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PubMed1998

Progression to overt proteinuria in microalbuminuric Koreans with non-insulin-dependent diabetes mellitus.

Long-term data concerning the progression of microalbuminuria are not available in Koreans with non-insulin-dependent diabetes mellitus (NIDDM). To elucidate potential risk factors of the development of overt proteinuria in microalbuminuric Koreans with NIDDM, we studied retrospectively 46 patients with NIDDM. Between 1989 and 1990, they were found to have persistent microalbuminuria, and then were followed up regularly. Urinary albumin excretion rates (UAEs) were measured on a 24-h urine sample. Microalbuminuria was defined as UAE between 20 and 200 microg/min, and overt proteinuria as UAE > 200 microg/min on two consecutive occasions. After a mean of 4.5 years (range 3-6), 23 patients progressed to overt proteinuria (progressors), and others remained microalbuminuric (nonprogressors). Duration of diabetes was significantly longer in progressors than in nonprogressors. Mean fasting plasma glucose and HbA1c levels during the follow-up were significantly higher in progressors compared with nonprogressors (11.5+/-3.6 vs. 8.7+/-2.5 mmol/l, P=0.006, and 8.9+/-1.5 vs. 7.5+/-1.4%, P=0.005, respectively). In addition, frequencies of overt proteinuria were significantly higher in patients with their mean HbA1c > 8% during follow-up than in patients with their mean HbA1c < or=80% during follow-up (65.2 vs. 30.4%, P=0.015). Mean systolic blood pressure and mean diastolic blood pressure during follow-up tended to be higher in progressors compared with nonprogressors. Multiple logistic regression analysis revealed that mean HbA1c levels and mean systolic blood pressure during the follow-up were the most significant predictors for the incidence of overt proteinuria at 4.5-year follow-up, when adjusted for various factors (P=0.023, P=0.038, respectively). We conclude that poor glycemic control, along with elevated systolic blood pressure, were powerful predictors for the development of overt proteinuria in microalbuminuric Koreans with NIDDM.

Albuminuria↗
PubMed1992

Long-term beneficial effects of angiotensin-converting enzyme inhibition in patients with nephrotic proteinuria.

Angiotensin-converting enzyme inhibitors (ACEI) can reduce proteinuria in diabetic and nondiabetic nephropathy. However, no studies have determined whether this antiproteinuric effect modifies the progression of renal insufficiency. We studied the evolution of 46 nondiabetic patients with nephrotic proteinuria treated with captopril for a minimum of 12 months. The follow-up period before captopril treatment was 12 to 18 months. At the end of follow-up, after captopril introduction (24.4 +/- 7.6 months), proteinuria had decreased from 6.3 +/- 2.5 to 3.9 +/- 3.1 g/24 h (P less than 0.001), with a mean decrease of 45% +/- 28%. The proteinuria decrease was higher in patients with reflux nephropathy, proteinuria associated with reduction of renal mass, inactive crescentic glomerulonephritis, nephroangiosclerosis, and IgA nephropathy, whereas patients with membranous glomerulonephritis and idiopathic focal glomerulosclerosis showed a poorer response. Patients were separated according to a proteinuria reduction greater (group A, 23 patients) or lower (group B, 23 patients) than 45% of the initial value. At the end of follow-up, renal function had not significantly changed in group A with respect to values at the start of treatment: serum creatinine (SCr) was 229 +/- 167 mumol/L (2.6 +/- 1.9 mg/dL) versus 203 +/- 97 mumol/L (2.3 +/- 1.1 mg/dL), and creatinine clearance (CrCl) was 0.80 +/- 0.52 mL/s (48 +/- 31 mL/min) versus 0.87 +/- 0.47 mL/s (52 +/- 28 mL/min). The slope of the reciprocal of Scr (1/SCr) showed a significantly beneficial change after captopril introduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Proteinuria in African Americans with type 1 diabetes.

