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PubMed2003

Unilateral renal cortical necrosis with contralateral hydronephrosis after surgery for uterus carcinoma.

Renal cortical necrosis (RCN) represents a rare cause of acute renal failure that is characterized by necrosis of the renal cortex with sparing of the medulla. Most previous RCN cases reported have been bilateral and have occurred in pregnancy. Unilateral RCN is a quite rare disorder. Here, we report a case of unilateral RCN with contralateral hydronephrosis after surgery for uterus carcinoma. In this patient it seems that hydronephrosis had been present before RCN occurrence. It is suggested that ureteric obstruction protects against RCN development.

Adenocarcinoma↗
PubMedDate not supplied

Renal cortical necrosis: a case series of nine patients & review of literature.

BACKGROUND: The purpose of this study is to review cases of renal cortical necrosis (RCN) which we came across during a period of five years, confirmed on needle biopsy specimens, with literature available so far. METHODS: All renal biopsy records between January 1996 to December 2001 at the Aga Khan University Hospital, Karachi, Pakistan were reviewed to identify patients with histologically proven renal cortical necrosis. Seven patients were also referred by the department of Nephrology, Lady Reading Hospital, Peshawar, Pakistan. Patients' medical records were reviewed for demographic, clinical, and follow up data. RESULTS: There were total of nine patients identified with renal cortical necrosis. The mean age was 26.21 +/- 13.01 year. Five cases (55.5%) were caused by obstetric complications. The most common histology type of RCN was patchy cortical necrosis in seven patients (77.8%). Three patients were alive at last follow up; remaining patients were lost to follow up. CONCLUSION: Obstetric complications remain the leading cause of renal cortical necrosis in our setting. The recognition of this entity and value of renal biopsy in cases of acute renal failure needs to be emphasized as this helps in establishing diagnosis, to assess prognosis and to aid in selection of a rational approach to therapy.

Acute Kidney Injury↗
PubMed1995

Protective effect of coconut oil on renal necrosis occurring in rats fed a methyl-deficient diet.

Weanling rats fed a methyl-deficient diet develop renal necrosis with acute renal failure. The aim of this experiment was to explore further the role of coconut oil in this experimental model. Weanling Wistar male rats were fed methyl-deficient and their controls were fed methyl-supplemented diets. Coconut oil was fed at 14% and 20%, the latter concentration with and without 1% safflower oil (rich in linoleic acid); other groups received similar diets but instead of coconut oil, a mixture of hydrogenated vegetable oil and corn oil (rich in unsaturated fatty acids) was employed. Coconut oil fed at a 14% concentration did not evidence any protective outcome in relation to the renal lesions. Coconut oil at a 20% concentration showed a protective effect, mainly when the diet included safflower oil. The renal protective effect was evidenced by less or no mortality and increased survival time in the methyl-deficient rats receiving coconut oil, as well as by a reduced incidence (%) and severity of the renal lesions as evaluated by renal weight, and type (tubular and cortical necrosis or repair) and extent (grade) of the renal damage. The lack of a protective outcome when coconut oil was fed at 14%, along with the fact that in those rats receiving coconut oil at 20% the protection was greater when the diet was supplemented with 1% safflower oil, indicates that the protective effect should be attributed to the type of fatty acids coconut oil has and not to their shortage of essential fatty acids.

Animals↗
PubMed1989

In vivo release of cisplatin from a needle-type copolymer formulation implanted in rat kidney.

Cisplatin, cis-dichlorodiamine platinum (II), was incorporated in a needle-type copolymer formulation (0.8 mm diameter, 6 mm long) by radiation-induced polymerization. The copolymer used was copoly(diethylene glycol dimethacrylate/polyethylene glycol #600 dimethacrylate, 80/20 vol%). This copolymer, containing 6 mg of cisplatin, was implanted into the kidney of adult male Wistar rats (420 +/- 20 g). A total of 70 d was required for 100% release of cisplatin in vivo. The kidney tissue surrounding the formulation was strongly necrotized by the action of cisplatin. Two layers of necrosis could be distinguished: necrotic tissue surrounding the formulation and necrobiotic tissue surrounding the necrotic tissue. The amount of necrotic tissue changed markedly over time, but no change was apparent in the amount of necrobiotic tissue. The maximal amounts of necrotized tissue were observed 14 d after implantation: 3100 microns and 600 microns thick for the necrotic and necrobiotic tissues, respectively.

