UMLS:C0033687 - FACTA Search

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Query: UMLS:C0033687 (proteinuria)
24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to evaluate the role of proangiogenic growth factors in an experimental model of ischemia/reperfusion injury (I/R) in both normotensive and hypertensive rats. Renal ischemic injury was induced in transgenic rats rendered hypertensive due to renin overproduction [TGR (mREN-2)-27] and in normotensive Hannover Sprague-Dawley rats (HanSD). Animals were treated for 12 weeks with either tacrolimus (TAC, 0.1 mg/kg per day, intramuscularly [IM]) or placebo. After 12 weeks, kidneys were harvested for morphologic, immunohistochemical, and RT-PCR analysis. Both normotensive and hypertensive untreated rats developed significantly greater proteinuria and glomerulosclerosis compared with TAC-treated rats. Immunohistologically, TGR showed higher basic fibroblast growth factor (bFGF) protein expression compared with normotensive HanSD. TAC-treated rats had higher bFGF protein expression than untreated rats. Vascular endothelial growth factor (VEGF) protein expression in glomeruli was more increased in TGR after I/R than in sham-operated animals. TAC-treated TGR hosts developed higher VEGF mRNA expression compared with both untreated and sham groups; however, there were no differences between treated and untreated normotensive HanSD animals. bFGF is involved in the fibrogenesis induced by hypertension and I/R injury. The nature of the increase in proangiogeneic growth factor expression among tacrolimus-treated animals remains to be elucidated.
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PMID:Regulators of angiogenesis in renal ischemia/reperfusion injury in normotensive and hypertensive rats: effect of tacrolimus. 1580 41

The aim of this study was to evaluate the outcome of treatment of pregnancy--induced hypertension (PIH) in rats by Ligustrazine collaborated with magnesium sulfate. PIH rat models were induced with Nomega-nitro-L-arginine methyl ester (L-NAME) infusing at 7 mg/kg per day via caudal vein for four days, then treated with Ligustrazine, magnesium sulfate, or both for three days. Rat blood pressure level was measured by the tail-cuff method, 24 hours urine protein was also assayed. The blood pressure and urine proteins of grouped PIH rats were recorded before the start and after the termination of therapy. The body length and the weight of fetal rats, the weight of placentals from pregnant rats were measured. The placental tissues, livers, kidneys of rats were investigated with integrated methods such as histopathologic observation with light microscopy, ultrastructural observation with transmission electron microscopy. L-NAME administration in pregnancy rats during the late pregnancy period had resulted in an rise of blood pressure, an increasing of urine protein, death rate of rat fetus, incidence of teratogenesis, and so on. Three groups of PIH rats treated with single magnesium sulfate, Ligustrazine, or Ligustrazine combined with magnesium sulfate showed an obvious dropping of the proteinuria, decompression of blood pressure (p<0.01, p<0.001), especially the treatment efficacy in the group of Ligustrazine combined with magnesium sulfate was more significant effective than other two groups (p<0.01, p<0.001). The treatment with both Ligustrazine and magnesium sulfate could increase the body length of newly born rats, the body weight of tomites and the placental weight, furthermore, reduce the rate of the teratosis of hindlimb-shortness (p<0.001). There were diffuse focal necrosis areas in the livers of PIH rats, their glomerular basement membrane had thickened extensively, the glomerular endothelium had swelled, extensive edema in the epithelia of renal tubule was demonstrated. The decidua and basal zone of the placentae of PIH rats all thickened, the microvilli of trophoblasts decreased. After treatment with ligustrazine especially with both Ligustrazine and magnesium sulfate, the necrosis of hepatocytes disappeared. The thickening of glomerular basement membrane in the group of ligustrazine or both Ligustrazine and magnesium sulfate treatment reduced; Moreover in the latter group the morphology of glomerular endothelium essentially recovered, the edema in cytoplasms of renal tubular epithelium reduced. The placental lesions were also relieved. The present results indicated the therapeutic effect by Ligustrazine collaborated with magnesium sulfate was better than a single use of Ligustrazine or magnesium sulfate. There were pathological alteration involved ischemia and anoxic in the placental tissues of PIH rats, resembled the placental pathological alteration of the human cases with PIH. The treatment with ligustrazine, and especially both Ligustrazine and magnesium sulfate in PIH rats could obviously relieve the lesions in lives, kidneys and placentae.
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PMID:[Evaluation of the efficacy of ligustrazine collaborated with magnesium sulfate in the treatment of pregnancy-induced hypertension in rats]. 1583 6

