53 ERA Poster printing financially sponsored by:  Focal segmental glomerulosclerosis (FSGS), a histologic pattern of glomerular injury, defines a number of clinicopathologic syndromes that may be primary (idiopathic) or secondary [1].  Early in the disease process, the pattern of glomerulosclerosis is focal, involving a minority of glomeruli, and segmental, involving a portion of the glomerular tuft [1].  Patients with primary FSGS present with asymptomatic proteinuria or full nephrotic syndrome. Hypertension is found in 30% to 50% of children and adults with FSGS at diagnosis. Microhematuria is found in 25% to 75% of these patients, and a decreased GFR is noted at presentation in 20% to30% [2].  Kidney transplantation is a treatment, not a cure as it does not necessarily remove the cause of the original kidney disease. Glomerulonephritis (GN) and diabetes are the two leading causes of end-stage renal disease (ESRD) worldwide and both diseases may recur [3].  Nowadays FSGS is the most common kidney disease known to recur after kidney transplantation. Recurrence rate of FSGS is 30% to 50% in adults. A reliable estimate is approximately 30% to 40% at a first graft, with an exponential increment of risk (up to 80%) at subsequent renal grafts [4]. 1-D’Agati VD (2011): "Podocyte injury can be catching". J Am Soc Nephrol. 22: 1181- 1183. 2-Johnson JR., Feehally J and Floege R (2014): "Primary and secondary causes of FSGS". Comprehensive clinical nephrology. 18: 220-222. 3-Cole EH., Johnston O., Rose CL and Gill JS (2008): "Impact of acute rejection and new- onset diabetes on long-term transplant graft and patient survival". Clin J Am Soc Nephrol.3: 814-821. 4-Hickson LJ., Gera M., Amer H., Iqbal CW., Moore TB., Milliner DS., Cosio FG., Larson TS., Stegall MD., Ishitani MB., Gloor JM and Griffin MD (2009): "Kidney transplantation for primary focal segmental glomerulosclerosis: Outcomes and response to therapy for recurrence". Transplantation. 87: 1232-1239. References: Methods:  FSGS group and non-glomerular diseases groups were comparable regarding demographic data, pre-transplant immunological data, pre-transplant medical disorders and frequency of acute rejection episodes. Post-transplant medical complications as hypertension, diabetes mellitus and 5- year graft function and survival were also comparable.  The use of steroids was significantly more frequent among FSGS group than the non-glomerular group. This could be explained by the more attention and precautions of FSGS recurrence by giving more steroids in such cases.  Graft survival was comparable between both groups with no clinically and statistically significant difference. At last follow up, 50 out of 88 patients with FSGS were living with functioning graft at while 64 out of 96 patients with non-glomerular diseases were living with functioning graft.  When the outcome of FSGS group was compared with other glomerular diseases group; demographic data, pre-transplant immunological data, pre-transplant medical disorders and frequency of acute rejection episodes were comparable. Likewise, post-transplant medical complications hypertension, diabetes mellitus, bacterial infection and CMV disease and 5-year graft survival and function were comparable.  On the other hand, there was a significant difference in the type of calcineurin inhibitors used in both groups. Cyclosporine was more frequently used among FSGS group while tacrolimus was more frequently used among the group of other glomerular diseases.  The data that was obtained from the last 2 comparison underline the fact that patients affected by FSGS can obtain a good graft survival even in the long term. Even if recurrence occurred, plasmapharesis and anti-CD 20 use improved the outcome.  We could conclude from this study that a good graft outcome could be obtained when kidney transplantation to FSGS patients and FSGS patients shouldn`t be excluded from transplantation.  Younger recipient age and younger onset of FSGS are the only risk factors have been proved in this study.  