PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10975307-2 2000 Currently, most children with FSGS are treated with cyclosporine and steroids after establishing steroid resistance, and approximately 60% of patients benefit from this therapy. Steroids 69-77 actinin alpha 4 Homo sapiens 30-34 10975307-2 2000 Currently, most children with FSGS are treated with cyclosporine and steroids after establishing steroid resistance, and approximately 60% of patients benefit from this therapy. Steroids 69-76 actinin alpha 4 Homo sapiens 30-34 10865418-12 2000 The prognosis of patients with FSGS varied and correlated with the degree of steroid responsiveness. Steroids 77-84 actinin alpha 4 Homo sapiens 31-35 10830556-0 2000 Focal segmental glomerulosclerosis in African Americans: effects of steroids and angiotensin converting enzyme inhibitors. Steroids 68-76 actinin alpha 4 Homo sapiens 0-34 10594798-0 1999 A randomized trial of cyclosporine in patients with steroid-resistant focal segmental glomerulosclerosis. Steroids 52-59 actinin alpha 4 Homo sapiens 70-104 9708606-3 1998 We performed six plasmapheresis treatments over 2 weeks in eight patients with a history of steroid-resistant idiopathic FSGS in native kidneys for an average of 12 +/- 2.3 months to determine whether treatment would decrease proteinuria or stabilize renal function. Steroids 92-99 actinin alpha 4 Homo sapiens 121-125 10516344-11 1999 005), renal insufficiency at presentation (P = 0.001), and steroid resistance (P = 0.0006) were significantly greater in children with FSGS. Steroids 59-66 actinin alpha 4 Homo sapiens 135-139 10454778-1 1999 A survey of North American pediatric nephrologists was conducted to assess the variability in the treatment of primary steroid-resistant focal segmental glomerulosclerosis (FSGS) of native kidneys. Steroids 119-126 actinin alpha 4 Homo sapiens 173-177 10594798-2 1999 UNLABELLED: A randomized trial of cyclosporine in patients with steroid-resistant focal segmental glomerulosclerosis. Steroids 64-71 actinin alpha 4 Homo sapiens 82-116 10594798-3 1999 BACKGROUND: A clinical trial of cyclosporine in patients with steroid-resistant focal segmental glomerulosclerosis (FSGS) was conducted. Steroids 62-69 actinin alpha 4 Homo sapiens 80-114 10594798-3 1999 BACKGROUND: A clinical trial of cyclosporine in patients with steroid-resistant focal segmental glomerulosclerosis (FSGS) was conducted. Steroids 62-69 actinin alpha 4 Homo sapiens 116-120 10594798-5 1999 METHODS: We conducted a randomized controlled trial in 49 cases of steroid-resistant FSGS comparing 26 weeks of cyclosporine treatment plus low-dose prednisone to placebo plus prednisone. Steroids 67-74 actinin alpha 4 Homo sapiens 85-89 10594798-13 1999 CONCLUSIONS: These results suggest that cyclosporine is an effective therapeutic agent in the treatment of steroid-resistant cases of FSGS. Steroids 107-114 actinin alpha 4 Homo sapiens 134-138 9708606-10 1998 These studies suggest that plasmapheresis may diminish proteinuria and stabilize renal function in a small minority of patients with steroid-resistant idiopathic FSGS. Steroids 133-140 actinin alpha 4 Homo sapiens 162-166 8897562-9 1996 Cyclophosphamide therapy for children with steroid-resistant FSGS is not recommended. Steroids 43-50 actinin alpha 4 Homo sapiens 61-65 8914044-9 1996 Idiopathic collapsing FSGS is a variant of FSGS with increasing incidence, distinct clinicopathologic features, black racial predominance, a rapidly progressive course and relative steroid resistance. Steroids 181-188 actinin alpha 4 Homo sapiens 22-26 8914044-9 1996 Idiopathic collapsing FSGS is a variant of FSGS with increasing incidence, distinct clinicopathologic features, black racial predominance, a rapidly progressive course and relative steroid resistance. Steroids 181-188 