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The purpose of this study was to determine the prevalence of bladder lesions diagnosed during transurethral resection of the prostate (TURP), to identify the associated risk factors, and to correlate the macroscopic descriptions with the pathological findings. This was a single-center retrospective case series conducted at a hospital in the city of Sao Paulo, Brazil. We reviewed the medical and surgical records of patients who underwent TURP between January 2012 and December 2017. The final sample comprised 513 patients, with a mean age of 70.8 years. Bladder lesions were identified during TURP in 109 (21.2%) of the patients, and 90 of those lesions were submitted for pathological examination. The most common macroscopic finding was bullous edema, which was seen in 57 (63.3%) of the 90 lesions examined. The pathological analysis revealed chronic cystitis in 61 lesions (67.8%) and malignant lesions in 16 (17.8%). Of the 57 lesions described as bullous edema, 5 (8.8%) were found to be malignant. Alterations in the bladder mucosa appear to be more common among elderly patients who use an indwelling urinary catheter for a prolonged period and among patients with recurrent urinary tract infections. In addition, the risk of a bladder lesion being malignant is apparently higher in current and former smokers than in never smokers. Our findings suggest that at-risk patients should undergo biopsy or resection of incidental bladder lesions even if those lesions seem to be benign, due to the low level of agreement between the visual analysis and the pathological examination.

IntroductionIgA nephropathy (IgAN) is the most common primary glomerulopathy worldwide. According to the Oxford Classification, changes in the kidney vascular compartment are not related with worse outcomes. This paper aims to assess the impact of thrombotic microangiopathy (TMA) in the outcomes of Brazilian patients with IgAN.Materials and methodsAnalysis of clinical data and kidney biopsy findings from patients with IgAN to assess the impact of TMA on renal outcomes.ResultsThe majority of the 118 patients included were females (54.3%); mean age of 33 years (25;43); hypertension and hematuria were observed in 67.8% and 89.8%, respectively. Median creatinine: 1.45mg/dL; eGFR: 48.8ml/min/1.73m2; 24-hour proteinuria: 2.01g; low serum C3: 12.5%. Regarding to Oxford Classification: M1: 76.3%; E1: 35.6%; S1: 70.3%; T1/T2: 38.3%; C1/C2: 28.8%. Average follow-up: 65 months. Histologic evidence of TMA were detected in 21 (17.8%) patients and those ones presented more frequently hypertension (100% vs. 61%, p ConclusionsIn this study patients with TMA had worse clinical manifestations and outcomes. In terms of histologic evidence, E1 distinguished patients with TMA from other patients. Further studies are necessary to analyze the impact of vascular lesions on IgAN prognosis.