Chronic renal failure represents a major problem of public health. Incidence for patients arrived at the terminal stage of the disease is in France 126.4/million inhabitants and the cost of medical care reaches 2 % of the expenses of the National Health Insurance. The progression of the disease is divided into 5 stages that are defined by the level of creatinine clearance from the stage of renal diseases with a normal renal function (clearance>90 ml/min) to the terminal stage (clearance <15 ml/min). Prevalence of patients at this ultimate stage is around 50,000. Prevalence for the totality of patients with a renal disease is evaluated between 2 and 3 millions. Renal diseases must be screened because they are silent and because an early pre-dialysis nephrological care allows renal replacement therapy to be delayed and the number of cardiovascular accidents to be diminished. Screening must be performed in the high-risk populations, essentially patients with diabetes, hypertension, coronary ischemia, renal tract diseases and all subjects treated with drugs toxic for the kidneys. Screening in the total population seems inadequate because of a high cost to benefit ratio. Screening is based on testing for the presence of proteinuria, quantifying the number of formed elements and plasma creatinine determination, the latter allowing, together with age and weight, glomerular filtration rate to be evaluated according to Cockcroft's formula. Prevention of renal diseases in the whole population necessitates the same life style as that recommended for prevention of cardiac and metabolic diseases. In the high-risk populations, one must control glycemia, blood pressure and cholesterol plasma level. In patients that have been already screened, renal function decay has to be slowed down by blocking the renin angiotensin system with converting enzyme inhibitors, controlling plasma cholesterol with statins and diminishing dietary proteins. In the light of these various data, the National Academy of medicine recommends: 1 - in the field of public health, to extend to the whole country the registries containing data on patients with terminal chronic renal failure, to support the creation of medical networks for the screening of renal diseases, to vaccine the patients against hepatitis B, flue and pneumococcal infections and to verify whether a low birth weight is associated with a greater risk of renal diseases in adulthood; 2 - in the field of teaching and research, to stop the decrease in the number of nephrologists, to promote research in genetics, to evaluate the efficacy of antifibrosis drugs and the possible renal toxicity of all new drugs.
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PMID:[Prevention and screening of chronic renal failure]. 1591 71

Chronic allograft nephropathy (CAN) is the leading cause of graft loss following kidney transplantation. One factor contributing to CAN is chronic alloimmune injury. However, the involvement of alloantigen-dependent and -independent factors in CAN is unclear. The pathomechanism of CAN has been extensively studied by utilizing the Fischer-to-Lewis (F344-to-LEW) rat model. Transplant capillaropathy (circumferential multiplication of the peritubular capillary basement membrane) and transplant glomerulopathy (reduplication of the glomerular basement membrane) have recently been validated clinicopathologically as ultrastructural indicators of chronic alloimmune injury. To investigate the presence of these markers, F344-to-LEW kidneys were examined by electron and light microscopy 32, 40 and 52 weeks after implantation. F344 rats with or without 30-min ischemia of the left kidney following right nephrectomy served as controls. All transplanted rats displayed marked proteinuria. On electron microscopy, transplant capillaropathy, transplant glomerulopathy, and T-cell cytotoxicity (indicator of ongoing cellular rejection) were absent. On light microscopy, the arteries were devoid of intimal fibrosis. Focal-segmental glomerulopathy resembling hyperfiltration injury was encountered, with mild interstitial infiltration, fibrosis, and tubular atrophy. The proteinuria and kidney pathology were more severe in transplanted than in ischemic or uninephrectomized rats. Because chronic-active rejection could not be detected between weeks 32 and 52, we propose that the alloantigen-dependent initial graft injury subsides, but induces the late events: glomerular hyperfiltration, proteinuria, and glomerulosclerosis. Accordingly, the model - in the late phase - is suitable to investigate alloantigen-independent factors of CAN and lacks markers of alloantigen-dependent processes.
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PMID:Ultrastructural analysis of the Fisher to Lewis rat model of chronic allograft nephropathy. 1594 67

