Search PubMed⌕ Search

Biomedical subjects

A Cases

Publications and source records attributed to A Cases.

At least 19 recordsLinked to original sources
PubMed2005

[Cytomegalovirus esophagitis in a patient on peritoneal dyalisis].

Symptomatic cytomegalovirus (CMV) infection usually affects immunocompromised patients, such as transplant recipients. From that point of view, the patient with endstage renal disease under maintenance dialysis is considered as immunocompetent. Thus, opportunistic infections, such as CMV infection, is not systematicaly searched in these patients, despite that an impaired cellular immunity has been reported in dialysis patients. We report a case of CMV esophagitis, clinically symptomatic, in a patient endstage renal disease under peritoneal dialysis, without other known immunosuppressive factors and with a good clinical response to gancyclovir treatment.

Aged↗
PubMed2005

[Recurrent vascular access trombosis associated with the prothrombin mutation G20210A in a adult patient in haemodialysis].

Vascular access-related complications are a frequent cause of morbidity in haemodialysis patients and generate high costs. We present the case of an adult patient with end-stage renal disease and recurrent vascular access thrombosis associated with the prothrombin mutation G20210A and renal graft intolerance. The clinical expression of this heterozygous gene mutation may have been favoured by inflammatory state, frequent in dialysis patients. In this patient, the inflammatory response associated with the renal graft intolerance would have favored the development of recurrent vascular access thrombosis in a adult heterozygous for prothrombin mutation G20210A. In the case of early dysfunction of haemodialysis vascular access and after ruling out technical problems, it is convenient to carry out a screening for thrombophilia.

Anticoagulants↗
PubMed2004

Cigarette smoke concentrate increases 8-epi-PGF2alpha and TGFbeta1 secretion in rat mesangial cells.

Epidemiological studies have shown that cigarette smoke, an oxidant agent, is a risk factor for the development of diabetic nephropathy (DN), in which pathogenesis transforming growth factor beta(1) (TGFbeta(1)) plays a key role. In our experimental model we exposed mesangial cell cultures to cigarette smoke concentrate (CSC) to study the effect of smoking on the pathogenesis of DN. Thus, we analyzed the effect of CSC on TGFbeta(1) and lipid peroxidation (8-epi-PGF(2alpha)) in rat mesangial cells. Furthermore, since the protein kinase C (PKC) pathway appears to be a key factor for the enhanced production of TGFbeta(1), we also analyzed the effect of the selective PKCbeta inhibitor LY379196 on TGFbeta(1) response to CSC. CSC induced an increase of both TGFbeta(1) and 8-epi-PGF(2) compared to basal conditions (5 mM glucose). The CSC-induced increase in TGFbeta(1) secretion was significantly suppressed by LY379196. These data suggest that smoking could increase TGFbeta(1) production, probably due to oxidative stress and PKCbeta activation. This finding supports the concept that smoking is a risk factor for DN development.

Animals↗
PubMed2004

The effects of smoking and its cessation on 8-epi-PGF2alpha and transforming growth factor-beta 1 in Type 1 diabetes mellitus.