actinin alpha 4 Homo sapiens 43-47 9686959-1 1998 Patients with steroid-resistant focal and segmental glomerulosclerosis (FSGS) have a poor prognosis but may benefit from high-dose methylprednisolone or cyclosporine A therapy. Steroids 14-21 actinin alpha 4 Homo sapiens 72-76 9686959-11 1998 Steroid-resistant FSGS may be successfully treated with the described protocol. Steroids 0-7 actinin alpha 4 Homo sapiens 18-22 8971906-1 1996 If not aggressively treated, oral steroid-resistant (SRst) nephrotic focal segmental glomerulosclerosis (FSGS) is likely to progress to end-stage renal failure. Steroids 34-41 actinin alpha 4 Homo sapiens 105-109 7563952-10 1995 The FSGS + DP subgroup had a high incidence of denudation, vacuolization and detachment of podocytes, partial collapse of the glomerular basement membrane, and a very high incidence of resistance to steroid therapy. Steroids 199-206 actinin alpha 4 Homo sapiens 4-8 34383125-1 2022 BACKGROUND: Steroid-resistant nephrotic syndrome (SRNS), commonly caused by focal segmental glomerulosclerosis (FSGS), is associated with progression to stage 5 chronic kidney disease, requirement for kidney replacement therapy and a risk of disease recurrence post-kidney transplantation. Steroids 12-19 actinin alpha 4 Homo sapiens 112-116 2206894-0 1990 Treatment of steroid-resistant focal segmental glomerulosclerosis with pulse methylprednisolone and alkylating agents. Steroids 13-20 actinin alpha 4 Homo sapiens 31-65 2206894-1 1990 In children, steroid-resistant nephrotic syndrome due to focal segmental glomerulosclerosis (FSGS) is frequently a progressive condition resulting in end-stage renal disease. Steroids 13-20 actinin alpha 4 Homo sapiens 57-91 8203357-2 1994 Based on past experience, many nephrologists have considered primary FSGS a lesion that is steroid resistant and therefore are reluctant to offer steroids as treatment. Steroids 91-98 actinin alpha 4 Homo sapiens 69-73 8203357-3 1994 Recent data, however, have demonstrated that patients with primary FSGS have a response to steroid therapy that is considerably better than had been described. Steroids 91-98 actinin alpha 4 Homo sapiens 67-71 1994534-1 1991 Steroid-resistant FSGS and its recurrence posttransplantation are predominantly seen in children. Steroids 0-7 actinin alpha 4 Homo sapiens 18-22 34944624-1 2021 No effective treatments are available for familial steroid-resistant Focal Segmental Glomerulosclerosis (FSGS), characterized by proteinuria due to ultrastructural abnormalities in glomerular podocytes. Steroids 51-58 actinin alpha 4 Homo sapiens 69-103 33539328-8 2021 The patient had several FSGS relapses that were treated by different combinations of plasmapheresis, pulse steroid, mycophenolic acid, tacrolimus, prednisolone, IVIG, and IV rituximab. Steroids 107-114 actinin alpha 4 Homo sapiens 24-28 3280767-3 1988 Although this lesion resembles focal segmental glomerulosclerosis (FSGS), Howie and Brewer suggested that it constitutes a distinct entity, differing also clinically from FSGS, in that it would have a better response to steroid treatment. Steroids 220-227 actinin alpha 4 Homo sapiens 67-71 3280767-3 1988 Although this lesion resembles focal segmental glomerulosclerosis (FSGS), Howie and Brewer suggested that it constitutes a distinct entity, differing also clinically from FSGS, in that it would have a better response to steroid treatment. Steroids 220-227 actinin alpha 4 Homo sapiens 171-175 31396499-3 2019 However, this traditional classification system overlooks the frequent clinical conundrum when, for example, one patient with FSGS responds briskly to steroids, and another quickly progresses to end stage kidney disease despite therapy. Steroids 151-159 actinin alpha 4 Homo sapiens 126-130 32984227-12 2020 Nineteen percent of whites with FSGS