Animals↗
PubMed1991

Erythropoietin deficiency in acute crescentic glomerulonephritis and in total bilateral renal cortical necrosis.

Six patients with acute renal failure, in five cases due to acute crescentic glomerulonephritis and in one case due to total bilateral renal cortical necrosis, were studied. All had serum erythropoietin (EPO) concentrations in the normal range, despite a relatively severe anaemia. Half-life and plasma clearance of intravenously injected recombinant human erythropoietin (rhEPO) were determined. The results indicate that the lack of compensatory increase in serum EPO to the anaemic stimulus is not due to increased catabolism, but to decreased synthesis of the renal hormone. Two patients were treated with rhEPO (Eprex). In marked contrast to untreated controls, both patients responded with vigorous reticulocytosis and normalization of haemoglobin levels while they were still in severe renal failure. These results are similar to our previous findings in patients with acute renal failure due to tubular necrosis. Under all three conditions the defective EPO synthesis is probably the dominant pathogenetic factor for the largely aregeneratory anaemia of prolonged cases, and for the sluggish restoration of red cell mass during recovery of renal function. It is concluded that defective synthesis of EPO is not only a permanent and irreversible feature of severe chronic renal failure, but that it is also present, usually in a transient and reversible form, in different types of acute renal failure.

Acute Disease↗
PubMed1973

Excretion urography in acute renal failure.

High-dose excretion urography has been carried out in 32 patients presenting with non-obstructive acute oliguric or non-oliguric renal failure. An early, dense, persisting nephrogram has been observed in all patients with acute uncomplicated tubular necrosis and in patients with acute oliguric pyelonephritis. This appearance is modified by the presence of pre-existing renal disease. Different patterns have been observed in patients with acute glomerular disease, severe renal ischaemia, and chronic glomerular disease. The study demonstrates that careful analysis of the evolution of the nephrogram in patients with acute renal failure provides valuable information as to the nature of the parenchymal disease.

Acute Kidney Injury↗
PubMedDate not supplied

Epidemiology of acute renal failure in hospitalized patients: experience from southern Saudi Arabia.

Despite advances in health care, morbidity and mortality associated with acute renal failure (ARF) remain high. This study determined the frequency and etiology of ARF in hospitalized patients in Saudi Arabia over 2 years. Of the 150 cases of ARF, 38.0% were community-acquired and 62.0% hospital-acquired. The main cause was acute tubular necrosis (ATN) in 93 patients, due to sepsis (24.7%), ischaemia (12.7%), rhabdomyolysis (mainly from road traffic accidents) (10.7%), drugs (7.3%) and malaria and snake-bites (4.6%). Overall, 40% died, 48% made a full recovery and 1 patient (0.7%) became dialysis-dependant. Factors associated with poor prognosis were: age 60+ years, community-acquired ARF, peak blood urea nitrogen > 160 mg/dL, duration of ARF > 1 week, need for dialysis and associated chronic liver disease.

Acute Kidney Injury↗
PubMed1983

Disseminated aspergillosis complicating hepatic failure.

Disseminated aspergillosis is not generally known as a complication of hepatic failure. Three patients with subacute hepatic necrosis died of clinically unrecognized disseminated aspergillosis. All of the patients had pulmonary aspergillosis and Aspergillus infections of the CNS. Focal neurologic deficits were clinically misconstrued as intracerebral hemorrhages caused by the coagulopathy of liver failure. Signs of invasive pulmonary aspergillosis were ascribed to refractory bacterial pneumonia. Each patient had a hospital course of longer than three weeks and each received treatment with corticosteroids and intravenous antibiotics. Invasive aspergillosis should be considered as a cause of refractory pneumonia and of new focal neurologic deficits in patients with hepatic failure.

