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Biomedical subjects

A Aguilera

Publications and source records attributed to A Aguilera.

At least 55 records · Page 3Linked to original sources
PubMed2000

RAD52-dependent and -independent homologous recombination initiated by Flp recombinase at a single FRT site flanked by direct repeats.

We have devised a system for isolating yeast DNA sequences that are able to act as initiators of recombination leading to deletions in mitotically growing yeast cells. This system has allowed us to identify the FRT site of the 2-micron site-specific recombinase Flp as such a sequence. We show that Flp is able to initiate recombination leading to deletions at a single FRT site in cir(o) strains. These results indicate that Flp is able to cleave a single FRT site, supporting the observation that the mechanism of cleavage by Flp is trans-horizontal. Interestingly, Flp can induce homologous recombination in both a RAD52-dependent and RAD52-independent manner. Our work provides a new system for the study of homologous recombination leading to deletions, in which the initiation step can be efficiently controlled. We discuss the possibility that Flp-induced, RAD52-independent events occur by single-strand annealing.

Binding Sites↗
PubMed2000

Susceptibility to drug-induced apoptosis correlates with differential modulation of Bad, Bcl-2 and Bcl-xL protein levels.

To define the responses of apoptotic regulatory proteins to different chemotherapeutic agents, we investigated the expression of Bcl-2 family gene products, the release of cytochrome c, and the activation of pro-caspase-3 during apoptosis induced by Taxol and Thiotepa, in the MCF-7 breast carcinoma and the HL-60 leukemia cell lines. The earliest event induced by drug exposure was increase in Bad protein levels, followed by Bcl-2 down-regulation, cytochrome c release, and Bcl-xL and Bax up-regulation. Bak accumulation was a late event. Activation of pro-caspase-3 and cleavage of Bcl-2 protein occurred in the HL-60 cells only, and followed the cytochrome c release. The overall responses were qualitatively similar in both cell types, but MCF-7 cells treated with Taxol showed a significant delay in apoptosis, correlating with early up-regulation of Bcl-2 and delayed release of cytochrome c. We conclude that Bad up-regulation is an early indicator of a cellular response that will lead to cell death, but may be modulated by survival mechanisms, which cumulatively govern the ultimate susceptibility to apoptosis.

14-3-3 Proteins↗
PubMed2000

Cholinergic modulation of growth hormone responses to growth hormone-releasing hormone in uraemic patients on peritoneal dialysis.

BACKGROUND: Hypothalamic cholinergic neurotransmission plays a major role in the regulation of GH secretion. Pyridostigmine, a cholinesterase inhibitor, is able to decrease hypothalamic somatostatinergic tone and release GH in normal subjects. Blockade of muscarinic receptor with pirenzepine blunts the GH release in several clinical situations. However, little information is available on the role played by central cholinergic pathways in GH regulation in uraemic patients. OBJECTIVE: We aimed to assess GH responses to GHRH after pretreatment with pyridostigmine and pirenzepine in a group of uraemic patients undergoing peritoneal dialysis (PD). GH responses of the patients treated with recombinant human erythropeitin (rhEPO) were compared to patients without treatment. DESIGN: We studied 14 male patients on PD and nine control subjects. All subjects underwent three endocrine test in random order after an overnight fast. Each subject received GHRH (100 microg, i.v. in bolus at 0 minutes). Sixty minutes before the injection of GHRH subjects were given oral placebo, pyridostigmine (120 mg), or pirenzepine (100 mg). MEASUREMENTS: Blood samples for GH were collected at -60, 0, 15, 30, 45, 60 and 90 minutes The hormonal secretory responses were studied by a time-averaged (area under the curves, AUC) and time-independent (peak values) analysis. RESULTS: Baseline GH concentrations were similar in patients and controls. GH responses to placebo plus GHRH were also comparable in patients and controls (peak 26.6 +/- 3.8 vs. 33.2 +/- 4.4 mU/l, AUC 28.2 +/- 3.4 vs. 27.8 +/- 4.6 mU/h/l). Pyridostigmine administration induced a significant potentiation of GH responses to GHRH both in patients (peak 43.2 +/- 5.2 mU/l, AUC 47.6 +/- 6.0 mU/h/l; P < 0.01) and in control subjects (peak 79.2 +/- 8.6 mU/l, AUC 78.0 +/- 9.4 mU/h/l; P < 0.01). However, the increment in GH peak and AUC was significantly (P < 0.05) greater in controls in relation to values found in patients. Pirenzepine administration induced an abolishment of GH release after GHRH stimulation both in PD patients (peak 5.4 +/- 2.6 mU/l, AUC 6.0 +/- 2.4 mU/h/l; P < 0.01) and in healthy controls (peak 3.8 +/- 0.6 mU/l, AUC 4.0 +/- 0.4 mU/h/l; P < 0.05). Responses to pyridostigmine plus GHRH and pirenzepine plus GHRH were similar in patients on chronic therapy with recombinant human erythropeitin and in patients without rhEPO therapy. CONCLUSION: These results suggest that the cholinergic regulation of GH release is preserved in uraemic patients on peritoneal dialysis. The significantly lower increase in GH response to GHRH induced by pyridostigmine suggests that cholinergic stimulatory tone is attenuated in patients in relation to control subjects. Long-term therapy with rhEPO seems not to affect GH responses to cholinergic stimulation or blockade.

