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Background: Scorpion venom causes renal injury and affects vascular ion-channels function. Centruroides margaritatus scorpion is found in Colombia and is frequently the cause of envenomation accidents; however, its renal impact has never been investigated., Objective: To evaluate the effects of C. margaritatus venom (CmV) on renal parameters using isolated rat kidney and renal cell culture models., Methods: Wistar rats (n = 5, weighing 240-300 g) were first perfused with Krebs-Henseleit solution containing 6 g 100 mL-1 bovine serum albumin. After 30 minutes, the kidneys were perfused with CmV to a final concentration of 10 μgmL-1; evaluation was performed by measuring Perfusion Pressure (PP), Renal Vascular Resistance (RVR), Urinary Flow (UF), Glomerular Filtration Rate (GFR), and percentage of electrolyte tubular transport. Moreover, kidney histological analyses and cell cytotoxicity in renal tubule epithelial cells (MDCK) and proximal tubular cells (LLC-MK2) were assessed., Results: CmV increased PP and RVR 60 min after perfusion. On the other hand, UF, GFR, and the percentages of sodium, potassium and chloride tubular transport decreased after experimental envenomation. UF dropped after 120 min, while GFR and percentage of electrolyte tubular transport diminished after 60, 90 and 120 min. CmV was not toxic to MDCK cell line but reduced the viability of LLC-MK2 cells at concentrations ranging from 6.25 to 200 μgmL-1. Histological analyses disclosed hydropic degeneration, edema, and protein deposits. Flow cytometry disclosed that cell death occurred predominantly by necrosis., Conclusion: Our results suggest that C. margaritatus venom can trigger renal impairment, mainly in the proximal kidney tubule., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

The optimal prophylactic induction immunosuppressive therapy to prevent renal transplant rejection remains controversial. Recently, basiliximab efficiency has been reported in several studies. We sought to evaluate the efficiency of induction immunosuppressive therapy with basiliximab in renal transplantation in our unit based upon the acute rejection rate, patient and graft survivals, first hospital admission length, and incidence of infectious or malignant complications during 4 years of follow-up. We retrospectively evaluated the outcome of two groups of renal transplant recipients treated with triple immunosuppressive therapy (cyclosporine, mycophenolate mofetil, and prednisolone) without (group 1, 149 patients) or with (group 2, 104 patients) induction immunosuppression with basiliximab. The two groups did not differ in demographic characteristics, number of hypersensitized patients, cold ischemia time, or donor age. The group receiving basiliximab displayed a significantly lower acute rejection rate (7.6% vs 24%, P = .001) and shorter first hospital admission (14.4 +/- 8 vs 19.5 +/- 11 days). There was no difference in graft or patient survival, death due to sepsis, or incidence of posttransplant malignancies. Although there was no difference in graft or patient survival, immunosuppressive induction therapy with basiliximab yielded a significant reduction in the acute rejection rate.

Mycophenolate mofetil (MMF) use in renal transplantation has allowed a significant decrease in early acute rejection rates. We retrospectively evaluated the incidence of acute rejection episodes, renal function at the first year posttransplant, patient and graft survivals, cytomegalovirus (CMV) infection rate, influence of the degree of sensitization, and number of MHC antigen mismatches on graft survival in two groups of patients receiving either MMF or azathioprine. Group 1 included 149 patients receiving cyclosporine, MMF, and prednisolone; group 2 included 191 patients receiving cyclosporine, azathioprine, and prednisolone. The two groups did not differ in terms of age, sex, degree of sensitization (expressed as percentage of antibodies reactive to panel), MHC mismatch number, cold ischemia time, donor age, or anti-thymocyte globulin induction. In group 1 (MMF) there was a significant decrease in early acute rejection rate (19% vs 57%, P < .0001), longer graft survival at 10 years (92% vs 75%, P = .006), and higher rate of CMV infection (22% vs 12%, P = .004). Renal function at the first year posttransplant and patient survival during follow-up did not differ between the groups. The degree of sensitization influenced graft survival in group 2. The number of MHC mismatches did not influence graft survival in either group. With MMF, there was a significant reduction in early acute rejection rate, a significant increase in graft survival at 10-year follow-up, and diminished impact of the degree of sensitization on graft survival.

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.

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.

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)