Pre-transplant plasmapharesis didn`t statistically affect the graft outcome but clinically, evaluation upon more patients is needed.  We recommend:  Performing pre-transplant plasmapharesis even only for high risk patients.  Strict follow up for proteinuria after kidney transplantation. Once recurrence is suspected, we recommend starting plasmapharesis sessions and/or anti-CD 20.  Genetic analysis is important and should be done especially for recurrent FSGS patient to determine whether to re-transplant or not on the base that recurrence occurs more frequently in patients with no NPHS2 gene mutation while no recurrence occur in patients with mutations particularly if homozygous.  Urinary podocyte specific mRNA P.C.R should be done as screen tests for all FSGS patients after kidney transplantation as early recurrence detector. Plasmapharesis should be started immediately if +ve results were obtained.  Protocol for prophylactic post-transplant plamapharesis for high risk patients is controversial. This retrospective single Centre study included 357 kidney transplant recipients who were transplanted at Mansoura urology & nephrology Centre, Egypt between June 1976 and December 2013.Patients divided into three groups according to the original kidney disease (OKD); group I all FSGS patients as OKD (88 patients),this group will be subdivided into 2 groups (non-recurrent FSGS group and recurrent FSGS group post-transplant, group II all glomerular disease other than FSGS (173 patients), group III Non-glomerular disease as OKD (96 patients). In each visit recipients were subjected to: Thorough clinical examination, Laboratory investigations: Renal profile ;S creatinine., Urine analysis: microscopy and dipstick, CBC , Immunosuppressive drug level (each visit). CsA, Tacrolimus:, Sirolimus assay for whole blood trough level. Liver function test (every 6 ms).Total serum cholesterol (annually).Radiological and Histopathological examination of the graft biopsy in cases of graft dysfunction: Statistical analysis: The findings were recorded, tabulated and analyzed using SPSS for windows (SPSS inc. Chicago). T test was used to compare the continuous data between the two groups. Categorical data were compared using chi square test. The graft and patient survival were computed using the Kaplan-Meier technique. P-value < 0.05 was considered statistically significant. Results: Conclusions: Objectives: FOCAL SEGMENTAL GLOMERULOSCLEROSIS AS ORIGINAL KIDNEY DISEASE FOR LIVING DONOR KIDNEY TRANSPLANTATION RECIPIENTS. I- Comparison between FSGS and non-glomerular diseases groups Comparison between recurrent FSGS and non-recurrent FSGS groups II- Comparison between FSGS and other glomerular diseases groups Demographic and immunological data FSGS (No=88) Non-glomerular disease (No=96) P-value Recipient age(M ± SD) years 26.19 ± 9.5 28.46± 10.93 0.137 Recipient gender 0.802 Male 62(70.5%) 66(68.8%) Donor age(M ± SD) years 37.02 ± 11.02 37.66 ± 9.86 0.683 Donor gender 0.969 Male 41 (46.6%) 45(46.9%) Immunological workup: A) HLA class I matching 0.82 Four mismatch 8(9%) 7(7.3%) Three mismatch 8(9%) 8(8.3%) Two mismatch 52(59%) 50(52%) One mismatch 9(10.2%) 12(12.5%) Zero mismatch 4(4.5%) 7(7.3%) Inapplicable 7(8.3%) 12(12.6%) B) HLA class II (DR) matching 0.507 Zero mismatch 16(18.2%) 14(14.3%) One mismatch 72(81.8%) 82(85.4%) Prior blood transfusion 38(42.2%) 41(42.7%) 0.578 Induction of immunosuppressive therapy: FSGS (No=88) Non-glomerular disease (No=96) P-value ATG 10(11.5%) 9(9.5%) 0.260 Basiliximab 28(32%) 46(48.4%) NO INDUCTION 50(56.5%) 41(42.1%) Immunosuppressive therapy: FSGS (No=88) Other glomerular diseases (No=173) P-value Steroid-based 83(94.3%) 144(83.2%) 0.012 Tacrolimus-based 19(21.6%) 67(38.7%) 0.005 Cyclosporine-based 53(60.2%) 76(43.9%) 0.013 Mycophenolate mofetil-based 29(33%) 66(38.2%) 0.410 Azathioprine-based 50(56.8%) 86(49.7%) 0.277 Sirolimus-based 5(5.7%) 11(6.4%) 0.829 Demographic and immunological data FSGS (No=88) Other glomerular diseases (No=173) P-value Recipient age(M ± SD) years 26.19 ± 9.5 25.8 ± 9.925 0.761 Recipient