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PubMed2001

Proteinuria and plasma total homocysteine levels in chronic renal disease patients with a normal range serum creatinine: critical impact of true glomerular filtration rate.

Conflicting data have been reported concerning the independent association between proteinuria and plasma total homocysteine (tHcy) levels, particularly among chronic renal disease (CRD) patients with a normal range serum creatinine. Studies of this potential relationship have been limited by failure to assess true GFR, failure to assess proteinuria in a quantitative manner, or arbitrary restriction of the range of proteinuria examined. We examined the potential independent relationship between plasma tHcy levels and a wide range of quantitatively determined proteinuria (i.e., 0.000-8.340 g/day), among 109 CRD patients with a normal range serum creatinine (range; 0.8-1.5 mg/dl; median=1.2 mg/dl). Glomerular filtration rate (GFR) was directly assessed by iohexol clearance, and plasma status of folate, pyridoxal 5'-phosphate, and B12, along with serum albumin, were also determined. Linear modeling with ANCOVA revealed that proteinuria was not independently associated with tHcy levels (partial R=0.127; P=0.201), after adjustment for potential confounding by GFR (partial R=0.408; P<0.001), age, sex, plasma B-vitamin status, and serum albumin. Moreover, descending across quartiles (Q) [from Q4 to Q1] of GFR, ANCOVA-adjusted (i.e., for age, sex, and folate status) geometric mean tHcy levels (micromol/l) were significantly increased: tHcy Q4 GFR=9.6; tHcy Q3 GFR=10.5; tHcy Q2 GFR=11.9; tHcy Q4 GFR=14.5; P<0.001 for overall Q difference. We conclude that across a broad spectrum of quantitatively determined proteinuria, after adjustment for true GFR, in particular, there is no independent relationship between proteinuria and tHcy levels among CRD patients with a normal range serum creatinine.

Adult↗
PubMed1999

Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria.

BACKGROUND: Stratum 2 of the Ramipril Efficacy in Nephropathy (REIN) study has already shown that in patients with chronic nephropathies and proteinuria of 3 g or more per 24 h, angiotensin-converting enzyme (ACE) inhibition reduced the rate of decline in glomerular filtration and halved the combined risk of doubling of serum creatinine or end-stage renal failure (ESRF) found in controls on placebo plus conventional antihypertensives. In REIN stratum 1, reported here, 24 h proteinuria was 1 g or more but less than 3 g per 24 h. METHODS: In stratum 1 of this double-blind trial 186 patients were randomised to a ramipril or a control (placebo plus conventional antihypertensive therapy) group targeted at achieving a diastolic blood pressure of less than 90 mm Hg. The primary endpoints were change in glomerular filtration rate (GFR) and time to ESRF or overt proteinuria (> or =53 g/24 h). Median follow-up was 31 months. FINDINGS: The decline in GFR per month was not significantly different (ramipril 0.26 [SE 0.05] mL per min per 1.73m2, control 0.29 [0.06]). Progression to ESRF was significantly less common in the ramipril group (9/99 vs 18/87) for a relative risk (RR) of 2.72 (95% CI 1.22-6.08); so was progression to overt proteinuria (15/99 vs 27/87, RR 2.40 [1.27-4.52]). Patients with a baseline GFR of 45 mL/min/1.73 m2 or less and proteinuria of 1.5 g/24 h or more had more rapid progression and gained the most from ramipril treatment. Proteinuria decreased by 13% in the ramipril group and increased by 15% in the controls. Cardiovascular events were similar. As expected, the rate of decline in GFR and the frequency of ESRF were much lower in stratum 1 than they had been in stratum 2. INTERPRETATION: In non-diabetic nephropathies, ACE inhibition confers renoprotection even to patients with non-nephrotic proteinuria.

Adult↗
PubMed1999

ACE inhibition induces regression of proteinuria and halts progression of renal damage in a genetic model of progressive nephropathy.

