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Biomedical subjects

A Ortiz

Publications and source records attributed to A Ortiz.

At least 127 records · Page 7Linked to original sources

Expression of leucocyte chemoattractants by interstitial renal fibroblasts: up-regulation by drugs associated with interstitial fibrosis.

Interstitial inflammation is a strong predictor of long-term renal damage. The potential role of renal interstitial fibroblasts in recruitment of inflammatory leucocytes into the interstitium is unclear. We have thus studied the mRNA expression of several leucocyte chemotactic factors by rat renal interstitial fibroblasts and its modulation by cytokines. In addition, the effects of two unrelated drugs associated with the development of interstitial fibrosis, namely puromycin aminonucleoside (PAN) and cyclosporin A (CsA), were also studied. Rat renal interstitial fibroblasts showed constitutive mRNA expression for the chemokines monocyte chemoattractant protein 1 (MCP-1) and interferon-inducible protein 10 (IP-10). In addition, these cells also exhibited constitutive mRNA expression for cyclophilin B, an immunophilin recently found to have leucocyte chemoattractant properties. The inflammatory cytokine tumour necrosis factor-alpha up-regulated IP-10 and MCP-1 mRNA expression (10- and four-fold, respectively), but had no effect on cyclophilin B mRNA levels. IP-10 and MCP-1 produced about a four-fold increase in MCP-1 and cyclophilin B mRNA expression, but did not affect IP-10 mRNA. PAN caused an augmentation in IP-10, MCP-1 and cyclophilin B mRNA levels (12-, 9.5, and two-fold, respectively), while CsA increased only cyclophilin B mRNA in a dose-dependent manner. In conclusion, rat renal interstitial fibroblasts express mRNA for chemotactic factors and this expression is up-regulated by inflammatory cytokines, PAN and CsA. The present findings suggest that renal interstitial fibroblasts may play an active role in the recruitment of inflammatory leucocytes into the interstitium.

Animals↗

Urinary excretion of platelet-activating factor in human and experimental nephrosis.

BACKGROUND: Platelet-activating factor (PAF) is a phospholipid that has been implicated in the pathogenesis of glomerulonephritis and can be synthesized by glomerular cells in response to different stimuli. PAF increases glomerular permeability to proteins and urinary PAF has been determined to be of renal origin. In order to assess whether urinary PAF can be found augmented in situations of glomerular damage without glomerular leukocyte infiltration, urinary PAF was quantified in human and experimental nephrosis. METHODS: Urinary PAF was quantified by platelet bioassay and glomerular PAF by incorporation of 3H-acetate into PAF. PAF was characterized by its behaviour on thin-layer chromatography and high performance liquid chromatography and the blockade of its bioactivity by receptor antagonists. RESULTS: Urinary PAF excretion was significantly higher in patients with active idiopathic nephrotic syndrome than in controls (5.8+/-1.5 versus 1.7+/-0.75 mg/24 h; P<0.05) and patients in remission (1.63+/-0.75 ng/24 h; P<0.02). In rats with nephrosis induced by puromycin aminonucleoside there was an early increase in urinary PAF excretion (138+/-19 versus 49+/-22 pg/24 h in controls; P<0.035) that coincided with the augmented glomerular PAF synthesis (67+/-3.4 versus 36+/-1.2 DPM/mg protein in controls; P<0.003). CONCLUSIONS: These results suggest that the synthesis of PAF in the kidney may be involved in the pathogenesis of the proteinuria in idiopathic nephrotic syndrome and that urinary PAF excretion may be a good marker of disease activity.

Animals↗

A Staphylococcus aureus capsular polysaccharide (CP) vaccine and CP-specific antibodies protect mice against bacterial challenge.