Chronic rejection is currently the most prevalent cause of renal transplant failure. Clinically, chronic rejection presents by chronic transplant dysfunction, characterized by a slow loss of function, often in combination with proteinuria and hypertension. The histopathology is not specific in most cases but transplant glomerulopathy and multilayering of the peritubular capillaries are highly characteristic. Several risk factors have been identified such as young recipient age, black race, presensitization, histoincompatability, and acute rejection episodes, especially vascular rejection episodes and rejections that occur late after transplantation. Chronic rejection develops in grafts that undergo intermittent or persistent damage from cellular and humoral responses resulting from indirect recognition of alloantigens. Progression factors such as advanced donor age, renal dysfunction, hypertension, proteinuria, hyperlipidemia, and smoking accelerate deterioration of renal function. At the tissue level, senescence conditioned by ischemia/reperfusion (I/R) may contribute to the development of chronic allograft nephropathy (CAN). The most effective option to prevent renal failure from chronic rejection is to avoid graft injury from both immune and nonimmune mechanism together with nonnephrotoxic maintenance immunosuppression.
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PMID:Chronic renal allograft rejection: pathophysiologic considerations. 1595 91

Proteinuria 1 year after transplantation is associated with poor renal outcome. It is unclear whether low-grade (<1 g/24 h) proteinuria earlier after transplantation and its short-term change affect long-term graft survival. The effects of proteinuria and its change on long-term graft survival were retrospectively assessed in 484 renal transplant recipients. One- and 3-month proteinuria correlated with donor age, donor cardiovascular death, prolonged cold and warm ischemia times and acute rejection. One- and 3-month proteinuria (per 0.1 g/24 h, hazard ratio (HR): 1.07 and 1.15, p<0.0001)-especially low-grade proteinuria (HR: 1.20 and 1.26, p<0.0001)-were powerful, independent predictors of graft loss. Its short-term reduction correlated with arterial pressure (AP) (the lower the 3-month diastolic and 12-month systolic AP, the lower the risk of increasing proteinuria during 1-3 months and 3-12 months periods, respectively: Odds ratio (OR) per 10 MmHg: 0.78, p=0.01 and 0.85, respectively, p=0.02), and was associated with decreased long-term graft loss (per 0.1 g/24 h: HR: 0.88 and 0.98, respectively, p<0.0001), independently of initial proteinuria. Early low-grade proteinuria due to pre-transplant renal lesions, ischemia-reperfusion and immunologic injuries is a potent predictor of graft loss. Short-term reduction in proteinuria is associated with improved long-term graft survival.
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PMID:Early low-grade proteinuria: causes, short-term evolution and long-term consequences in renal transplantation. 1668 77

Sensitive and specific biomarkers are needed to detect early kidney injury. The objective of the present work was to develop a sensitive quantitative urinary test to identify renal injury in the rodent to facilitate early assessment of pathophysiological influences and drug toxicity. Two mouse monoclonal antibodies were made against the purified ectodomain of kidney injury molecule-1 (Kim-1), and these were used to construct a sandwich Kim-1 ELISA. The assay range of this ELISA was 50 pg/ml to 5 ng/ml, with inter- and intra-assay variability of <10%. Urine samples were collected from rats treated with one of three doses of cisplatin (2.5, 5, or 7.5 mg/kg). At one day after each of the doses, there was an approximately three- to fivefold increase in the urine Kim-1 ectodomain, whereas other routinely used biomarkers measured in this study [plasma creatinine, blood urea nitrogen (BUN), urinary N-acetyl-beta-glucosaminidase (NAG), glycosuria, proteinuria] lacked the sensitivity to show any sign of renal damage at this time point. When rats were subjected to increasing periods (10, 20, 30, or 45 min) of bilateral ischemia, there was an increasing amount of urinary Kim-1 detected. After only 10 min of bilateral ischemia, Kim-1 levels on day 1 were 10-fold higher (5 ng/ml) than control levels, whereas plasma creatinine and BUN were not increased and there was no glycosuria, increased proteinuria, or increased urinary NAG levels. Thus urinary Kim-1 levels serve as a noninvasive, rapid, sensitive, reproducible, and potentially high-throughput method to detect early kidney injury in pathophysiological studies and in preclinical drug development studies for risk-benefit profiling of pharmaceutical agents.
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PMID:Urinary kidney injury molecule-1: a sensitive quantitative biomarker for early detection of kidney tubular injury. 1617 63