Abscess↗
PubMed1984

Focal renal cortical necrosis associated with zomepirac.

Anaphylactoid shock, disseminated intravascular coagulation, and anuric renal failure requiring dialysis occurred in a patient receiving zomepirac sodium for toothache. Although renal function showed gradual improvement after seven days of anuria, the recovery was slow and incomplete. Renal biopsy three weeks after the onset of renal failure revealed evidence of focal renal cortical necrosis. Association of zomepirac administration with renal cortical necrosis is not known to have been previously demonstrated. This observation adds another dimension to the previously reported renal complications of nonsteroidal anti-inflammatory agents, especially zomepirac. The proportions of lymphocyte subsets, as defined with monoclonal antibodies, and the proliferative response to mitogens were normal. The patient's lymphocytes showed no proliferative response to zomepirac. Serum complement components and immunoglobulin levels were within normal limits, and radioallergosorbent testing gave negative results. The mechanism of anaphylactoid reaction to zomepirac in this case, therefore, remains unclear.

Analgesics↗
PubMedDate not supplied

Renal cortical necrosis and Purtscher's retinopathy in hemorrhagic pancreatitis.

A patient presented with acute hemorrhagic pancreatitis complicated by both renal cortical necrosis and Purtscher's retinopathy. Either of these two complications is rare and never before have both been reported in the same patient. The patient's renal insufficiency required hemodialysis; it gradually improved over two years when dialysis could be discontinued. The patient's retinopathy included bilateral hemorrhages and cotton wool spots; visual fields and acuity remained normal. Funduscopic lesions disappeared by three months after the acute event. These two rare vasculo-occlusive complications of pancreatitis simultaneously occurring in one individual might suggest complement-mediated leukostatic mechanisms.

Acute Disease↗
PubMed1976

Bilateral renal cortical necrosis: a report of 2 cases.

Two cases of renal cortical necrosis, one of which occurred after an obstetric complication (abruptio placentae) and the other after postpartum haemorrhage, are described. The diagnosis was made by percutaneous renal biopsy, intravenous pyelography and selective nephro-angiography. Immunofluorescence studies of the kidney showed no abnormality in one patient, but showed the presence of IgM in the glomerular basement membrane in the second patient. Hypotension was not observed when anuria occurred. Both patients survived. The importance of prolonged haemodialysis is stressed, since one patient was oliguric for 57 days and required intermittent haemodialysis for 5 months, while the second patient was oliguric for 17 days, required haemodialysis for 5 months and now has established hypertension.

Abruptio Placentae↗
PubMed1987

Inhibition of fibrinolytic system by liquoid (polyanetholesulfonate). A contributing factor in the liquoid-induced renal cortical necrosis.

Liquoid induces microvascular thrombosis and renal cortical necrosis in experimental animals. We hypothesized that thrombosis and renal cortical necrosis may, at least in part, result from the inhibition of the fibrinolytic system by liquoid. Effects of liquoid on plasminogen activation by rat kidney, purified human tissue plasminogen activator (TPA), urokinase, streptokinase, and on the amidolytic activities of TPA, urokinase, and plasmin were studied using chromogenic substrates and clot lysis. Liquoid had a strong inhibitory effect on the fibrinolytic system in vivo and in vitro. The inhibition was most effective at the plasminogen activation level, with activation by streptokinase being most susceptible. The demonstrated stoichiometric binding between liquoid and plasminogen, and to a lesser degree the direct inactivation of plasminogen activators and plasmin, is probably responsible for the reduction of plasminogen activation in circulation and in the kidneys.

Animals↗
PubMed2005

ApoSense: a novel technology for functional molecular imaging of cell death in models of acute renal tubular necrosis.