were steroid-sensitive and none of the blacks with FSGS responded to corticosteroids. Steroids 42-49 actinin alpha 4 Homo sapiens 32-36 32943589-3 2020 METHODS: This historical cohort was carried out on 69 children affected by steroid resistant FSGS. Steroids 75-82 actinin alpha 4 Homo sapiens 93-97 31372025-11 2019 More importantly, the predominant histopathologic lesions associated with steroid resistance are FSGS (West Africa) and MCN/FSGS (South Africa), with mean prevalence rates of 57.2% and 36.1% respectively. Steroids 74-81 actinin alpha 4 Homo sapiens 97-101 31372025-11 2019 More importantly, the predominant histopathologic lesions associated with steroid resistance are FSGS (West Africa) and MCN/FSGS (South Africa), with mean prevalence rates of 57.2% and 36.1% respectively. Steroids 74-81 actinin alpha 4 Homo sapiens 124-128 31040189-1 2019 BACKGROUND: The etiology of steroid-resistant nephrotic syndrome, which manifests as FSGS, is not completely understood. Steroids 28-35 actinin alpha 4 Homo sapiens 85-89 27213154-1 2016 Focal segmental glomerulosclerosis (FSGS) is a common cause of end-stage renal disease and a common pathologic diagnosis of idiopathic nephrotic syndrome (NS), especially in steroid-resistant cases. Steroids 174-181 actinin alpha 4 Homo sapiens 0-34 31190951-2 2019 This steroid resistance among Nigerian children also reflects underlying renal histopathology, revealing a rare minimal-change disease and a varying burden of membranoproliferative glomerulonephritis and focal segmental glomerulosclerosis (FSGS). Steroids 5-12 actinin alpha 4 Homo sapiens 240-244 31190951-6 2019 Monogenic FSGS is primarily resistant to steroids, and this foreknowledge obviates the need for steroids, other immunosuppressive therapy, and renal biopsy. Steroids 41-49 actinin alpha 4 Homo sapiens 10-14 31190951-6 2019 Monogenic FSGS is primarily resistant to steroids, and this foreknowledge obviates the need for steroids, other immunosuppressive therapy, and renal biopsy. Steroids 96-104 actinin alpha 4 Homo sapiens 10-14 31056594-0 2019 THE METABOLOMICS SIGNATURE ASSOCIATED WITH RESPONSIVENESS TO STEROID THERAPY IN FOCAL SEGMENTAL GLOMERULOSCLEROSIS: A PILOT STUDY. Steroids 61-68 actinin alpha 4 Homo sapiens 80-114 31056594-1 2019 Background: Focal segmental glomerulosclerosis (FSGS) is considered one of the most severe glomerular diseases and around 80% of cases are resistant to steroid treatment. Steroids 152-159 actinin alpha 4 Homo sapiens 12-46 30550036-0 2018 [FSGS collapsing variant during anabolic steroid abuse: Case Report]. Steroids 41-48 actinin alpha 4 Homo sapiens 1-5 26467726-1 2016 Steroid-resistant nephrotic syndrome (SRNS) represents glomerular disease resulting from a number of different etiologies leading to focal segmental glomerulosclerosis (FSGS). Steroids 0-7 actinin alpha 4 Homo sapiens 169-173 28540445-8 2017 The FSGS group had a higher proportion of hypertension (40 vs. 15%; p = 0.02), hematuria (80 vs. 47%; p = 0.01), and nephritis (22 vs. 2%; p = 0.004) and was more likely to be steroid resistant after 6 weeks of treatment than the MCD group (67 vs. 19%; p < 0.001). Steroids 176-183 actinin alpha 4 Homo sapiens 4-8 28540445-11 2017 CONCLUSION: Steroid resistance after 6 weeks of therapy and/or nephritis at initial presentation is an accurate predictor of FSGS in children with NS and will be used as the indication for kidney biopsy in our newly developed clinical pathway. Steroids 12-19 actinin alpha 4 Homo sapiens 125-129 28776307-4 2017 Adult-onset FSGS/NS is often associated with low response to steroid treatment and immunosuppressive medication and poor renal survival. Steroids 61-68 actinin alpha 4 Homo sapiens 12-16 28405841-1 2017 BACKGROUND: Mutations in the AarF domain containing kinase 4 gene (ADCK4), one of the novel