We examined the influence of chronic treatment with ANG-(1-7) on development of hypertension and end-organ damage in spontaneously hypertensive rats (SHR) chronically treated with the nitric oxide synthesis inhibitor L-NAME (SHR-L-NAME). L-NAME administered orally (80 mg/l) for 4 wk significantly elevated mean arterial pressure (MAP) compared with SHR controls drinking regular water (269 +/- 10 vs. 196 +/- 6 mmHg). ANG-(1-7) (24 microg x kg(-1) x h(-1)) or captopril (300 mg/l) significantly attenuated the elevation in MAP due to L-NAME (213 +/- 7 and 228 +/- 8 mmHg, respectively), and ANG-(1-7) + captopril completely reversed the L-NAME-dependent increase in MAP (193 +/- 5 mmHg). L-NAME-induced increases in urinary protein were significantly lower in ANG-(1-7)-treated animals (226 +/- 6 vs. 145 +/- 12 mg/day). Captopril was more effective (96 +/- 12 mg/day), and there was no additional effect of captopril + ANG-(1-7) (87 +/- 5 mg/day). The abnormal vascular responsiveness to endothelin-1, carbachol, and sodium nitroprusside in perfused mesenteric vascular bed of SHR-L-NAME was improved by ANG-(1-7) or captopril, with no additive effect of ANG-(1-7) + captopril. In isolated perfused hearts, recovery of left ventricular function from 40 min of global ischemia was significantly better in ANG-(1-7)- or captopril-treated SHR-L-NAME, with additive effects of combined treatment. The beneficial effects of ANG-(1-7) on MAP and cardiac function were inhibited when indomethacin was administered with ANG-(1-7), but indomethacin did not reverse the protective effects on proteinuria or vascular reactivity. The protective effects of the ANG-(1-7) analog AVE-0991 were qualitatively comparable to those of ANG-(1-7) but were not improved over those of captopril alone. Thus, during reduced nitric oxide availability, ANG-(1-7) attenuates development of severe hypertension and end-organ damage; prostaglandins participate in the MAP-lowering and cardioprotective effects of ANG-(1-7); and additive effects of captopril + ANG-(1-7) on MAP, but not proteinuria or endothelial function, suggest common, as well as different, mechanisms of action for the two treatments. Together, the results provide further evidence of a role for ANG-(1-7) in protective effects of angiotensin-converting enzyme inhibition and suggest dissociation of factors influencing MAP and those influencing end-organ damage.
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PMID:Angiotensin-(1-7) prevents development of severe hypertension and end-organ damage in spontaneously hypertensive rats treated with L-NAME. 1640 46

We report a 22 years old male with chronic allergic rhinitis, who presented with asthma, prolonged fever, eosinophilia, cutaneous vasculitis, subcutaneous nodules, polyarthritis, ulcers in the nasal mucosa and external auditory canal, hematuria, proteinuria, renal failure, severe hypertension, pulmonary infiltrates and mesenteric ischemia with a perforation of the sigmoid colon. Arteriography showed multiple aneurysmae of intrarenal arteries and a skin biopsy showed a leukocytoclastic vasculitis. A diagnosis of Churg-Strauss syndrome was made. He was initially treated with steroids and cyclophosphamide but abandoned therapy. Eighteen years after the onset of the disease, he required hemodialysis. Eight months after being on dialysis, he suffered a reactivation of the disease with lung hemorrhage and finally died, due to an upper gastrointestinal bleeding caused by a duodenal ulcer.
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PMID:[Late reactivation of Churg-Strauss syndrome]. 1653 66

Uninephrectomy is associated with increased glomerular filtration rate in both the donated and the remaining contralateral kidney. The long-term effects of ischemic acute renal failure (ARF) following uninephrectomy are unknown. This study examined renal function, histology and proteinuria 52 weeks after an episode of reversible ischemic ARF. Ischemic ARF was induced in uninephrectomised mice by renal pedicle clamping. At 52 weeks inulin clearance (muL/min/g) was 7.2+/-0.2 in sham, 5.0+/-0.1 in uninephrectomy (P<0.01 vs. sham) and 3.9+/-0.1 in uninephrectomy + ischemia (P<0.01 vs. sham, P<0.05 vs. uninephrectomy). Thus, mice subjected to uninephrectomy alone demonstrated compensatory hyperfiltration following reduction in renal mass. This response was prevented by ischemic ARF. At 52 weeks there was no difference in urine protein/creatinine, mean arterial pressure or scores of glomerulosclerosis or interstitial fibrosis. In conclusion, ischemic ARF following uninephrectomy in mice impairs long-term renal function.
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PMID:Ischemic acute renal failure following nephrectomy impairs long-term renal function. 1653 86

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