AIMS: African Americans with type 1 diabetes are at a high risk for end-stage renal disease (ESRD). Factors associated with the presence of (any) proteinuria were examined in this ethnic group. METHODS: Proteinuria and creatinuria were measured in both first-voided and 4-h timed urine specimens in African Americans with type 1 diabetes (N=717). Other evaluations included clinical interview, ocular examination, fundus photography, blood pressure, and glycosylated hemoglobin measurements. RESULTS: Of the 717 patients, 357 (49.8%) had any proteinuria. Frequency of any proteinuria increased significantly with (a). age, from 34.2% of patients 20-30 years of age to 84.7% in those >or=45 years of age, and (b). duration of diabetes from 24.1% in those with 0-4 years of diabetes to 77.5% in those with >or=25 years of diabetes. Multivariate logistic regression showed that any proteinuria was significantly and independently associated with male sex, systemic hypertension, poor glycemic control, and longer duration of diabetes. CONCLUSION: Proteinuria is common in African Americans with type 1 diabetes. Risk factors include male sex, systemic hypertension, poor glycemic control, and longer duration of diabetes. Whether early protection of renal function, in addition to glycemic control, may prevent such morbidity in this ethnic group requires study.

Adolescent↗
PubMed1992

The diagnostic value of haematuria and proteinuria in Schistosoma haematobium infection in southern Nigeria.

Haematuria and proteinuria as detected by chemical reagent strips correlated moderately (r = 0.7) with prevalence and intensity of infection with Schistosoma haematobium in an area of Anambra State, Nigeria. Differences attributable to age and sex were also reflected in a similar pattern, all peaks occurring in the 5-14 year age group. The differences observed with varying levels of intensity and haematuria at both 10 and 50 erythrocytes/microliter (p < 0.001) and proteinuria at 0.3 g/dl (p < 0.01) were statistically significant. At a proteinuria level of 1 g/dl, the observed differences were however not statistically significant (p > 0.5). The percentage of specimens from children (0-14 years) positive for S. haematobium eggs and with at least traces of haematuria and proteinuria (63.4% and 95%, respectively) was higher than in adults (33.3% and 80.2%, respectively). All individuals with more than 50 eggs/10 ml of urine were correctly identified using both indices either separately or in combination. For egg counts of less than 50 eggs/10 ml of urine, false diagnosis occurred in only 5% of all specimens examined. The sensitivity and specificity of haematuria and proteinuria at trace quantities was very high, but haematuria had a higher predictive value for a positive test (PvPt) and was considered the overall better indicator. A combination of both indices did not significantly increase the PvPt. When trace haematuria and moderate proteinuria were combined, both the sensitivity, specificity and PvPt were all above 90%, giving the best overall values in all the combinations made.

Adolescent↗
PubMed1987

Indomethacin reduces proteinuria in passive Heymann nephritis in rats.

Indomethacin has been used to lower proteinuria in human glomerular diseases with controversial results. The mechanism of indomethacin beneficial effects has not been established. A possible explanation is that indomethacin reduces proteinuria by inhibiting the synthesis of renal prostaglandins (PGs); however, appropriate studies to address this issue have never been done. The objectives of the present study were: to investigate whether indomethacin influences protein excretion in an experimental model of immunologically-mediated glomerular disease; to establish if the possible favorable effect of indomethacin on proteinuria is related to a reduction in glomerular filtration rate (GFR); to establish the possible association between the antiproteinuric effect of indomethacin and its inhibitory effect on arachidonic acid (AA) metabolites of renal or extrarenal origin; and to further investigate the relationship between proteinuria and renal thromboxane (Tx) synthesis previously demonstrated in experimental models of nephrotoxic nephritis and adriamycin (ADR) nephrosis. To this purpose we used an experimental immune-complex disease, passive Heymann nephritis (PHN) which was induced in the rat by a single intravenous (i.v.) injection of heterologous serum directed against a brush border component (gp 330 antigen). Indomethacin at a dose of 6 mg/kg intraperitoneally (i.p.) administered for four consecutive days to PHN animals during the period of heavy proteinuria, effectively reduced urinary protein excretion. The reduction in proteinuria does not appear to be a consequence of a reduction in GFR as documented by inulin clearance. Glomerular synthesis and urinary excretion of vasodilatory prostacyclin (PGI2) and PGE2 were decreased or unchanged in PHN animals in respect to control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Evidence suggesting a role for hydroxyl radical in puromycin aminonucleoside-induced proteinuria.

