Simvastatin in an experimental spinal cord injury model: a histopathological and biochemical evidence based study.

AIM: In this study we tried to determine the possible neuroprotective effects of simvastatin in a rat model of Spinal Cord Injury (SCI) with the help of biochemical and histopathological tests. METHODS: Rats were divided into 5 groups:1) SCI control, 2) Sham operated, 3) SCI with 10 mg/kg intraperitoneal simvastatin, 4) SCI with 10 mg/kg oral simvastatin, 5) SCI with 10 mg/kg subcutaneous simvastatin. After the treatment period, all rats were sacrificed; their blood and spinal cord samples were taken for biochemical and histopathological assessment. RESULTS: When the groups were compared in terms of oedema and inflammation status, the scores of groups receiving simvastatin were better than the control and sham groups (p = 0.001 and p = 0.038 respectively). When the 3 treatment groups (oral, intraperitoneal and subcutaneous simvastatin groups) were compared with each other in terms of inflammation, haemorrhage and oedema, there were no significant differences between groups (p = 0.112, p = 0.797 and p = 0.188, respectively). NSE and S100B levels were significantly lower in the treatment groups compared to the sham group (p = 0.039 and p = 0.004 respectively). CONCLUSION: According to our biochemical and histopathological findings, simvastatin 10 mg/kg has a positive impact in the spinal cord injury model in rats, regardless of route of application (Tab. 1, Fig. 5, Ref. 26).

The Effects of O6-methyl Guanine DNA-methyl Transferase Promotor Methylation and CpG1, CpG2, CpG3 and CpG4 Methylation on Treatment Response and their Prognostic Significance in Patients with Glioblastoma.

This retrospective study examined the prognostic significance and treatment effect of promoter methylation of O6- methyl guanine methyl transferase (MGMT) and meth-ylation of CpG 1, CpG2, CpG3 and CpG4 in glioblastoma (GB) patients received postoperative radiotherapy (PORT), with or without adjuvant temozolomide (TMZ). One hundred patients with GB who received PORT with concomitant TMZ plus adjuvant TMZ or PORT alone, were included. The MGMT promoter methylation of CpG1, CpG2, CpG3 and CpG4 islands were examined. Overall, MGMT-methylation emerged as a significant prognostic factor for better overall survival (OS) and progression-free survival (PFS) [odds ratio (OR): 0.609, 95% confidence interval (95% CI): 0.395-0.939, p = 0.02; OR: 0.662,95% CI: 0.430-1019, p = 0.5, respectively]. The methylation of each CpG1, CpG2, CpG3 and CpG4 islands was found to have no significant effects on OS and the methylation of each CpGl, CpG2 and CpG4 islands had no significant effect on PFS (p <0.05 for all). On the other hand, the methylation of CpG3 had a positive prognostic effect on PFS (OR: 2.1, 95% CI: 0.99-4.67, p = 0.04). In the group that only received radiotherapy (RT), CpG1 and CpC3 methylations were found to have a positive prognostic significance in terms of PFS (OR: 266, 95% CI: 1.05-6.75, p -0.03 for CpG1; OR: 2.4, 95% CI: 1.01-5.92, p = 0.04 for CpG3). The MGMT promoter methylation represents an important biomarker for predicting response to therapy. Individual islands, particularly CpG3, deserves further investigation as a prognostic marker. Further studies need to be done with larger sample sizes to clarify the results.

Spinal intradural abscess caused by hematogenous spread of Prevotella oralis in a 3-year-old child with an asymptomatic congenital spinal abnormality.

STUDY DESIGN: Case Report. OBJECTIVES: To report a case of spinal intradural abscess caused by hematogenous spread of Prevotella oralis and discuss the treatment. SETTING: Department of Neurosurgery, Ankara Education and Research Hospital, Ankara, Turkey. METHOD: We report a 3-year-old child with progressive paraparesis who was diagnosed with an intradural spinal abscess, epidermoid cyst and dermal sinus. The patient was treated surgically followed by antimicrobial treatment. RESULT: Intraoperative abscess culture was positive for Prevotella oralis, which has not been reported before as a single isolate in literature. The patient's neurologic status was significantly improved after surgical treatment. CONCLUSION: Prophylactic antimicrobial therapies should cover the anaerobic bacteria in spinal intradural abscess. Surgical decompression with laminectomy and duraplasty may be warranted to achieve immediate neurologic improvement in such cases.