Experimental data consistently indicate that renal disease progression is fully prevented in proteinuric glomerulopathies by long-enough angiotensin-converting enzyme (ACE) inhibition therapy. Whether regression of established proteinuria to normal can be achieved is, however, ill defined. The current study was designed with the aim to clarify whether ACE inhibition may induce regression of established proteinuria and renal structural damage in MWF rats, a genetic model of progressive proteinuria and renal injury. Animals treated with the ACE inhibitor lisinopril from 20 weeks of age (time when proteinuria is already important) and age-matched untreated rats were followed for 10 weeks. ACE inhibition normalized systolic blood pressure and progressively reduced proteinuria (from 172 +/- 79 to 81 +/- 23 mg/24 hours). In these animals, a highly significant correlation was obtained between baseline proteinuria and antiproteinuric response. At variance in untreated rats, proteinuria showed a marked increase in the 10-week follow-up period (from 165 +/- 57 to 325 +/- 86 mg/24 hours). Lisinopril prevented the progression of renal damage, as documented by a significantly lower incidence of glomeruli affected by sclerotic lesions (P < 0.01) than in untreated animals after the 10-week study period. Kidney tissue damage was comparable in lisinopril-treated rats and in untreated animals at 20 weeks of age, indicating that structural changes were arrested by the treatment. Thus, in proteinuric MWF rats, late-onset ACE inhibition normalized blood pressure, effectively and progressively restored high protein excretion rate toward normal values, and arrested progression of tissue damage.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Risk factors for development of proteinuria in chronic spinal cord injury.

A retrospective, case-control study was performed to investigate the risk factors that may contribute to the development of proteinuria in patients with chronic spinal cord injury (SCI). During an 18-month period, 31 subjects with a 24-hour protein excretion of 1.0 g or greater were identified. Three control subjects with SCIs with a 24-hour urinary protein excretion of less than 1.0 g during the same time period were randomly selected for each study subject with proteinuria. Clinical data, including level and duration of injury, age, presence of indwelling bladder catheter, number of decubitus ulcer procedures, serum albumin and creatinine concentrations, hematocrit, creatinine clearance, and the presence of hypertension and diabetes mellitus, were obtained from medical records. Subjects with proteinuria had other evidence of renal dysfunction with greater serum creatinine concentrations and reduced creatinine clearances, serum albumin concentrations, and hematocrits. Proteinuric subjects were older, had a longer duration of injury, had undergone a greater number of decubitus ulcer procedures, and were more likely to have hypertension and indwelling bladder catheters. The independent predictors for the development of proteinuria using logistic stepwise multiple linear regression analysis were the use of chronic indwelling bladder catheters, number of decubitis ulcer procedures, presence of hypertension, and older age. These data suggest that inflammatory complications associated with complications of chronic SCI, rather than SCI per se, contribute to the development of proteinuria. SCI patients with proteinuria have more impaired renal function and increased mortality compared with SCI patients without proteinuria.

Catheters, Indwelling↗
PubMed1988

Proteinuria in IgA nephropathy.

Clinicopathological data in 74 patients with IgA nephropathy were analyzed with special attention to level of proteinuria and its prognostic significance in this disease. Excretion rates exceeding 3 g per day (heavy), in the range of 1 to 2.9 g (moderate) and under 1 g per day (mild) each occurred in approximately equal proportions of patients. One-sixth of those with more than 1 g developed end-stage renal failure, while serum creatinine never exceeded 2 mg/dl in any with mild proteinuria. "Renal survival" (serum creatinine of 2 mg/dl or less) at five years after presentation was 100% in patients with persistently mild proteinuria, 87% in those whose protein excretion reached the moderate range, and 69% when heavy or nephrotic range proteinuria developed. Of significance, only rarely did mild proteinuria at presentation increase to higher levels. A correlation existed between level of protein excretion and severity of mesangial, segmental or global proliferation, glomerulosclerosis, podocyte effacement, interstitial infiltration, tubular atrophy and vascular sclerosis, even in patients with unimpaired renal function. Moderate or heavy proteinuria typically preceded the onset of hypertension and occurred prior to the development of renal insufficiency. Our results underscore magnitude of proteinuria as an early marker of glomerular damage in the prognosis of IgA nephropathy.