PURPOSE: Acute renal tubular necrosis (ATN), a common cause of acute renal failure, is a dynamic, rapidly evolving clinical condition associated with apoptotic and necrotic tubular cell death. Its early identification is critical, but current detection methods relying upon clinical assessment, such as kidney biopsy and functional assays, are insufficient. We have developed a family of small molecule compounds, ApoSense, that is capable, upon systemic administration, of selectively targeting and accumulating within apoptotic/necrotic cells and is suitable for attachment of different markers for clinical imaging. The purpose of this study was to test the applicability of these molecules as a diagnostic imaging agent for the detection of renal tubular cell injury following renal ischemia. METHODS: Using both fluorescent and radiolabeled derivatives of one of the ApoSense compounds, didansyl cystine, we evaluated cell death in three experimental, clinically relevant animal models of ATN: renal ischemia/reperfusion, radiocontrast-induced distal tubular necrosis, and cecal ligature and perforation-induced sepsis. RESULTS: ApoSense showed high sensitivity and specificity in targeting injured renal tubular epithelial cells in vivo in all three models used. Uptake of ApoSense in the ischemic kidney was higher than in the non-ischemic one, and the specificity of ApoSense targeting was demonstrated by its localization to regions of apoptotic/necrotic cell death, detected morphologically and by TUNEL staining. CONCLUSION: ApoSense technology should have significant clinical utility for real-time, noninvasive detection of renal parenchymal damage of various types and evaluation of its distribution and magnitude; it may facilitate the assessment of efficacy of therapeutic interventions in a broad spectrum of disease states.

Acute Disease↗
PubMed2000

Waterhouse-Friderichsen syndrome and bilateral renal cortical necrosis in meningococcal sepsis.

Waterhouse-Friderichsen syndrome and bilateral renal cortical necrosis (BRCN) are rare complications of meningococcal sepsis associated with high mortality rates. We describe a 20-year-old man who presented with a 1-day history of fever, chills, malaise, and vomiting. He collapsed in the emergency room, requiring mechanical ventilation and intravenous vasopressors for resuscitation. He was noted to be anuric, and computed tomography showed adrenal hemorrhage and BRCN. Blood cultures later confirmed Neisseria meningitidis sepsis, and a biopsy confirmed renal cortical infarction. The patient was treated aggressively with intravenous antibiotics, corticosteroids, and immunoglobulins, in addition to plasmapheresis, dialysis, and supportive measures. He recovered his adrenal function and was discharged from the hospital, but he remains dialysis dependent. To our knowledge, this is the first reported case of concomitant Waterhouse-Friderichsen syndrome and BRCN in a patient with meningococcal sepsis.

Adult↗
PubMed1996

CT scan as an important diagnostic tool in the initial phase of diffuse bilateral renal cortical necrosis.

The serious clinical circumstances and coagulopathy generally accompanied by diffuse bilateral renal cortical necrosis (BRCN), especially during the early period, do not allow renal biopsy being well known as a gold standard diagnostic method for BRCN. Therefore, other noninvasive diagnostic modalities in the initial phase of BRCN have been tried, and, among them, contrast-enhanced computerized tomography (CT) was found to provide very characteristic representative findings, i.e., low attenuation of cortex sparing thin rim of subcapsular cortex and medulla, correlating well with histological findings of renal biopsy performed in the late somewhat stable clinical status or at autopsy. These specific CT findings were reported consistently with or without renal biopsy in several articles recently. Herein, we present a 38-year-old woman of massive automobile accident victim, developed protracted total anuria as well as shock with disseminated intrasvascular coagulation (DIC), and diagnosed as BRCN by the specific CT findings without renal biopsy in the second day of admission. Simultaneously, all the scattered cases of BRCN diagnosed by CT are reviewed and contrast to the findings of other diagnostic procedures performed for the same cases. The importance of contrast-enhanced CT as noninvasive diagnostic procedure during the initial phase of BRCN is stressed.

Adult↗
PubMedDate not supplied

Comparisons of models of cortical necrosis with segmental infarction.