Ultrastructural evaluation of urine alkalinization versus hydration on colistin-induced nephrotoxicity.

OBJECTIVES: Colistin is a vital antibiotic used in multidrug-resistant infections. Its most important side effect is nephrotoxicity. Colistin is a weak acid. This study aims to evaluate whether urine alkalinization is protective in the nephrotoxicity of colistin. METHODS: Twenty-eight male Sprague-Dawley rats were divided into groups. Group I (n = 4) was injected with intramuscular distilled water twice a day for 7 days. Group II (n = 8) was injected with 750,000 IU/kg/day colistin for 7 days. Group III (n = 8) was injected with the same dose of colistin after their urinary pH was ≥7 through the addition of bicarbonate in their drinking water. Group IV (n = 8) was injected with the same dose of colistin after their urine density fell below 1010 through the addition of NaCl molds in their food and 12.6 mg/L NaCl in their drinking water. RESULTS: According to tubular degenerations (scored 0-5), group I scored 0, group II scored 4.25, group III scored 2, and group IV scored 1.5. In groups III and IV, protection was achieved (p = 0.001). The bicarbonate group was not superior to the NaCl group (p = 0.789). In transmission electron microscopy, group III had more microvilli integrity and autophagic vacuoles compared to group IV. Group IV had mitochondrial swelling and cristae lysis. A lower urine density was related to lower tubular scores (p = 0.001). CONCLUSIONS: Colistin was highly nephrotoxic without protection. Light microscopy findings revealed that urinary alkalinization and NaCl hydration were similarly protective. Urine alkalinization further prevents ultrastructural changes as revealed by electron microscopy.

Utility of the Doppler ultrasound parameter, resistive index, in renal transplant histopathology.

BACKGROUND: Doppler ultrasonography is routinely used by many clinicians during long-term follow-up to identify high-risk patients without diagnosing the exact cause of graft dysfunction. Despite a number of studies showing a correlation between intrarenal resistive index (RI) and renal function in patients with kidney diseases, correlations between RI and renal histopathologic characteristics have not been sufficiently evaluated in renal transplant recipients. The aim of this study was to examine this relationship in grafted kidneys. PATIENTS AND METHODS: The intrarenal RI was retrospectively compared with biopsy findings in 28 kidney recipients. All renal biopsy specimens were reviewed by light microscopy and immunofluorescence staining. For glomerulosclerosis, we considered the percentage of glomeruli showing this change; for interstitial fibrosis/tubular atrophy and interstitial infiltration, we graded abnormalities according to the methods of Kliem et al (Kidney Int 49:666, 1996). RESULTS: The percentage of globally sclerosed glomeruli was significantly greater among patients with RI values higher than 0.75 than below this level (23% vs 47%; P = .022). Patients with grade 1 interstitial fibrosis and tubular atrophy (n = 14) showed lower RI values (0.68 +/- 0.03 vs 0.74 +/- 0.06; P = .047) than those with grade 3 fibrosis (n = 12). Similarly, lower RI values (0.66 +/- 0.02 vs 0.73 +/- 0.05; P = .014) were observed among patients with grade 1 (n = 13) compared with grade 3 interstitial infiltration (n = 13). CONCLUSION: RI seemed to provide a prognostic marker for the graft rather than yielding an exact diagnosis of renal graft dysfunction.

Anterior sacral meningocele. A case report.

A case of anterior sacral meningocele in a 6-year-old girl is reported. The laminotomies of L5, S1, and S2 vertebrae were performed through a median posterior approach. The communication between the subarachnoid space and the meningocele was closed using dural fibrin patch, which has not yet been described in the literature. The relevant literature is reviewed.

Urinary Type III Procollagen Is Associated With Chronic Allograft Dysfunction and Predicts Graft Survival.