Adult↗
PubMed1996

Elastase, but not proteinase 3 (PR3), induces proteinuria associated with loss of glomerular basement membrane heparan sulphate after in vivo renal perfusion in rats.

Elastase, but not PR3, induces proteinuria associated with loss of glomerular basement membrane (GBM) heparan sulphate after in vivo renal perfusion in rats. PR3 and elastase are cationic neutral serine proteinases present in the azurophilic granules of polymorphonuclear leucocytes. Release of these proteolytic enzymes along the glomerular capillary wall may induce glomerular injury. Here, we investigated the effects of PR3 and elastase on the induction of proteinuria and glomerular injury after renal perfusion of these enzymes in Brown-Norway rats. Perfusion of active elastase induced a dose-dependent proteinuria 24h after perfusion, while inactivated elastase did not. Perfusion of comparable amounts of active PR3 did not induce proteinuria. Light and electron microscopy showed no morphological abnormalities in any experimental group. However, immunohistology revealed that proteinuria occurring after perfusion of active elastase was associated with a strong reduction in intraglomerular expression of the heparan sulphate side chain and, to a lesser extent, of the protein core of heparan sulphate proteoglycans (HSPG). In vitro, both elastase and PR3 digested HSPG. However, PR3 bound to a lesser extent to HSPG than elastase. We conclude that elastase, but not PR3, induces proteinuria after in vivo renal perfusion. This differential effect probably relates to different binding to the GBM of those enzymes due to differences in their isoelectric points. Degradation of heparan sulfate proteoglycans, leading to the disappearance of their side chains that contribute to the polyanionic structure of the GBM, appears to be involved in the induction of proteinuria after perfusion of elastase.

Animals↗
PubMed1998

Effects of an ACE inhibitor/calcium antagonist combination on proteinuria in diabetic nephropathy.

BACKGROUND: The degree of proteinuria in patients with diabetes correlates strongly with both an increase in progression of nephropathy as well as cardiovascular events. Moreover, post hoc analyses of recent clinical trials support the concept that reductions of blood pressure and proteinuria correlate with a slowed progression of nephropathy. Both angiotensin converting enzyme (ACE) inhibitors and the nondihydropyridine calcium antagonists, (non-DHPCAs) reduce both arterial pressure and proteinuria in those with diabetic nephropathy. METHODS: The present randomized, open label, parallel group designed study tests the hypothesis that, at similar levels of blood pressure, the combination of an ACE inhibitor, trandolapril (T) with the non-DHPCA, verapamil (V) produces a greater reduction in proteinuria over either agent alone at one year. Thirty-seven participants, mean age 59.6 +/- 5.8 years, with nephropathy (baseline creatinine 1.4 +/- 0.3 mg/dl and proteinuria of 1342 +/- 284 mg/dl) secondary to type 2 diabetes completed the study. Doses of drug were titrated in each group over eight weeks to achieve a goal blood pressure of < 140/90 mm Hg. All participants were counseled to ingest a sodium diet of < 120 mEq/day. RESULTS: Proteinuria reduction from baseline was significantly greater in the T+V group compared to either T alone (-33 +/- 8%, T vs. -62 +/- 10%, T+V; P < 0.001) or V alone (-27 +/- 8%, V vs. -62 +/- 10%, T+V; P < 0.001). No significant differences in either glomerular filtration rate, arterial pressure, fasting blood glucose or urinary sodium excretion were noted at one year. The mean daily dose of the individual components of T+V (2.9 +/- 0.8 mg, T/219 +/- 21.1 mg V) was significantly lower than the dose of either T alone 5.5 +/- 1.1 mg/day (P < 0.01) or V alone 314.8 +/- 46.3 mg, given in two divided doses (P < 0.01). CONCLUSION: These data support the concept that the combination of an ACE inhibitor with a non-DHPCA reduce proteinuria to a greater extent than either agent alone. This added antiproteinuric effect occurs at lower doses of each drug and is independent of further reductions in arterial pressure. These findings could have ramifications for slowing renal disease progression in patients with nephropathy from type 2 diabetes.