Background Schistosoma mansoni schistosomiasis (SM) remains a public health problem in Brazil. Renal involvement is classically manifested as a glomerulopathy, most often membranoproliferative glomerulonephritis or focal and segmental glomerulosclerosis. We report a case of collapsing glomerulopathy (CG) associated with SM and high-risk APOL1 genotype (HRG). Case report A 35-year-old male was admitted for hypertension and an eight-month history of lower-limb edema, foamy urine, and increased abdominal girth. He had a recent diagnosis of hepatosplenic SM, treated with praziquantel, without clinical improvement. Laboratory tests revealed serum creatinine 1.89mg/dL, blood urea nitrogen (BUN) 24mg/dL, albumin 1.9g/dL, cholesterol 531mg/dL, low-density lipoprotein 426mg/dL, platelets 115000/mm3, normal C3/C4, antinuclear antibody (ANA), rheumatoid factor (RF), and antineutrophil cytoplasmic antibodies (ANCA), negative serologies for hepatitis C virus (HCV) and human immunodeficiency virus (HIV), HBsAg negative and AntiHBc IgG positive, no hematuria or leukocyturia, 24 hour proteinuria 6.56g and negative serum and urinary immunofixation. Kidney biopsy established the diagnosis of CG. A treatment with prednisone was started without therapeutic response, progressing to end-stage kidney disease 19 months later. Molecular genetics investigation revealed an HRG. Conclusions This is the first report of CG associated with SM in the setting of an HRG. This case highlights the two-hit model as a mechanism for CG pathogenesis, where the high-risk APOL1 genotype exerts a susceptibility role and SM infection serves as a trigger to CG., Author summary Schistosomiasis mansoni is still a public health problem in Brazil and renal involvement is described. In such cases, a glomerulopathy is the typical manifestation, most often membranoproliferative glomerulonephritis. In the current article, we report a patient with a recent diagnosis of hepatosplenic SM who was admitted for nephrotic syndrome associated with reduced renal function and hypertension. Kidney biopsy established the diagnosis of collapsing glomerulopathy (CG) and molecular genetics investigation identified a high-risk APOL1 genotype (HRG). Of note, HRG has been associated with increased risk to develop CG, and a two-hit model has been proposed for the genesis of this glomerulopathy. According to this model, a HRG represents the increased-susceptibility component, while an infection or other environmental factors could act as triggers for the development of CG. Based on those data and model, our case raises SM infection as a new trigger for this severe form of glomerulopathy. This is the first description of a case of CG associated with SM in a patient with an HRG. This case corroborates the interactive role between genetic and environmental factors in the pathogenesis of CG but also identifies SM infection as an additional trigger for its development.

Introduction: there is evidence linking silicosis and autoimmune diseases, such as systemic lupus erythematosus, systemic sclerosis, and rheumatoid arthritis. More recently, there are some reports and studies associating chronic kidney disease and silica exposure, but, until now, the mechanisms of renal lesion by silica have not been well elucidated. We bring a case of a patient with silicosis who developed acute renal injury related to autoimmune renal disease. Case Report: a 37-year old man came to a routine evaluation. He had been diagnosed with silicosis for the past three years, after a six-year history of silica exposure and compatible chest tomography. He maintained his usual dyspnea for moderate efforts, but in the past 15 days refered fever, without other systemic or localized symptoms. His physical exam was unremarkable. His serum creatinine (SCr) was 5.49 mg/dL (previous SCr was 0.98 mg/dL two years before). Urinalysis showed hematuria and proteinuria. An autoimmune investigation revealed positive antinuclear factor 1/1560, rheumatoid factor 119 IU/mL and negative antineutrophil cytoplasmic antibody (ANCA). Renal ultrasonography showed normal-sized kidneys, with normal thickness but hyperechogenic parenchyma. Renal biopsy revealed a pauci-immune crescentic glomerulonephritis. He underwent pulse therapy with methylprednisolone for three days followed by cyclosporine monthly for 06 months. His SCr and urea levels decreased progressively with treatment to normal levels and ANCA turned positive (1/40) 03 months later. Conclusion: Silica can be associated with autoimmune diseases and this case brings the association with an autoimmune renal disease (vasculitis) in silicotic patients.

Alport syndrome (AS) is a disorder of collagen IV, a component of glomerular basement membrane (GBM). The association of AS and immunocomplex nephropathies is uncommon. This is a case of a 37-year-old woman with family history of X-linked AS, including 4 affected sons. This patient developed full-blown nephrotic syndrome along a 3-month period, a presentation not consistent with AS progression. This scenario suggested an alternative diagnosis. A kidney biopsy was therefore performed, showing membranous nephropathy (MN) in addition to GBM structural alterations compatible with AS. Whole exome sequencing also confirmed the diagnosis of X-linked AS, revealing a heterozygous pathogenic mutation in COL4A5. While a negative serum anti-phospholipase A2 receptor did not rule out a primary form of MN, it was also uncertain whether positive serologic tests for syphilis could represent a secondary factor. It is currently unknown whether this unusual association represents AS susceptibility to immunocomplex-mediated diseases or simply an association of 2 disorders.

