.98%). The Perinatal Mortality was greater with proteinúria (175 vs 19,7) and, when = 2.0g (297.8 vs 19.6). CONCLUSIONS: The presence of proteinuria in the hipertensives syndromes during gestation and the elevation of their levels increase the risks of maternal complications, especially HELLP syndromes and eclampsia. Besides, it was observed a significative incidence of premature birth, newborn with Apgar < 7, weight < 2500g, IUGR, stillborn and neonatal deaths.

Adult↗
PubMed2001

Renal endothelin-1 and endothelin receptor type B expression in glomerular diseases with proteinuria.

The endothelin (ET) system has been studied extensively in experimental models of progressive chronic renal disease, but there is limited information regarding the ET system in renal patients. First, the expression of human ET-1, as well as ET receptor type A (ET-R(A)) and ET-R(B), was studied in 26 renal biopsies from patients with different renal diseases. Gene expression was assessed by quantitative reverse transcription-PCR. Second, ET-1 and ET-R(B) protein expression and localization were examined, by immunohistochemical analyses, among a homogeneous cohort of 16 patients with IgA nephropathy and different degrees of proteinuria. ET-R(B) mRNA expression was threefold higher among patients with higher-grade proteinuria [> or =2 g/24 h, n = 10; OD ratio (ODR), i.e., wild-type/mutant mRNA ratio, 1.81 +/- 0.3], compared with patients with lower-grade proteinuria (<2 g/24 h, n = 8; ODR, 0.63 +/- 0.1; P < 0.01) or control subjects (n = 9; ODR, 0.57 +/- 0.1; P < 0.01). ET-1 gene expression was significantly higher among patients with higher-grade proteinuria, compared with patients with lower-grade proteinuria (P < 0.01) or control subjects (P < 0.05). ET-R(A) mRNA expression was not different among the groups. Patients with higher-grade proteinuria who were receiving angiotensin-converting enzyme inhibitors exhibited significantly (P < 0.05) lower ET-1 and ET-R(B) mRNA expression, which was comparable to that of control subjects. By using immunohistochemical analyses, an association between proteinuria and expression of ET-1 and ET-R(B) in proximal tubular epithelial cells and of ET-1 in glomeruli was confirmed in the separate cohort of patients with IgA nephropathy. It is concluded that the increased ET-R(B) and ET-1 mRNA and protein expression observed in animal models of renal disease is also demonstrable among patients with renal disease and high-grade proteinuria.

Adult↗
PubMedDate not supplied

Assessment and management of proteinuria in dogs and cats: 2004 ACVIM Forum Consensus Statement (small animal).

Emerging data indicate that more attention should be given to the detection, evaluation, monitoring, and treatment of dogs and cats with proteinuria. The purposes of this consensus statement are to describe an appropriate approach for accomplishing these tasks and to provide specific recommendations for assessing and managing dogs and cats with proteinuria based on data that are currently available. Because proteinuria and albuminuria have numerous possible causes, they must be assessed appropriately to determine their implications for the patient. This assessment involves localization of the origin of the proteinuria as well as determination of its persistence and magnitude. Because persistent renal proteinuria usually indicates presence of chronic kidney disease, which sometimes is a progressive disorder, its detection identifies dogs and cats that have increased risk for adverse health outcomes. Thus, urine testing that will detect proteinuria should be a component of the clinical evaluations of dogs and cats under all circumstances that prompt their veterinarians to also perform comprehensive hematologic and serum biochemical evaluations. At a minimum, this testing should consist of a complete urinalysis that includes a satisfactorily accurate semiquantitative test for protein, and positive reactions should be properly followed with further testing. The appropriate response to persistent renal proteinuria depends on the magnitude of proteinuria and the status of the patient. The recommended response generally involves continued monitoring, further investigation, and therapeutic intervention, which should be implemented as an escalating series of inclusive, stepwise responses.

Animals↗
PubMed2005

Insulin resistance contributes to obesity-related proteinuria.