gender 0.268 Male 62(70.5%) 110(63.6%) Donor age(M ± SD) years 37.02 ± 111.02 36.47 ± 10.022 0.683 Donor gender 0.683 Male 41(46.6%) 77(44.8%) Immunological workup: A) HLA class I matching 0.483 Four mismatch 4(4.55%) 11(6.36%) Three mismatch 9(10.23%) 18(10.4%) Two mismatch 51(57.95%) 81(46.82%) One mismatch 8(9.09%) 25(14.45%) Zero mismatch 8(9.09%) 14(8.1%) Inapplicable 8(9.09%) 24(13.87%) B) HLA class II (DR) matching 0.396 Zero mismatch 16(18.2%) 24(13.87%) One mismatch 72(81.8%) 149(86.13%) Prior blood transfusion 38(42.2%) 76(43.9%) 0.229 Induction of immunosuppressive therapy: FSGS (No=88) Other glomerular diseases (No=173) P-value ATG 10(11.5%) 19(11%) 0.399 Basiliximab 2832%) 78(45.3%) NO INDUCTION 50(56.5%) 76(43.7%) Immunosuppressive therapy: FSGS (No=88) Other glomerular diseases (No=173) P-value Steroid-based 83(94.3%) 144(83.2%) 0.012 Tacrolimus-based 19(21.6%) 67(38.7%) 0.005 Cyclosporine-based 53(60.2%) 76(43.9%) 0.013 Mycophenolate mofetil-based 29(33%) 66(38.2%) 0.410 Azathioprine-based 50(56.8%) 86(49.7%) 0.277 Sirolimus-based 5(5.7%) 11(6.4%) 0.829 Demographic and immunological data Recurrent FSGS (No=35) Non-recurrent FSGS (No=53) P-value Recipient age(M ± SD) years 23.74 ± 8.4 27.8 ± 9.87 0.042 Recipient gender 0.871 Male 25(71.4%) 37(69.8%) Donor age(M ± SD) years 34.46 ± 11.18 38.7 ± 10.68 0.076 Donor gender 0.314 Male 14(40%) 27(50.9%) Age at diagnosis of FSGS 19.13 ± 10.5 24.028± 10.22 0.03 Immunological workup: A) HLA class I matching 0.173 Four mismatch 3(8.6%) 1(2%) Three mismatch 5(14.3%) 4(7.8%) Two mismatch 19(54.3%) 33(62.7%) One mismatch 4(11.4%) 4(7.8%) Zero mismatch 4(11.4%) 4(7.8%) Inapplicable 0 7(11.9%) B) HLA class II (DR) matching 0.417 One mismatch 30(85.7%) 42(78.8%) Zero mismatch 5(14.3%) 11(21.2%) P-value Non-recurrent FSGS (No=53) Recurrent FSGS (No=35) Pre-transplant medical disorders 0.457 26(49.1%) 20(57.1%) Pre-transplant hypertension 0.882 4(7.6%) 3(8.6%) Pre-transplant diabetes mellitus 0.804 2(3.8%) 1(2.9%) Pre-transplant HCV infection 0.23 12(63%) 13(86%) Mesangial proliferation in native kidney biopsy (36 patients) 0.245 51(96.2%) 35(100%) Pre-transplant dialysis 0.831 12(0, 96) 21(1, 48) Dialysis duration (months) Median, range 0.224 18 (2, 120) 24(2, 168) Duration between FSGS diagnosis and starting dialysis (months) Median, range Induction of immunosuppressive therapy: Recurrent FSGS (No=35) Non-recurrent FSGS (No=53) P-value ATG 3(8.8%) 7(13.8%) 0.106 Basiliximab 12(34.3%) 16(31.4%) NO INDUCTION 20(56.9%) 30(54.9%) Pre-transplant plasma exchange 8(22.9%) 7(13.2%) 0.239 Immunosuppressive therapy: Recurrent FSGS (No=35) Non-recurrent FSGS (No=53) P-value Steroid-based 35(100%) 48(90.6%) 0.061 Tacrolimus-based 7(20%) 12(22.6%) 0.768 Cyclosporine-based 26(74.3%) 27(50.9%) 0.029 Mycophenolate mofetil-based 10(28.6%) 19(35.8%) 0.477 Azathioprine-based 19(54.3%) 31(58.5%) 0.697 Sirolimus-based 2(5.7%) 3(5.7%) 0.991 Number and types of rejection episodes: Recurrent FSGS (No=35) Non-recurrent FSGS (No=53) P-value Number of acute rejection No rejection 13(36.4%) 23(43.4%) 0.711 One episode 14(40%) 17(32%) Two episodes 6(17.7%) 9(17.1%) Three episodes 2(5.9%) 2(3.75%) Four episodes 0 2(3.75%) Chronic rejection 13(37.1%) 13(25%) 0.155 Response to treatment modalities of FSGS recurrence post-transplant: No response Partial remission Complete remission ACEI`s & lipid lowering drugs (17 patients) 8 9 0 I.V pulse steroid (3 patients) 0 1 2 I.V Cyclophosphamide (3 patients) 2 0 1 Plasmapharesis (9 patients)* 0 4 5 Anti-CD20 (3 patients)** 0 1 2 *Protocol of 10 sessions every other day then monthly for 6 to 12 months **375mg/m^2 weekly for 4 weeks Figure (1): Graft survival among the three groups Figure (2): Patient survival among the three groups 729--MP AYMAN NAGIB DOI: 10.3252/pso.eu.53era.2016 Renal transplantation. Clinical. Dept. of dialysis and transplantation, The Urology & Nephrology Center, Mansoura University, Egypt . Ahmed Yahia Elmowafy, Amir Mohamed El-Okely, Ayman Maher Nagib, Mohammed Fouad Ahmed, Mohamed Hamed Abbas and Ayman Fathy Refaie.