Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One group of male Wistar rats (Group B) was pretreated by a daily subcutaneous injection with CdCl2 during 5 days with increasing doses (0.5, 1, 1, 2 and 2 mg Cd/kg). Another group of rats (Group A) was daily given normal saline subcutaneously for 5 days. On the second day after the last injection, a single s.c. injection of 109Cd-metallothionein (CdMT, 0.4 mg Cd/kg) was given to each animal in both groups. Urinary calcium, protein, metallothionein (MT), N-acetyl-beta-D-glucosaminidase (NAG) and gamma glutamyltransferase (gamma-GT) were measured. In Group A, calciuria, proteinuria, metallothioneinuria and enzymuria was induced by CdMT. Calciuria reached a peak during 0-6 h after the administration of CdMT, thus appearing earlier than other effects. Enzymuria was displayed at 6-12 h for gamma-GT and 12-24 h for NAG. A prominent increase of proteinuria appeared at 24-48 h after the challenge of CdMT. In Group B, no significant increase of urinary calcium, protein, or NAG was observed after the CdMT injection and urinary gamma-GT was only slightly elevated, thus demonstrating the protective action of pretreatment. This study demonstrates for the first time that calciuria, one of the signs of cadmium nephrotoxicity, can be prevented by cadmium pretreatment. Urinary MT increased slightly during the 4-5 days of CdCl2 pretreatment. This is in accordance with previous observations that cadmium pretreatment induces new synthesis of MT which is likely to constitute the background for the resistance to the CdMT challenge to the kidney.
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PMID:Modulation of calciuria by cadmium pretreatment in rats with cadmium-metallothionein-induced nephrotoxicity. 136 Jul 15

Patients with diffuse, proliferative lupus nephritis (DPLN) were subjected to differential solute clearances (n = 22) and serial renal biopsy (n = 11) before and again after 6-12 mo of immunosuppressive therapy. Glomerular sieving of dextrans of graded size was analyzed with a heteroporous membrane model. This revealed active DPLN to be associated with 1) a reduction of overall pore density accompanied by a 53% depression of glomerular filtration rate (GFR), and 2) appearance of a subset of large, nondiscriminatory pores, which accounted for the observed nephrotic level of proteinuria. Morphometric analysis of biopsy tissue provided evidence of reduced filtration surface area due to global or segmental occlusion of capillary loops in glomerular tufts. Activity of DPLN resolved posttreatment. A computed increase in pore density was associated with a 24% increment in GFR; a marked reduction in the fraction of shuntlike pores was accompanied by a parallel reduction of proteinuria into a subnephrotic range. Repeat biopsy revealed diminished glomerular cellularity, fewer immune deposits, and an ensuing increase in the fraction of tuft area occupied by patent loops. Epithelial filtration slit frequency also increased. Neither functional nor structural recovery was complete, however. Residual pore density approximated only 23-35% of that in healthy controls, and corresponding shuntlike pores were threefold more prominent. We conclude that severe DPLN is only partially reversible by current modalities of treatment and that the ensuing residual injury is far more severe than suggested by conventional tests of renal function.
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PMID:Extent of glomerular injury in active and resolving lupus nephritis: a theoretical analysis. 203 58

We investigated the effect of proteolytic enzyme treatment on the course of passive Heymann nephritis (PHN). PHN was induced by intravenous injection of Heymann antibody into Sprague Dawley rats. Protease-treated rats received intraperitoneal chymopapain and subtilisin. In rats given subnephritogenic doses of Heymann antibody (5 or 10 mg, insufficient to cause proteinuria), glomerular immune deposits were assessed by immunofluorescence and electron microscopy. In rats given 5 mg Heymann antibody and treated with protease in the heterologous phase of the disease (days 1-7), fewer animals were positive for rabbit IgG and rat IgG, as determined by immunofluorescence on day 12, compared with controls (p less than 0.01). Rats given 10 mg Heymann antibody and treated on days 1-5 were less frequently positive for rabbit IgG on day 5 than controls (p less than 0.05). When treatment was given on days 6-12 (autologous phase), fewer rats had glomerular rabbit and rat IgG compared with controls (p less than 0.025). Protease treatment of rats given nephritogenic doses of Heymann antibody (greater than or equal to 40 mg, causing proteinuria) did not result in significant differences in immunofluorescence deposits. However, protease treatment significantly reduced the number of electron dense deposits at all doses of antibody (p less than 0.01). Furthermore, rats given 60 mg Heymann antibody followed by enzyme treatment in the heterologous phase (days 1-7) or throughout the autologous phase (days 6-18) had significantly reduced protein excretion during the autologous phase compared with control rats (p less than 0.05). After onset of significant proteinuria on day 15 in rats given 40 mg Heymann antibody and treated from day 15 until day 25, there was significantly less (p less than 0.05) proteinuria on days 21-22 and 24-25 than in control rats; thus, enzymes could reverse proteinuria. In normal rats, administration of proteases did not have significant effects on urinary protein excretion, serum creatinine, or renal morphology, nor did protease affect anti-rabbit IgG antibody production in rats injected with Heymann antibody. The overall results indicate that proteolytic enzyme treatment can prevent or remove glomerular immune deposits and can prevent or reverse proteinuria.
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PMID:Proteolytic enzyme treatment reduces glomerular immune deposits and proteinuria in passive Heymann nephritis. 353 93

