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10.1007/s13730-016-0235-0 http://scihub22266oqcxt.onion/10.1007/s13730-016-0235-0 C5438800!5438800!28509120     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 280.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 280.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 280.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 280.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 280.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 314.4 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       CEN+Case+Rep 2017 ; 6 (1): 12-7 Nephropedia Template TP {{tp|p=28509120|t=2017. Complex glomerular pathology of thrombotic microangiopathy and focal segmental glomerulosclerosis forms tumor-like mass in a renal transplant donor with severe renovascular hypertension |pdf=|usr=}}{{28509120}} gab.com Text Complex glomerular pathology of thrombotic microangiopathy and focal segmental glomerulosclerosis forms tumor-like mass in a renal transplant donor with severe renovascular hypertension JO: CEN Case Rep http://www.kidney.de/pget.php?&tw=1&pmid=28509120 #FOAvip The pathogenesis of glomerular hypertension-mediated FSGS and its histological variations in humans remains unknown. A 47-year-old man developed nephrotic syndrome, renal dysfunction, and malignant hypertension 2 years after donating a kidney to his son. The donor?s remnant kidney developed renal mass at an upper pole which was fed by an aberrant artery that branched from the root of the renal artery. Furthermore, the main non-aberrant renal artery demonstrated severe stenosis that caused renovascular hypertension, resulting in malignant hypertension. Upon radiological examinations, a tumorous mass was detected. Because of progressive renal dysfunction, nephrectomy was performed. The kidney revealed a diffuse distribution of complex FSGS lesions, i.e., a random combination of cellular/collapsing FSGS and glomerular thrombotic microangiopathy, confined to the renal mass, whereas such lesions were absent in the non-mass portion. This indicated that severe glomerular hypertension alone caused FSGS with TMA features. Heterogeneous FSGS lesions let us surmise that glomerular hypertension promoted simultaneous damages in endothelial cells and podocytes, which synergistically progressed to glomerulosclerosis. This unique case uncovers causal relationships between unusual glomerular hypertension and severe forms of FSGS that was possibly caused by the disruption of homeostasis sustained by podocytes and endothelial cells. Twit Text FOAVip Complex glomerular pathology of thrombotic microangiopathy and focal segmental glomerulosclerosis forms tumor-like mass in a renal transplant donor with severe renovascular hypertension ????CEN Case Rep http://www.kidney.de/pget.php?&tw=1&pmid=28509120 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28509120 #FOAvip English Wikipedia <ref>{{Cite pmid|28509120}}</ref> Complex glomerular pathology of thrombotic microangiopathy and focal segmental glomerulosclerosis forms tumor-like mass in a renal transplant donor with severe renovascular hypertension #MMPMID28509120 Nagata M; Yamaguchi Y; Toki D; Yamamoto I; Shinmura H; Kawaguchi H CEN Case Rep 2017[May]; 6 (1): 12-7 PMID28509120show ga The pathogenesis of glomerular hypertension-mediated FSGS and its histological variations in humans remains unknown. A 47-year-old man developed nephrotic syndrome, renal dysfunction, and malignant hypertension 2 years after donating a kidney to his son. The donor?s remnant kidney developed renal mass at an upper pole which was fed by an aberrant artery that branched from the root of the renal artery. Furthermore, the main non-aberrant renal artery demonstrated severe stenosis that caused renovascular hypertension, resulting in malignant hypertension. Upon radiological examinations, a tumorous mass was detected. Because of progressive renal dysfunction, nephrectomy was performed. The kidney revealed a diffuse distribution of complex FSGS lesions, i.e., a random combination of cellular/collapsing FSGS and glomerular thrombotic microangiopathy, confined to the renal mass, whereas such lesions were absent in the non-mass portion. This indicated that severe glomerular hypertension alone caused FSGS with TMA features. Heterogeneous FSGS lesions let us surmise that glomerular hypertension promoted simultaneous damages in endothelial cells and podocytes, which synergistically progressed to glomerulosclerosis. This unique case uncovers causal relationships between unusual glomerular hypertension and severe forms of FSGS that was possibly caused by the disruption of homeostasis sustained by podocytes and endothelial cells. äComplex glomerular pathology of thrombotic microangiopathy and focal s(epmc).pdf DeepDyve Pubget Overpricing