Acute renal failure following myeloablative autologous and allogeneic hematopoietic cell transplantation.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M M Prata.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: The long-term effect of recombinant human erythropoietin (rhEPO) on the blood-lipid profile has not been well documented. The aim of this study was to evaluate whether rhEPO therapy affects the lipid pattern. METHODS: A group of 102 maintenance haemodialysis patients were treated for 2 years with rhEPO given intravenously at the end of the dialysis session. Attempts were made to keep the haemoglobin (Hb) at 10-11 g/dl and/or the haematocrit (Hct) at 30-35%. Twenty maintenance haemodialysis patients not treated with rhEPO were examined as controls. Total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, apolipoproteins A1 and B, and lipoprotein (a)[Lp (a)] were assessed at baseline (without rhEPO), and 1 and 2 years after the beginning of treatment. Hb, Hct and ferritin were measured monthly, and Kt/v was evaluated monthly and kept above 1.1. RESULTS: During follow-up, in both groups, there was a significant increase in Apo A1 and no significant changes in the other lipid parameters. In the treated group, Hb and Hct increased significantly after the fourth month of treatment. CONCLUSIONS: Erythropoietin therapy does not affect significantly the levels of total cholesterol, LDL- and HDL-cholesterol, triglycerides, Apo B and Lp (a) in maintenance hemodialysis patients.
Explore the source record for details and available documents.
Autosomal dominant polycystic kidney disease is characterized by clinical and genetic heterogeneity. Two loci implicated in the disease have previously been mapped (PKD1 on chromosome 16 and PKD2 on chromosome 4). By two point and multipoint linkage analysis, negative lod scores have been found for both chromosome 16 and chromosome 4 markers in a large Portuguese family, indicating that a third PKD locus is involved in the development of the disease.
Explore the source record for details and available documents.
Eight patients with biopsy-proven primary nephrotic syndrome were included in an open, prospective, two-year study of lovastatin. One patients was withdrawn after 6 months due to an asymptomatic rise in creatinine phosphokinase, which was rapidly reversed after interruption of lovastatin. In the remaining patients, treatment was well-tolerated and produced no side effects. After 2 years of treatment, these 7 patients had decreases in total cholesterol from 446 +/- 165 to 250 +/- 57 mg/dl (p < 0.001), LDL cholesterol from 343 +/- 121 to 174 +/- 49 mg/dl (p < 0.001), Apo B lipoprotein from 162 +/- 60 to 108 +/- 42 mg/dl (p < 0.05), triglycerides from 336 +/- 273 to 182 +/- 71 mg/dl (p < 0.04). There was no change in HDL cholesterol. The LDL/HDL cholesterol and the total/HDL cholesterol ratios fell from 15.0 +/- 12.1 and 19.1 +/- 17.2 mg/dl before the study to 4.4 +/- 1.2 and 6.3 +/- 1.6 mg/dl, respectively, at 2 years. A decrease in proteinuria from 8.6 +/- 4.6 to 5.0 +/- 3.7 g/24 h (p < 0.02) was noted in 4 patients on concomitant ACE inhibitor therapy. Renal function remained stable in all patients throughout the study, except for one whose moderate impairment progressed to end-stage renal failure requiring dialysis 3 months poststudy. We conclude that long-term lovastatin in patients with primary nephrotic syndrome is an effective and generally safe treatment for accompanying dyslipidemia.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The effect of indomethacin-induced inhibition of endogenous prostaglandin synthesis on the antihypertensive activity of pindolol (15 mg daily) and propranolol (80--160 mg daily) was studied in 7 hypertensive patients. In four test phases of 10 days each, patients received beta-blocker alone, placebo, beta-blocker plus indomethacin (100 mg daily), and beta-blocker alone. Mean supine diastolic blood-pressure rose from 82 +/- 2 mm Hg in the first beta-blocker phase to 98 +/- 3 mm Hg in the placebo phase, remained elevated (96 +/- 3 mm Hg) in the beta-blocker-plus-indomethacin phase, and fell to 83 +/- 3 mm Hg in the last beta-blocker phase. Diastolic blood-pressure values obtained in the beta-blocker-plus-indomethacin phase were not significantly different from those obtained in the placebo phase but were significantly different from the values measured in both beta-blocker phases (P less than 0-01). The changes in systolic blood-pressure and pulse-rate were not significant. These preliminary results suggest that the antihypertensive effect of these two beta-blockers in some hypertensive patients may be related to the endogenous prostaglandin system.
Explore the source record for details and available documents.