BACKGROUND: Chronic allograft dysfunction (CAD) is the most important clinical problem in solid organ transplantation. Interstitial fibrosis and tubular atrophy contribute to long-term renal allograft failure. Urinary type III procollagen N-terminal propeptide (PIIINP), has been shown to associate fibrotic processes. METHODS: One hundred sixty patients with CAD who underwent allograft biopsies were evaluated, and 52 patients with chronic or sclerosing allograft nephropathy were enrolled in the study. The subjects were divided into 2 groups according to the level of urinary PIIINP to creatinine (u-PIIINP-to-Cr): high procollagen group and low procollagen group. The association between u-PIIINP-to-Cr level at the time of biopsy and renal endpoints during 36 months of follow-up was assessed by multivariate Cox analysis. RESULTS: Interstitial fibrosis and proteinuria were higher in the high procollagen group compared with the low urinary procollagen group. Correlation analysis showed that levels of u-PIIINP-to-Cr were positively associated with fibrosis scores. During the follow-up, glomerular filtration rate (GFR) decreased in both study groups; however, GFR declined more in the high procollagen group than in low procollagen group. Cox regression model showed that the u-PIIINP-to-Cr levels, GFR, and proteinuria were independent risk factors associated with graft survival. CONCLUSION: u-PIIINP-to-Cr level is a potentially useful noninvasive marker for graft survival in patients with CAD.

The role of proinflammatory cytokine gene polymorphisms for development of insulin resistance after renal transplantation.

BACKGROUND: Insulin resistance, a frequent prediabetic metabolic complication after renal transplantation, is generally linked to immunosuppressive drugs including corticosteroids, cyclosporine (CsA) or tacrolimus, as well as to age, cadaveric donors and ethnic factors. Cytokines are known to be inflammation modulatory substances that contribute to metabolic derangements after transplantation. The present study investigated the effects of cytokine gene polymorphisms on insulin resistance in renal transplant recipients. PATIENTS AND METHODS: Sixty-one renal transplant recipients (37 men, 24 women; mean age: 39.3 +/- 10.8 years) who attended regular clinical visits without a known history of diabetes were enrolled in the study. All patients were on a regimen of steroid, CsA, and mycophenolate mofetil. Venous blood samples were collected for biochemical analyses after an overnight fast at 08:00 pm. CsA trough levels, C-reactive protein, and fibrinogen were also estimated. Additional 10 mL of blood was withdrawn into an ethylenediamine tetraacetic acid-containing tube to determine cytokine genotypes (tumor necrosis factor-alpha [TNF-alpha] -238 G/A, transforming growth factor-beta [TGF-beta] codon 10 -869 T/C). Insulin resistance was calculated by the homeostasis model assessment (HOMA) method using the values of fasting blood glucose (FBG) and insulin levels. Anthropometric indices as well as body height, weight, waist and hip circumferences were measured simultaneously to calculate body mass index (kg/m2) and waist-to-hip ratio. Impaired fasting glucose (IFG) was described as an FBG > or = 110 but < 126 mg/dL. RESULTS: IFG was detected in 27.9% of this study group. The HOMA index was significantly higher among patients with IFG compared with normal FBG (NoGT) (6.3 +/- 4.5 vs 3.7 +/- 1.5; P = .01). Neither FBG and insulin nor HOMA values correlated with antrophometric, metabolic, or inflammatory parameters. Cytokine genotype allele frequencies, age, sex, immunosuppressive and antihypertensive drug type and doses, CsA trough levels, and donor source (cadaveric/living) were similar for patients with IFG and NoGT. Mutant allele carrier genotypes (AA + GA) for TNF-alpha -238 G/A showed higher fasting insulin (14.0 +/- 7.9 vs 34.1 +/- 17.7 microIU/mL; P = .04) and HOMA (4.01 +/- 2.01 vs 7.95 +/- 5.44; P = .002) levels than GG homozygote subjects. FBG, HOMA, and other metabolic and anthropometric indices were similar between TGF-beta codon 10 -869 T/C genotypes. The daily dose of steroid (mg/d) and A allele frequency for TNF-alpha -238 G/A genotype were significant predictors of HOMA index in linear regression analysis. CONCLUSION: The present study revealed that beside the daily dose of steroids, TNF-alpha -238 G/A genotype may contribute to insulin resistance in renal transplant recipients. Further investigations may highlight the effects of cytokine gene heterogenity on insulin resistance in those patients.