genes causing steroid-resistant nephrotic syndrome (SRNS), usually manifest as isolated adolescent-onset focal segmental glomerulosclerosis (FSGS). Steroids 106-113 actinin alpha 4 Homo sapiens 233-237 28405841-10 2017 CONCLUSIONS: ADCK4 mutations should be considered in older children presenting with steroid resistant FSGS. Steroids 84-91 actinin alpha 4 Homo sapiens 102-106 28937082-1 2017 Various immunomodulating agents have been tried for the treatment of steroid-resistant focal segmental glomerulosclerosis (FSGS) in the native kidney. Steroids 69-76 actinin alpha 4 Homo sapiens 123-127 28937082-3 2017 We report on the case of a 76-year-old male with steroid-resistant FSGS successfully treated with rituximab and remained in remission at the end of six months. Steroids 49-56 actinin alpha 4 Homo sapiens 67-71 28937082-5 2017 We conclude that rituximab is a potentially useful treatment for steroid resistant FSGS and larger controlled studies are needed to further define its role in this setting. Steroids 65-72 actinin alpha 4 Homo sapiens 83-87 27190346-1 2017 Background: NUP107 is a novel gene associated with autosomal recessive steroid-resistant nephrotic syndrome (SRNS) with focal segmental glomerulosclerosis (FSGS) in children. Steroids 71-78 actinin alpha 4 Homo sapiens 156-160 26820844-4 2017 Podocin gene (NPHS2) mutations cause childhood-onset steroid-resistant FSGS and MCD to adult-onset FSGS. Steroids 53-60 actinin alpha 4 Homo sapiens 71-75 27294131-1 2016 Focal segmental glomerulosclerosis (FSGS) is the most common cause of steroid resistant nephrotic syndrome in children. Steroids 70-77 actinin alpha 4 Homo sapiens 0-34 27294131-1 2016 Focal segmental glomerulosclerosis (FSGS) is the most common cause of steroid resistant nephrotic syndrome in children. Steroids 70-77 actinin alpha 4 Homo sapiens 36-40 26613029-1 2015 Primary focal segmental glomerulosclerosis (FSGS) is one of the major causes of steroid-resistant nephrotic syndrome, and renal prognosis in patients with steroid-resistant FSGS is poor. Steroids 80-87 actinin alpha 4 Homo sapiens 44-48 26670137-8 2015 75 % of the patients had idiopathic NS and among the patients that had idiopathic steroid resistant NS, FSGS was the most common followed by MPGN. Steroids 82-89 actinin alpha 4 Homo sapiens 104-108 26613029-1 2015 Primary focal segmental glomerulosclerosis (FSGS) is one of the major causes of steroid-resistant nephrotic syndrome, and renal prognosis in patients with steroid-resistant FSGS is poor. Steroids 155-162 actinin alpha 4 Homo sapiens 173-177 26115618-4 2015 METHODS: This was a study of 60 individuals, ages 3-38 years, with steroid-resistant FSGS enrolled in the FSGS clinical trial. Steroids 67-74 actinin alpha 4 Homo sapiens 85-89 25182141-0 2014 Predictive urinary biomarkers for steroid-resistant and steroid-sensitive focal segmental glomerulosclerosis using high resolution mass spectrometry and multivariate statistical analysis. Steroids 56-63 actinin alpha 4 Homo sapiens 74-108 25687382-7 2015 Resistance to steroids was higher in children with FSGS. Steroids 14-22 actinin alpha 4 Homo sapiens 51-55 25182141-2 2014 Since there is currently no diagnostic test that can accurately predict steroid responsiveness in FSGS, prediction of the responsiveness of patients to steroid therapy with noninvasive means has become a critical issue. Steroids 72-79 actinin alpha 4 Homo sapiens 98-102 23380388-1 2014 Our patient appears to represent a previously unrecognized variant of steroid-responsive minimal change disease (MCD)/focal and segmental glomerulosclerosis (FSGS) in which severe AKI developed even though the serum albumin was essentially normal and proteinuria was minimal. Steroids 70-77 actinin alpha 4 Homo sapiens 158-162 23380388-3 2014 To explain this paradox, it is suggested