Multiple Myeloma (MM) causes a wide range of serious clinical, alterations, including acute renal failure (ARF) often present and contributing to the global mortality of this neoplasm. ARF usually occurs well after MM is diagnosed. We describe a case of ARF in a 42 years old male patient requiring urgent hemodialysis that subsequently proved to have MM. The singularity of this case lead us to review cases of ARF admitted to the Nephrology Department between 1978 and 1990. We describe 7 patients (4 male) with ARF as presenting form of MM. Their mean +/- SD age was 60.0 +/- 10.6 (range 42-73). ARF with conserved diuresis was the presenting form in 6, 5 has systemic infection, and none was hypertensive. Replacement therapy with hemodialysis was needed in 6 patients and plasmapheresis was performed in 3. 4 patients died while admitted, 2 were discharged on chronic hemodialysis and there was recovery of renal function in 1 patient.
End-stage chronic renal failure (CRF) is often associated with platelet' disfunction and therefore with impaired hemostasis. Several investigators have reported that rHu Epo, used in the treatment of CRF anaemia, is able to activate a broad spectrum of hematopoietic stem cells, and therefore is able to increase the number of platelets and to induce correction of platelet disfunction. In order to investigate hemostasis changes associated with rHu Epo we studied 8 dialysis patients before and 12 weeks after rHu Epo. RHu Epo did not induce any change in the number of platelets (187710 +/- 52690 vs 204430 +/- 68710; p = NS), but seemed to improve its function (MI% of aggregation with ADP: 46.3 +/- 4.4% vs 49.1 +/- 5.3%; p less than 0.05). There was an improvement in PT (79.0 +/- 3.0% vs 87.5 +/- 8.9%; p less than 0.02) and aPTT (33.3 +/- 5.9" vs 29.3 +/- 2.1"; p less than 0.05) suggesting an improvement in platelet coagulant activities. These preliminary results indicate that rHu Epo does not increase the number of platelets but can induce a correction of platelet disfunction.
In this study we analyse the effects of the administration of recombinant human erythropoietin (rHuEpo) during 12 months to correct the anaemia in a group of 17 patients (9 men and 8 women; mean age 52.7 +/- 13.7; range 23 to 68 years) with end-stage renal disease (ESRD) on chronic haemodialysis (HD) for a range of 14 to 126 months (mean 43.1 +/- 29.6). In the correction period the rHuEpo was started at 50 U/Kg i.v. 3 times a week, immediately after each HD. This dose was maintained during 4 weeks and then increased in 25 U/Kg steps until haemoglobin (Hb) levels of 12 g/dl or a maximum dose of 100 U/Kg were reached. During the long-term maintenance period the individual rHuEpo dose was adjusted to keep the Hb constant at the target level of 10-12 g/dl. Baseline blood tests were done before the beginning of the treatment and every months afterwards. The levels of Hb increased significantly in week 4 and at the end of the first 3 month only 4 patients had no answer to rHuEpo. These patients had baseline serum ferritin levels below 100 ng/ml and responded well when this defficiency was corrected with oral iron. When levels of 30-35 vol% haematocrit (Hct) were reached the dose of rHuEpo could be reduced (150 to 200 U/Kg/week). The serum ferritin levels decreased 51% from a mean baseline level of 247.8 +/- 196 to 121.1 +/- 154.9 ng/ml with the onset of the maintenance phase (p less than 0.05).
A group of 50 patients (26 men and 24 women, mean age 50 +/- 19 years and range 21 to 67) on chronic hemodialysis (HD) and with basal levels of hemoglobin (Hb) less than or equal to 8 g/dl was treated with recombinant human erythropoietin (r-HuEpo) during 3 months. r-HuEpo was started at 50 U/kg I.V. 3 times a week, immediately after each session of HD, for 4 weeks, and this dose was increased in steps of 25 U/kg until a Hb level of 12 g/dl or a maximum dose of 100 U/kg were reached. Complete blood counts and biochemical profile were performed before the first dose of r-HuEpo and once weekly and monthly respectively during the period of treatment. In 8 patients the red-cell life span was studied with cromium 51 labelled erythrocytes just before and after treatment. One patient had a grand mal seizure and the r-HuEpo was discontinued. In 44 patients the mean hematocrit increased from 21.8% to 32.1% and in the other 5 there were no response because of iron deficiency. There were no changes in leucocytes and platelets counts and consistent decreases in iron and ferritin serum concentrations were observed despite oral supplementation of iron. In the 8 patients studied the shortened erythrocyte survival did not suffer any significant variation with r-HuEpo. Predialysis creatinine, urea and phosphorus blood levels increased significantly at 3th month of treatment but there was no increase in potassium. In 32.6% of previously normotensive and hypertensive patients an increase in blood pressure was founded. Thrombosis of arteriovenous fistulas and other severe clinical side effects were not observed.(ABSTRACT TRUNCATED AT 250 WORDS)