Adult↗
PubMed2000

Short-term recombinant human growth hormone therapy does not modify growth hormone, thyrotropin and prolactin responses to thyrotropin-releasing hormone in adult dialysis patients.

BACKGROUND: We recently have reported the first randomized, controlled study on the effects of short-term recombinant human growth hormone (rhGH|| therapy on the nutritional status of a group of malnourished adult dialysis patients. In order to evaluate whether rhGH administration exerts any influence on GH, thyrotropin (TSH|| and prolactin (PRL|| responses to TSH-releasing hormone (TRH||, we assessed these responses before and after rhGH therapy. METHODS: GH, PRL and TSH responses to TRH before and 1 month after rhGH therapy in a group of adult dialysis patients were evaluated. Seventeen dialysis patients (11 on continuous ambulatory peritoneal dialysis/six on haemodialysis|| were studied (rhGH group, n=8; control group, n=9||. In the rhGH group, 0.2 IU/kg/day rhGH was administered subcutaneously. Each patient was tested with TRH (400 microg bolus i.v.|| on two separate occasions, just before and immediately after the treatment period. RESULTS: rhGH treatment did not modify baseline serum GH concentrations (6.6+/-2.7 vs 4.1+/-1.1 microg/l||, paradoxical GH responses to TRH (six out of eight patients||, GH peak (11.9+/-4.6 vs 11.2+/-5.3 microg/l, NS|| or area under the secretory curve of GH (GH AUC; 19.1+/-4.5 vs 12.1+/-3.1 microg/h/l||. Both basal PRL (35.5+/-7.1 vs 36.7+/-8.6 microg/l|| and TSH (2.3+/-1.1 vs 2.8+/-1.7 mU/l|| concentrations, as well as their responses to TRH stimulation (PRL peak, 59.9+/-16.6 vs 59. 5+/-11.8 microg/l; TSH peak, 6.2+/-2.6 vs 7.1+/-3.9 mU/l||, were also unaffected by rhGH therapy. CONCLUSION: These results suggest that short-term rhGH therapy does not significantly influence the magnitude of the somatotropic, lactotropic or thyrotropic response to TRH in adult dialysis patients. However, this finding has to be interpreted with caution due to the two different patient groups included in this study.

Adult↗
PubMed2000

Prevalence, patterns, and course of past hepatitis B virus infection in intravenous drug users with HIV-1 infection.