The efficacy of capsular polysaccharide (CP)-specific antibodies elicited by active immunization with vaccines composed of Staphylococcus aureus types 5 and 8 CP linked to Pseudomonas aeruginosa exoprotein A or with immune immunoglobulin G (I-IgG) obtained from vaccinated plasma donors was tested in lethal and sublethal bacterial mouse challenge models. A dose of 2 x 10(5) CFU of S. aureus type 5 CP per mouse administered intraperitoneally (i.p.) with 5% hog mucin was found to cause 80 to 100% mortality in BALB/c mice within 2 to 5 days. Mice passively immunized i.p. 24 h earlier or subcutaneously 48 h earlier with 0.5 ml of I-IgG showed significantly higher average survival rates than animals receiving standard IgG or saline (P < 0.01) following the bacterial challenge. Animals actively immunized with the monovalent type 5 CP-P. aeruginosa exoprotein A conjugate showed a survival rate of 73% compared with 13% in phosphate-buffered saline-immunized animals. The prechallenge geometric mean titer of type 5 CP antibodies in animals that died was significantly (P < 0.05) lower than that of animals which survived the challenge (95.7 versus 223.6 micrograms/ml, respectively). The IgG was further evaluated in mice challenged i.p. with a sublethal dose of 5 x 10(4) CFU per mouse. Serial blood counts were performed on surviving animals at 6, 12, 24, and 48 h. Surviving animals were sacrificed at 72 h, and bacterial counts were performed on their kidneys, livers, and peritoneal lavage fluids. Animals receiving I-IgG had lower bacterial counts in blood samples and lower bacterial densities in kidneys, livers, and peritoneal lavage samples than mice immunized with standard IgG (P < 0.05). These data suggest that S. aureus type 5 CP antibodies induced by active immunization or administered by passive immunization confer protection against S. aureus infections.

Animals↗

Acute renal failure due to sulphadiazine crystalluria in AIDS patients.

We report two AIDS patients who developed acute renal failure while receiving sulphadiazine for cerebral toxoplasmosis. Renal ultrasound revealed diffuse bilateral echogenic shadowing material. 'Sheaves of wheat' crystals, typical of sulphadiazine crystalluria, were present in the urine. One patient required a percutaneous nephrostomy. Hydration and urine alkalinisation resulted in rapid improvement of renal function and ultrasonographic findings. Sulphadiazine-induced crystalluria and acute renal failure is increasingly frequent. Awareness of its existence may lead to prevention and early conservative treatment.

AIDS-Related Opportunistic Infections↗

Interferon-inducible protein-10 is highly expressed in rats with experimental nephrosis.

Interferon-inducible protein (IP)-10 is a small glycoprotein member of a family of chemotactic cytokines structurally related to interleukin-8. We have recently described the induction of IP-10 mRNA in mouse mesangial cells stimulated with lipopolysacharide, interferon-gamma, and tumor necrosis factor-alpha. To further evaluate a possible role for this chemokine in renal injury, we have studied IP-10 in an experimental model of nephrosis induced in rats by adriamycin. High levels of glomerular IP-10 mRNA expression and glomerular and tubulointerstitial IP-10 protein were seen on day 21, coinciding with maximal proteinuria, glomerular tumor necrosis factor mRNA expression, and interstitial cellular infiltrates. Maintenance on a low protein diet not only delayed the appearance of proteinuria and interstitial cellular infiltrate but also decreased glomerular IP-10 mRNA expression. Isolated normal glomeruli and cultured glomerular epithelial and mesangial cells from normal rats expressed IP-10 mRNA upon stimulation with 100 U/ml interferon or 1 microgram/ml lipopolysaccharide for 3 hours. IP-10 mRNA expression was also inducible by lipopolysaccharide and cytokines in NRK 49F renal interstitial fibroblasts and, to a lesser extent, in NRK 52E tubular epithelial cells. Furthermore, IP-10 protein was inducible in murine mesangial cells. We conclude that IP-10 is highly inducible in vitro and in vivo in resident glomerular and tubulointerstitial cells. IP-10 may participate in the modulation of renal damage in experimental nephrosis.

Animals↗

Conservative treatment versus antireflux surgery in Barrett's oesophagus: long-term results of a prospective study.

The results obtained for the treatment of 59 patients diagnosed with Barrett's oesophagus, randomized to receive medical treatment (n = 27) or antireflux surgery (n = 32) were assessed prospectively. Median follow-up for the patients undergoing medical treatment was 4 (range 1-11) years and for patients undergoing surgical treatment 5 (range 1-11) years. Satisfactory symptomatic control (excellent to good results) was achieved in 24 patients after medical therapy and in 29 after antireflux surgery. The proportion of patients with persistent inflammatory lesions (54 per cent) and persistent or recurrent stenosis (47 per cent) was significantly higher after conservative treatment than after surgery (5 and 15 per cent, respectively). A decrease in the length of the segment of columnar mucosa was observed in eight of the patients who underwent antireflux surgery, and in only two of those given medical therapy. Conversely, an upward progression of the columnar lining was more frequent in the latter group (11 versus three). Mild dysplasia was observed in five patients, all from the group undergoing medical treatment. Severe dysplasia was detected in two patients, one undergoing medical treatment and the other following surgical therapy, in whom an antireflux procedure had failed previously. Both patients underwent oesophageal resection, with confirmation of a carcinoma in situ. The patients in whom antireflux surgery proved effective showed no dysplastic change or progression to adenocarcinoma. These results, despite the small number of patients and methodological limitations, question the systematic conservative approach in the initial management of patients with Barrett's oesophagus.

