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PubMed1975

Renal cortical necrosis induced in rabbits by local perfusion followed by systemic administration of endotoxin.

In an experimental model adapted to avoid severe systemic lesions, renal cortical necrosis was frequently induced in rabbits by repeated administration of endotoxin. The experimental model involves perfusion of the kidney in situ with endotoxin. Another dose of endotoxin was given intravenously 24-28 h before or after the perfusion. A significant effect of the perfusion or the endotoxin administered first was reflected by the pronounced unilateral morphological alterations appearing after the second administration of endotoxin. Some of the kidneys with cortical necrosis had band- or ring-shaped areas of preserved juxtamedullary tissue. Heavy infiltration of leukocytes at the borders of these areas called for commentation of the histological picture of infarcts, incorrectly described even in most modern textbooks.

Animals↗
PubMed1983

[Characteristics of kidney involvement in disseminated intravascular coagulation (morphogenesis of cortical necrosis)].

Morphological examinations of 72 autopsy observations of the disseminated intravascular blood coagulation (DIVBC) syndrome (a combination of microthrombosis in renal glomeruli, adrenals, gastrointestinal tract and other organs with the hemorrhagic syndrome) led to a conclusion on the role of DIVBC in the formation of cortical renal necroses. All the observations presented capillary thrombosis of the renal glomeruli the extent and dissemination of which had influenced the size of cortical necroses. Cortical ischemia in early stages is manifested by nephrothelium dystrophy followed at 3-5 days by the development of necrosis of the tubules, glomeruli, and stroma. The formed cortical necroses of the kidneys (CNK) are demarkated, their healing occurs at the expense of the interstitial tissue, whose cells proliferate, and later collagen genesis is observed. Scars from CNK have been shown to contain tubules with an undifferentiated epithelium.

Adult↗
PubMed1982

Effects of continuous intravenous infusion of Escherichia coli endotoxin into swine.

Escherichia coli endotoxin was continuously infused IV into 31 pigs. The response was related to the infusion rate. Of 13 pigs given endotoxin at the rate of 15.4 and 23.1 micrograms/kg of body weight/hour, 10 had bilateral renal cortical necrosis similar to a generalized Shwartzman lesion. All 13 pigs given endotoxin at the rate of 6.6 to 12.1 micrograms/kg/hour survived the infusion and were euthanatized 7 to 12 days later. Most of the pigs that developed chronic neurologic disturbances were given the smaller dose of endotoxin. Of 5 pigs given endotoxin at the rate of 22.0 to 23.1 micrograms/kg/hour after receiving 200 U of sodium heparin/kg of body weight, 1 died during the 48-hour period of infusion and the 4 pigs euthanatized 8 to 12 days later had lesions that were similar to those produced by endotoxin without heparin. The 4 control pigs given continuous IV infusion of isotonic saline solution at a rate of 30 dl/hour had no clinical signs or pathologic lesions. The continuous IV infusion of endotoxin into pigs at various doses produced similar clinical signs of endotoxic shock. Pigs that died acutely had widespread thrombosis. The hematologic findings indicated an intravascular coagulopathy and some of the clinical signs and lesions in the pigs resembled changes in the CNS in pigs with spontaneous edema disease (ED); however, distinct differences were also observed. Fibrinoid vascular necrosis did not occur in the CNS, and this lesion is consistently present in naturally occurring ED. The exact nature of the causal substance or substances causing ED is still unknown, but is considered an angiotoxin associated with hemolytic E coli.

Animals↗
PubMed1989

The roles of glucocorticosteroid and of fibrinolytic activity in the development of bilateral renal cortical necrosis in cycloheximide-treated mice challenged with a submicrogram dose of endotoxin.

