Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28509120
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
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
): 12-17
PMID28509120
show 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.
free
free
free