Adolescent↗

Relationships between plasma ferritin and aminotransferase profile in haemodialysis patients with hepatitis C virus.

BACKGROUND: HCV infection is a major complication among patients undergoing dialysis therapy throughout the world. In the years prior to the use of human recombinant erythropoietin (rHuEpo), patients undergoing haemodialysis were subjected to an excessive iron load as a consequence of frequent blood transfusions. Recent data in the non-dialysis population have shown a positive correlation between iron deposits and the severity of HCV hepatitis and between iron deposition and an impaired response to interferon therapy. METHODS: One hundred and five haemodialysis patients were studied. Every patient was screened for HCV infection by ELISA II and HCV RNA. Serum biochemistries were analysed by SMAC20. Ferritin was measured by radioimmunoassay. RESULTS: The aminotransferase levels for the HCV positive (n = 39) and negative patients (n = 66) were below the normal levels for the general population. The mean values of aminotransferases and plasma ferritin were, however, higher in the HCV-positive patients than in the HCV-negative patients. A positive correlation between aminotransferases and plasma ferritin was evident in HCV-positive patients, which was absent in the HCV-negative individuals. The histological severity of liver disease (n = 7) was, however, not statistically related with the levels of either ferritin or aminotransferases. CONCLUSION: HCV infection is a relevant variable when estimating iron deposits by measuring plasma ferritin. Accordingly, a misinterpretation of the actual amount of iron deposits may occur in HCV-positive patients, which should be taken into account at the time of planning their iron reposition therapy. On the other hand, the level of iron deposits might have a significant role in the evolution of HCV-related liver disease.

Aged↗

Hepatic and erythrocytic glutathione peroxidase activity in liver diseases.

Hepatic and erythrocytic glutathione peroxidase activity, together with malondialdehyde levels, were determined as indicators of peroxidation in 83 patients from whom liver biopsies had been taken for diagnostic purposes. On histological study, the patients were classified into groups as minimal changes (including normal liver), steatosis, alcoholic hepatitis, hepatic cirrhosis, light to moderately active chronic hepatitis, and severe chronic active hepatitis. The glutathione peroxidase activity in erythrocytes showed no significant changes in any liver disease group. In the hepatic study, an increased activity was observed in steatosis with respect to the minimal changes group, this increased activity induced by the toxic agent in the initial stages of the alcoholic hepatic disease declining as the hepatic damage progressed. There was a negative correlation between the levels of hepatic malondialdehyde and hepatic glutathione peroxidase in subjects with minimal changes. This suggested the existence of an oxidative equilibrium in this group. This equilibrium is broken in the liver disease groups as was manifest in a positive correlation between malondialdehyde and glutathione peroxidase activity.

Erythrocytes↗

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis.