Sieving effect of heat-denatured milk proteins during ultrafiltration of skim milk. I. The preliminary approach.

The effect of heat treatment of skim milk on the ultrafiltration process was examined. The change in permeate collection rate was explained as a function of heat-induced modifications of the milk protein system. It is suggested that there was a sieving effect which contributed to the acceleration of permeate flow-down during membrane filtration. It is thought that this resulted from formation of complex structures between heat-denatured whey proteins and casein micelles.

Endothelial dysfunction in renal transplant recipients: role of vitamin D and fibroblast growth factor-23.

BACKGROUND: Endothelial dysfunction can be detected at early stages of chronic kidney disease. Although endothelial functions improve after successful renal transplantation, renal transplant recipients have still worse endothelial functions compared to healthy subjects. Vitamin D deficiency and high fibroblast growth factor-23 (FGF-23) levels may have a role on endothelial dysfunction in chronic kidney disease patients. The aim of this study is to investigate the association between endothelial functions, vitamin D, and FGF-23 levels in renal transplant recipients. METHODS: One hundred nine renal transplant recipients (71 male, 38 female) underwent brachial flow-mediated dilatation (FMD), serum 25-OH vitamin D, and FGF-23 level measurements. Vitamin D and FGF-23 levels were compared between patients with normal and abnormal endothelial functions. Correlations between FMD, vitamin D, and FGF-23 were also investigated. RESULTS: Endothelial functions were abnormal in 72.5% of the patients. Prevalence of vitamin D deficiency was 80.7%. Vitamin D levels were significantly lower in patients with endothelial dysfunction compared to patients with normal endothelial functions (12.6 ± 6.6 µg/L vs 17.3 ± 10.0 µg/L respectively, P = .02). FGF-23 levels were not different between the two groups. 25-OH vitamin D levels had a significant positive correlation with amount of FMD (r = 0.218 and P = .02) and were an independent predictor of FMD after adjusting for potential confounding factors including age, transplantation duration, body mass index, mean blood pressure, glomerular filtration rate, proteinuria, hemoglobin, and FGF-23 in multivariate regression analysis (beta = 0.194, P = .04). FGF-23 levels were not predictive of FMD in this model (beta: -0.125, P = .197) CONCLUSION: Vitamin D deficiency is associated with endothelial dysfunction in renal transplant recipients. Further clinical and experimental studies are necessary to define a causal relationship between the parameters, discover the potential mechanisms, and observe the effect of vitamin D replacement on endothelial functions in renal transplant recipients.

Urologic Disorders in Living Renal Donors and Outcomes of Their Recipients.

BACKGROUND: There is an expanding gap between the number of patients listed for kidney transplantation and the number of kidney transplantations performed annually. The use of sensitive imaging methods results in increased discovery of many urologic asymptomatic problems, such as urolithiases, renal cysts, and solid renal masses. This result has brought the question of whether all donors with these urologic disorders should be rejected for donation. METHODS: We retrospectively analyzed donor and recipient records of all living kidney transplantations performed from 2004 to 2014. RESULTS: Among 251 living-related donor kidney transplantations, 51 donors (20.3%) had urologic disorders. Mean donor age was significantly higher in donors with urologic disorders than in the standard donor group (50 y vs 41 y). The identified disorders were 32 renal cysts, 8 urolithiases, 3 renal tumors, 6 adrenal adenomas, and 2 microscopic hematurias. After nephrectomy, the graft kidneys with cysts were inspected carefully and all of the cortical-peripheral cysts were decorticated. Renal tumors were excised in 3 renal units. Transplantations had proceeded after the confirmation of low malignancy potentials of the lesions with safe surgical margins. Two out of 8 patients had undergone stone removal with ex vivo ureteroscopy and 1 by means of pyelotomy incision because of calix neck stenosis. None of those donors and recipients developed clinically significant renal stone disease with a mean follow-up of 28 months. Neither donors nor recipients of asymptomatic microscopic hematuria patients developed any problem with a mean 28 months' follow-up period. CONCLUSIONS: Asymptomatic urologic problems are very common. The significance of these asymptomatic pathologies is unclear. Our results suggest that in a selected group, at least some of these candidates can be accepted for donation.