A general method for calculating incidences of the more common adverse reactions during long-term therapy with disease suppressive agents is presented. With D-penicillamine treatment, the incidence of proteinuria rises during 6-12 months and then declines, but with aurothiomalate treatment the incidence of proteinuria and rash progressively decline. Low-dose chloroquine treatment was associated with a much lower withdrawal rate due to adverse reactions compared to D-penicillamine. However, the efficacy at mean doses of chloroquine less than 250 mg day-1 has not been formally evaluated. A formal, well-controlled trial comparing D-penicillamine, at current dosage, and of chloroquine, at low dosage, seems warranted in order to place the usefulness of D-penicillamine in perspective.
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PMID:A method of comparing the toxicities of disease suppressive agents: possible application to a comparison between D-penicillamine and chloroquine. 642 36

The cadmium-metallothionein (CdMT) injection model was used to examine whether multiple short-interval injections of CdMT, instead of a single dose, could better reproduce the features of chronic exposure to inorganic cadmium. Male Wistar rats were given an initial CdMT dose and four subsequent doses subcutaneously at 2-h intervals. A control group, given saline, was compared with a low dose group (0.2 + 4 x 0.1 mg Cd/kg b.w.) and high dose group (0.4 + 4 x 0.1 mg Cd/kg b.w.). Nephrotoxic effects were seen at the high dose. A marked proteinuria began 6-12 h after the first injection and extended to day 9. A progressive, unreversed calciuria appeared at 6 h and reached its maximum at day 13. This was a marked increase in duration compared with the transient peaks of proteinuria and calciuria observed in previous single dose studies. The unreversed calciuria and the marked proteinuria are suggestive of residual tubular damage, which may be irreversible. In conclusion, the model with multiple short-interval CdMT injections more closely reproduces the situation in long-term exposure to inorganic cadmium, compared to the single dose models previously employed.
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PMID:Nephrotoxic impact of multiple short-interval cadmium-metallothionein injections in the rat. 881 44

Nephropathy is the major life-threatening complication of insulin-dependent diabetes mellitus (IDDM). The clinical syndrome is characterized by persistent albuminuria (greater than 300 mg day), a rise in arterial blood pressure, and a relentless decline in glomerular filtration rate leading to end-stage renal failure. The availability of a radioimmunoassay for detecting albumin in low concentrations in urine has allowed the study of urinary albumin excretion rates in diabetics well before clinically persistent proteinuria develops. An albumin excretion rate greater than that in normal subjects and lower than that in macroalbuminuric subjects is called microalbuminuria (range 20-200 microg/min or 30-300 mg/24 h). Although recent studies have challenged the predictive value of microalbuminuria for later development of overt diabetic nephropathy, albumin excretion rate in the microalbuminuric range and its tracking (i.e. annual increase) are still considered reliable markers for prediction of later overt diabetic kidney disease. Overnight urinary collection is preferred for calculation of the rate of albumin excretion, but may be difficult to perform precisely. The albumin:creatinine ratio of the first morning urine sample is a reliable screening method: the microalbuminuric range is considered to be 2.5-25 mg/mmol or 30-300 mg/g (3.5 mg/mol has been proposed as lower limit in females because of their lower creatinine excretion). Irrespective of the procedure used, at least two samples over a 3-6-month period should test positive before microalbuminuria is confirmed and 'persistent microalbuminuria' defined. If the albumin excretion rate is persistently in the microalbuminuric range it is of crucial importance to define strategies and carry out interventions for prevention of decline in kidney function. The goal of achieving the best glycaemic control as early as possible in as many IDDM patients as is safely possible is particularly important in microalbuminuric patients. Although it is unsafe to reduce dietary protein intake drastically, particularly in children and adolescents, moderate decrease of protein intake (i.e. 0.9-1.1/g/kg day) is advisable in diabetic patients from the very beginning of the disease. Timely treatment with an angiotensin-converting enzyme inhibitor, independently of rise in arterial blood pressure, should be considered if improvement of glycaemic control and moderate decrease of dietary protein intake for 6-12 months have failed to reduce the albumin excretion rate. Screening programmes for microalbuminuria and early intervention can substantially modify the natural history of diabetic renal involvement and disease and possibly reduce the incidence of end-stage renal failure.
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PMID:The importance of microalbuminuria as an indicator of incipient diabetic nephropathy: therapeutic implications. 945 92