Very few patients with familial hypomagnesemia, hypercalciuria and nephrocalcinosis have been described. Information about clinical course, familial studies or evolution after renal transplantation is very scant. We have studied eight patients with this syndrome who belong to five different families. The mean age at diagnosis was 15 +/- 7 years (5 to 25 years). The primary clinical data were polyuria-polydipsia (8 cases), ocular abnormalities (5), recurrent urinary tract infections (5) and recurrent renal colics with stone passage (2). Bilateral nephrocalcinosis was observed in all cases. Every patient showed hypomagnesemia (1.1 +/- 0.2 mg/dl) with inappropriately high urinary magnesium (Mg) excretions (70 +/- 17 mg/day), Mg clearances (4.4 +/- 1.2 ml/m) and Mg fractional excretions (16.2 +/- 7.1%). Hypercalciuria was present in every case except in those with advanced renal insufficiency. Serum parathormone levels were abnormally high. Serum calcium (Ca), phosphorus and potassium, and urinary excretions of uric acid and oxalate were normal. Neither chronic oral Mg administration nor thiazide diuretics normalized serum Mg levels or urinary Ca excretions, respectively. Follow-up was 6 +/- 4.5 years. Renal function worsened in every case with six patients starting on chronic dialysis after 4.3 +/- 3.8 years. The progression rate of renal insufficiency correlated with the severity of nephrocalcinosis. Five patients have received a kidney graft, and their serum Mg and urinary Ca have always been within normal values after transplantation. Twenty-six members of four of the affected families were studied: none of them showed hypomagnesemia, renal insufficiency or nephrocalcinosis. However, eleven cases (42%) had hypercalciuria and four of them presented with recurrent renal stones. Two family members had medullary sponge kidneys. In conclusion, progression to renal insufficiency is common in this syndrome; oral Mg and thiazide diuretics are ineffective to correct abnormalities. After kidney graft, tubular handling of Mg and Ca was normal. A striking incidence (42%) of hypercalciuria was found in the familial study.

Adolescent↗

ACE inhibition reduces proteinuria, glomerular lesions and extracellular matrix production in a normotensive rat model of immune complex nephritis.

We studied the effect of the angiotensin converting enzyme (ACE) inhibitor, quinapril, on the clinical and morphological lesions of a normotensive model of immune complex nephritis. Untreated rats developed massive nephrotic syndrome, intense cell proliferation and glomerular and tubulointerstitial lesions. In the renal cortex of nephritic rats there was a significant increase in gene expression of TGF-beta 1, fibronectin and collagens, and ACE activity. Systolic blood pressure remained normal with progression of the disease. Administration of quinapril for three weeks to animals with glomerular lesions (proteinuria 20 to 50 mg/day) avoided the development of intense proteinuria (79 +/- 28 vs. 589 +/- 73 mg/day, P < 0.001) and decreased cell proliferation, glomerulosclerosis, tubulointerstitial lesions, and inflammatory infiltrates. Cortical gene expression of TGF-beta 1 and matrix proteins was also diminished. ACE activity was inhibited by 68% in renal cortex. These results show that quinapril administration to normotensive rats with immune complex nephritis decreases proteinuria and glomerular and tubulointerstitial lesions, probably modulating the local angiotensin II generation and its effects on cell growth, TGF beta and matrix protein synthesis.

Angiotensin-Converting Enzyme Inhibitors↗

Reversibility of the alterations induced by chronic alcoholism and malnutrition in rats after alcohol withdrawal and proper nutrition.

OBJECTIVE: The specific influence of malnutrition on the cellular damage induced by alcoholism has been poorly defined; therefore, the possible degree of improvement that could be obtained after the institution of proper nutrition and after alcohol withdrawal remains unclear. We studied both conditions in several combinations, either after chronic alcoholism, chronic malnutrition or both, and after reversal of each condition or of both. METHOD: Using experimental models of alcoholism and malnutrition, we studied the alterations induced by each condition and on the combination of both in five histological locations and in 10 hematological and biochemical parameters; afterwards, we studied the possible restorative effect on each parameter after 4 months of alcohol withdrawal or proper nutrition or both. RESULTS: Our results showed that chronic alcoholism induced a mean of 31% deviation from values obtained in controls, malnutrition induced 17%, and alcoholism and malnutrition combined induced 52%. Upon the removal of the offending condition, alcohol withdrawal brought 13% improvement and proper nutrition 5% improvement; in the animals with alcoholism and malnutrition, alcohol withdrawal and proper nutrition brought 26% improvement, alcohol withdrawal but continuation of malnutrition 10% improvement, and continuation of alcoholism but proper nutrition led to a further 8% worsening from the alterations already found during alcoholism and malnutrition. CONCLUSIONS: Multivariate statistical comparisons demonstrated that chronic malnutrition produced an important, independent and difficult to reverse effect on the damage induced by alcoholism in several histological and physiological parameters.

Alcoholism↗

Involvement of tumor necrosis factor-alpha in the pathogenesis of experimental and human glomerulonephritis.