A single intravenous injection of puromycin aminonucleoside (PAN) results in marked proteinuria and glomerular morphological changes that are similar to minimal change disease in humans. We examined the effect of hydroxyl radical scavengers and an iron chelator on PAN-induced proteinuria. PAN in a dose of 5 mg/100 g body wt significantly increased urinary protein by day 5 (saline: 15 +/- 2, N = 24: PAN: 63 +/- 17, N = 23, P less than 0.001); the proteinuria rapidly increased thereafter, reaching 216 +/- 34, N = 23 by day 7. Concurrent administration of hydroxyl radical scavengers dimethylthiourea, (DMTU 500 mg/kg followed by 125 mg/kg i.p. twice a day) and sodium benzoate (BENZ, 150 mg/kg followed by 125 mg/kg i.p. twice a day) starting the evening before PAN injection markedly reduced proteinuria throughout the course of the study (urinary protein, mg/24 hours on day 7, mean +/- SEM: PAN: 229 +/- 45, N = 15; PAN + DMTU: 30 +/- 5, N = 18; PAN + BENZ: 80 +/- 18, N = 16. Because of the participation of iron in biological systems to generate hydroxyl radical, we also examined the effect of deferoxamine (DFO, 30 mg/day), an iron chelator, on the PAN-induced proteinuria. Concurrent administration of DFO was also protective. In a second series of experiments, DMTU and DFO (administered as described above and then for two additional days after the PAN) provided marked protection even when they were stopped prior to the onset of proteinuria. The protective effects of two hydroxyl radical scavengers and iron chelator implicate an important role for hydroxyl radical in PAN-induced nephrotic syndrome.

Animals↗
PubMed1989

Incidence of proteinuria in type 2 diabetes mellitus in the Pima Indians.

Little is known of the natural history of nephropathy in type 2 (non-insulin-dependent) diabetes, yet type 2 diabetes is a major cause of end-stage renal disease in the United States. The incidence rate of heavy proteinuria was determined in Pima Indians participating in a longitudinal population study of diabetes and its complications. Heavy proteinuria was defined by a urine protein (g/liter) to urine creatinine (g/liter) ratio greater than or equal to 1.0 (greater than or equal to 113 mg protein/nmol creatinine), a level which corresponds to a urine protein excretion rate of about 1 g/day. The incidence rates of proteinuria in diabetic Pimas were 4, 12, 37, and 106 cases/1,000 person-years at risk in the periods 0 to 5, 5 to 10, 10 to 15, and 15 to 20 years after the diagnosis of diabetes. The cumulative incidence rates were 2%, 8%, 23%, and 50% at 5, 10, 15, and 20 years, respectively. The duration of diabetes, severity of diabetes as determined by the degree of hyperglycemia and type of treatment, and blood pressure were risk factors for proteinuria. The presence of heavy proteinuria was strongly associated with the development of renal insufficiency, defined by serum creatinine greater than or equal to 2.0 mg/dl (greater than or equal to 177 mumol/liter). The incidence of proteinuria in type 2 diabetes in Pima Indians was as high as that reported in type 1 diabetes in other populations and represents a frequent, serious complication of the disease.

Adult↗
PubMed1993

Fish oil has protective and therapeutic effects on proteinuria in passive Heymann nephritis.

