4th International Conference on Nephrology & Therapeutics September 14-16, 2015 Baltimore, USA

Ali Manouchehri has completed his MD at the age of 25 years from Hormozgan University of Medical Sciences ,Bandar Abbas School of Medicine. He is the registered physisian of C-ICU at Namazi hospital (shiraz medical university hospital).He has had many presentations at reputed domestic and international medical conferences.

Objective: Antithymocyte globulin (ATG) is an effective induction therapy after renal transplantation which reduces the rates of acute rejection. In this article a prospective study is designed to investigate the effectiveness and complications of ATG use compared with those who received steroid after transplantation. Material and Method: All kidney allograft recipients who underwent transplantation from June 2009 till June 2012 were enrolled for the study (n=167). Of the recipients, those who experienced kidney rejection during the first 24 hours after operation were excluded (n=15).The recipients were allocated to the high risk group for rejection received ATG (n=54) while low risk group received steroid therapy (n=98). The final efficacy end point consisting of acute rejection, graft loss, death and treatment side effects including thrombocytopenia, leukopenia and cytomegalovirus infection (CMV) were studied for 12 months after transplantation. Results: Here, it is shown that the use of ATG was accompanied by lower incidence of acute rejection (3.7% vs. 21.4%), graft loss (11.1% vs. 17.3%), cytomegalovirus infection (12.9% vs. 14.2%), leukopenia (12.9% vs. 24.4%) and thrombocytopenia (14.8% vs. 24.4%) in the high risk recipients receiving ATG. Furthermore, it is demonstrated that indicators of long term renal function including BUN and Cr are less reduced in the high risk population (2.98 and 3.74 vs. 2.22 and 1.89 for Cr; P-value: 0.002 and 0.17; 56.88 and 39.11 vs. 36.66 and 28.41 for BUN; P-value < 0.05). The use of ATG improved these parameters before the first year of transplantation (1.75 and 1.54 vs. 1.61 and 1.43 for Cr; P-value: 0.65, 0.72; 23.20 and 18.59 vs. 22.30 and 18.90 for BUN; P-value: 0.74, 0.90). Conclusion: ATG was accompanied by lower rates of leukopenia, thrombocytopenia, CMV infection and acute graft rejection compared to those who received steroid therapy for induction of immunosuppression after renal transplantation. Therefore it is concluded that the ATG induction therapy is a reasonable approach especially in high risk recipients for the prevention of graft rejection , improving long term prognosis with similar side effects as with steroid therapy, all of which indicate ATG effectiveness, especially in the recipients with high risk of graft rejection.

Zafer Demirer has completed his MD at the age of 35 years Gulhane Medical Faculty, School of Medicine and postdoctoral studies from Gulhane Medical Faculty, School of Medicine. He is the director of Eskisehir Military Hospital. He has published more than 20 papers in reputed journals. Also, he has published 5 articles about kidney disease.

Background & Aims: Adult’s kidneys tumor classification expands rapidly with new categories which are including recently being incorporated tumors also. Mixed epithelial stromal tumor of the kidney (MESTs) was recently described and unusual entity. This rare complex renal neoplasm composed of a mixture of cystic and solid components. Although mesoblastic nephroma mostly detected in during the first few weeks of life, the first case of adult mesoblastic nephroma which was grossly and microscopically similar to congenital mesoblastic nephroma was described in 1973 (2). These tumors also termed as benign mixed epithelial and stromal tumor (MESTs) by Michal and Syrucek in 1998 (3). Since then, it has been reported with different names which are leiomiyomatous renal hamartoma, adult type congenital mesoblastic nephroma, adult metanephric stromal tumor, cystic hamartoma of renal pelvis, solitary multilocular cysts of the kidney and multilocular renal cyst with mullerian-like stroma (2-4). Herein, we report unusual tumor of the kidney which abundant stroma and devoid of epithelial component. Material & Methods or Patient & Methods: A 22-year old female presented with a palpable right-sided abdominal mass and microscopic hematuria. She had no history of hipertension, and all laboratuary values were normal. A 15 cm heterogenous solid, right renal mass which was displacing the renal parenchyma revealed by contrast-enhanced CT scan without adenopathies Renal mass was also confirmed by MR imaging and there was marked displacement of the inferior vena cava without tumoral infiltration (Figure 1A). A: Upper abdominal MR showing large solid renal mass pushing the renal parenchyma to the posteromedially. B and C: Radical nephrectomy material (A) and on the cut surface there were seen a huge tan-grey mass compressing to normal renal parenchyma Histological sections representing mesenchymal component of the tumor: Results: We performed open right radical nephrectomy. Gross examination revealed a large, tan-gray solid mass, compressing the adjacent renal parenchyma (Figure 1B). On the cut surface, an encapsulated tan-gray renal mass with 14x13x12 cm in dimension was detected (Figure 1C). There was no any cystic change and it had completely solid appearance. Microscopic examination revealed a well-circumscribed mesenchymal tumor consisting of mostly intersecting fascicles of spindle cells with abundant intercellular collagen (Figure 2 A and B). The lesion also focally consisted of hypocellular areas with myxoid changes (Figure 2 C and D). The lesion was devoid of epithelial component and tubule or gland like epithelial structures within the Müllerian stroma at periphery of the tumor (Figure 2 E and F). The final pathologic diagnosis was adult mesoblastic nephroma with no atypical features. Convalescence was uneventfull and she discharged 4 th day of the surgery. The patient was free of disease on the 18-months follow-up examination. Conclusions: (MEST) is a rare neoplasm of the kidney. 25% of the subjects were detected incidentally and they consist 0.20 to 0.28 percent of renal tumors. The main differential diagnosis of (MEST) is renal cell carcinoma. For accurate diagnosis, histopathologic examination is a gold standard Key words: Adulthood kidney tumor, mesoblastic nephroma, mixed epithelial and stromal tumor