OBJECTIVE: Proteinuria is a recognized complication of obesity, but the pathogenesis remains unclear. We undertook the present study to clarify the factors contributing to proteinuria associated with obesity. METHODS: We studied 12 obese patients with proteinuria. Twenty-seven age-matched obese subjects without proteinuria served as controls. A glucose tolerance test and renal biopsy were performed in all patients. Fasting serum insulin and homeostasis model assessment-insulin resistance (HOMA-IR) were regarded as reflecting insulin resistance. To delineate the relation between insulin resistance and proteinuria, troglitazone, which acts an insulin sensitizer was given to 6 of 12 patients with a regular diet for 8 weeks. The 6 others were observed without receiving troglitazone. RESULTS: The 12 patients showed the presence of a cluster of insulin resistance factors: higher blood pressure, higher body mass index, higher fasting plasma glucose, higher fasting serum insulin, and higher HOMA-IR than controls. The renal biopsy specimens exhibited no histological abnormalities in 7, focal segmental glomerulosclerosis in 3 and benign nephrosclerosis in 2. Troglitazone attenuated HOMA-IR and ameliorated proteinuria, but did not affect body weight, creatinine clearance, or blood pressure. In contrast, the parameters in the patients not given troglitazone did not change. CONCLUSION: Insulin resistance is a factor contributing to obesity-related proteinuria. The role of insulin resistance as a factor reducing proteinuria remains to be clarified.

Adult↗
PubMed1981

Plasma renin and aldosterone in adult-onset diabetics with persistent proteinuria.

Plasma renin activity (PRA) and plasma aldosterone (PA) were measured under conditions of bed rest and after administration of furosemide and/or angiotensin II to adult-onset diabetics and age-matched controls. Seventeen of the diabetics had no proteinuria (non-proteinuria group) while in the other ten subjects, there was a persistent proteinuria, but no hypertension and renal dysfunction (proteinuria group). In the non-proteinuria group, changes in PRA and PA levels during both bed rest time and after the stimulation with furosemide did not significantly differ from findings in the control group. In the proteinuria group, PRA and PA levels were significantly lower than in the other two groups. PA and diastolic pressure responses to angiotensin II were slightly increased in diabetics (N.S.). PA responses to furosemide had significant positive correlation with those to angiotensin II. These findings suggest that the renin-aldosterone system responds normally in adult onset diabetics without proteinuria, but shows lower response in diabetics with persistent proteinuria, even without complications of hypertension and a decreased renal function.

Aldosterone↗
PubMedDate not supplied

[Effect of proteinuria on transport of sodium, potassium and chloride ions in renal tubules].

Functional and structural damages of tubulointerstitium are caused by proteinuria. The aim of this study was to assess the influence of different proteinuria levels on Na+, K+, Cl- tubular transport. We examined 50 patients (24 males, 26 females), mean age 46.50 +/- 13.08 years, with mean creatinine clearance of 87.29 +/- 31.17 mL/min. They were separated in three groups, depending on proteinuria value. The first group with proteinuria less than 0.3 g/24 h included 19 persons (7 males, 12 females), mean age 45.12 +/- 13.28 years, with mean creatinine clearance of 94.27 +/- 34.70 mL/min. The second group of 18 patients (8 males, 10 females), mean age 45.39 +/- 12.64 years, had proteinuria of 0.3-3.0 g/24 h and mean creatinine clearance of 90.07 +/- 31.89 mL/min. The third group had proteinuria level higher than 3.0 g/24 h and mean creatinine clearance of 73.25 +/- 20.44 mL/min. It included 13 patients (9 males, 4 females), mean age 50.08 +/- 13.73 years. As a parameter of proteinuria influence on tubular transport of Na+, K+ and Cl-, fractional excretion of these electrolytes, was studied. Student's T test, Mann Whitney U test and c2 test were used for statistical analysis. No statistically significant influence of proteinuria was found on Na+, K+ and Cl tubular transport.

Biological Transport, Active↗
PubMed1988

Epidemiology of persistent proteinuria in type II diabetes mellitus. Population-based study in Rochester, Minnesota.

Clinical risk factors for nephropathy were assessed in a population-based study of Rochester, Minnesota, residents with diabetes mellitus initially diagnosed between 1945 and 1969 (incidence cohort). The 1031 Rochester residents with non-insulin-dependent diabetes mellitus (NIDDM) were followed through their complete medical records in the community to 1 January 1982. The prevalence of persistent proteinuria was 8.2% at the diagnosis of NIDDM. Among those initially free of persistent proteinuria, the subsequent incidence was 15.3/1000 person-yr. Twenty years after the diagnosis of diabetes, the cumulative incidence of persistent proteinuria was 24.6%. A proportional hazards model identified the following risk factors for persistent proteinuria in NIDDM: elevated initial fasting blood glucose (P less than .01); older age at onset of diabetes (P less than .01); male gender (P = .05); and presence of macrovascular disease (P = .05), diabetic retinopathy (P = .05), or glycosuria (P = .07) at the diagnosis of diabetes. Separate analyses controlling for attained age indicated no association between duration of NIDDM and the incidence of persistent proteinuria. Stratified analysis of the two most significant risk factors (fasting blood glucose and age) indicated that hyperglycemia was a stronger risk factor for proteinuria in younger diabetic subjects, perhaps because of a competing risk of death in the elderly diabetic patient. In contrast to a recently described decreasing secular trend of proteinuria in Danish insulin-dependent diabetes mellitus patients, there was no decrease over the past 40 yr in proteinuria risk in this NIDDM incidence cohort.