Passive Heymann nephritis (PHN) is a rat model of membranous nephropathy induced by injecting anti-Fx1A. The onset of proteinuria in PHN is caused by complement-mediated injury to glomerular epithelial cells (GEC) accompanied by enhanced glomerular eicosanoid production. In addition, sublethal injury by complement of rat GECs in culture leads to phospholipase activation, phospholipid hydrolysis and release of arachidonic acid and dienoic prostanoids. Based on these findings, we undertook to determine if substituting arachidonic acid (omega-6) in GEC membrane phospholipids with omega-3 fatty acids derived from fish oil would alter the development and course of proteinuria in PHN. We found that rats fed a diet containing 10% fish oil for four weeks prior to antibody injection developed 50 to 60% less proteinuria between two and six weeks after anti-Fx1A than rats fed an equivalent diet containing 10% safflower oil, and had substantial enrichment of glomerular phospholipids with omega-3 fatty acids and displacement of arachidonic acid. This outcome was associated with a 50% reduction in release of glomerular thromboxane B2 (stable metabolite of thromboxane A2) in the fish oil group. More importantly, when PHN rats with well established proteinuria while on regular chow were randomized to three dietary groups, those fed fish oil had a 25 to 50% decline in proteinuria as compared to those fed lard or safflower oil. This difference was evident within two weeks of randomization and persisted until the end of the study after eight weeks. In neither study could the differences in urine protein excretion be accounted for by protein or calorie deprivation, or by differences in blood pressure, renal function, immune response to sheep IgG, or glomerular deposition of IgG or complement. Thus, our results indicate that dietary fish oil has protective and therapeutic effects with regard to proteinuria in PHN. These benefits may relate to alterations in membrane phospholipid composition in favor of omega-3 fatty acids and release of less reactive trienoic eicosanoids.

Animals↗
PubMed2006

The relationships of proteinuria, serum creatinine, glomerular filtration rate with cardiovascular disease mortality in Japanese general population.

Proteinuria, high serum creatinine, and reduced glomerular filtration rate (GFR) have been associated with increased mortality from cardiovascular disease (CVD) and all causes. However, the combined effect of proteinuria with serum creatinine and GFR on CVD or all-cause mortality has not been well investigated. We conducted a 10-year prospective cohort study of 30,764 men and 60,668 women aged 40-79 years who participated in annual health checkups in 1993. The Cox proportional hazards model was used to estimate the relative risk (RR) after adjusting for age, smoking, and other cardiovascular risk factors. The multivariable RR (95% confidence interval (CI)) of CVD death for positive vs negative proteinuria was 1.38 (1.05-1.79) among men and 2.15 (1.64-2.81) among women. The respective RR for the highest vs lowest creatinine groups (> or = 1.3 vs < or = 0.8 mg/dl for men and > or = 1.1 vs < or = 0.6 mg/dl for women) was 1.56 (1.19-2.04) among men and 2.15 (1.58-2.93) among women. The respective RR for GFR < 60 vs > r = 100 ml/min/1.73 m2 was 1.65 (1.25-2.18) among men and 1.81 (1.39-2.36) among women. For individuals with proteinuria combined by hypercreatininemia or reduced GFR, the risk of CVD death was two-fold higher in men and 4-6-fold higher in women compared to those without proteinuria and with normal creatinine level or GFR. Similar associations were observed for stroke, coronary heart disease, and all-cause mortality. Proteinuria, and hypercreatininemia or reduced GFR and their combination were significant predictors of CVD and all-cause mortality.

Antihypertensive Agents↗
PubMed2006

Increasing incidence of proteinuria and declining incidence of end-stage renal disease in diabetic Pima Indians.

The introduction of more efficacious treatments for diabetic kidney disease may slow its progression, but evidence for their effectiveness in populations is sparse. We examined trends in the incidence of clinical proteinuria, defined as a urinary protein-to-creatinine ratio >0.5 g/g, and diabetic end-stage renal disease (ESRD), defined as death from diabetic nephropathy or onset of dialysis, in Pima Indians with type 2 diabetes between 1967 and 2002. The study included 2189 diabetic subjects >/=25 years old. During follow-up, 366 incident cases of proteinuria occurred in the subset of 1715 subjects without proteinuria at baseline. The age-sex-adjusted incidence rate of proteinuria increased from 24.3 cases/1000 person-years (pyrs) (95% confidence interval (CI) 18.7-30.0) in 1967-1978 to 35.4 cases/1000 pyrs (95% CI 28.1-42.8) in 1979-1990 and 38.9 cases/1000 pyrs (95% CI 31.2-46.5) in 1991-2002 (P(trend)<0.0002). In each period, the age-sex-adjusted incidence of proteinuria increased with diabetes duration, but diabetes duration-specific incidence was stable throughout the study period (P=0.8). The age-sex-adjusted incidence of ESRD increased between 1967 and 1990 and declined thereafter. The incidence of proteinuria increased over 36 years in Pima Indians as the proportion of people with diabetes of long duration increased. On the other hand, the incidence of ESRD declined after 1990, coinciding with improved control of blood pressure, hyperglycemia, and perhaps other risk factors.