Aged↗
PubMed1999

Proteinuria induces tubular cell turnover: A potential mechanism for tubular atrophy.

BACKGROUND: Proteinuria and tubular atrophy have both been closely linked with progressive renal failure. We hypothesized that apoptosis may be induced by tubular cell exposure to heavy proteinuria, potentially leading to tubular atrophy. Apoptosis was studied in a rat model of "pure" proteinuria, which does not induce renal impairment, namely protein-overload proteinuria. METHODS: Adult female Lewis rats underwent intraperitoneal injection of 2 g of bovine serum albumin (BSA, N = 16) or sham saline injections (controls, N = 8) daily for seven days. Apoptosis was assessed at day 7 in tissue sections using in situ end labeling (ISEL) and electron microscopy. ISEL-positive nuclei (apoptotic particles) were counted in blinded fashion using image analysis with NIH Image. Cell proliferation was assessed by detection of mRNA for histone by in situ hybridization, followed by counting of positive cells using NIH Image. RESULTS: Animals injected with saline showed very low levels of apoptosis on image analysis. BSA-injected rats had heavy proteinuria and showed both cortical and medullary apoptosis on ISEL. This was predominantly seen in the tubules and, to a lesser extent, in the interstitial compartment. Overall, the animals injected with BSA showed a significant 30-fold increase in the number of cortical apoptotic particles. Electron microscopy of tubular cells in a BSA-injected animal showed a progression of ultrastructural changes consistent with tubular cell apoptosis. The BSA-injected animals also displayed a significant increase in proximal tubular cell proliferation. This increased proliferation was less marked than the degree of apoptosis. CONCLUSION: Protein-overload proteinuria in rats induces tubular cell apoptosis. This effect is only partially balanced by proliferation and potentially provides a direct mechanism whereby heavy proteinuria can induce tubular atrophy and progressive renal failure.

Animals↗
PubMed2000

Proximal tubular epithelial hyperplasia in patients with chronic glomerular proteinuria.

BACKGROUND: Proteinuria is known to affect the proximal tubular epithelial structure and function. The present study tested the hypothesis that chronic proteinuria leads to hyperplasia of proximal tubular epithelium. METHODS: This hypothesis was tested by morphometric analysis of the renal biopsy specimens in two groups of patients. Group A (N = 15) was composed of patients with chronic glomerular proteinuria who, for clinical indications, underwent renal biopsy of their native kidneys on two separate occasions. The proteinuria was sustained during the first and second renal biopsies in all but two of the patients with minimal change nephrotic syndrome who experienced transient remission. Group B (N = 10) was composed of patients with little or no proteinuria who underwent renal biopsy because of unexplained hematuria and whose renal biopsy showed only thin glomerular basement membrane (GBM) disease. RESULTS: In Group A, the mean number of epithelial cell nuclei per proximal tubule cross-section increased significantly from the first to the second renal biopsy (11.0 +/- 2.7 vs. 13.0 +/- 2.2, P = 0.005, paired t-test). Also, those with severe proteinuria showed proximal tubules with reactive epithelium (large pale nuclei with a high nucleus to cytoplasm ratio) and marked hyperplasia (double and triple layers of epithelium). Such changes were not seen in group B renal biopsies. Compared with group A biopsies, group B biopsies showed a lower mean value for proximal tubular epithelial cell nuclei per tubular cross-section (P = 0.056) and a higher mean proximal tubular volume (P = 0.049). As a consequence, the mean number of nuclei per relative tubular volume was significantly greater in group A compared with group B (0.55 +/- 0.14 vs. 0.40 +/- 0.06, P = 0.003, by Wilcoxon rank sum). CONCLUSIONS: Chronic heavy proteinuria is associated with hyperplasia of proximal tubular epithelium and contraction of proximal tubular volume. These events may impair glomerular filtration and represent another mechanism of progression of renal disease.