OBJECTIVE: Hepatitis B virus (HBV) and human immunodeficiency virus (HIV) share common routes of transmission. Therefore, markers of either active or past HBV infection are present in many HIV-infected patients, particularly in intravenous drug users (IDUs). The aim of this study was to analyze the serological pattern of past HBV infection (presence or absence of anti-HBs) and the course of past HBV infection (changes in anti-HBs status, and HBV reactivation) in two cohorts of IDUs with and without HIV infection. METHODS: HBV serum markers were studied in 388 HIV-positive and 197 HIV-negative IDUs. Among them, 263 HIV-positive and 50 HIV-negative patients with past HBV infection (serum HBsAg negative and anti-HBc positive, with or without anti-HBs) were followed-up for a median of 21 and 13 months, respectively, to detect changes in anti-HBs status and HBV reactivation. RESULTS: The prevalence of HBV infection (either active or past) was higher in HIV-positive than in HIV-negative cases (90% vs 62%, p < 0.001), even when stratified by years of drug use. Most cases (92% of HIV-positive and 89% of HIV-negative) had markers of past infection. Among those patients with past HBV infection, 60% of HIV-positive and 72% of HIV-negative presented serum anti-HBs (p = 0.03). The incidence of anti-HBs loss was 1.8 cases/100 person-year in HIV-positive, and 1.8 cases/100 person-year in HIV-negative patients (RR 1.0, 95% CI 0.1-94, p = NS). Incidence of anti-HBs development was 17.6 cases/100 person-year in HIV-positive and 25.6 cases/100 person-year in HIV-negative IDUs (RR, 1.5, 95% CI, 0.6-3.5, p = NS). Only one HIV-positive patient with markers of past HBV infection developed an active infection (0.2 events/100 person-year). CONCLUSIONS: HBV infection (either active or past) is particularly frequent in HIV-positive IDUs. Most cases have markers of past infection. Isolated detection of anti-HBc (absence of anti-HBs) is more common in HIV-positive than in HIV-negative IDUs. Despite their progressive immunosuppression, both anti-HBs loss and HBV reactivation are rare in HIV-infected IDUs.

Adolescent↗
PubMed2000

Prevalence of HTLV infection in pregnant women in Spain.

OBJECTIVE: To estimate the prevalence of HTLV infection among pregnant women in Spain. METHODS: A commercial ELISA incorporating HTLV-I and HTLV-II antigens was used for HTLV antibody screening. Repeatedly reactive samples were further examined by western blot. Moreover, confirmation with PCR was performed when cells were available. RESULTS: 20,366 pregnant women in 12 different Spanish cities were tested in a 3 year period (July 1996 to August 1999). 32 samples were repeatedly reactive by ELISA, and 10 of them were confirmed as positive by western blot (eight for HTLV-II and two for HTLV-I). In addition, three of 13 women who had an indeterminate western blot pattern yielded positive results for HTLV-II by PCR. All 11 HTLV-II infected women had been born in Spain, and all but one were former drug users. Seven of them were coinfected with HIV-1. One HTLV-I infected woman was from Peru, where HTLV is endemic and where she most probably was infected during sexual intercourse. CONCLUSION: The overall prevalence of HTLV infection among pregnant women in Spain is 0.064% (13/20,366), and HTLV-II instead of HTLV-I is the most commonly found variant. A strong relation was found among HTLV-II infection and specific epidemiological features, such as Spanish nationality and injecting drug use. Although HTLV-II can be vertically transmitted, mainly through breast feeding, both the low prevalence of infection and its lack of pathogenicity would not support the introduction of HTLV antenatal screening in Spain.

Blotting, Western↗
PubMed2000

Serum level of vascular endothelial growth factor is influenced by erythropoietin treatment in peritoneal dialysis patients. (Grupo de Estudios Peritoneales de Madrid).

Some patients on long-term peritoneal dialysis (PD) develop a hyperpermeability state, owing to peritoneal neoangiogenesis. Vascular endothelial growth factor (VEGF), a potent mitogen for endothelial cells, has been implicated in most diseases characterized by microvascular neoformation. Erythropoietin (EPO) is able to induce endothelial proliferation in vitro. Our aim was to elucidate whether VEGF serum levels are influenced by EPO treatment, and whether VEGF serum level maintains a relationship with peritoneal transport data. We analyzed serum levels of VEGF in 35 PD patients (18 males, 17 females). Mean age was 58 years, with a mean time on PD of 98 +/- 75 months. Of the 35 patients, 19 were on automated peritoneal dialysis, and 16 were on continuous ambulatory peritoneal dialysis. Seven patients had diabetes. Peritoneal transport parameters were: urea mass transfer coefficient (MTC), 19.5 +/- 6.6 mL/min; creatinine MTC, 9.9 +/- 4.7 mL/min; net ultrafiltration, 491 +/- 166 mL per 4-hour dwell. Twenty seven patients were under therapy with recombinant human erythropoietin (rHuEPO). Mean serum VEGF levels were 347 +/- 203 pg/mL (range 66-857 pg/mL), with most patients in the normal range (60-700 pg/mL). VEGF levels did not correlate with age, sex, primary renal disease, diabetes, type of PD, time on PD, peritonitis, and cumulative glucose load. We found no correlation with urea MTC, creatinine MTC, ultrafiltration rate, or protein effluent levels. However, a significant negative correlation with residual renal function was seen (r = -0.39, p < 0.05). Patients treated with rHuEPO showed significantly higher serum levels of VEGF than non treated patients (375 +/- 220 pg/mL vs 251 +/- 75 pg/mL, p < 0.05), although they had similar residual renal function. We conclude that increased serum VEGF levels are associated with EPO treatment. Consequently, VEGF might have a role in the EPO effects found in PD patients. Whether both agents are related to peritoneal neoangiogenesis requires further research.