that our patient is a rare variant of a phenomenon that is well documented in steroid-responsive MCD/FSGS, specifically, glomerular permeability to large molecules is increased (accounting for the proteinuria) but decreased to small molecules (accounting for the low glomerular filtration rate). Steroids 119-126 actinin alpha 4 Homo sapiens 142-146 21178977-1 2011 Optimal therapy of patients with steroid-resistant primary focal segmental glomerulosclerosis (FSGS) remains controversial. Steroids 33-40 actinin alpha 4 Homo sapiens 59-93 22895884-1 2013 An 11 y -old boy with steroid resistant nephrotic syndrome (SRNS) secondary to focal segmental glomerulosclerosis (FSGS) developed pericardial tamponade during the course of illness. Steroids 22-29 actinin alpha 4 Homo sapiens 79-113 22895884-1 2013 An 11 y -old boy with steroid resistant nephrotic syndrome (SRNS) secondary to focal segmental glomerulosclerosis (FSGS) developed pericardial tamponade during the course of illness. Steroids 22-29 actinin alpha 4 Homo sapiens 115-119 21804085-14 2012 CONCLUSIONS: Results from this study show that half of adults with primary FSGS achieve sustained remission with prolonged steroid treatment and consequently exhibit an excellent prognosis for long-term outcome. Steroids 123-130 actinin alpha 4 Homo sapiens 75-79 22288013-3 2012 However, with the recognition of hereditary FSGS caused by mutations podocyte slit diaphragm genes, it is increasingly clear that the steroid-resistant form of FSGS that recurs in the renal allografts (R-FSGS) constitutes a distinct clinical entity. Steroids 134-141 actinin alpha 4 Homo sapiens 44-48 22288013-3 2012 However, with the recognition of hereditary FSGS caused by mutations podocyte slit diaphragm genes, it is increasingly clear that the steroid-resistant form of FSGS that recurs in the renal allografts (R-FSGS) constitutes a distinct clinical entity. Steroids 134-141 actinin alpha 4 Homo sapiens 160-164 22669525-6 2011 The authors suggest that anabolic steroid abuse is a direct cause of FSGS. Steroids 34-41 actinin alpha 4 Homo sapiens 69-73 21110043-1 2011 Focal and segmental glomerulosclerosis (FSGS) is an important cause of steroid-resistant nephrotic syndrome in adults and children. Steroids 71-78 actinin alpha 4 Homo sapiens 40-44 23760382-14 2013 There was mixed response of collapsing FSGS to steroids. Steroids 47-55 actinin alpha 4 Homo sapiens 39-43 23689573-12 2013 Steroid-resistant FSGS patients had a worse histological severity of glomerular sclerosis than steroid-dependent patients (p < 0.01). Steroids 0-7 actinin alpha 4 Homo sapiens 18-22 22334613-1 2012 Focal segmental glomerulosclerosis (FSGS) is a common cause of steroid-resistant nephrotic syndrome in children and adults. Steroids 63-70 actinin alpha 4 Homo sapiens 0-34 22334613-1 2012 Focal segmental glomerulosclerosis (FSGS) is a common cause of steroid-resistant nephrotic syndrome in children and adults. Steroids 63-70 actinin alpha 4 Homo sapiens 36-40 21960168-1 2011 Patients with steroid-resistant focal segmental glomerulosclerosis (FSGS) may benefit from treatment with calcineurin inhibitors. Steroids 14-21 actinin alpha 4 Homo sapiens 32-66 21960168-1 2011 Patients with steroid-resistant focal segmental glomerulosclerosis (FSGS) may benefit from treatment with calcineurin inhibitors. Steroids 14-21 actinin alpha 4 Homo sapiens 68-72 21355056-1 2011 Steroid-resistant focal segmental glomerulosclerosis (FSGS) often recurs after renal transplantation. Steroids 0-7 actinin alpha 4 Homo sapiens 54-58 21178977-1 2011 Optimal therapy of patients with steroid-resistant primary focal segmental glomerulosclerosis (FSGS) remains controversial. Steroids 33-40 actinin alpha 4 Homo sapiens 95-99 20733489-1 2010 PURPOSE OF REVIEW: Steroid-resistant nephrotic syndrome/focal