Clinical diabetic nephropathy is a well-recognized cause of increased morbidity and mortality in patients with type 1 diabetes. The finding that microalbuminuria predicts progression to overt nephropathy has allowed early diagnosis and preventive interventions. Several studies have demonstrated that treatment with angiotensin-converting enzyme (ACE) inhibitors slows down the rate of decline of the glomerular filtration rate in type 1 diabetes patients with established proteinuria. The renoprotective properties of the ACE inhibitor captopril extend beyond its antihypertensive effects. ACE inhibitors represent the most appropriate class of antihypertensive drugs for treating type I diabetes patients because of their efficacy and safety. When microalbuminuria is detected and confirmed in a diabetic child or adolescent, and if it persists despite 6-12 months of improved metabolic control, treatment with ACE inhibitors should be started, even if the child is normotensive. Careful follow-up of renal function is essential.
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PMID:Diabetic nephropathy in children and adolescents: a critical review with particular reference to angiotensin-converting enzyme inhibitors. 982 93

We retrospectively studied the clinical course and treatment outcome of idiopathic membranous nephropathy (IMN) amongst 38 Chinese patients (25 male, 13 female, age 51.6 +/- 14.6 years, follow-up duration 58.2 +/- 51.1 months) who presented over a 10-year review period. Eight never received any form of specific treatment (group I), seven received oral corticosteroid alone for 6-9 months (group II), 17 were given corticosteroid plus cyclophosphamide for 6-12 months (group III), and six were treated with methylprednisolone alternating with chlorambucil every other month for 6 months (group IV). No untoward effect from drugs sufficient to alter the dosage used was recorded. After 6 months of treatment, over 50% of patients went into remission: a significant reduction in proteinuria (p = 0.01, 0.01, 0.02) with a corresponding rise in serum albumin levels (p = 0.01, 0.01, 0.04) was observed in groups II, III, and IV, respectively, but not in group I. During follow-up, one patient in each of groups I, III, IV, and two of group II developed renal function deterioration, which correlated with an abnormal presenting serum creatinine. In six group I and eight group III patients who have been followed for at least 5 years, there was progressive reduction in proteinuria in group III (p < 0.05), but not in group I: serum creatinine has remained unchanged in both groups. IMN runs a benign course in Chinese patients in Hong Kong, with 2.6% of patients going into end-stage renal failure during the study period. Contrary to reports in Caucasians, there is similar treatment response to steroid alone or a combination of steroid and cytotoxic agents.
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PMID:Clinical features and treatment outcome of idiopathic membranous nephropathy in Chinese patients. 1062 90

The differential diagnosis of hematuria with or without proteinuria is extensive, and isolated hematuria is a common problem in children and adolescents. Extensive evaluation is often necessary for the child presenting with macroscopic plus microscopic hematuria including nonglomerular and glomerular etiologies, while children with only isolated microscopic hematuria can generally be followed after baseline evaluation to rule out infection, hypercalciuria, familial hematuria, sickle cell disease, post-streptococcal glomerulonephritis (GN), and structural abnormalities (cysts, stones, obstruction, Wilms tumor). Children with the combination of hematuria and proteinuria require rapid systematic evaluation, generally including renal biopsy, except in cases where post-streptococcal GN can be clearly documented. Post-streptococcal GN occurs 7-21 days after a streptococcal infection, is associated with an acute fall in C3 levels with return to normal by approximately 8 weeks, rarely causes acute renal failure, and in children has a pattern of gradual resolution of hypertension, hematuria, and proteinuria over a course of 6-12 months.
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PMID:Asymptomatic hematuria in childhood: a practical approach to evaluation. 1079 63

The CD154/CD40 pathway is required for the development and progression of disease in a variety of autoimmune model systems. We have demonstrated previously that long-term anti-CD154 treatment of nephritic (SWRxNZB)F1 mice prolonged survival and preserved kidney function. Herein we ask if long-term treatment is required and further characterize the protective effect on renal pathology by examining alpha-smooth muscle actin, collagen and TGF-beta1 expression in renal tissue. The effects of anti-CD154 on brain and heart inflammation are also examined. Three dosing strategies of anti-CD154 mAb were compared in SNF1 mice that exhibited moderate or severe nephritis: (1) weekly for 6 weeks; (2) monthly; (3) weekly for 6-12 weeks followed by monthly dosing. Proteinuria, serum anti-DNA, anti-CD154 pharmacokinetics and serum soluble CD154 analyses were performed. Anti-CD154 treatment of moderate disease increased survival across all regimens, although weekly followed by monthly maintenance dosing proved most efficacious. This regime also inhibited renal alpha-smooth muscle actin and collagen deposition. Only the most aggressive anti-CD154 treatment protocol increased survival in severely nephritic mice. Long-term anti-CD154 treatment significantly inhibits key mediators of kidney fibrosis and is required to maximize survival and renal function. Potential reasons for differential therapeutic efficacy in moderately vs severely nephritic mice are discussed.
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PMID:Long-term anti-CD154 dosing in nephritic mice is required to maintain survival and inhibit mediators of renal fibrosis. 1124 13


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