Adult↗
PubMed2007

Effect of combining ACE inhibition with aldosterone blockade on proteinuria and renal damage in experimental nephrosis.

Aldosterone has pro-fibrotic properties and is a potential target for additional intervention in patients with chronic renal disease showing resistance to therapy during treatment with angiotensin-converting enzyme inhibitors (ACEi). Combining ACEi and aldosterone receptor blockade (aldoRB) in proteinuric renal disease reduces proteinuria, but effects on proteinuria-induced renal damage are unknown. We studied the effect of ACEi/aldoRB in adriamycin nephrosis (AN). Six weeks after injection of adriamycin in Wistar rats, randomized treatment with vehicle (VEH, n=8), aldoRB (n=12), ACEi (n=10), or a combination of ACEi/aldoRB (n=14) was given for 12 weeks. Healthy rats served as controls (n=6). Renal damage was quantified by markers of tubular injury (osteopontin (OPN) and kidney injury molecule-1 (Kim-1)), pre-fibrotic lesions (alpha-smooth muscle actin (SMA)), interstitial fibrosis (IF), and focal glomerulosclerosis (FGS). In AN animals, proteinuria was increased compared with controls. ACEi and ACEi/aldoRB significantly reduced proteinuria compared with VEH, whereas aldoRB monotherapy was without effect. Blood pressure was reduced in ACEi and ACEi/aldoRB compared with VEH and aldoRB. OPN and Kim-1 were increased in AN animals, but significantly reduced by ACEi/aldoRB. Treatment with ACEi and ACEi/aldoRB prevented an increase of SMA, IF, and FGS. In conclusion, ACEi/aldoRB effectively reduced proteinuria and markers of tubular injury and prevented renal damage in this rat model of chronic proteinuria-induced renal damage.

Actins↗
PubMed1998

An epidemic of proteinuria in Pima Indians with type 2 diabetes mellitus.

BACKGROUND: The risk of proteinuria in Type 1 diabetes declined > or = 30% over the past 50 years, and improvements in metabolic control are believed to be largely responsible. Little is known about secular changes in the risk of proteinuria in Type 2 diabetes. METHODS: We examined trends in the incidence rate of proteinuria in Pima Indians > or = 20 years of age with diabetes diagnosed between January 1, 1955 and December 31, 1994. RESULTS: Among 1305 initially non-proteinuric diabetic subjects, 433 developed proteinuria during a median follow-up of 8.0 years (range 0.8 to 30.2 years). With subjects with diabetes diagnosed between 1955 and 1964 serving as the reference group, the rate of proteinuria was similar (rate ratio 1.0; 95% confidence interval, 0.79 to 1.3) in the cohort diagnosed between 1965 and 1974, 1.5 times as high (95% confidence interval, 1.1 to 2.0) in the cohort diagnosed between 1975 and 1984, and 1.9 times as high (95% confidence interval, 1.1 to 3.0) in the cohort diagnosed between 1985 and 1994, after adjusting for potential confounders in a generalized additive proportional hazards model. Between the first and last cohorts, plasma glucose concentration declined, on average, by 17% (P = 0.0001) and the mean arterial pressure declined by 11% (P = 0.0001). CONCLUSIONS: The incidence rate of proteinuria in Pima Indians with Type 2 diabetes increased nearly twofold in the last 40 years, despite improvements in plasma glucose and blood pressure. Rapidly changing environmental or behavioral factors must play an important role in the pathogenesis of diabetic renal disease in this population.

