Bilateral Cortical Necrosis of the Kidneys

Duff, G. W.; Murray, Edward

doi:10.1097/00000441-194103000-00033

Cited by 81 publications

(12 citation statements)

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“…Diseases such as subacute bacterial endocarditis (23), malaria (24), Rocky Mountain spotted fever (25), typhoid fever (26), Gram-negative septicemias (27), Dengue fever (28), and meningococcal infections (29) have been noted to be associated with thrombocytopenia. Consequences of overwhelming sepsis such as renal cortical necrosis and adrenal hemorrhagic thrombosis of the Waterhouse-Friderichsen type have been attributed to intravascular coagulation (30)(31)(32)(33) and may well evolve in part at least from platelet injury.…”

Section: Discussionmentioning

confidence: 99%

Effects of Bacterial Endotoxin on Rabbit Platelets

Prez

Bryant

1966

The Journal of Experimental Medicine

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When endotoxin is injected by vein it is immediately fixed onto platelets (1). Both in vivo and in vitro studies have further shown that endotoxin causes rapid aggregation and disappearance of blood platelets, accelerates coagulation, and promotes release of several intracellular platelet factors with physiological activity (2-5). It has thus appeared likely that this platelet-endotoxin ~nteraction may play a role in the earliest phases of removal of endotoxin from the blood stream.While a superficially similar form of platelet aggregation and release of platelet factors is produced by thrombin, previous studies have shown that the effects of endotoxin and of thrombin on platelets differ in several important respects (6). The blood of most mammals contains antibodies to endotoxin (7). Because antigen-antibody interactions also produce platelet aggregation and release of intraceUular components (8-11), the present studies explored the thesis that platelet-endotoxin interaction might be a special instance of platelet damage by antigen-antibody complexes. These experiments compare the divalent ion requirements of these two types of platelet injury. They have led to the tentative hypothesis that antigen-antibody and endotoxin injury may be identical in nature, and secondary to platelet phagocytosis. Materials and MethodsRabbit blood obtained by cardiac puncture was delivered directly through plastic tubing into cold sterile siliconized centrifuge tubes containing anticoagulant solutions to provide a final mixture of one part anticoagulant to nine parts blood. Piatelet-rich plasma and plateletpoor plasma were prepared by centrifugation as previously described and contained from 4 to 8 X 10 s platelets per milliliter (2). Platelet-rich plasma prepared directly from heparinized blood contained a much lower concentration of platelets due to spontaneous platelet clumping in this anticoagulant under the conditions employed. Accordingly, heparinized platelet-rich plasma was prepared by collection of blood in NaEDTA, preparation of platelet-rich plasma,

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Section: Discussionmentioning

confidence: 99%

Effects of Bacterial Endotoxin on Rabbit Platelets

Prez

Bryant

1966

The Journal of Experimental Medicine

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“…There is also growing evidence that males and females have different abilities to tolerate the renal injury (15). Sexual dimorphism in renal injury has been a recognized clinical entity for at least 65 years, and sex steroid effects on renal tissue have been investigated for at least 30 years (5,11). However, there is no information concerning sex differences about the protective effect of new methods of conditionings in the kidney.…”

mentioning

confidence: 99%

Postconditioning is protective in renal reperfusion injury only in male rats. A gender difference study

Mahmoudi¹,

Kadkhodaee²,

Golab³

et al. 2015

Acta Physiologica Hungarica

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Purpose:We investigated the impact of sex on the protective effect of postconditioning (POC), a series of brief ischemia-reperfusion (IR) cycles at the reperfusion onset, as a recently described novel approach to attenuate renal IR injury. In this study, the left renal pedicles of uni-nephrectomized male and female rats were clamped for 45 minutes followed by 24 hours of reperfusion as IR groups. Uni-nephrectomized, sham-operated male and female rats served as control groups. Ischemic postconditioning was performed using 4 cycles of 10 seconds IR of renal pedicle at the end of the ischemia. Twenty-four hours later, BUN (blood urea nitrogen), plasma creatinine (Cr), and renal histological changes, as well as kidney levels of MDA (malondialdehyde) and SOD (superoxide dismutase) as oxidative stress markers were evaluated to detect the protective effect of POC against IR injury in rats. Results: Induction of IR resulted in significant reduction in renal function, demonstrated by increase in plasma Cr and BUN, histological changes and oxidative stress in both genders. Application of POC afforded significant protection against these injuries in male rats, namely decreased levels of BUN and Cr, histological improvements and less oxidative damages. However, there were no significant differences in the above-mentioned parameters in female rats. Conclusion: While POC is shown to be beneficial against renal IR injury in male rats, it did not show any protective effect in female rats.

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“…The causation of the ischaemia is uncertain. The theories that have been postulated to explain the ischaemia have been reviewed by Duff & Murray (1941) and Lauler & Schreiner (1958). The renal lesion in our patient must have occurred soon after the bite, because the anuria commenced on the day that he was bitten.…”

Section: Necropsymentioning

confidence: 85%