Adolescent↗
PubMed2002

Proteinuria is preceded by decreased nitric oxide synthesis and prevented by a NO donor in cholesterol-fed rats.

BACKGROUND: Hypercholesterolemia decreases nitric oxide (NO) availability in the circulation and induces podocyte activation and renal injury in rats. It is unknown whether hypercholesterolemia decreases renal NO availability. To dissociate the injury-independent effect of hypercholesterolemia on renal NO availability from secondary effects of proteinuria, increasing concentrations of cholesterol were administered. To determine whether podocyte activation and renal injury were associated with NO deficiency, molsidomine, an exogenous NO donor, was administered to hypercholesterolemic rats. METHODS: Female rats were fed 0, 0.5, 1, or 2% cholesterol for 24 weeks. Rats fed 2% cholesterol were also studied for two weeks. In addition rats fed 0 or 1% cholesterol received 120 mg molsidomine/L drinking water. Renal NO availability was determined by measuring renal NO synthesis and superoxide activity. Podocyte activation was monitored by desmin staining. RESULTS: Hypercholesterolemia dose-dependently increased proteinuria. In the absence of proteinuria, hypercholesterolemia decreased renal NO synthesis (4.2 +/- 0.5 in 0.5% cholesterol vs. 6.8 +/- 0.6 pmol/min/mg protein in controls; P < 0.05). With the exception of neuronal nitric oxide synthase (nNOS), renal NOS protein mass remained unaffected. Renal superoxide activity was dose-dependently increased, thus further lowering renal NO availability. Podocyte injury was dose-dependently increased even in the absence of proteinuria (score, 40 +/- 4 in 0.5% cholesterol vs. 9 +/- 4 in controls; P < 0.05). After two weeks, hypercholesterolemia caused no proteinuria, but did cause some podocyte injury. Renal NOS activity was decreased, but glomerular endothelial NOS (eNOS) staining was unchanged. Molsidomine prevented proteinuria, podocyte activation, and all further renal injury. CONCLUSIONS: Hypercholesterolemia decreases renal NO synthesis, and induces podocyte activation before proteinuria appears. Renal superoxide activity is increased once rats are proteinuric, further lowering renal NO availability. All of these changes can be prevented by a NO donor.

Animals↗
PubMed2002

Losartan in patients with type 2 diabetes and proteinuria: observations from the RENAAL Study.

BACKGROUND: Recently, the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) Study demonstrated the benefit of losartan in reducing renal outcomes in patients with type 2 diabetes and proteinuria. Additional questions concerning the reduction of proteinuria and its relationship to end-stage renal disease (ESRD) as well as cardio-renal outcomes and the safety and tolerability of losartan remain to be addressed. METHODS: Three analyses were performed: (a) the impact of losartan on the relationship between the reduction of proteinuria and ESRD; (b) a time-to-event analysis of the cardio-renal composite endpoint of ESRD, myocardial infarction, stroke or all-cause death; and (c) additional analyses of adverse events, particularly in patients with serum creatinine >or=2.0 mg/dL. RESULTS: After adjusting the values for proteinuria over the entire study, the reduction of proteinuria accounted for approximately half of the treatment effect of losartan on the risk reduction for ESRD. In addition, losartan was associated with a 21% risk reduction for the composite cardio-renal outcome (P=0.003). The addition of losartan to a conventional antihypertensive regimen did not increase the overall incidence of adverse events, regardless of severity of renal impairment. CONCLUSIONS: Losartan significantly reduced the risk of cardiorenal outcomes and was well tolerated by patients, including those with serum creatinine levels >or=2.0 g/dL. In addition, although this study shows that the reduction of proteinuria does not completely explain the impact of intervention on outcomes such as ESRD, reduction of proteinuria must remain an important consideration when treating patients with type 2 diabetes and nephropathy. However, the reduction of outcomes such as ESRD should remain the goal of therapy when evaluating renal protection in this patient population.

