Recovery of Minimal Change Nephrotic Syndrome and Acute Renal Failure in a Patient withRenal Cell Carcinoma

1998 ◽  
Vol 18 (5) ◽  
pp. 433-435 ◽  
Author(s):  
Teresa Auguet ◽  
Alfons Lorenzo ◽  
Enrique Colomer ◽  
Alberto Zamora ◽  
Carmen García ◽  
...  
1989 ◽  
Vol 4 (10) ◽  
pp. 914-916 ◽  
Author(s):  
M. Praga ◽  
M. A. Martinez ◽  
A. Andres ◽  
M. Alvarez de Buergo ◽  
I. Bello ◽  
...  

Nephron ◽  
1998 ◽  
Vol 80 (2) ◽  
pp. 234-236
Author(s):  
Gakusen Nishihara ◽  
Masahiko Nakamoto ◽  
Chikao Yasunaga ◽  
Harumichi Higashi ◽  
Shunya Matsuo ◽  
...  

1988 ◽  
Vol 139 (6) ◽  
pp. 1382-1382
Author(s):  
J.E. Springate ◽  
J.F. Coyne ◽  
M.P. Karp ◽  
L.G. Feld

2008 ◽  
Vol 67 (2) ◽  
pp. 137-140
Author(s):  
Takashi Maruyama ◽  
Machiko Uga ◽  
Jin Ikeda ◽  
Yuuki Matsumi ◽  
Chinami Nagura ◽  
...  

1988 ◽  
Vol 77 (7) ◽  
pp. 1031-1036
Author(s):  
Masahito TSUJI ◽  
Shigeru MOTOHASHI ◽  
Shigeru YOMOGIDA ◽  
Yoshihiro ARIMURA ◽  
Akio INOUE ◽  
...  

1984 ◽  
Vol 246 (3) ◽  
pp. F272-F281 ◽  
Author(s):  
R. A. Zager ◽  
L. A. Baltes ◽  
H. M. Sharma ◽  
W. G. Couser

To determine whether preexistent glomerular injury and the nephrotic syndrome increase renal susceptibility to ischemic renal injury, normal rats and rats with either experimental minimal-change disease (Adriamycin nephropathy) (AN) or membranous nephropathy (passive Heymann nephritis) (PHN) underwent renal functional and histologic studies under either basal conditions or 18 h after bilateral renal artery occlusion (over 30 min). Prior to renal ischemia AN and PHN rats had minimally depressed glomerular filtration rate (GFR), normal (AN) or increased (PHN) renal blood flow (RBF), heavy proteinuria, hypoalbuminemia, decreased urine sodium excretion, extensive glomerular foot process fusion, and intratubular hyalin cast formation. Losses of GFR in response to ischemia were comparable among the three groups of rats (controls, 0.29; AN, 0.28; PHN, 0.25 ml X min-1 X 100 g body wt-1) despite prevailing differences in postischemic hemodynamics. Neither light nor transmission electron microscopy showed any differences in the degree of ischemic renal injury. These results suggest that 1) glomerulopathy and the nephrotic syndrome do not significantly increase renal susceptibility to ischemic renal injury; 2) the syndrome of acute renal failure that occurs in patients with minimal-change glomerulopathy is not due to a marked susceptibility of these kidneys to clinically occult ischemic events; and 3) foot process fusion is probably not a pathophysiologically significant lesion in ischemic acute renal failure, as previously suggested.


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