Mice given cycloheximide and 0.2 microgram of endotoxin simultaneously developed ischaemic bilateral renal cortical necrosis as part of a fatal syndrome. Endotoxin given 2 h after cycloheximide, although fatal, failed to produce renal cortical necrosis. Investigation suggested that, following endotoxin challenge in cycloheximide-treated mice, the occurrence or non-occurrence of bilateral renal cortical necrosis was determined by the concentration of circulating glucocorticoids at the time of endotoxin challenge. Thus, below a certain, as yet undefined, glucocorticoid concentration, endotoxin does not cause renal cortical necrosis in cycloheximide-treated mice. Inhibition of the fibrinolytic system by epsilonaminocaproic acid (EACA) indicated that protection against renal cortical necrosis was directly mediated by increased fibrinolytic activity. Since this increased activity occurred during a period of profound cycloheximide-mediated inhibition of protein synthesis, it was postulated that pre-existing plasminogen activator was released from inhibition, and that this release could only occur when the glucocorticoid concentration fell below a certain critical value.

Aminocaproic Acid↗
PubMed1985

[Characteristics of destructive-regenerative processes in the kidneys of albino rats in conditions of necronephrosis caused by corrosive sublimate].

Study of serial semi-thin (0.5 micron) metacrylate and paraffinic (8 microns) of rat kidney sections 6, 12, 24 and 48 h after subcutaneous injection of mercury bichloride at a dose of 0.6 mg/100 g bw has revealed that injury to different parts of the canalicular nephron is of heterogeneous character. The proximal part of the nephron demonstrates both complete and partial necrosis of nephrocyte cytoplasm. The distal parts of the nephron and collecting tubules are characterized by partial necrosis of the apical cytoplasm. Within the period between 12 and 24 h after the mercury bichloride injection, intracellular reparative processes are observed, in addition to destruction, in partially damaged but viable nephrocytes, which is confirmed by the enlargement of the nucleolic size. Regeneration of the tubular epithelium due to cellular restoration was unmarked 24 h after the mercury bichloride injection.

Animals↗
PubMed1994

Acute renal cortical necrosis--a study of 113 patients.

Over a 28-year period, 113 out of 2986 (3.8%) patients dialysed for acute renal failure at a referral center in North India were diagnosed to have acute renal cortical necrosis (ACN). Obstetric causes were responsible for ACN in 56.6% patients and nonobstetric causes in 43.4%. Within the obstetric group, ACN developed in association with complications of late pregnancy in 37.1% and following septic abortion in 19.5%. The various nonobstetric causes included viperine snake bite in 14.2%, hemolytic uremic syndrome in 11.5%, renal allograft rejection in 5.3%, acute gastroenteritis in 4.4%, acute pancreatitis in 3.5%, septicemia in 2.7%, and trauma and drug-induced IV hemolysis in 0.9% patients. Total anuria was the commonest presenting feature and was noted in 78.8% of patients. Renal histology showed diffuse cortical necrosis in 62.8% and patchy lesions in 37.2% patients. Computerized tomography (CT scan) of the kidneys revealed characteristic diagnostic findings in all the 5 patients in whom it was done. Dialytic support could be withdrawn as a result of improvement in renal function in 19 patients with patchy cortical necrosis. Dialysis-free survival of as long as 12 years has been recorded. The present study shows that, in contrast to the Western world, ACN continues to be a common cause of acute renal failure in developing countries. CT scan of the kidneys is helpful in establishing an early diagnosis.

Acute Kidney Injury↗
PubMed1995

Case report: the diagnostic value of contrast-enhanced computed tomography in acute bilateral renal cortical necrosis.

Acute bilateral renal cortical necrosis is a relatively rare cause of acute renal failure accounting for only 2% of cases in the Western World. The pathophysiology of this condition is complex, but ultimately leads to the destruction of the renal cortex with sparing of the renal medulla. A definitive diagnosis is based on renal histology. In this report we describe a patient in whom this diagnosis was made using contrast-enhanced computed tomography as renal biopsy was contraindicated.

Acute Kidney Injury↗
PubMed1985

An animal model of haemolytic--uraemic syndrome in shigellosis: lipopolysaccharides of Shigella dysenteriae I and S. flexneri produce leucocyte-mediated renal cortical necrosis in rabbits.