Adult↗
PubMed2005

Antagonists of aldosterone and proteinuria in patients with CKD: an uncontrolled pilot study.

BACKGROUND: Experimental evidence suggests that aldosterone may contribute to progressive kidney disease. Although angiotensin-converting enzyme (ACE) inhibitors and angiotensin type 1 receptor antagonists (ARBs) suppress the renin-angiotensin system, these agents do not adequately control plasma aldosterone levels. Hence, administration of aldosterone receptor antagonists may provide additional renal benefits to the ACE inhibitors and ARBs. METHODS: In the present uncontrolled pilot study, we evaluate the short-term (8 weeks) effects of spironolactone on proteinuria in 42 patients with chronic kidney disease (CKD) already treated with ACE inhibitors and/or ARBs. RESULTS: Spironolactone (25 mg/d for 8 weeks) decreased proteinuria from protein of 2.09 +/- 0.16 to 1.32 +/- 0.08 g/24 h after 2 weeks and 1.05 +/- 0.08 g/24 h after 8 weeks. Four weeks after discontinuation of spironolactone therapy, proteinuria returned to close to baseline values. Baseline proteinuria correlated significantly with plasma aldosterone level (r = 0.81; P < 0.0001). Moreover, baseline aldosterone level correlated significantly with degree of reduction in proteinuria after treatment with spironolactone (r = 0.70; P < 0.0001). Spironolactone caused a significant increase in serum potassium levels (from 4.4 +/- 0.1 mEq/L [mmol/L] at baseline to 4.8 +/- 0.1 mEq/L [mmol/L] after 8 weeks of treatment; P < 0.01). CONCLUSION: This study shows that spironolactone may effectively reduce proteinuria in patients with CKD. Concerns remain in regard to the risk for hyperkalemia in patients with CKD. Prospective randomized trials are necessary to confirm the efficacy and safety of antagonists of aldosterone on proteinuria and progression of CKD.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

The impact of accepting living kidney donors with mild hypertension or proteinuria on transplantation rates.

BACKGROUND: As waiting times for kidney transplantation increase, individuals with hypertension or proteinuria may be considered as eligible living donors. We set out to determine how frequently donors are excluded because of hypertension or proteinuria and to what extent accepting such donors would increase transplantation rates. METHODS: Wait lists from 4 Canadian transplantation centers were examined for causes of living kidney donor exclusion. Donors with hypertension (clinic blood pressure >140/90 mm Hg or requiring antihypertensive medication) or proteinuria historically have been excluded at these centers. We define potentially acceptable hypertension as a clinic blood pressure less than 150/100 mm Hg or less than 140/90 mm Hg if administered a single antihypertensive medication and define acceptable proteinuria as protein of 0.15 to 0.3 g/d. RESULTS: Only 35% (124 of 352 patients) of wait-listed patients had a living donor evaluated (n = 180 potential donors). Primary reasons for donor exclusion were immunologic: a positive cross-match (32%; n = 59) or blood group type incompatibility (22%; n = 40). Hypertension or proteinuria were less common (17%; n = 31). Of 31 donors excluded for hypertension or proteinuria, only 13 had results in the acceptable range. Acceptance of these donors would have resulted in transplantation of 3% (12 of 352 patients) of the wait-list population. CONCLUSION: Accepting living donors with mild hypertension and proteinuria will lead to a slight increase in transplantation rates. Efforts to improve living donor awareness and overcome immunologic barriers to transplantation may have a greater impact.