Sodium and water excretion were studied by standard clearance techniques in three experimental models where renal mass was reduced by superficial cortical necrosis (CN) or ischemic segmental infarction (SI). During hydropenia either CN or SI were able to conserve and regulate sodium to a very similar degree. After expansion of extracellular volume, CN reabsorbed less sodium and water than SI. In free-water clearance (CH2O) experiments, the 'apparent distal' sodium delivery was higher in CN than in SI, suggesting a decreased sodium and water reabsorption in the proximal tubules of juxtamedullary nephrons (JM). Both kidneys had similar CH2O when factored for inulin clearance but when CH2O was corrected for 'apparent distal' sodium delivery it was lower in CN than in SI, demonstrating an incapacity of JM to dilute urine. CN also showed less capacity to reabsorb free water than SI. Thus, the use of CN and SI within the same animal was useful to study functional differences between superficial and juxtamedullary nephrons. The present study also suggests that the kidney with superficial CN was unable to perform maximal urine dilution and concentration.

Absorption↗
PubMed2000

Protective effect of myristic acid on renal necrosis occurring in rats fed a methyl-deficient diet.

Weanling rats fed a methyl-deficient diet develop acute renal failure, the morphological features of which vary from focal tubular necrosis to widespread cortical necrosis. We and others have shown that coconut oil, rich in saturated fatty acids, has a renal protective effect in this experimental model. In the experiment we are reporting now, we studied which fatty acid is involved in the protection afforded by coconut oil by feeding five groups of methyl-deficient rats a mixture of corn oil and hydrogenated vegetable oil, C6-C8-C10 fatty acids, C12 fatty acid, C14 fatty acid and C16-C18 fatty acids. Five groups of rats receiving the same diets supplemented with choline chloride were used as controls. The group of methyl-deficient rats fed C14 fatty acid (myristic acid) showed a greater percentage of surviving animals and lower renal damage than the other groups of methyl-deficient rats, indicating that the protective effect of coconut oil found in previous experiments is due to its high content of myristic acid.

Analysis of Variance↗
PubMed1977

Inhalation toxicity of vinyl chloride and vinylidene chloride.

Exposure of mice to 1000 ppm of vinyl chloride (VC), 6 hr/day, 5 days/week, caused some acute deaths with toxic hepatitis and marked tubular necrosis of the renal cortex. Starting the sixth month, mice exposed to 1000, 250, or 50 ppm of VC became lethargic, lost weight quickly, and died. Only a few mice exposed to 50 ppm survived for 12 months. Pulmonary macrophage count was elevated in some mice. There was a high incidence of bronchiolo-alveolar adenoma, mammary gland tumors including ductular adenocarcinoma, squamous and anaplastic cell carcinomas with metastasis to the lung, and hemangiosarcoma in the liver, and, to a lesser extent, in some other organs. The incidence of these tumors quickly increased, and the severity was in direct proportion to the levels of VC and the length of exposure. Malignant lymphoma involving various organs was observed in a few mice. Rats were more resistant to the toxic effects of VC. Exposure to 1000 ppm slightly depressed the body weight of the females. Exposures of 250 or 1000 ppm caused a number of deaths and hemangiosarcoma in the liver starting the ninth month. Most rats with hepatic hemangiosarcoma also developed hemangiosarcoma in the lung. Hemangiosarcoma occasionally occurred in other tissues of one or two rats exposed to 50 ppm or higher level of VC. Exposure of mice to 55 ppm of vinylidene chloride (VDC) also caused a few acute deaths and a few hepatic hemangiosarcomas. Inflammatory, degenerative, and mitotic changes occurred in the liver. No mouse exposed to VDC developed any mammary gland tumors. Several mice had bronchioloalveolar adenoma. Exposure of rats to 55 ppm of VDC slightly depressed the body weight. Hemangiosarcoma occurred in the mesenteric lymph node or subcutaneous tissue in two rats.

Adenoma↗