segmental glomerulonephritis (FSGS) is the primary renal disease in approximately 10% of pediatric patients receiving a renal allograft. Steroids 19-26 actinin alpha 4 Homo sapiens 92-96 20419325-2 2010 Of 21 girls with steroid-resistant nephrotic syndrome secondary to focal segmental glomerulosclerosis (FSGS) who were screened for mutations in the WT1 gene, two showed Frasier syndrome. Steroids 17-24 actinin alpha 4 Homo sapiens 103-107 20419325-6 2010 This report highlights the need for screening for mutations in the WT1 gene in girls with steroid-resistant FSGS. Steroids 90-97 actinin alpha 4 Homo sapiens 108-112 17504846-1 2007 BACKGROUND: The rate of complete remission after induction therapy for steroid-resistant nephrotic syndrome (SRNS) due to either focal segmental glomerulosclerosis (FSGS) or minimal change nephrotic syndrome (MCNS) has been reported to be <50%. Steroids 71-78 actinin alpha 4 Homo sapiens 165-169 20718182-13 2010 The use of immunosuppressive treatment in conjunction with prolonged steroid seems beneficial in primary FSGS in children. Steroids 69-76 actinin alpha 4 Homo sapiens 105-109 19956976-0 2010 Analysis of recessive CD2AP and ACTN4 mutations in steroid-resistant nephrotic syndrome. Steroids 51-58 actinin alpha 4 Homo sapiens 32-37 20061699-9 2010 Steroid therapy increases the chances of remission and preserves renal function in patients with sporadic primary FSGS. Steroids 0-7 actinin alpha 4 Homo sapiens 114-118 19303679-4 2009 We describe results for 3 patients treated with a combination of low-dose steroids and rapamycin for FSGS, focusing on the importance of maintaining low drug (rapamycin) levels by using a twice-daily regimen. Steroids 74-82 actinin alpha 4 Homo sapiens 101-105 18785907-2 2009 The main clinical findings are spondyloepiphyseal dysplasia with disproportionate growth restriction, defective cellular immunity, and steroid-resistant nephrotic syndrome secondary to biopsy proven FSGS leading to ESRF. Steroids 135-142 actinin alpha 4 Homo sapiens 199-203 18853198-6 2009 We speculate that infants with steroid-resistant nephrotic syndrome due to FSGS may benefit from tight control of hypertension, mainly though early blockade of the renin-angiotensin axis. Steroids 31-38 actinin alpha 4 Homo sapiens 75-79 18443213-0 2008 Bigenic heterozygosity and the development of steroid-resistant focal segmental glomerulosclerosis. Steroids 46-53 actinin alpha 4 Homo sapiens 64-98 18443213-1 2008 BACKGROUND: Focal segmental glomerulosclerosis (FSGS) is a major cause of steroid-resistant nephrotic syndrome in childhood with a central role for the podocytes in the pathogenesis. Steroids 74-81 actinin alpha 4 Homo sapiens 12-46 17995521-14 2007 In this viewpoint, it can also be said that FSGS is the most severe form of MCNS in which the initial injury is the greatest, so the majority of patients with FSGS are non-responders to steroid and progress to chronic renal failure. Steroids 186-193 actinin alpha 4 Homo sapiens 44-48 17995521-14 2007 In this viewpoint, it can also be said that FSGS is the most severe form of MCNS in which the initial injury is the greatest, so the majority of patients with FSGS are non-responders to steroid and progress to chronic renal failure. Steroids 186-193 actinin alpha 4 Homo sapiens 159-163 17437129-2 2007 There are, however, limited longitudinal pediatric data on prevalence, demographics, and steroid responsiveness in FSGS. Steroids 89-96 actinin alpha 4 Homo sapiens 115-119 17437129-4 2007 Compared with non-FSGS children, FSGS children were older at diagnosis (6.9 years vs 4.4 years, P<0.02), more likely girls (54% vs 28%, P<0.02), Black or Hispanic (42% vs 16%, P<0.001), and the FSGS was more likely to be steroid resistant (73% vs 10%, P<0.001). Steroids 230-237 actinin alpha 4 Homo sapiens 33-37 