Cross-Sectional Studies↗
PubMed2006

Increased pulse wave velocity is associated with low creatinine clearance and proteinuria in a screened cohort.

BACKGROUND: Chronic kidney disease (CKD) is a risk factor for future cardiovascular disease. Although pulse wave velocity (PWV), which reflects arterial stiffness, was increased in subjects with CKD, little is known regarding whether renal function is associated with PWV in a low-risk population and whether proteinuria and decreased renal function synergistically affect PWV. METHODS: Subjects are 3,387 persons (mean age, 52 years) who attended a health checkup program in Okinawa, Japan. We measured brachial-ankle PWV (baPWV) by using an automatic oscillometric method. Proteinuria was semiquantified by using the dipstick method. Creatinine clearance (CCr) was estimated by using the Cockcroft-Gault formula. RESULTS: baPWV was accelerated with increases in age, systolic blood pressure, fasting glucose level, and total cholesterol level; male sex; presence of proteinuria; and decrease in CCr. All these factors independently predicted baPWV in multiple regression analysis. When subjects were divided into 6 groups according to CCr of 90 or greater, 60 to 89, or 30 to 59 mL/min (> or =1.50, 1.00 to 1.48, or 0.50 to 0.98 mL/s) and the absence or presence of proteinuria, baPWV, after adjustment for age, sex, and systolic blood pressure, increased in a stepwise fashion corresponding to decreases in CCr regardless of proteinuria, with the relationship exaggerated in the presence of proteinuria. CONCLUSION: Arterial stiffness increases with a decrease in renal function or with proteinuria independently of other risk factors.

Adult↗
PubMed1992

[Proteinuria and atherogenic risk].

The relationship between blood-lipid levels and severity of proteinuria was examined retrospectively in 30 patients (12 males, 18 females; mean age 39 [18-58] years). All patients had histologically confirmed glomerulonephritis (minimal change: n = 7, perimembranous: n = 8, focal sclerosing: n = 6, rapid progressive: n = 3, mesangio-proliferative: n = 4, membrano-proliferative: n = 1, diabetic glomerulosclerosis: n = 1). None was taking lipid-lowering drugs. Patients were classified according to the degree of proteinuria. In group 1 (proteinuria less than 5 g/d, n = 13) the LDL-HDL ratio averaged 4.4; in group 2 (proteinuria 5.0-10.0 g/d, n = 10) the average ratio was 8.8, and in group 3 (proteinuria greater than 10.0 g/d, n = 7) 13.3. Total cholesterol concentration also rose with increasing proteinuria (to 300 +/- 87 mg/dl, 375 +/- 168 mg/dl and 464 +/- 143 mg/d, respectively). The size of the LDL-HDL ratio and the level of total cholesterol did not correlate with the degree of excretory renal failure. These results point to an impressive correlation between the degree of proteinuria and the level of LDL-HDL ratio as a measure of atherogenic risk for a given patient.

Adult↗
PubMed2001

Use of a random urinary protein-to-creatinine ratio for the diagnosis of significant proteinuria during pregnancy.

OBJECTIVE: The purpose of this study was to evaluate whether a random urinary protein-to-creatinine ratio is a clinically useful predictor of significant proteinuria (300 mg/24 hour). STUDY DESIGN: The medical records of 138 women who completed both a random urinary protein-to-creatinine ratio and a 24-hour urine collection for the evaluation of preeclampsia were reviewed. Urine samples for the random protein-to-creatinine ratio were collected before the 24-hour urine collection. With the use of a protein level of at least 300 mg in the 24-hour urine sample as the gold standard, the sensitivity and specificity of the random protein-to-creatinine ratio for the diagnosis of significant proteinuria were determined with a range of cutoffs. RESULTS: Fifty percent of the study population had significant proteinuria. The data suggest that a cutoff below 0.14 ruled out significant proteinuria. The best cutoff of > or = 0.19 yields a sensitivity of 90% and a specificity of 70%. All of the false-negative test results had 24-hour urine protein levels below 400 mg; 13 of the 21 false-positive results had levels that ranged from 250 to 300 mg. CONCLUSION: The random urinary protein-to-creatinine ratio is strongly associated with the 24-hour total protein excretion. A level below 0.14 can rule out significant proteinuria. A best cutoff of > or = 0.19 is a good predictor of significant proteinuria. With further study, the random urinary protein-to-creatinine ratio could replace the 24-hour urine collection as a simpler, faster, more useful method for the diagnosis of significant proteinuria.