BACKGROUND: Oxidative stress and transforming growth factor-beta 1 (TGF-beta1) are associated with diabetic complications, and smoking is a risk factor. AIMS: This study aimed (i) to compare urinary 8-epi-PGF2alpha and plasma and urinary TGF-beta1 levels obtained in heavy smokers with Type 1 diabetes with those observed in age-matched non-smoker patients with Type 1 diabetes and controls, and (ii) to investigate the effects of smoking cessation (SC) on the above-mentioned parameters in patients with Type 1 diabetes. METHODS AND RESULTS: Compared with control subjects (n = 12), non-smoker diabetic patients (n = 12) presented higher values of urinary 8-epi-PGF2alpha (74.2 +/- 29.6 vs. 29.6 +/- 11.1 pg/mg urinary creatinine, P = 0.01), plasma TGF-beta1 (7.7 +/- 4.7 vs. 3.6 +/- 1.7 ng/ml, P = 0.001) and urinary TGF-beta1 (15.3 +/- 6.3 vs. 8.1 +/- 4.4 ng/mg urinary creatinine, P = 0.02). Compared with non-smoker diabetic patients, smoker diabetic patients (n = 16) showed higher levels of urinary 8-epi-PGF2alpha (107.8 +/- 40.2 vs. 74.2 +/- 29.6 pg/mg urinary creatinine, P = 0.0001), plasma TGF-beta1 (12.6 +/- 4.9 vs. 7.7 +/- 4.7 ng/ml, P = 0.001) and urinary TGF-beta1 (27.5 +/- 16.0 vs. 15.3 +/- 6.3 ng/mg urinary creatinine, P = 0.01). Smoker patients were included in a smoking cessation programme. In the 10 patients that gave up smoking there was a reduction of urinary 8-epi-PGF2alpha (basal: 110.47 +/- 47.0 vs. week 12: 73.2 +/- 25.6; P < 0.001), plasma TGF-beta1 (basal: 11.2 +/- 5.9 vs. week 12: 4.89 +/- 2.25; P < 0.01) and urinary TGF-beta1 (basal: 18.12 +/- 9.27 vs. week 12: 10.32 +/- 2.0; P < 0.01) levels. CONCLUSIONS: In patients with Type 1 diabetes, smoking increased oxidative stress, evaluated by lipid peroxidation, and TGF-beta1 production. Smoking cessation decreased these parameters, providing additional support to encourage diabetic patients to give up smoking.

Adult↗
PubMed2004

[Superior vena cava thrombosis in a patient on hemodialysis].

We present a patient with end-stage renal disease on maintenace hemodialysis through a permanent catheter (Permcath) on the right subclavian vein. One month after the catheter placement the patient exhibited a superior vena cava syndrome due to a pericatheter thrombosis. The patient was initially managed with anticoagulation with early clinical improvement. Nevertheless, the reappearance of the symptoms forced the removal of the catheter and percutaneous angioplasty of the superior vena cava. After those measures and anticoagulation with coumarin the patient remains stable with complete clinical resolution and angiographical improvement.

Angioplasty, Balloon↗
PubMed2003

[Pure red blood cell aplasia associated with neutralizing antibodies against erythropoietin induced by epoetin alfa:a new form of acquired erythroblastopenia in auremic patients].

We report the case of a woman with end-stage renal disease on maintenance hemodialysis and treated with recombinant human erythropoietin (epoetin alfa) administered subcutaneously, who developed a pure red cell aplasia secondary to the development of neutralizing antibodies anti-erythropoietin after 8 months of treatment. Despite epoetin withdrawal and immunosuppressive treatment with corticosteroids and gammaglobulins the patient still has high red blood cell transfusion requirements and undetectable plasma erythropoietin levels. Pure red cell aplasia secondary to the development of neutralizing antibodies anti-erythropoietin is a rare but severe complication associated with the use of recombinant human erythropoietin in uremic patients. In recent years, the incidence of this complication has sharply increased, specially associated with the use of epoetin alfa administered subcutaneously. For this reason, the Spanish Drug Agency has recently contraindicated treating uremic patients with epoetin alfa administered subcutaneously.

Adult↗
PubMed2002

[Cardiovascular risk factors in chronic renal failure].

Cardiovascular complications are the main cause of death in patients with chronic renal disease. These complications are due to two important morphological changes. Firstly, left ventricular hypertrophy together with the changes in the cardiac remodelling and myocardiac fibrosis constitute the lesion with the highest incidence in renal chronic disease. Secondly, disease in the large arteries (macrovascular disease) involve two types lesions: Artherosclerosis, which is characterised by the formation of plaques in the intima arterial membrane and artherosclerosis due to lesions in the media arterial membrane, which causes a loss in elasticity of the arterial tree.

Arteriosclerosis↗
PubMed2002

[Cardiovascular risk in patients with chronic renal failure. Patients in renal replacement therapy].

