Focal segmental glomerulosclerosis: molecular genetics and targeted therapies

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Term Occurence Count Dictionary
Reflux nephropathy 1 nephrologydiseases
cyclosporine 1 nephrologydiseasesdrugs
focal segmental glomerulosclerosis 1 nephrologydiseases
lupus nephritis 2 nephrologydiseases
mycophenolate mofetil 1 nephrologydiseasesdrugs
nephrotic syndrome 1 nephrologydiseases
rituximab 1 nephrologydiseasesdrugs
chronic kidney disease 2 nephrologydiseases
glomerulonephritis 2 nephrologydiseases
prednisone 6 nephrologydiseasesdrugs
tacrolimus 2 nephrologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
cyclosporine 16533 immunosuppressive therapy with alkylating agents. However, mutation analysis should not be used to discard cyclosporine (CSA) as a therapeutic agent. Recently, it has been shown that the APOL1 risk genotype does not influence
mycophenolate mofetil 16684 Recently, it has been shown that the APOL1 risk genotype does not influence proteinuria responses to CSA or mycophenolate mofetil (MMF)/dexamethasone in idiopathic FSGS patients enrolled in the National Institutes of Health (NIH)-sponsored
prednisone 23113 considered only in idiopathic FSGS associated with clinical features of the NS (1C). KDIGO suggested prednisone be given at a daily single dose of 1 mg/kg (maximum 80 mg) or alternate-day dose of 2 mg/kg (maximum
prednisone 24106 C-low, and D-very low [[91]]). A variety of nonrandomized retrospective studies have reported that prednisone induces 40 to 80 % rates of complete or partial remission.Treatment of SR FSGSFor SR FSGS, the KDIGO
prednisone 24893 patients previously failed to achieve a remission of the proteinuria after a minimum of eight weeks of prednisone at ≥ 1 mg/kg/day. The major entry criteria were proteinuria ≥ 3.5 g/d and creatinine clearance ≥ 42 ml/min/1.73 m2.
prednisone 25115 clearance ≥ 42 ml/min/1.73 m2. Patients with CG were excluded. 26 weeks of CSA treatment plus low-dose prednisone was compared to placebo plus prednisone. Despite relapses after CSA was discontinued, at the end of
prednisone 25155 CG were excluded. 26 weeks of CSA treatment plus low-dose prednisone was compared to placebo plus prednisone . Despite relapses after CSA was discontinued, at the end of long term follow-up of 104 weeks, there
prednisone 26128 given in addition to 46 pulse doses of DEX for 12 months. In addition, both arms were treated with prednisone , 0.3 mg/kg, every other day for the first 6 months and angiotensin-converting enzyme inhibitor (or
rituximab 27467 against the CD20 antigen expressed in human B cells. There are conflicting results regarding the use of rituximab in FSGS, and it has been unclear exactly how this drug achieves success in some patients, but not others
tacrolimus 25480 directly stabilize podocyte actin cytoskeleton [[93]]. There are no randomized clinical trials using tacrolimus . Uncontrolled studies suggest that tacrolimus may be an alternative in patients intolerant of CSA [[94],
tacrolimus 25526 [[93]]. There are no randomized clinical trials using tacrolimus. Uncontrolled studies suggest that tacrolimus may be an alternative in patients intolerant of CSA [[94], [95]].In a recent NIH-funded multicenter
Select Disease Character Offset Disease Term Instance
Reflux nephropathy 4089 hyperfiltration4.1 Reduced kidney mass Oligomeganephronia Unilateral kidney agenesis Kidney dysplasia Reflux nephropathy Surgical kidney ablation Chronic allograft nephropathy Any advanced kidney disease with reduction
chronic kidney disease 14073 sometimes. For example, patients with two APOL1 renal risk alleles are prone to develop hypertension and chronic kidney disease complicated by FSGS [[61]]. In such patients, is FSGS primarily due to a specific genetic predisposition
chronic kidney disease 29410 APOL1 genetic risk variants in conferring susceptibility to common kidney diseases, including FSGS, chronic kidney disease , and hypertension, is evolving. In addition, the development of NGS has revealed that FSGS can arise
focal segmental glomerulosclerosis 271 date (pmc-release): 7/2015Publication date (collection): /2015AbstractRecent advances show that human focal segmental glomerulosclerosis (FSGS) is a primary podocytopathy caused by podocyte-specific gene mutations including NPHS1, NPHS2,
glomerulonephritis 4469 anemia5. Malignancy (lymphoma)6. Nonspecific pattern of FSGS caused by kidney scarringFocal proliferative glomerulonephritis (IgA nephropathy, lupus nephritis, pauci-immune focal necrotizing and crescentic glomerulonephritis)Hereditary
glomerulonephritis 4569 glomerulonephritis (IgA nephropathy, lupus nephritis, pauci-immune focal necrotizing and crescentic glomerulonephritis )Hereditary nephritis (Alport syndrome)Membranous glomerulopathyThrombotic microangiopathyModified from
lupus nephritis 4506 Nonspecific pattern of FSGS caused by kidney scarringFocal proliferative glomerulonephritis (IgA nephropathy, lupus nephritis , pauci-immune focal necrotizing and crescentic glomerulonephritis)Hereditary nephritis (Alport syndrome)Membranous
lupus nephritis 10533 historically attributed to hypertension, FSGS or the collapsing variant, sickle cell nephropathy, and severe lupus nephritis in AAs. The risk variants G1 (S342G:I384M) and G2 (del.N388/Y389) are two coding variants in the APOL1
nephrotic syndrome 1132 recognized in the 20th century as a histopathological pattern of glomerular injury associated with nephrotic syndrome (NS) [[1]]. It is a lesion rather than a disease with morphologic variations including tip, perihilar,

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