To develop an animal model of the haemolytic-uraemic syndrome during shigellosis, rabbits were injected with lipopolysaccharides (LPS) extracted by the hot phenol-water method from Shigella dysenteriae I and from S. flexneri. Two intravenous injections of LPS spaced by 24 h elicited renal cortical necrosis in a generalized Shwartzman reaction characterized by fibrin deposition in glomerular capillaries and by elevated plasma creatinine concentration. Rabbits rendered leucopenic by busulphan treatment were protected against renal cortical necrosis after injection with LPS derived from S. dysenteriae I. Both LPS preparations derived from Shigella species were also active in producing fever in rabbits, death in rabbits, and gelation of limulus lysate with approximately the same potency as a standard LPS of E. coli 055:B5. These results demonstrated that the LPS of Shigella species given intravenously to rabbits produces renal cortical necrosis, which is caused by leucocyte-mediated intravascular fibrin deposition in renal blood vessels and which resembles histologically the renal lesion in the haemolytic-uraemic during shigellosis in humans.

Animals↗
PubMed1995

[Renal arterial disease-induced tubulo-interstitial lesions].

Renal arterial disease-induced tubulo-interstitial lesions described in this chapter include benign arterio- and/or arteriolo-sclerotic and malignant nephrosclerosis, renal infarction and renal cortical necrosis. In these conditions renal glomeruli as well as tubules are always involved, and consequent loss of nephrons, or renal parenchyma results in interstitial fibrotic changes. The parenchymal lesions have a spectrum from slowly progressive atrophy and loss to necrosis of abrupt onset and disappearance of glomeruli and tubules. As for glomerular reactions to the ischemia, the intermediate type consisted of mesangial degeneration and epithelial cell proliferation described as "alterative glomerulitis" is noteworthy. Briefly, in renal arterial diseases, glomeruli are rather variably involved than tubules and loss of the parenchyma results in interstitial fibrosis.

Arteriosclerosis↗
PubMed1987

Renal and cerebral necrosis in survivor after in utero death of co-twin.

A newborn with bilateral renal cortical necrosis and severe cerebral damage in association with a macerated stillborn twin is reported. The alterations in the kidneys and brain of the twin born alive suggest that the primary event took place before birth. Thromboplastic material and embolizing particles derived from the dead fetus may have passed the monoamnionic-monochorionic twin placenta and caused disseminated intravascular coagulation in the living twin, followed by infarction in other organ systems.

Brain Diseases↗
PubMed1989

Factors involved in the fatal susceptibility to submicrogram doses of endotoxin in cycloheximide-treated mice.

Analysis of fatal sensitivity to 0.2 microgram of S. enteritidis lipopolysaccharide in cycloheximide-treated mice identified two independent lethal elements. First, an absolute requirement for steroid supplementation to ensure survival suggests a crucial role for cycloheximide-mediated inhibition of steroidogenesis. The second factor is the development of virtually total bilateral renal cortical necrosis, itself a consequence of glomerular capillary occlusion with fibrin-like material. The survival of cycloheximide and endotoxin-challenged mice requires both hydrocortisone treatment and defibrination with ancrod. Cycloheximide and a smaller dose of endotoxin (0.1 microgram per mouse) is also fatal, but here steroid deficiency is not a crucial factor, protection being conferred by ancrod defibrination alone.

Ancrod↗
PubMed1985

Acute renal failure with polyarteritis nodosa and multiple myeloma.

A patient who presented with acute renal failure due to renal cortical necrosis is described. Renal biopsy showed cortical infarction and angiography demonstrated aneurysms in the renal, splenic and hepatic circulations. Concurrently he was found to have an IgA kappa paraprotein with bone marrow changes diagnostic of multiple myeloma. He was treated with haemodialysis, immunosuppressive drugs and plasma exchange but died 3 months after presentation.

Acute Kidney Injury↗
PubMed1984

Renal cortical necrosis in systemic lupus erythematosus.

A patient with active systemic lupus erythematosus had acute and irreversible renal failure after an uncomplicated cholecystectomy, and renal biopsy established the diagnosis of acute cortical necrosis. Patients with lupus have a diathesis for intravascular coagulation, and the interactive effects of immune complex or endotoxin-induced vascular injury, change in platelet dynamics, impairment of fibrinolysis, alterations in the mononuclear phagocytic system, and/or concomitant use of corticosteroids may have singularly or in combination been important in generating this rare renal complication of systemic lupus erythematosus in our patient.