Adult↗
PubMed1988

Proteinuria and activated T-lymphocytes in diabetic nephropathy.

The reasons for the presence of activated T-lymphocytes (ATL) in some long-standing insulin-dependent diabetic (IDDM) patients are unknown. These cells have been implicated in the genesis of proteinuria in some forms of immune-mediated renal disease. We measured ATL in 18 IDDM patients with diabetic nephropathy, 10 with nonnephrotic proteinuria (total urinary protein excretion rate greater than 0.5 and less than 3.5 g/24 h) and 8 with nephrotic proteinuria (total urinary protein excretion rate greater than 3.5 g/24 h), and in 17 age-, sex-, and duration-of-diabetes-matched diabetic control subjects without clinical proteinuria (total urinary protein less than 0.5 g/24 h). T-lymphocytes purified from peripheral blood were stained by direct immunofluorescence with the fluorescein-labeled monoclonal antibody anti-HLA-DR. Absolute number and percent of DR-positive T-lymphocytes were significantly higher in patients with nonnephrotic proteinuria (median and range 162 x 10(6)/ml, 40-320 x 10(6)/ml; 13.9%, 8.1-19.4%) compared with nonproteinuric control subjects (81 x 10(6)/ml, 2-240 x 10(6)/ml, P less than .05; 6.2%, 0-13.1%, P less than .01). In 8 patients with nephrotic proteinuria, absolute and percent DR-positive T-lymphocytes tended to be lower (36 x 10(6)/ml, 14-56 x 10(6)/ml; 3.4%, 1.1-5.4%) than in nonproteinuric control subjects. An increased number of activated T-lymphocytes may be part of an immune-mediated process associated with the development of proteinuria in diabetic nephropathy. In advanced renal disease with nephrotic proteinuria, this immune process may become exhausted.

Adult↗
PubMed1996

Prevalence and prognostic significance of proteinuria in patients with lung cancer.

The purpose of the present study was to ascertain the prevalence and prognostic significance of proteinuria in patients with lung cancer. Results of urinary dipstick testing were retrospectively reviewed in 1026 consecutive out-patients with histologically proven primary lung cancer and 475 consecutive out-patients with benign pulmonary disorders. Postoperative urinary dipstick test results were recorded in 243 surgically resected patients. Proteinuria was significantly more frequent in patients with lung cancer than in controls (30.1% vs 8.8%, p < 0.0001). The presence of proteinuria was significantly correlated with advanced disease stage (p < 0.0001). The frequency of proteinuria was significantly higher in patients with small cell carcinoma than in patients with other histologic types (p < 0.01). In the surgically resected patients, preoperative and postresection proteinuria occurred in 25.5% and 10.7% respectively (p < 0.0001). Patients with malignancies and proteinuria had significantly poorer survival than patients with normal urinary protein excretion (p < 0.0001). In a multivariate analysis including TNM stage, histologic type, sex, and age, proteinuria continued to be a significant predictor of reduced survival time. Our results suggest a high prevalence of increased urinary protein excretion in patients with primary lung cancer. Proteinuria may also be an independent predictor of poor survival.

Adult↗
PubMed1984

The relationship between aurothioglucose- and D-penicillamine-induced proteinuria.

We studied patients with rheumatoid arthritis who have been treated with aurothioglucose (Au) and subsequently with D-penicillamine (DP), and who developed drug-induced proteinuria, over a 10-year period. Twelve patients developed Au-induced and 19 DP-induced proteinuria. Of the 12 patients with Au-induced proteinuria, only 2 (17%) developed DP-induced proteinuria, indicating a slightly increased risk as compared with the overall incidence (9.3%) of this reaction in 168 DP-treated patients. In addition, only a minority (2 out of 19, 10.6%) of patients with DP-induced proteinuria had previous Au-induced proteinuria. These data may indicate that different mechanisms are operative in Au and DP-induced proteinuria, as is also suggested by the finding that HLA-DR3 was present more frequently in the latter (50%) than in the former (21%). A history of previous Au-induced proteinuria is insufficient reason to deny these patients the benefits of subsequent treatment with DP.

Arthritis, Rheumatoid↗