Association between urinary angiotensinogen, hypertension and proteinuria in pregnant women with preeclampsia.

INTRODUCTION: Preeclampsia is a life-threatening disorder of pregnancy. The pathogenic mechanisms of preeclampsia remain uncertain. The aim of this study is to investigate the relation between urinary angiotensinogen (UAGT) levels, an indicator of local renin-angiotensin system (RAS) activity in the kidney, and blood pressure and urinary protein excretion in preeclampsia. MATERIALS AND METHODS: For this study, 90 women aged between 20-39 years were recruited. Spot urine samples were collected to measure urinary angiotensinogen/creatinine ratio (UAGT/UCre). Log(UAGT/UCre) was compared in pregnancies with and without preeclampsia and non-pregnant controls. Factors affecting log(UAGT/UCre) in pregnancies were also investigated. RESULTS: In all pregnancies log(UAGT/UCre) levels were significantly higher than in non-pregnant controls (0.58±0.19 vs. 0.33±0.14, respectively, p=0.002). However, log(UAGT/UCre) levels in pregnancies with preeclampsia were slightly lower than in normal pregnancies (0.52±0.18 vs. 0.64±0.19, respectively, p=0.012). Log(UAGT/UCre) levels were correlated positively with blood pressure and proteinuria in pregnancies with preeclampsia. However, log(UAGT/UCre) levels were not correlated with age, height, body weight, gestational age, body mass index, and serum creatinine. CONCLUSION: This study showed that elevated local RAS activity in kidney was correlated with high blood pressure and proteinuria in preeclampsia. Local RAS activation in the kidneys may be one of the contributing factors in the development of preeclampsia.

Does allograft size really matter in the long-term outcome of living donor kidney transplantation?

BACKGROUND: Increased allograft mass in living donor kidney transplantation has been recognized as a predictor factor of better short-term allograft function. We evaluated whether donor kidney volume adjusted for recipient body weight is associated with long-term allograft function in living donor kidney transplantation. METHODS: We analyzed 67 living donors and their recipients who underwent transplantation between 2003 and 2007. Estimated glomerular filtration rate (eGFR) and serum creatinine levels at 1, 2, 3, 4, and 5 years post-transplantation were recorded for all recipients. Transplanted kidney volumes were measured using 3-D helical computed tomography scanning. A transplant kidney volume-recipient body weight (Vol/Wt) ratio was calculated for each donor-recipient pair. The subjects were divided into tertiles according to Vol/Wt ratios: low (<2.16), medium (2.16-2.88), and high (>2.88). RESULTS: Vol/Wt ratio significantly correlated with recipient eGFR and serum creatinine levels at 1, 2, 3, and 4 years post-transplantation (r = .48, P < .0001; r = .46, P < .0001; r = .47, P < .0001; r = .26, P = .037, respectively, for eGFR; r = -.53, P < .0001; r = -.50, P < .0001; r = -.44, P < .0001; r = -.37, P = .003, respectively, for serum creatinine) but not at 5 years (r = .12, P = .406 for eGFR; r = -.21, P = .110 for serum creatinine). Whereas recipient eGFR increased significantly in a graded fashion among low to high Vol/Wt ratio groups during 1 to 3 years post-transplantation, there was no difference in eGFR values between Vol/Wt ratio groups at 4 and 5 years (P = .21 and .71, respectively). CONCLUSION: Vol/Wt ratio is not associated with long-term allograft function in living donor kidney transplantation.

Effects of angiotensin converting enzyme and angiotensin II receptor inhibition on impaired fibrinolysis in systemic hypertension.