Adult↗
PubMed2000

Interstitial fibrosis in mice with overload proteinuria: deficiency of TIMP-1 is not protective.

BACKGROUND: Progressive renal interstitial fibrosis is characterized by up-regulated expression of the gene that encodes the tissue inhibitor of metalloproteinases-1 (TIMP-1), a regulator of extracellular matrix remodeling, suggesting that impaired matrix turnover contributes to the fibrogenic process. The present study was designed to develop a murine model of renal interstitial fibrosis, and to determine the functional significance of up-regulated Timp-1 expression by comparing the severity of this renal disease in wild-type mice and mice genetically deficient in Timp-1. METHODS: Initial pilot studies developed and characterized a murine model of bovine serum albumin (BSA)-induced protein-overload proteinuria with respect to the degree of proteinuria, severity of interstitial fibrosis, and renal mRNA levels for genes encoding matrix proteins, transforming growth factor-beta1 (TGF-beta1), and TIMP-1, -2, -3, and -4. In the final study, the severity of interstitial fibrosis was compared in wild-type and Timp-1-deficient mice after six weeks of proteinuria. RESULTS: Mice injected with large daily intraperitoneal doses of BSA developed proteinuria, interstitial inflammation, and progressive interstitial fibrosis. A time course study based on measurements after one, two, and six weeks of BSA injections showed increased renal mRNA levels for the matrix genes procollagens alpha1(I), alpha1(III), and alpha2(IV) and TGF-beta1 and Timp-1. Timp-2 and Timp-3 genes were constitutively expressed at high levels in the normal kidneys and showed little change in the proteinuric kidneys. Timp-4 transcripts were not detected in any of the kidneys. After six weeks of BSA overload-proteinuria, the groups (N = 8 per group) of wild-type and Timp-1-deficient mice developed significant interstitial fibrosis compared with the control saline-injected groups. The severity of the interstitial fibrosis was similar in both proteinuric groups based on an assessment of the final kidney weight, total kidney collagen content, and the number of interstitial fields with increased fibronectin staining. CONCLUSIONS: Results of the present study indicate that TIMP-1 deficiency does not alter the degree of interstitial fibrosis in the murine overload proteinuria model. Potential explanations include Timp-1 genetic redundancy, as suggested by the observation that, despite significant intrarenal induction of the Timp-1 gene expression, net renal metalloproteinase-9 (MMP-9) activity was not significantly altered. TIMP-1 is a multifunctional protein that may play a metalloproteinase-independent role in response to renal injury.

Animals↗
PubMed2000

Effects of current smoking and smoking discontinuation on renal function and proteinuria in the general population.

BACKGROUND: Smoking may adversely affect the progression of renal diseases. However, it is unknown whether smoking affects renal function in subjects without nephropathy. METHODS: In 1998, 28,409 volunteers from the general population were examined at the Institut Régional pour la Santé (IRSA). Renal function was estimated with creatinine clearance using the Cockcroft formula. Dipstick proteinuria was assessed on an overnight urine sample by a trained technician. RESULTS: Adjusted creatinine clearance was higher in current smokers than in former smokers and never smokers (100.6 +/- 13.6 vs. 98.8 +/- 13.9 mL/min/1.73 m2, P < 0.0001, and vs. 98.5 +/- 14.0 mL/min/1. 73 m2, P < 0.0001, respectively). This difference was predominant in men and weak in women, and was associated with the number of cigarettes smoked daily. The slope of the projected age-related decline in the creatinine clearance accelerated with age, but it was similar in current smokers, former smokers, and never smokers. Creatinine clearance was associated with a relative risk of proteinuria [for each mL/min/1.73 m2, the relative risk was 1.007 (95% CI, 1.000 to 1.015), P = 0.056, for 1+ or higher proteinuria; and 1.018 (1.004 to 1.030), P = 0.0078, for 2+ or higher proteinuria]. Current and former smokers had a marked risk of 2 or higher proteinuria [adjusted RR (95% CI), 3.26 (1.66 to 6.80), P = 0. 0009, and 2.69 (1.24 to 5.99), respectively, P = 0.013, vs. never smoking], which was independent of the daily or cumulative cigarette consumption. CONCLUSIONS: In the general population, smokers do not exhibit lower creatinine clearance than never smokers. In fact, creatinine clearance is slightly higher in current smokers at least in men, even when normotensive and hypertensive subjects are analyzed separately, but the difference is small, especially in women. This effect seems reversible upon smoking discontinuation. Chronic smoking results in a marked risk of irreversible proteinuria that may occur despite moderate smoking.