The evidence supporting a role for TNF-alpha in glomerular diseases can be summarized with the following: TNF-alpha can be secreted in the kidney by intrinsic renal cells and infiltrating phagocytes, as has been shown in vitro and in vivo during glomerular injury. TNF-alpha has proinflammatory actions which include cell death, chemotactic properties, and modulation of secretion of other inflammatory mediators, and extracellular matrix (Fig 5). Administration of exogenous TNF-alpha or agents that induce release of endogenous TNF alpha, such as endotoxin, increase the severity of experimental glomerular injury. Furthermore, the blockade of TNF-alpha action with specific antibodies, soluble receptors, or inhibitors improves the outcome of glomerulonephritis. Finally, several of the agents currently in use for the therapy of glomerular injury, such as corticosteroids and cyclosporine, are known to modulate the production of TNF-alpha. Specific TNF-alpha antagonists or inhibitors may have a role in the management of glomerulonephritis in the future.

Animals↗

Factors involved in the return of peristalsis in patients with achalasia of the cardia after Heller's myotomy.

OBJECTIVE: To assess the reappearance of peristalsis in a group of 45 patients with achalasia of the cardia undergoing surgery and to analyze the factors involved in this phenomenon. METHODS: According to the postoperative manometric data, the 45 patients were divided into two groups, depending on whether or not they presented a return of peristalsis. A statistical comparison of age, sex, duration of the disease, pre- and postoperative radiological diameter of the esophagus, classic or vigorous nature of the achalasia, and manometric data of the lower esophageal sphincter and esophageal body was made. RESULTS: In 46.6% of the patients, peristalsis returned to the upper esophagus, and 100% of the waves were progressive; in 24.4%, peristalsis returned to the middle third also, but only 50% of the waves were progressive; and in 8.8% (four patients), peristalic activity returned to the whole esophagus, but only 40% of the waves were progressive. The group of patients with a return of peristalsis had a shorter duration of dysphagia, less preoperative dilation of the esophagus, and a greater contractile activity of the esophageal body. CONCLUSIONS: Return of peristalsis is a frequent phenomenon after myotomy in patients with achalasia of the cardia, especially in cases of short clinical evolution, little esophageal dilation, and a conserved contractile capacity, although its accurate production mechanism is unknown.

Adolescent↗

Health record problem-oriented information system.

Health Record refers to the recording of the medical and relevant social history of the patient, obtained directly or indirectly. It is an instrument of frequent use that must guarantee the quality of assistance provided, reflecting all information pertinent to forming the patient's medical history. It must be designed so that data is easily and effectively retrieved for everyday use, without compromising the patient's privacy. The Health Record Problem Oriented model achieves all of these objectives. This model comprises: 1. Initial data: the relevant medical histories and biography is recorded. 2. Problems list: the patient provides reasons why she is seeking medical attention. 3. Performance plans: these include diagnostic, therapeutic, pharmacological, dietetic, physiotherapist, and surgical plans, as well as the education of the patient. 4. Evolution notes: the progress of the condition. This model guarantees multi-professional registration, an integral focus on the health, and a continued focus on the patient. These characteristics make it the model par excellence of Primary Care. Prior to the implementation of this model, existing information must be analyzed so that it can eventually be converted to a relational database. The Entity-Relationship Model (E/R Model) has been used to represent the database. Here, the basic concepts involved are entities, relationships, and attributes. Entities represent classes or objects from the real world that have common characteristics. The relationships represent the aggregation of two or more entities. The attributes are elemental properties of both entities and relationships. The E/R Diagram graphically represents the conceptual model of a database; the one built for the Health Record Problem Oriented reflects all the entities that compound the attending processes and the relationships existing between them. The Patient is the central axis of the attending process. The record contains the identifying data of the subject and his habits. We can know his medical history by means of his past Illness (personal and family record), Vaccine (what he is vaccinated against), and Case History (each patient has a case history). The other important component is the Consult Motive. A patient has a reason for every consultation, and this reason is added to her medical history as part of the Consult Motive. Each consult motive produces different events that are shown as relations with the other entities. So, for example, by analyzing a patient's history of complaints, a doctor can more suitably determine if she should recommend Cardiac or Anthropometric Exploration, request an Analysis, request a Radiography or Specialist Report, or prescribe a Treatment. The various elements that are part of a Consult Motive are expressed as different entities. Once the conceptual schema of the database is defined, the next step is to convert this schema to a logical schema, suitable for the Relational Model.

Medical Records Systems, Computerized↗