17437129-4 2007 Compared with non-FSGS children, FSGS children were older at diagnosis (6.9 years vs 4.4 years, P<0.02), more likely girls (54% vs 28%, P<0.02), Black or Hispanic (42% vs 16%, P<0.001), and the FSGS was more likely to be steroid resistant (73% vs 10%, P<0.001). Steroids 230-237 actinin alpha 4 Homo sapiens 33-37 17437129-8 2007 In contradistinction to non-FSGS children, there was a marked increase in steroid resistance with FSGS (43% vs 62% vs 86%; P=0.03). Steroids 74-81 actinin alpha 4 Homo sapiens 98-102 17942957-1 2007 Mutations in NPHS2, the gene that encodes podocin, are well-established causes of both familial and sporadic steroid-resistant focal segmental glomerulosclerosis (FSGS) in the pediatric population, but have not been well-characterized in late-onset disease. Steroids 109-116 actinin alpha 4 Homo sapiens 127-161 17942957-1 2007 Mutations in NPHS2, the gene that encodes podocin, are well-established causes of both familial and sporadic steroid-resistant focal segmental glomerulosclerosis (FSGS) in the pediatric population, but have not been well-characterized in late-onset disease. Steroids 109-116 actinin alpha 4 Homo sapiens 163-167 17699384-8 2007 In this latter cohort, compound heterozygous mutations were detected only in one patient with steroid-sensitive FSGS (R229Q and Q285fsX302) and no homozygous mutations. Steroids 94-101 actinin alpha 4 Homo sapiens 112-116 17498006-0 2007 A case report of plasmapheresis and cyclophosphamide for steroid-resistant focal segmental glomerulosclerosis: recovery of renal function after five months on dialysis. Steroids 57-64 actinin alpha 4 Homo sapiens 75-109 18336100-14 2007 IN CONCLUSIONS: our results suggest that abnormal distribution and reduced expression of synaptopodin may be associated with poor response to steroid therapy in MCD and FSGS. Steroids 142-149 actinin alpha 4 Homo sapiens 169-173 16874699-7 2006 The absence of mutations in all other patients evaluated suggests its rarity in sporadic cases of adult-onset (steroid sensitive or resistant) FSGS in our population. Steroids 111-118 actinin alpha 4 Homo sapiens 143-147 16939069-10 2006 CONCLUSIONS: This report demonstrates the useful role of cyclophosphamide in the treatment of steroid-resistant nephrotic syndrome due to FSGS with glomerular tip lesion. Steroids 94-101 actinin alpha 4 Homo sapiens 138-142 16792133-1 2006 BACKGROUND: Steroid resistance and steroid dependence constitute a major problem in the treatment of minimal-change disease and focal segmental glomerulosclerosis (FSGS). Steroids 12-19 actinin alpha 4 Homo sapiens 164-168 16792133-1 2006 BACKGROUND: Steroid resistance and steroid dependence constitute a major problem in the treatment of minimal-change disease and focal segmental glomerulosclerosis (FSGS). Steroids 35-42 actinin alpha 4 Homo sapiens 164-168 16429836-1 2006 AIMS: We herein report the results of intravenous pulse cyclophosphamide (IVCP) therapy of 5 patients with steroid-resistant focal segmental glomerulosclerosis (FSGS). Steroids 107-114 actinin alpha 4 Homo sapiens 161-165 16429836-12 2006 CONCLUSION: We found that IVCP had a limited beneficial effect in treatment of steroid-resistant FSGS and it may be suggested that IVCP can be tried to treat steroid-resistant patients, also for patients with primary steroid resistance and those who do not respond to other immunosuppressive therapies. Steroids 79-86 actinin alpha 4 Homo sapiens 97-101 17699197-1 2006 Calcineurin inhibitors are effective therapy for steroid-resistant focal segmental glomerulosclerosis (FSGS) but are associated with significant morbidity and nephrotoxicity. Steroids 49-56 actinin alpha 4 Homo sapiens 103-107 17699197-11 2006 In patients with steroid-resistant FSGS, sirolimus reduced proteinuria and glomerular pore size and