Adult↗
PubMed2002

Rapid and persistent reduction of proteinuria following plasma exchange in a case of steroid-resistant focal segmental glomerulosclerosis.

We report on the case of a 45 year old male with focal segmental glomerulosclerosis (FSGS) in whom steroid-resistant proteinuria was reduced rapidly by plasma exchange. In 1994, he was admitted to our hospital because of massive proteinuria of several years' duration. Renal biopsy confirmed the diagnosis of FSGS. Proteinuria was suppressed partially with the use of dipyridamole. Though oral prednisolone (PSL, 30 mg/day) was effective initially, relapse occurred during PSL tapering. Doses of PSL up to 30 mg/day or additional mizoribine were ineffective. The patient was readmitted for a trial of plasma exchange in April 2000. Four sessions of plasma exchange with albumin replacement over 2 weeks immediately reduced the proteinuria from 3.2 g/day to 0.6 g/day without any change in medication. After discharge, proteinuria remained suppressed for more than 6 months despite a reduction of PSL dose to 15 mg. The rapid and long lasting effect of plasma exchange in the present case argues for the role of a putative circulatory factor in the pathogenesis of proteinuria in FSGS.

Drug Tolerance↗
PubMed2001

Urinary excretion of IgG and alpha(1)-microglobulin predicts clinical course better than extent of proteinuria in membranous nephropathy.

In idiopathic membranous nephropathy (MN), the main predictors for progression to chronic renal failure (CRF) are the amount of proteinuria and extent of tubulointerstitial damage. The aim of this study is to evaluate whether urinary excretion of proteins reflecting the alteration of permselectivity in the glomerular capillary wall, such as immunoglobulin G (IgG), and the reabsorption impairment of low-molecular-weight proteins, such as alpha(1)-microglobulin (alpha(1)m), correlates with the extent of tubulointerstitial damage and have a predictive value for functional outcome and response to therapy better than 24-hour proteinuria. In 78 patients with MN, urinary excretion of albumin, transferrin, IgG, and alpha(1)m was measured by immunonephelometry in second-morning urine samples and expressed in milligrams per gram of urinary creatinine (uCr). In 48 patients with characterization of proteinuria and renal biopsy performed at the same time, excretion of IgG (P = 0.0087) and alpha(1)m (P = 0.0024), but not albumin (P = 0.37), transferrin (P = 0.38), or 24-hour proteinuria (P = 0.32), was associated significantly with the extent of tubulointerstitial damage (score, 0 to 1 versus >/=2). Only alpha(1)m excretion was associated significantly with global glomerular sclerosis (P = 0.0032) and arteriolar hyalinosis (P = 0.0004). Moreover, urinary excretion of alpha(1)m was significantly dependent on IgG excretion (r = 0.67; P = 0.0001), but not on albumin (P = 0.66) or 24-hour proteinuria (P = 0.07). Functional outcome could be evaluated in 38 patients with nephrotic syndrome and baseline normal renal function (serum creatinine, 0.99 +/- 0.20 mg/dL; follow-up, 44 +/- 22 months). Remission was 100% versus 20% in patients with IgG excretion less than 110 mg/g uCr versus 110 mg/g uCr or greater (P = 0.0001) and 77% versus 17% in patients with alpha(1)m excretion less than 33.5 mg/g uCr versus 33.5 mg/g uCr or greater (P = 0.0009), respectively. In patients with IgG and alpha(1)m excretion less than or greater than the cutoff value, progression to CRF was 0% versus 35% (P = 0.0026) and 0% versus 58% (P = 0.0001), respectively. Nineteen patients treated with immunosuppressive therapy were compared with 19 untreated patients. There was no difference in remission or progression between treated and untreated patients when IgG and alpha(1)m excretion were less than the cutoff value. There was a significant difference for progression to CRF between treated and untreated patients when alpha(1)m excretion was greater than the cutoff value (17% versus 100%; P = 0.0076). In conclusion, IgG excretion is associated significantly with the extent of tubulointerstitial damage and alpha(1)m excretion. This observation supports the hypothesis that IgG may be the toxic moiety of proteinuria. Excretion of IgG and alpha(1)m has a significant predictive value for both remission and progression and is useful to identify patients who are at risk for progression and for whom treatment with immunosuppressive therapy is indicated soon after diagnosis.