Dialysis patients constitute a high-risk subset of patients for developing cardiovascular disease, which accounts for nearly 50% of deaths. After stratification for age, race and gender, cardiovascular mortality is 10-20 times higher in dialysis patients than in the general population. Cardiovascular disease in this population cannot be fully explained by the high prevalence of classical cardiovascular risk factors (age, hypertension, diabetes, hyperlipidemia, smoking, etc.). Thus, the involvement of "new" cardiovascular risk factors (hyperhomocysteinemia, hyperfibrinogenemia, high lipoprotein (a) levels, oxidative stress, inflammation, etc.), and uremia-related factors (anemia, impaired calcium-phosphorus metabolism, hyperparathyroidism, accumulation of endogenous inhibitors of nitric oxide synthesis, etc.) has been also invoked to play a role in the increased cardiovascular risk in these patients. Endothelial dysfunction is the initial event in the development of atherosclerosis. Uremic patients exhibit an endothelial dysfunction, even before starting dialysis, which persists o is even aggravated under dialysis treatment. Uremic patients must be considered at high risk of developing cardiovascular disease. Thus cardiovascular risk factors in these patients should be managed early, aggressive and multifactorially in order to reduce their high cardiovascular morbidity and mortality.

Arteriosclerosis↗
PubMed2002

[Uremic media affects hemostatic properties of human endothelial cells in culture and increases the production of von Willebrand factor].

We have investigated the ability of serum from uremic patients to modify the thrombogenic properties of the endothelium. The effect of the uremic media on the morphology of ECs, and their resistance to flow was analyzed. The reactivity of the extracellular matrix (ECM) generated by ECs towards normal platelets was evaluated in a parallel-plate perfusion chamber. Exposure of ECs to uremic media resulted in abnormal morphology and signs of accelerated growth. Detachment of ECs exposed to circulating blood was increased when cells had been grown with media supplemented with uremic serum (22% vs 13%). Platelet deposition and formation of aggregates were significantly elevated on ECMs generated in the presence of uremic media (40.23 +/- 6.43% vs 25.42 +/- 2.69%, p < 0.05, n = 5). Immunocytochemical methods detected an enhanced expression of von Willebrand factor antigen on uremic ECMs (uremic 17.1 +/- 4.2% vs control 13.57 +/- 3.98%, p < 0.05) and its mRNA expression in endothelial cells (uremic 213.24 +/- 6.13 vs control 200.77 +/- 7.52, p < 0.05). These results suggest that uremic medium alters endothelial function and impairs the antithrombotic functions of cultured endothelial cells. This effect may contribute to the increased cardiovascular and thrombotic risk reported in ESRD patients.

Cells, Cultured↗
PubMed2001

Effect of angiotensin II receptor blockade on renal disease progression in patients with non-diabetic chronic renal failure.

BACKGROUND: The aim of the present study was to investigate the effect of losartan on the progression of renal function in non-diabetic patients with chronic renal failure in an open, prospective, follow-up study of 1 year. METHODS: Twenty-nine hypertensive patients (14 females and 15 males; mean age 63 years.) with non-diabetic chronic renal failure of several causes received losartan 50 mg/day (plus other antihypertensive agents if needed) and were followed-up prospectively during 13+/-1 months. Eighteen patients received angiotensin-converting enzyme inhibitors plus other antihypertensive drugs at baseline. Patients had been followed-up for 44+/-4 months prior to the treatment with losartan. The rate of progression of renal insufficiency was evaluated as the slope of the reciprocal of serum creatinine vs time in months. RESULTS: Blood pressure, creatinine clearance and urinary protein excretion at baseline and after 1 year of treatment with losartan were: 149+/-3/90+/-1 vs 142+/-2/84+/-1 mmHg (P<0.01/P<0.05), 29+/-3 vs 29+/-3 ml/min (P=NS), and 1.7+/-0.4 vs 1.2+/-0.2 g/24 h (P=0.11, NS). Serum creatinine at baseline, and after 6 months and 1 year of treatment with losartan was: 3.18+/-0.24, 3.24+/-0.27 (P=NS vs baseline) and 3.49+/-0.32 mg ml (P<0.05 vs baseline). The rate of progression of renal disease before and after 1 year of treatment with losartan was -0.0039+/-0.0058 vs -0.0012+/-0.0073 mg/month (P<0.01). Changes in proteinuria after 1 year of treatment with losartan correlated with the change in renal disease progression (r=-0.519, P<0.01). CONCLUSIONS: The rate of progression of renal function in patients with non-diabetic chronic renal failure is slowed down after 1 year of treatment with losartan. The results of this preliminary study suggest that AT1 receptor blockade treatment offers renoprotection in this subset of patients, although these results need to be confirmed in appropriate controlled trials.