Khalid elsiddig Khalid has completed his Bachelor of medicine and surgery by the age of 23 from the university of Khartoum faculty of medicine, had an extensive bioinformatics workshop conducted by Phd holder in Moleculr genetics.

Nephrotic syndrome is a nonspecific kidney disorder characterized by a number of signs of disease: proteinuria, hypoalbuminemia and edema.It is characterized by an increase in permeability of the capillary walls of the glomerulus leading to the presence of high levels of protein in the urine.NPHS2 is encoding Podocin an important protein in renal filtration function. Analysis of the genetic variation that can alter the expression and the function of the NPHS2 gene was done using computational methods. Genomic analysis of NPHS1 was initiated By Sift and Polyphen-2 servers and yielded 18 mutations to be damaging , the mutant amino acids biophysical characteristics and multiple sequence alignment were demonstrated to be affecting the protein function using Align-GVGD and Panther platforms.11 mutations affected protein function the most. Genetic co-expression profile and interactions were demonstrated by GeneMANIA server, and NPHS2 is found to be co-expressed with a neuronal protein,3D structure molding was done using Phyre2 and Chimera. Computational methods yield accurate results which can be a basis of diagnosis of steroid resistant nephrotic syndrome.

The nephron numbers individually varies in various mammalian species. In any renal diseases with reduced nephron mass, nephrons never regenerate because mature kidneys already lose their stem cells. Recently it has been reported that birth weight is related to nephron mass. The low birth weight leads to reduced nephron numbers and high risks for chronic kidney disease (CKD). Thus, the pathogenesis of CKD caused by nephron reduction is thought to be important for prognosis of such CKD patients. So we focused on hypoplastic kidney (HPK) with 80% nephron reduction in affected rats of HGNII strain. The affected HPK rats have a loss-of-function mutation on the gene encoding a microtubule-associated protein, Astrin. Although it has been reported that Astrin is required for mitotic progression in HeLa cells, in vivo function of Astrin especially in renal development and its’ involvement to renal diseases have not yet been established. Based on our previous reports (NDT 2005; 20: 1362-9, Pediatric Nephrol 2006; 21: 637-42, Congenit Anom (Kyoto) 2007; 47: 34-44), we have hypothesized that the defect of Astrin might be related with development and prognosis of CKD. In the present study, we immunohistologically examined the progression of CKD in HPK rats at 5-30 weeks of age. In HPK rats at 5 weeks of age, the glomerulus already hypertrophied and exhibited infiltration of macrophages, increased TGF-β and fibronectin levels and desquamation of podocytes (discontinuity of podocin staining in glomerulus). In affected glomerulus at 20 weeks of age afterward, we found high levels of PDGF and its receptor, increases of mesangial cells and extracellular matrixes (ECMs) including collagen type 1, collagen type 4 and fibronectin and epithelial-mesenchymal transition in Bowman’s capsule. In the interstitium of HPK, we found increases of PDGF receptor β-positive fibroblasts at all week’s examined and α-SMA positive myofibroblasts after 10 weeks afterwards, indicating the transition from fibroblast to myofibroblast. Then we observed age-related accumulation of ECMs with increased levels of PDGF. Consisting with these changes, we observed hematological symptoms of renal dysfunction with age-related deterioration. These results suggested that congenital 80% nephron reduction due to loss of Astrin results in progressive renal fibrosis and glomerulosclerosis and that genetic abnormality of Astrin is one of the possible risk factors for CKD. Recently, it has been reported that Astrin is a negative mTOR regulator of stress response in HeLa cells (Cell 2013; 154: 859-74).We will discuss the possibility that Astrinis related with embryonic pathogenesis of HPK.