Abnormalities in fibrinolysis have been reported in hypertension. Angiotensin converting enzyme (ACE) inhibitors have been shown to improve altered fibrinolytic balance in hypertensive patients. It has not been documented, however, whether this is due to a decrease in angiotensin II (Ang-II) generation or is a consequence of elevated local levels of bradykinin. Accordingly, the aim of this study was to determine the effects of an ACE inhibitor (perindopril) and an Ang-II receptor antagonist (losartan) on fibrinolytic kinetics. We have examined the serum levels of the plasminogen activator inhibitor type-1 (PAI-1) antigen and activity, tissue plasminogen activator (t-PA) antigen and activity, soluble thrombomodulin (sTM), and tissue factor pathway inhibitor (TFPI) before and after reaching the target blood pressure (<140/90 mm Hg) in 13 hypertensive patients receiving perindopril (mean age 40+/-11 years, 6 women, 7 men) and in 12 patients receiving losartan (mean age 38+/-9 years, 6 women, 6 men). We also compared the baseline fibrinolytic activity of hypertensive patients with that of 12 normotensive control persons (mean age 40+/-9 years, 6 women, 6 men). The mean basal plasma levels of PAI-1 antigen, PAI-1 activity, and sTM were significantly higher in the hypertensive patients than in normal controls (P<.005). The values of other analytes were similar in both groups. Increased plasma levels of PAI-1 antigen, PAI-1 activity, and sTM were reduced in patients after they were given perindopril and losartan (P<.005); the reductions in losartan-receiving group were more pronounced (P<.05). There were no significant effects on the plasma levels of t-PA antigen, t-PA activity, and TFPI in patients receiving the two therapeutic regimens (P>.05). In conclusion, chronic hypertension is associated with hypofibrinolysis. The beneficial effect of ACE inhibitors on fibrinolysis seems to be related to the blockade of Ang-II, and increased kinin activity does not appear to play a major role.

Environmentally-induced malignant pleural mesothelioma and HLA distribution in Turkey.

SETTING: A large university hospital in Ankara, Turkey. OBJECTIVE: To investigate the potential links, if any, between the occurrence of malignant pleural mesothelioma (MPM) and the presence and distribution of human leukocyte antigens (HLA) in patients environmentally exposed to asbestos and erionite in rural Anatolia, Turkey. DESIGN: A case-control study design was used to compare the relative frequency and distribution of HLA among 31 MPM patients originating from the fibrous zeolite (erionite) and asbestos villages in central Anatolia, and two sets of controls. The cases represented all of the MPM cases diagnosed between 1995 and 1997 in our clinic at the Hacettepe University Hospital. One control group of 119 healthy individuals was drawn from Tuzköy, which has the largest population of three erionite villages, a very high prevalence of mesothelioma due to environmental exposure to erionite, and accounted for 16 of the MPM cases in the study. A second control group composed of 118 renal transplant donors was formed for external comparison. RESULTS: A significant relation was found with the HLA-B41 antigen in 19.4% of the patients compared to 0.8% of the Tuzköy inhabitants (odds ratio [OR] 28.3; 95% confidence interval [CI] 3.1-652.5) and 1.7% of the referent renal donor population (OR 13.9; 95% CI 2.3-106.7). The frequency of the HLA-B58 and -DR16 antigens was also observed to be significantly higher in patients with MPM compared to the two control groups. The odds ratios of MPM in those with HLA-B58 were 8.6 (95% CI 1.2-72.4) and 8.5 (95% CI 1.2-71.8), respectively, compared to those of the Tuzköy inhabitants and renal donors. CONCLUSION: The predictive role of the HLA antigens -B41, -B58 and -DR16 for MPM needs to be further investigated. This will help in screening the population at risk, and facilitate preventive measures such as family counselling and gene therapy.

Thrombopoietin and thrombospondin in renal allograft recipients.

Recipients of renal transplants appear to be at increased risk of thromboembolic events. Despite accumulating evidence for the hyperreactivity of platelets, the primary regulator of thrombopoiesis, thrombopoietin (TPO), has not yet been studied in renal transplant recipients. Thus, the aim of the present study was to quantify the levels of TPO and to assess its contribution to increased platelet reactivity in recipients of renal allografts. Serum concentrations of thrombospondin (TSP) were also determined in patients undergoing renal transplants in order to evaluate the role of this multifunctional protein in platelet hyperaggregability. Serum levels of TPO were significantly lower in renal transplant recipients (n = 27) than in healthy controls (30.8+/-20.6 pg/ml versus 129.9+/-113.6 pg/ml, P = 0.001). Serum concentrations of TPO were correlated neither with serum levels of creatinine nor duration of transplantation. However, levels of TPO were negatively correlated with platelet counts (r = -0.50, P = 0.007) in recipients of renal transplants. Plasma levels of TSP were higher in renal transplant patients than in the control group (104.5+/-54.7 ng/ml versus 63.4+/-41.5 ng/ml, P = 0.003). No significant correlation was found between levels of TPO and TSP. We conclude that, rather than the allograft function, the platelet mass determines the levels of TPO in recipients of renal transplants. Despite the low serum levels of TPO, and increased concentrations of TSP, TPO might still play a role in the hyperaggregability of platelets in patients undergoing renal transplants.