Angiotensin Receptor Antagonists↗
PubMed2001

Hemodynamic and renal effects of acute and progressive nitric oxide synthesis inhibition in anesthetized dogs.

This study evaluated the effects of progressive nitric oxide (NO) inhibition in the regulation of systemic and regional hemodynamics and renal function in anesthetized dogs. The N(G)-nitro-L-arginine methyl ester group (n = 9) received progressive doses of 0.1, 1, 10, and 50 microg. kg(-1). min(-1). Renal (RBF), mesenteric (MBF), iliac (IBF) blood flows, mean arterial pressure (MAP), pulmonary pressures, cardiac output (CO), and systemic and pulmonary vascular resistances were measured. During N(G)-nitro-L-arginine methyl ester infusion, MAP and systemic vascular resistances increased in a dose-dependent manner. Mean pulmonary pressure and pulmonary vascular resistances increased in both the N(G)-nitro-L-arginine methyl ester and the control group, but the increase was more marked in the N(G)-nitro-L-arginine methyl ester group during the last two infusion periods. CO decreased progressively, before any significant change in blood pressure was noticeable in the N(G)-nitro-L-arginine methyl ester group. IBF decreased significantly from the first N(G)-nitro-L-arginine methyl ester dose, whereas RBF and MBF only decreased significantly during the highest N(G)-nitro-L-arginine methyl ester dose. Urinary volume and sodium excretion only increased significantly in the time control group during the two last time periods. The pulmonary vasculature was more sensitive than the systemic vasculature, whereas skeletal muscle and renal vasculatures showed a greater sensitivity to the inhibition of NO production than the mesenteric vasculature. NO synthesis inhibition induces a progressive antidiuretic and antinatriuretic effect, which is partially offset by the increase in blood pressure.

Anesthesia↗
PubMed2001

Uremic medium disturbs the hemostatic balance of cultured human endothelial cells.

We have investigated the ability of serum from uremic patients to modify the thrombogenic properties of the endothelium. The effects of uremic medium on the morphology of endothelial cells (ECs), and their resistance to flow was analyzed. The influence of uremic media on the reactivity of the extracellular matrix (ECM) generated by ECs towards normal platelets was evaluated in a parallel-plate perfusion chamber. Exposure of ECs to uremic medium resulted in abnormal cell morphology and signs of an accelerated growth. Detachment of ECs exposed to circulating blood was increased when cells had been grown with media supplemented with uremic serum (21% vs. 14% non exposed). Platelet deposition was significantly elevated on ECMs generated in the presence of uremic media (uremicECMs) (p<0.01 vs. control studies). Effects of uremic serum were not observed at short incubation periods (5 h) but were evident after 24 or 72 h of incubation. Northern blot analysis revealed increased expression of tissue factor (TF) mRNA in ECs exposed to uremic conditions. Immunocytochemical methods detected an augmented expression of TF antigen on uremic ECMs. Incubation of ECMs with an antibody to human tissue factor prevented the increase in platelet deposition observed in uremic ECMs, suggesting that the presence of TF in ECM could be responsible for the enhanced platelet deposition. Results from our study indicate that uremic medium impairs the antithrombotic functions of cultured endothelial cells.

Biological Factors↗