Acute Disease↗
PubMed1987

Acute renal failure in pregnancy: 1987.

Acute renal failure has become a rare complication of pregnancy due to the virtual disappearance of septic abortion and to better prenatal care, including prevention of blood volume contraction. The incidence of bilateral renal cortical necrosis also decreased in recent years. Severe preeclampsia-eclampsia may be accompanied by acute tubular necrosis. Acute fatty liver of pregnancy is often associated with renal failure. It is a medical emergency. The diagnosis should be made promptly, before liver failure becomes too severe. This should be followed by immediate delivery. In postpartum hemolytic uremic syndrome, plasma infusion, plasma exchange, and/or antiplatelet drug therapy may be of value.

Acute Kidney Injury↗
PubMed2002

Renal artery dissection after blunt abdominal trauma: a rare cause of acute cortical necrosis.

Renal artery injury is an uncommon complication of blunt abdominal trauma. We present a case of a 19-year-old man who developed acute cortical necrosis in a congenital single kidney after a motorcycle accident. On initial presentation, he had signs of splenic injury and required immediate laparotomy and splenectomy. His renal function deteriorated, and he became dialysis dependent. Computed tomography followed by percutaneous angiography showed a dissection of a single renal artery causing the formation of a large pseudoaneurysm. A second angiogram showed an increase in the size of the pseudoaneurysm. We performed a laparotomy and attempted in situ vein graft repair of the renal artery. A wedge biopsy specimen taken at laparotomy revealed acute cortical necrosis, and plain radiographs showed cortical calcification. Renal artery dissection and pseudoaneurysm formation are rare events after blunt trauma. Iatrogenic damage is the most common cause of pseudoaneurysm. Traumatic pseudoaneurysms have a poor prognosis without prompt surgical intervention. Renal arterial damage may occur after blunt trauma, and early imaging and intervention are essential to salvage renal function.

Abdominal Injuries↗
PubMed1991

Bilateral renal cortical necrosis in two patients with Neisseria meningitidis sepsis.

Two patients who developed bilateral renal cortical necrosis as a consequence of Neisseria meningitidis infections are described: 1 patient had meningococcemia and the other had meningococcal meningitis. Both patients developed a Shwartzman-like reaction, disseminated intravascular coagulation and irreversible renal failure. Renal biopsy showed sclerosis of the majority of glomeruli; some glomeruli showed capillary congestion, thrombosis and an increased number of neutrophils; the intralobular arterioles showed thrombotic occlusions.

Adult↗
PubMed2001

Acute bilateral renal cortical necrosis as a cause of postoperative renal failure.

Acute renal failure after a major intra-abdominal operation is, unfortunately, not an infrequent occurrence. Acute tubular necrosis, the most common cause of postoperative renal failure, usually follows a predictable clinical course, with most patients recovering full renal function. We describe a patient who developed acute renal failure after orthotopic liver transplantation. Subsequent workup revealed the patient to have acute bilateral renal cortical necrosis. Bilateral renal cortical necrosis is an extremely rare cause of renal failure and an even rarer cause of postoperative renal failure. We discuss the diagnosis and management of this uncommon disorder and review the salient literature. Of the approximately 15 known reported cases involving native kidneys after a major nonobstetric abdominal operation in the world literature, we believe this is the first to be related to an orthotopic organ transplant.

Acute Kidney Injury↗
PubMedDate not supplied

[A periventricular tumor associated with acute kidney failure and bilateral renal cortical necrosis].

The authors present a case in which the clinico-evolutive particularity was an association between a periventricular tumour (multiform glioblastoma) and acute renal failure. Considerations are made on clinical signs determined by the neoplastic process (apraxia-agnosia hyperthermia, etc.), and on the disseminated intravascular coagulation syndrome related to the acute renal failure.

Acute Kidney Injury↗