Biological Transport↗
PubMed2000

Peritoneal dialysis is the therapy of choice for end-stage renal disease patients with hereditary clotting disorders.

Chronic renal failure is an unusual complication of hereditary clotting disorders (HCDs), but this situation could change in the near future. The modality of dialysis for end-stage renal disease (ESRD) in patients with an HCD is a difficult choice. Hemodialysis (HD) may be considered, but intensive treatment with coagulation factors is required for vascular access execution and for each HD procedure. Peritoneal dialysis (PD) has been infrequently proposed. However, PD requires coagulation replacement therapy only during peritoneal catheter placement. The aim of this paper is to describe our experience of three patients with ESRD and HCD, successfully treated with chronic PD in the medium term. Case 1 was a 58-year-old man with moderate hemophilia A, type 2 diabetes mellitus, and hepatitis C virus (HCV) infection. His ESRD was secondary to glomerulonephritis. A double-cuff peritoneal catheter was surgically placed with pre-emptive factor VIII administration. He began treatment with continuous ambulatory peritoneal dialysis (CAPD). An inguinal hernia was repaired without complications. After eleven months of follow-up, no hemorrhage episodes have been observed and clinical outcome is optimal. Case 2 was a 46-year-old man with severe hemophilia A, type 2 diabetes mellitus, and HCV and human immunodeficiency virus (HIV) infections. He developed a diabetic nephropathy that required renal replacement therapy. A permanent silicone catheter was inserted in the left internal jugular vein, and the patient started HD treatment. Later on, PD therapy was proposed. A peritoneal catheter was implanted with simultaneous factor VIII infusion. Minimal bleeding was observed at the subcutaneous tunnel over the following 48 hours. The patient started PD treatment without complications, and two months later, remaining asymptomatic, transferred to another center. Case 3 was a 41-year-old woman diagnosed with von Willebrand disease type 2A, HCV infection, and polycystic kidney disease, who presented with ESRD. An internal arteriovenous fistula was performed under coagulation factor cover. During a fistulography, and despite coagulation factor substitutive treatment, the patient showed an important hematoma. Afterwards, PD was considered. A peritoneal catheter was implanted under coagulation factor cover. The postoperative course was uncomplicated, and the patient started CAPD treatment. During follow up, she suffered two hemoperitoneum episodes that were resolved with cold dialysate. After nine months, she uneventfully continued on PD. In conclusion, PD is the therapy of choice for patients with hereditary clotting disorders and ESRD requiring dialysis. Peritoneal dialysis therapy avoids many of the complications related to HD therapy.

Adult↗
PubMed1999

Construction and genetic analysis of S. cerevisiae deletants of six novel ORFs from chromosome II.

We have constructed S. cerevisiae strains carrying genomic deletions of six ORFs from the left arm of chromosome II (YBL018c, YBL019w, YBL024w, YBL042c, YBL043w and YBL046w) in both FY1679 and W303 backgrounds. We have found that YBL018c is an essential gene in yeast, whereas the other five genes are non-essential. We have developed plasmids carrying deletion cassettes that can be used to delete any of the six genes in S. cerevisiae by transforming to G418-resistance, as well as centromeric plasmids containing the cognate genes.

Blotting, Southern↗
PubMed1999

Long-term effects of recombinant human erythropoietin therapy on growth hormone secretion in uremic patients undergoing peritoneal dialysis.

