Glomerulopathy does not increase renal susceptibility to acute ischemic injury

1984 ◽  
Vol 246 (3) ◽  
pp. F272-F281 ◽  
Author(s):  
R. A. Zager ◽  
L. A. Baltes ◽  
H. M. Sharma ◽  
W. G. Couser
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Nephrotic Syndrome ◽  
Renal Injury ◽  
Artery Occlusion ◽  
Minimal Change ◽  
Glomerular Injury ◽  
Bilateral Renal Artery ◽  
Foot Process ◽  
Ischemic Renal Injury

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.

Acute Renal Failure and Tubular Dysfunction Associated with Minimal Change Nephrotic Syndrome

1989 ◽  
Vol 4 (10) ◽  
pp. 914-916 ◽  
Author(s):  
M. Praga ◽  
M. A. Martinez ◽  
A. Andres ◽  
M. Alvarez de Buergo ◽  
I. Bello ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Nephrotic Syndrome ◽  
Minimal Change Nephrotic Syndrome ◽  
Minimal Change ◽  
Tubular Dysfunction

Minimal-Change Nephrotic Syndrome with Acute Renal Failure Associated with Missed Abortion

Nephron ◽  
1998 ◽  
Vol 80 (2) ◽  
pp. 234-236
Author(s):  
Gakusen Nishihara ◽  
Masahiko Nakamoto ◽  
Chikao Yasunaga ◽  
Harumichi Higashi ◽  
Shunya Matsuo ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Nephrotic Syndrome ◽  
Minimal Change Nephrotic Syndrome ◽  
Minimal Change ◽  
Missed Abortion

Hepatocyte growth factor accelerates recovery from acute ischemic renal injury in rats

1994 ◽  
Vol 266 (1) ◽  
pp. F129-F134 ◽  
Author(s):  
S. B. Miller ◽  
D. R. Martin ◽  
J. Kissane ◽  
M. R. Hammerman
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Renal Injury ◽  
Artery Occlusion ◽  
Brdu Incorporation ◽  
Tubular Epithelium ◽  
Nitrogen Levels ◽  
Bilateral Renal Artery ◽  
Ischemic Renal Injury ◽  
Hepatocyte Growth

Effects of hepatocyte growth factor (HGF) administration were examined in a model of acute ischemic renal injury induced by bilateral renal artery occlusion in rats. Compared with rats administered vehicle, rats administered 20 micrograms HGF subcutaneously 30 min postischemia had significantly lower serum creatinine and blood urea nitrogen levels over the course of 7 days postocclusion, enhanced insulin clearances measured on day 2 postocclusion, reduced mortality, and much less injury evident by examination of kidney histologies 7 days postinjury. The tubular regeneration that occurred postischemic injury was reflected by increased incorporation of 5-bromo-2'-deoxyuridine (BrdU) in cortical tubular epithelium compared with incorporation in kidneys from noninjured rats. HGF enhanced BrdU incorporation compared with vehicle, indicating enhanced mitogenesis. The weight loss that occurs postischemic injury was not ameliorated by the dose of HGF we employed. We conclude that administration of HGF postischemic injury to rats stimulates the recovery of normal kidney function and the regeneration of proximal tubular epithelium.

Acute Renal Failure in Minimal Change Nephrotic Syndrome

1988 ◽  
Vol 139 (6) ◽  
pp. 1382-1382
Author(s):  
J.E. Springate ◽  
J.F. Coyne ◽  
M.P. Karp ◽  
L.G. Feld
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Nephrotic Syndrome ◽  
Minimal Change Nephrotic Syndrome ◽  
Minimal Change

Escherichia coli endotoxin injections potentiate experimental ischemic renal injury

1986 ◽  
Vol 251 (6) ◽  
pp. F988-F994 ◽  
Author(s):  
R. A. Zager
Keyword(s):  
Escherichia Coli ◽  
Adverse Effect ◽  
Renal Injury ◽  
Tissue Injury ◽  
Maintenance Phase ◽  
Artery Occlusion ◽  
E Coli ◽  
Initiation Phase ◽  
Bilateral Renal Artery ◽  
Ischemic Renal Injury

The purpose of this study was to assess the influence of Escherichia coli endotoxin on the evolution of ischemic acute renal failure (ARF). Rats were subjected to 25 min of bilateral renal artery occlusion (RAO) plus subcutaneous/intraperitoneal injections of either boiled E. coli or purified E. coli endotoxin (1.5 mg). Boiling the E. coli renders them nonviable but leaves endotoxin intact. Ischemic controls were injected with saline. The E. coli injections exacerbated ischemic ARF, doubling the degree of azotemia and increasing the extent of tubular necrosis and cast formation. This occurred without an adverse effect on renal blood flow or blood pressure during the initiation phase or maintenance phase of the ARF. Endotoxin tolerant rats were totally protected against the E. coli-ARF potentiating effect. Neither Staphylococcus aureus nor E. coli with denatured endotoxin adversely affected ischemic injury. Purified E. coli endotoxin reproduced the E. coli-ARF potentiating action. Neither E. coli nor purified endotoxin induced azotemia in the absence of renal ischemia. Conclusion: E. coli endotoxin can exacerbate ischemic renal injury without compromising renal hemodynamics. This action appears to be mediated by an adverse effect of endotoxin on critical subcellular determinants of ischemic tissue injury.

Body temperature: an important determinant of severity of ischemic renal injury

1986 ◽  
Vol 251 (1) ◽  
pp. F87-F93 ◽  
Author(s):  
R. A. Zager ◽  
R. Altschuld
Keyword(s):  
Body Temperature ◽  
Renal Injury ◽  
Degradation Products ◽  
Oxidant Stress ◽  
High Energy ◽  
Artery Occlusion ◽  
High Energy Phosphates ◽  
Renal Histology ◽  
Bilateral Renal Artery ◽  
Ischemic Renal Injury

To assess the effects of body temperature on renal susceptibility to ischemic injury, rats were rendered acutely hypothermic (90-93 degrees F), normothermic (98-99 degrees F), or hyperthermic (101-103 degrees F) with a heat-controlled surgical board and then were subjected to 25 min of bilateral renal artery occlusion (RAO). Renal high-energy phosphates, their degradation products, and nonprotein sulfhydryl (NPSH) content were assessed at selected times during the peri-ischemic period. The severity of acute renal failure (ARF) was determined for 48 h following RAO by blood urea nitrogen (BUN) and plasma creatinine determinations and by renal histology. Ischemic ATP, ADP, AMP, GTP, GDP, UTP, and NAD levels and postischemic NPSH levels (15 min reflow) inversely correlated with temperature (P less than 0.001). BUN, creatinine concentrations (at 24 and 48 h), and histological injury (at 48 h) directly correlated with temperature (P less than 0.01). Hyperthermia in the absence of RAO had no demonstrable adverse renal effects. We conclude that hyperthermia potentiates ischemic renal injury, whereas hypothermia confers protection. These effects are associated with, and may be influenced by, temperature-induced changes in renal high-energy phosphate availability and oxidant stress during the ischemic/postischemic period.

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