Renal Evaluation in Women with Preeclampsia

Background/Aims: Preeclampsia (PE) is a cause of glomerulopathy worldwide. Urinary retinol-binding protein (RBP) is a marker of proximal tubular dysfunction, albuminuria is an endothelial injury marker, urine protein:creatinine ratio (PCR) may have a predictive value for renal disease later in life, and, recently, podocyturia has been proposed as a sensitive tool in pregnancy, but it needs to be tested. The aim of this study was to evaluate renal involvement in PE and healthy pregnancy. Methods: Case-control study with 39 pregnant women assessed after 20 weeks of gestation (25 in the control group, CG, and 14 in the PE group) by performing urinary tests. Results: Mean (±SD) age and gestational age of the CG were 26.9 ± 6.4 years and 37.1 ± 5.0 weeks, and of the PE group 26.4 ± 6.9 years and 30.6 ± 5.6 weeks, respectively (p = 0.001). Mean (±SD) urinary RBP (p = 0.017), albuminuria (p = 0.002), and urinary albumin concentration (UAC) ratio (p = 0.006) of the CG were 0.4 ± 0.7 mg/l, 7.3 ± 6.9 mg/l, and 8.2 ± 6.7 mg/g and of the PE group 2.0 ± 4.4 mg/l, 2,267.4 ± 2,130.8 mg/l (p = 0.002), and 3,778.9 ± 4,296.6 mg/g (p = 0.006), respectively. Mean (±SD) urine PCR in the PE group was 6.7 ± 6.1 g/g (p Conclusions: Urinary RBP, PCR, albuminuria, and UAC ratio were elevated in the PE group in comparison to the CG. Podocyturia did not predict PE

Are the current chronic allograft nephropathy grading systems sufficient to predict renal allograft survival?

A major problem in renal transplantation is identifying a grading system that can predict long-term graft survival. The present study determined the extent to which the two existing grading systems (Banff 97 and chronic allograft damage index, CADI) correlate with each other and with graft loss. A total of 161 transplant patient biopsies with chronic allograft nephropathy (CAN) were studied. The samples were coded and evaluated blindly by two pathologists using the two grading systems. Logistic regression analyses were used to evaluate the best predictor index for renal allograft loss. Patients with higher Banff 97 and CADI scores had higher rates of graft loss. Moreover, these measures also correlated with worse renal function and higher proteinuria levels at the time of CAN diagnosis. Logistic regression analyses showed that the use of angiotensin-converting enzyme inhibitor (ACEI), hepatitis C virus (HCV), tubular atrophy, and the use of mycophenolate mofetil (MMF) were associated with graft loss in the CADI, while the use of ACEI, HCV, moderate interstitial fibrosis and tubular atrophy and the use of MMF were associated in the Banff 97 index. Although Banff 97 and CADI analyze different parameters in different renal compartments, only some isolated parameters correlated with graft loss. This suggests that we need to review the CAN grading systems in order to devise a system that includes all parameters able to predict long-term graft survival, including chronic glomerulopathy, glomerular sclerosis, vascular changes, and severity of chronic interstitial fibrosis and tubular atrophy

Impact of therapeutic changes on renal graft survival with posttransplant glomerulonephritis

Introduction. Posttransplant glomerulonephritis (GN) is the third cause of graft loss after 1 year of transplant follow-up; few approaches have been efficient in reversing this outcome. the aim of this study was to evaluate whether the modification of the immunosuppressive therapy for treating posttransplant GN had an impact on allograft survival. Patients andMethods. Forty-nine patients who underwent renal transplantation and developed posttransplant GN were divided into two groups: group 1, 22 patients with modified immunosuppressive treatment (72.3%, pulse of methylprednisolone; 13.6%, high-dose oral corticosteroid), and group 2, where it was maintained. Additionally, the impact of the concomitant use of drugs that promote the renin-angiotensin-aldosterone system blockade (RAASB) was analyzed in terms of graft survival.Results. We established the diagnosis of GN at 17.9 months (range, 0.57 to 153.4) after transplantation, when serum creatinine (Cr) was 2.2 mg/dL (range, 0.8 to 12.5) and proteinuria 3.2 g/L (range, 0.2 to 24.2). Graft survivals at 1 and 3 years after diagnosis were 69.2% and 52.9%, respectively. the patients of group 1 showed a lower prevalence of graft loss (27.2% versus 48.1%, P =.40) and better survival at the end of 1 year (73.2% versus 60.4%) and 3 years (62.5% versus 38.0%, P =.26), but the differences were not significant. RAASB showed a positive impact on survival at the end of 3 years in both groups: for group 1, 83.8 % with RAASB, 41.4% without RAASB; and for group 2, 75 % with RAASB and 14.8% without RAASB (P < .001).Conclusion. Although treatment of posttransplant GN with modification of immunosuppression seemed to improve graft survival in the first 3 years after diagnosis, RAASB improved this effect.Universidade Federal de São Paulo, Clin & Expt Immunol Lab, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Glomerulopathies Sect, Div Nephrol, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Pathol, BR-04023900 São Paulo, BrazilUniv São Paulo, Dept Immunol, Lab Transplantat Immunobiol, São Paulo, BrazilUniversidade Federal de São Paulo, Clin & Expt Immunol Lab, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Glomerulopathies Sect, Div Nephrol, BR-04023900 São Paulo, BrazilUniversidade Federal de São Paulo, Dept Pathol, BR-04023900 São Paulo, BrazilWeb of Scienc

Supplementary Material for: Thrombomodulin gene mutation and associated predisposing factors in familial collapsing glomerulopathy

Introduction: Collapsing glomerulopathy (CG) is a rare glomerular disease and its familial form is even rarer. CG and non-collapsing forms of focal segmental glomerulosclerosis (FSGS) may both be caused by pathogenic variants in the same genes, but there is less information on genetics of the former disease. We hypothesized that different hits (viral infection and genetic variants) may be involved in the development of a familial CG here described. Methods: Renal and etiological routine evaluation, PVB19 serology, genetic tests including whole exome analysis and dosage of serum thrombomodulin (THBD) were performed in two siblings with CG, one healthy sister and their mother. Results: The THBD gene variant p.A43T in homozygosity was identified in the proband and her affected brother, both with CG. The same mutation was identified in their mother in heterozygosity. Thrombomodulin levels were elevated in the serum of both affected siblings. They also had PVB19 positive serology and the G1 high-risk apolipoprotein L1 (APOL1) alelles in homozygosity. Their healthy sister had no PVB19 positive serology and no THBD nor APOL1 gene variants. Conclusion: In this case of familial CG, THBD and APOL1 gene variants, and a previous PVB19 infection may be associated with the development of CG in a multi-hit process. In addition, the p.A43T THBD variant, identified in the affected siblings, has never been previously described in homozygosis, pointing to a likely autosomal recessive CG trait caused by this gene mutation

Treatment Outcomes of FSGS Recurrence.

Univ Fed Sao Paulo, Hosp Rim, Sao Paulo, BrazilUniv Peruana Cayetano Heredia, Hosp Nacl Cayetano Heredia, Lima, PeruUniv Fed Sao Paulo, Hosp Rim, Sao Paulo, BrazilWeb of Scienc