increased K(f) in patients with steroid-resistant FSGS. Steroids 17-24 actinin alpha 4 Homo sapiens 35-39 16020995-0 2005 Effects of steroids in focal segmental glomerulosclerosis in a predominantly African-American population. Steroids 11-19 actinin alpha 4 Homo sapiens 23-57 17699197-11 2006 In patients with steroid-resistant FSGS, sirolimus reduced proteinuria and glomerular pore size and increased K(f) in patients with steroid-resistant FSGS. Steroids 132-139 actinin alpha 4 Homo sapiens 150-154 16020995-2 2005 Prolonged treatment with steroids is recommended for FSGS in those with nephrotic-range proteinuria, but strong evidence for this recommendation, especially in African-American adults, is lacking. Steroids 25-33 actinin alpha 4 Homo sapiens 53-57 16020995-3 2005 We reviewed our experience with steroids in FSGS in a predominantly African-American cohort. Steroids 32-40 actinin alpha 4 Homo sapiens 44-48 16245248-1 2005 We report our experience in using mycophenolate mofetil (MMF) for the treatment of steroid-resistant focal segmental glomerulosclerosis (FSGS) in two patients. Steroids 83-90 actinin alpha 4 Homo sapiens 137-141 15942677-3 2005 We studied 7 sera from patients with steroid-resistant FSGS, 3 from patients with nephrotic syndrome caused by non-immune disease, and 6 from healthy subjects. Steroids 37-44 actinin alpha 4 Homo sapiens 55-59 16245248-4 2005 Our observation illustrates that MMF could be useful in treating steroid-resistant FSGS if administered at an early phase of the disease, well before histologic damage becomes irreversible. Steroids 65-72 actinin alpha 4 Homo sapiens 83-87 12607970-0 2002 [A case of focal segmental glomerulosclerosis(FSGS) complicated with chronic hepatitis B and treated with steroid and LDL apheresis]. Steroids 106-113 actinin alpha 4 Homo sapiens 46-50 14738302-0 2003 Nephrotic syndrome after conversion to alternate day steroids in two children with a history of recurrent FSGS. Steroids 53-61 actinin alpha 4 Homo sapiens 106-110 15585516-12 2005 CONCLUSION: MtDNA abnormalities can cause a steroid-resistant nephrotic syndrome, histologically characterized by FSGS. Steroids 44-51 actinin alpha 4 Homo sapiens 114-118 12704575-1 2003 The pathologic diagnosis of focal segmental glomerulosclerosis (FSGS) is associated with a syndrome of steroid-resistant nephrotic syndrome and progressive renal insufficiency. Steroids 103-110 actinin alpha 4 Homo sapiens 64-68 12704583-0 2003 Primum non nocere: Should adults with idiopathic FSGS receive steroids? Steroids 62-70 actinin alpha 4 Homo sapiens 49-53 12704583-1 2003 Corticosteroids have been widely recommended for the treatment of patients with idiopathic focal segmental glomerulosclerosis (FSGS), despite the lack of evidence-based data to support the use of steroids in this disease. Steroids 7-15 actinin alpha 4 Homo sapiens 127-131 12704583-5 2003 The Glomerular Disease Collaborative Network"s experience with steroids in idiopathic FSGS has shown a low rate of remission even when steroids were used in the recommended doses and for prolonged periods. Steroids 63-71 actinin alpha 4 Homo sapiens 86-90 12704583-5 2003 The Glomerular Disease Collaborative Network"s experience with steroids in idiopathic FSGS has shown a low rate of remission even when steroids were used in the recommended doses and for prolonged periods. Steroids 135-143 actinin alpha 4 Homo sapiens 86-90 12704583-7 2003 The controversies regarding steroids in idiopathic FSGS will only be resolved with data from controlled clinical trials. Steroids 28-36 actinin alpha 4 Homo sapiens 51-55 11729243-0 2001 Prevalence, genetics, and clinical features of patients carrying podocin mutations in steroid-resistant nonfamilial focal segmental glomerulosclerosis. Steroids 86-93 actinin alpha 4 Homo sapiens 116-150