Adolescent↗
PubMedDate not supplied

Role of proteinuria reduction in the progression of IgA nephropathy.

UNLABELLED: Proteinuria has been shown to play a causal role in the progression towards ESRD of IgA nephropathy (IgAN). We demonstrated that steroids are effective in reducing proteinuria and preserving renal function. AIM: to evaluate the long-term effect of steroids in IgAN patients (6th year evaluation) and better clarify the role of proteinuria reduction in slowing down the progression. METHODS: multicenter randomized controlled trial of 86 adult IgAN patients with serum creatinine < or = 1.5 mg/ dL and moderate proteinuria. They received either supportive therapy or methylprednisolone 1-g i.v. for three days at months 1, 3, and 5, plus oral prednisone (0.5 mg/kg every other day for six months). RESULTS: Proteinuria significantly decreased in the treated patients (from 2.0+/-0.60 g/24 h at baseline to 1.0+/-0.68 g/24 h at six months) and remained stable till the 6th year (0.67+/-0.5 g/24 h), it slightly decreased in the control group. Six-year renal survival was significantly better in the steroid than in the control group: 9 patient (20.9%) in the steroid group and 15 (34.8%) in the control group reached the primary end-point of a 50% increase in serum creatinine from baseline. Five controls and none of the steroid-treated patients started dialysis. Steroid-treated patients did not experience any major side effects during follow-up. CONCLUSIONS: Steroids significantly reduce proteinuria and protect against renal function deterioration in IgAN patients. Early reduction of proteinuria could also be marker of a persistent reduction in its levels over time and of a better outcome in the long term.

Adult↗
PubMed2000

Severe proteinuria, sustained for 6 months, induces tubular epithelial cell injury and cell infiltration in rats but not progressive interstitial fibrosis.

BACKGROUND: Sustained proteinuria is reported to be very harmful to the tubulointerstitium, leading to severe interstitial injury. However, it remains unclear whether sustained proteinuria itself is responsible for severe interstitial injury because, in the previously reported models, the development of factors other than proteinuria in tubulointerstitial lesions could not be excluded completely. METHODS: After treatment to induce immune tolerance to mouse immunoglobulin, 20 rats were injected with anti-rat slit diaphragm monoclonal antibody (mAb) 5-1-6 twice a week for 6 months and were then sacrificed. RESULTS: mAb 5-1-6 induced massive proteinuria in 11 rats. In nine rats with mild proteinuria, no histological alteration could be detected with light microscopy and immunofluorescence. In nephrotic rats, light microscopy showed minor glomerular abnormalities, with interstitial oedema, tubular epithelial cell degeneration and interstitial cell infiltration. Immunofluorescence revealed increased expression of vimentin and an increased number of OX1-, OX19- and ED1-positive cells. However, we could not detect any accumulation of type I and IV collagen or laminin in the tubulointerstitium. RT-PCR showed that the expression of mRNA for type I collagen was not increased, compared with that in control rats. CONCLUSIONS: We succeeded in developing a model of persistent nephrosis without severe glomerular abnormalities, nephrectomy or other manoeuvres known to induce disturbed haemodynamics, using an agent without tubulointerstitial toxicity, and considered it to be suitable for investigating the direct toxicity of proteinuria. In this model, isolated massive proteinuria induced interstitial injury. However, the degree of injury was suggested to be much less than that observed in other previously developed models.

Animals↗