Recombinant human erythropoietin (rhEPO) is being successfully used for the treatment of uremic anemia. Short-term studies have proved that correction of anemia with rhEPO therapy is accompanied by several changes in growth hormone (GH) secretion in uremic patients. The present study aimed to assess the influence of long-term rhEPO therapy on baseline and stimulated GH concentrations in a group of uremic patients undergoing continuous ambulatory peritoneal dialysis (CAPD). Seven well-nourished and clinically stable CAPD patients were studied. Ten normal subjects were studied as controls. GH responses to direct pituitary stimulation with GH-releasing hormone (GHRH) (100 microg intravenously [i.v.]) and indirect hypothalamic stimulation with insulin-induced hypoglycemia (0.1 U/kg body weight i.v.) and clonidine (0.15 mg/m2 orally), were assessed before and after 3, 6, and 12 months of subcutaneously administered rhEPO therapy. After rhEPO administration, an increase of the hemoglobin concentration was observed in all patients and maintained at about 12 g/dL throughout the study period. rhEPO therapy did not induce any significant change in baseline concentrations of GH and insulin-like growth factor I. Correction of the anemia was accompanied by a clear increase in the area under the curve (AUC) and the area above the baseline (AAB) of GH secretion in response to GHRH stimulation. These changes were statistically significant after 3 and 6 months of therapy, although at 12 months no significant differences in relation to pretreatment values could be observed. rhEPO treatment was associated with a progressive decrement in the GH AUC and AAB in response to hypoglycemic challenge, reaching statistically significant values at months 6 and 12. On the other hand, compared with the control group, GH responses to clonidine were blunted at the start of the study in CAPD patients, and rhEPO therapy was not accompanied by any modification. In conclusion, long-term treatment with rhEPO in CAPD patients is associated with complex and profound effects on somatotrope cell function, characterized by diverse effects on GH responses to stimuli that release GH through different mechanisms. Some of these rhEPO-induced alterations in somatotrope function are dependent on the duration of treatment.

Adrenergic alpha-Agonists↗
PubMed1999

Effects of cholinergic muscarinic blockade on growth hormone responses to growth hormone-releasing hormone in uraemic patients.

BACKGROUND: Several alterations in growth hormone (GH) secretion have been reported in patients with chronic renal insufficiency. However, cholinergic modulation of somatotopic cell function has not been fully clarified in uraemic patients. To gain further insight into the disrupted mechanism of GH regulation in chronic renal failure, we investigated whether the blockade of cholinergic muscarinic receptor with pirenzepine could modify the response of GH to its physiological releasing hormone. METHODS: Eight uraemic male patients on peritoneal dialysis and six normal controls were studied. All subjects underwent two endocrine tests in random order. In one of them placebo was administered 60 min before the injection of GH-releasing hormone (GHRH, 100 microg, i.v. in bolus at 0 min). In another the muscarinic blocking agent pirenzepine, 100 mg p.o., was administered at that time. Blood samples for GH were collected at -60, 0, 15, 30, 45, 60 and 90 min. RESULTS: Baseline plasma GH concentrations were similar in patients and controls. GH responses to GHRH were characterized by great interindividual variability in uraemic patients with regard to the amount and the time to maximal peak. In the placebo plus GHRH test, the maximum GH concentrations in patients (14.0 +/- 3.2 microg/l) were similar to those reached by controls (18.0 +/- 3.1 microg/l), although GH secretion was more sustained in patients. The area under the secretory curve (AUC) of GH secretion in patients was also similar to that found in controls (14.4 +/- 2.9 vs 15.4 +/- 3.3 microg/h/l). When subjects were given pirenzepine before GHRH injection an abolishment of GHRH-induced GH release was observed in all controls and in all but one of the uraemic patients. The AUC of GH secretion was, therefore, significantly reduced both in uraemic patients (4.1 +/- 2.0 microg/h/l, P<0.05) and in control subjects (2.0 +/- 0.3 microg/h/l, P<0.05). CONCLUSION: These results suggest that GH secretion in uraemic patients is modulated, at least in part, by a cholinergic mechanism. The muscarinic blockade, possibly acting via an increase in somatostatin release, is able to inhibit GH release in response to direct pituitary stimulation with GHRH.

Administration, Oral↗
PubMed1999

Human immunodeficiency virus type 2 infection in Spain. The HIV-2 Spanish Study Group.

The first cases of human immunodeficiency virus type 2 (HIV-2) infection in Spain were identified in 1988, in 3 African immigrants living in Barcelona. Since then, up to December 1998, 92 individuals with HIV-2 infection have been reported in Spain. Most are adult men, infected through heterosexual contacts, originating from West African countries, and currently living in the largest urban Spanish cities. Fifteen individuals have developed AIDS, meanwhile the rest remain asymptomatic. For 22 subjects, HIV-2 subtyping was performed on proviral DNA, 16 being infected with subtype A (8 Spanish born and 8 African immigrants) and the remaining with subtype B (two Spanish born and 4 originating from Equatorial Guinea). Coinfection with HIV-1 was demonstrated in 9 individuals. In conclusion, HIV-2 is currently circulating in Spain with a low prevalence and without evidence for increase over time.