Albuminuria↗
PubMed2005

Proteinuria and hemoglobin levels in patients with primary glomerular disease.

BACKGROUND: Anemia in association with nephrotic syndrome has been described in small patient series and case reports. Whether nephrotic patients develop anemia has not been formally investigated. METHODS: We undertook a retrospective cross-sectional study of patients with biopsy-proven primary glomerular disease, various degrees of proteinuria, and creatinine levels less than 2 mg/dL (< 177 micromol/L). In addition to proteinuria, values for hemoglobin (Hb), age, body mass index (BMI), serum albumin and protein, and estimated glomerular filtration rate (eGFR) were derived from patient charts. RESULTS: We studied 297 patients, 187 men and 110 women, aged between 16 and 81 years. Univariate analysis showed no correlation between Hb level and proteinuria in either sex. Stratification of women and men into quartiles according to proteinuria showed no differences in Hb levels among the 4 groups. Three of 52 non-nephrotic women (6%) were anemic (Hb < 12 g/dL [< 120 g/L]) compared with 11 of 58 nephrotic women (19%; P = 0.047). Multiple regression analysis of all patients showed Hb level to have a correlation with sex (P < 0.001), BMI (P < 0.001), and eGFR (P = 0.005); negative correlation with age (P = 0.028); and borderline negative correlation with proteinuria (P = 0.054). In women, BMI showed a positive correlation with Hb level (P = 0.030). Proteinuria did not reach statistical significance (P = 0.093). In men, BMI (P = 0.001) and eGFR (P = 0.013) were associated positively and age (P = 0.031) was associated negatively with Hb level. CONCLUSION: These results indicate that nephrotic syndrome is not associated with anemia in men, but with a tendency to decrease Hb levels in women.

Adolescent↗
PubMed2007

Antihypertensive therapy in the presence of proteinuria.

The presence of proteinuria is a well-known risk factor for both the progression of renal disease and cardiovascular morbidity and mortality, and decreases in urine protein excretion level were associated with a slower decrease in renal function and decrease in risk of cardiovascular events. Increased blood pressure has a major role in the development of proteinuria in patients with either diabetic or nondiabetic kidney disease, and all recent guidelines recommend a blood pressure goal less than 130/80 mm Hg in patients with proteinuria to achieve maximal renal and cardiovascular protection. Drugs interfering with the renin-angiotensin system, ie, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, should be used as first-line antihypertensive therapy in patients with proteinuria because they seem to have a blood pressure-independent antiproteinuric effect, and if blood pressure levels are still out of goal, a diuretic should be added to this regimen. A combination of an angiotensin-converting enzyme inhibitor with an angiotensin receptor blocker or other classes of medications shown to decrease protein excretion, such as nondihydropyridine calcium antagonists or aldosterone receptor blockers, should be considered to decrease proteinuria further. This review provides an extended summary of current evidence regarding the associations of blood pressure with proteinuria, the rationale for currently recommended blood pressure goals, and the use of various classes of antihypertensive agents in proteinuric patients.

Angiotensin Receptor Antagonists↗