Cyclical acute renal failure due to bilateral ureteral endometriosis.

Endometriosis is a common disease but ureteral involvement is relatively rare. Ureteric endometriosis is mostly unilateral. Endometriotic ureteral obstruction is a serious event commonly diagnosed late and therefore associated with a major risk of hydronephrotic renal atrophy. We present the cyclical acute renal failure associated with menstruation in a patient who developed severe bilateral ureteral obstruction due to endometriosis. Physicians should be aware of this uncommon but serious manifestation of endometriosis, especially if the clinical presentation is cyclical acute renal dysfunction in a premenopausal woman.

Rapidly progressive glomerulonephritis associated with hepatitis C virus infection.

Glomerular disease often accompanies a wide variety of liver diseases, including acute or chronic hepatitis. A striking association between hepatitis B virus and glomerulonephritis particularly membranous glomerulonephritis has been reported by various authors. It is not surprising, therefore, that hepatitis C virus (HCV) infection has been recently associated with the development of various types of glomerulonephritis. The principal type of glomerulonephritis associated with HCV infection is either cryoglobulinemic or non-cryoglobulinemic membranoproliferative glomerulonephritis. However, other types of glomerular lesions were seen in the clinical course of HCV infection. We report a rare case of a 20-year-old woman who developed rapidly progressive glomerulonephritis (RPGN) during the course of the active HCV infection. Whether this case represents a true association or a coincidental association is not known.

Determinants of soluble CD23 antigen levels in hemodialysis patients: effect of 1.25 dihydroxyvitamin D3 and recombinant human erythropoietin treatment.

BACKGROUND: The immunodeficiency of end-stage renal disease (ESRD) paradoxically coexists with T cell and monocyte activation. In spite of well known defective antibody responses in ESRD, the functional status of B cells in the immune system dysregulation of uremia is still controversial. Soluble CD23 (sCD23) antigen is a recently identified B cell activation marker and is also involved in T cell activation process. Effects of parathyroid hormone (PTH), red blood cells and ferritin on T and B cell functions have been shown both in vivo and in vitro. PATIENTS AND METHODS: In this study, serum levels of sCD23 in hemodialysis patients were determined to evaluate the functional status of B cells and possible linkages between this cytokine and PTH levels, ferritin levels, red blood cell counts were investigated. RESULTS: Serum sCD23 levels were significantly elevated in hemodialysis patients relative to healthy controls (12.5+/-8.4 micro/l vs. 2.4+/-1.1 micro/l, p<0.001). Serum sCD23 levels were negatively correlated with red blood cell count (r = -0.61, p = 0.009) and serum PTH levels (r = -0.62, p = 0.008), while positively correlated with serum ferritin levels (r = 0.63, p = 0.007) in hemodialysis patients. We also investigated the immunumodulator effects of 1.25 dihydroxyvitamin D3 (1.25OHD3) and recombinant human erythropoietin (rHu-Epo) treatment in hemodialysis patients. 1.25OHD3 treatment for eight weeks did not change serum sCD23 levels in hemodialysis patients (n = 8). On the other side, rHu-Epo administration for 16 weeks led to a decrease in serum sCD23 levels (17.7+/-8.6 microg/l vs. 9.8+/-3.5 microg/l, p = 0.007) in these patients (n = 9). CONCLUSION: These results suggests that similar to T cells, B cells are activated in uremia and the degree of this activation is correlated with red blood cell count, serum parathyroid hormone levels and iron status of the hemodialysis patients. Moreover, B cell activation could be altered by recombinant human erythropoietin therapy in hemodialysis patients.