Adult↗
PubMed1999

Effects of recombinant human erythropoietin on functional and injury endothelial markers in peritoneal dialysis patients.

Clinical effects of recombinant human erythropoietin (rHuEPO) such as thrombosis, convulsions, hyperviscosity, hypertension, and angiogenic effect in culture cells have been described. We studied the rHuEPO effect on endothelial damage markers and endothelial function markers: tissue-type plasminogen activator (t-PA), nitrate (NO3), thrombomodulin (TM), and von Willebrand factor (vWF). Twenty-six peritoneal dialysis patients treated with rHuEPO and 19 controls were included. The study design for rHuEPO patients consisted of four periods: long-term treatment (rHuEPO-1); 2 months of withdrawal (rHuEPO-2); and 4 months on 5000 IU/week rHuEPO subcutaneously, with markers being measured after 2 months (rHuEPO-3) and after 4 months (rHuEPO-4). After 2 months of rHuEPO withdrawal, a decrease in hemoglobin level appeared (11+/-1.8 g/dL to 9.2+/-1.5 g/dL, p < 0.01). After rHuEPO reintroduction, this value reached 10.6+/-1.5 g/dL at two months, and 11.1+/-1.4 g/dL at four months. A significant increase in t-PA ratio was observed from two months without rHuEPO to two months on rHuEPO, returning to previous values after four months. Similarly, TM increased for patients with creatinine clearances (CrC) < 5 mL/min. No changes in the higher-than-normal plasma vWF levels were found during the various periods. A statistically significant lower value was found in controls compared with rHuEPO-4 patients. A statistically significant increase in NO3 levels was observed in the pre-venous occlusion (VO) test immediately after the re-introduction of rHuEPO. This increment returned to prior values four months after rHuEPO was reintroduced. Our results show that rHuEPO treatment causes an increase in some endothelial damage markers (TM, t-PA) and modifies endothelial function markers (t-PA ratio, NO3). These changes might favor thrombosis and atherosclerosis.

Adult↗
PubMed1999

Tumor necrosis factor alpha as a uremic toxin: correlation with neuropathy, left ventricular hypertrophy, anemia, and hypertriglyceridemia in peritoneal dialysis patients.

Tumor necrosis factor alpha (TNF alpha) is usually excreted by the kidney. In dialysis patients, it accumulates. TNF alpha has been implicated in the pathogenesis of malnutrition, diabetic neuropathy, and erythropoietin resistance. We studied TNF alpha plasma levels in 49 stable peritoneal dialysis (PD) patients, with the aim of correlating those levels with the presence and severity of peripheral neuropathy, hypertrophic cardiomyopathy, and anemia. Kt/Vurea' residual renal creatinine clearance (CrC), nutritional markers, and general biochemistry were also determined. The average plasma level of TNF alpha was 67 +/- 32 pg/mL (range: 18.1-156.3 pg/mL; normal value 3-20 pg/mL). No correlation was observed between TNF alpha and KT/Vurea' but a negative correlation with CrC was seen (r: -0.37, p < 0.05). TNF alpha levels were higher in patients with neuropathy as compared to patients with normal results (72.5 +/- 32 pg/mL vs 44 +/- 22 pg/mL, p < 0.05). Patients with neuropathy also showed a lower CrC value (1.5 +/- 1.7 mL/min vs 3.9 +/- 2.6 mL/min, p < 0.01). TNF alpha levels were higher in patients with left ventricular hypertrophy (LVH) with respect to normal individuals (70.4 +/- 32 pg/mL vs 38.5 +/- 20.8 pg/mL, p < 0.05). Patients with severe LVH showed the lowest CrC value. A direct, significant relationship was found between TNF alpha levels and weekly erythropoietin dose (r: 0.41, p < 0.05). Patients with hypertriglyceridemia or taking lipid-lowering agents showed a positive linear correlation between TNF alpha and triglycerides (r = 0.7, n = 14, p < 0.05). These data suggest that accumulation of TNF alpha may contribute to the development or maintenance of some neurologic, hematologic, and cardiac complications of uremic syndrome. Loss of residual renal function conditions an increment in TNF alpha levels. These data continue to add support to the idea that TNF alpha may be considered a uremic toxin.

Adult↗