Renal histology of proliferative lupus nephritis (LN) shows increased macrophage infiltration, but its association with renal outcome is a matter of debate. Here, we investigate the potential relationship that macrophage expression has with renal prognosis in patients with proliferative LN. Fifty patients newly diagnosed with proliferative LN were followed for a median of 8 years. Laboratory testing was conducted at diagnosis, after induction therapy and at the final follow-up evaluation. Renal biopsies were obtained at diagnosis and underwent immunohistochemical analysis with anti-CD68 and monocyte chemoattractant protein 1 monoclonal antibodies. Patients were stratified at final follow-up evaluation into glomerular filtration rate (GFR) >60 ml/min/1.73 m2 (non-progressor group; n = 24) and GFR ≤60 ml/min/1.73 m2 (progressor group; n = 26). All patients were treated with prednisone and six pulses of cyclophosphamide on induction therapy. Conventional maintenance therapy was administered in both groups. Compared to progressors, the non-progressor group showed a lower chronicity index (p = 0.01) and fewer CD68-positive cells in the renal tubules (p = 0.01) and particularly in the renal interstitium (p = 0.0003). Baseline and final serum creatinine correlated positively with the chronicity index (r = 0.3, p = 0.01 and r = 0.3, p = 0.04, respectively), and final serum creatinine correlated positively with interstitial expression of CD68 (r = 0.4, p = 0.0006). Renal expression of CD68 and the chronicity index are associated with progression to chronic kidney disease in patients with proliferative LN.

Figure 2 | Ultrastructural findings showing glomerular capillaries with subepithelial and intramembranous electron-dense deposits besides intervening projections (spikes) regularly distributed on the glomerular basement membrane. Original magnification 8000. A 53-year-old Brazilian man presented with lower limb edema that progressed to anasarca. He had no personal or family history of renal disease. Laboratory tests revealed urea level, 35 mg/dl; hemoglobin value, 9.8 g/dl; leukocyte count, 7500/mm; platelet count, 204,000/mm; serum albumin level, 1.2 g/dl; total cholesterol level, 239 mg/dl; and low-density lipoprotein cholesterol level, 92 mg/dl. Urinalysis showed no leukocyturia or hematuria; the 24-hour urinary protein level was 19.7 g. Serum complement levels were normal. Autoantibody testing and serologic test results were negative for hepatitis B, hepatitis C, and HIV. Light microscopy in a renal biopsy sample revealed mesangial hypercellularity, diffuse chain-like thickening with some spikes of the basement membrane, and interstitial lymphocytes (Supplementary Figure S1 online). A foreign body giant cell reaction was seen around an elliptical structure with a lateral spicule, consistent with a Schistosoma mansoni egg (Figure 1). Immunofluorescence showed granular deposits of IgG, IgA, IgM, C1q, C3, kappa, and lambda in the glomerular capillary loop. The pathologic diagnosis was of stage III membranous nephropathy (Figure 2) with tubulointerstitial

Background Fibroblast growth factor 23 (FGF23), a phosphate-regulating hormone is an established cardiovascular risk factor. Recently, FGF23 has been related to inflammation. Lupus is an inflammatory disease, and whether FGF23 is associated with Lupus nephritis (LN) activity is unknown. Materials and methods We studied 15 pre-menopausal patients with recent LN diagnose (⩽2 months) and compared them to 1:1 age-matched healthy control group. We measured serum levels of intact FGF23, interleukin-6 (IL-6), tumor necrosis factor α (TNFα), and urinary levels of monocyte chemotactic protein (MCP1). Results LN patients (29.5 ± 10 years) presented proteinuria of 4.7 ± 2.9 g/day, and estimated glomerular filtration rate of 37 (31–87) ml/min/1.73 m 2 . They demonstrated higher FGF23 levels when compared to healthy controls [106.7 (80.3–179) vs. 33.6 (25.8–60.9) pg/ml, p Conclusion Newly diagnosed LN patients demonstrated elevated FGF23 levels that were positively correlated to urinary MCP1, independently of vitamin D levels and kidney function. If FGF23 may predict clinical outcomes in LN warrants further evaluation.