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A rare case of acute intrapartum twin-twin transfusion occurred. The well-recognized criteria of long-standing chronic twin-twin transfusion were absent. Although a cesarean section was performed for obstetric reasons, the hyperperfused twin, A, died intrapartum. Twin B, the hypoperfused twin, although liveborn, died neonatally of renal failure attributed to renal cortical necrosis as a sequel to hypotension.
Acute renal cortical necrosis is a rare cause of acute renal failure that is usually associated with third trimester obstetrical complications. The appearance of this condition on contrast-enhanced computed tomography (CT) has rarely been described. A case of acute cortical renal necrosis is presented and the findings on contrast-enhanced CT are described. The pathologic correlation is also presented.
Two patients with presumed impending cortical necrosis, after haemolytic uraemic syndrome in one and after concealed accidental haemorrhage in the other, were treated by local infusion of urokinase and heparin into the renal artery. Both recovered and one regained normal renal function. Local infusion of anticoagulants or thrombolytic drugs into one renal artery offers the possibility of a controlled examination of the efficacy of this treatment in preventing cortical necrosis.
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A 16 year-old-boy was admitted to the ICU of university hospital with acute renal failure following snakebite. The clinical evolution of the patient associated with radiological findings of renal calcification suggested bilateral cortical necrosis of the kidneys. The biopsy findings were compatible with this diagnosis. The patient was discharged 86 days after his admission, with chronic renal failure, since a kidney transplantation was not possible.
Acute bilateral renal cortical necrosis is a very rare cause of acute renal failure. We report here for the first time a case related to antiphospholipid syndrome, paraneoplastic of a lung neoplasia. A 46-year-old male smoker without medical history was admitted for acute dyspnea and anuria. Biological examination showed acute renal failure associated with hyperkalemia, high serum lactate dehydrogenase level, and prolonged activated thrombin time (ratio 1.29). Chest radiograph showed a right laterotracheal round lesion. A percutaneous left renal biopsy showed cortical necrosis, and renal arteriography confirmed bilateral cortical necrosis. Blood examination showed antiphospholipid antibodies type anticardiolipin. Chest computed tomographic scan confirmed the presence of a lung tumor. Two years after tumor surgery, the patient was still anuric and on long-term hemodialysis therapy, but antiphospholipid antibody results were negative. This case describes the first association of antiphospholipid syndrome to epidermoid lung cancer, shown by cortical bilateral necrosis. It also emphasizes the utility of renal biopsy in case of an unusual acute renal failure.
In this study we have analyzed incidence, causes and clinical course of ARF due to primary intrarenal disease other than acute tubular necrosis. Thousand hundred and twenty two cases of ARF of diverse etiology were studied over a period of 16 years; July 1984 to Dec, 1999. Surgical ARF 231 (20.6%) were not included in the present study. Intrinsic renal diseases were responsible for ARF in 891 (79.4%) of cases. The most common intrinsic renal diseases 705 (79.4%) causing ARF were ischemic/toxic acute tubular necrosis, but not included in this study. Acute renal failure was related to acute glomerulonephritis (9.3%), acute interstitial nephritis (7%), and renal cortical necrosis in (4.6%) of cases. Therefore intrinsic renal diseases other than ATN were the causative factor for acute renal failure in 186 (20.8%) patients in our study. Crescentic (51.8%) and endocapillary proliferative glomerulonephritis (34.9%), were the main glomerular diseases responsible for ARF and 75.9% of GN was related to infectious etiology. Fifty three percent of acute interstitial nephritis was drug induced and in 25 (40%) patients it was related to an infectious etiology. Renal cortical necrosis due to HUS was observed in 16 (39%) children and majority (76.47%) of the cases had a diarrhoeal prodrome. Obstetrical complications were the main causes (61%) of cortical necrosis in adults with acute renal failure. Thus, intrinsic renal diseases other than ATN were responsible for ARF in 186 (20.8%) cases. Post-infectious glomerulonephritis, acute interstitial nephritis and renal cortical necrosis (complicating HUS in children and obstetrical complications in adult) are the main causes of acute renal failure in our study. Both acute GN and interstitial nephritis had excellent prognosis, however renal cortical necrosis was associated with a very high mortality.
Renal involvement is rare in patients with type III cryoglobulinemia. We report a case of renal cortical necrosis in a patient with type III cryoglobulinemia. Renal function improved partially after treatment with plasma exchange, steroids, and cyclophosphamide. Renal magnetic resonance imaging was a valuable tool in the evaluation of the extent of renal cortical necrosis and improvement in renal vascularization after treatment.
We report a serioangiographic method in rats which permits assessment of the course and dimensions of the renal arteries, the durations of the arterial and venous phases, and the intensity and uniformity of the renal parenchymal filling. The procedure was employed to study the mechanism by which administration of vasopressin to rats pretreated with estrin leads to renal cortical necrosis. The pathogenetic significance of the spasm localized on the larger renal arteries was proved directly; the possible role of the arteriovenous shunt in the development of the renal ischemia was excluded.
Renal cortical necrosis is an uncommon cause of acute renal failure. We report 23 cases of biopsy-proven renal cortical necrosis which constituted 6.3% (23/363) of all cases of acute renal failure studied over a period of seven years (1985-92). The patients were divided into two groups: obstetric and non-obstetric. Obstetric complications were responsible for renal cortical necrosis in 15 (65.2%) patients while non-obstetric conditions accounted for the remaining eight (34.8%) cases. The overall incidence of cortical necrosis in obstetric acute renal failure was 15/63 (23.8%) patients, the incidence being nearly equal in early (20.5%) and late (29%) pregnancy. Post-abortum renal failure was the sole cause of cortical necrosis in early pregnancy in the obstetric group. Haemolytic uraemic syndrome (three patients) and septicaemia (two patients) were the main cause of necrosis in the non-obstetric group. The cortical necrosis was diffuse and patchy in 17 and six patients, respectively. The disease had a fatal prognosis in 20 (87%) patients; mortality was due to uraemic complications and infections in the majority of patients. The high frequency of post-abortum renal cortical necrosis in our patients is similar to the experience of other Indian workers.
Experimental studies on mitomycin-C nephrotoxicity are scanty and mention the occurrence of cortical hemorrhage, tubular necrosis, or hydronephrosis secondary to papillomatous hyperplasia of the uroepithelium. To our knowledge, only one experimental study has mentioned morphological lesions similar to the hemolytic uremic syndrome in the human. In the present study 40 female Wistar rats were studied following unilateral renal perfusion of the left kidney with 2 mg/kg of mitomycin-C. Renal lesions corresponded to cortical necrosis with the presence of large bizarre nuclei. The presence of these nuclear atypias supports a direct toxic effect (alkylation) of the mitomycin or its metabolites on cells.
One case of symmetrical, synchron, antenatal thrombosis of the renal veins and haemorrhagic necosis of the kidneys in a 4 hours-old newborn is reported. In the pathomechanism of the process in addition to perinatal shock, asphyxia-hypoxia Schwartzmann's phenomenon may also play a part.
The procoagulant activity of rabbit peritoneal leukocytes significantly increased when the leukocytes were incubated in suspension cultures at 37 C for 24 hours. Intravenous infusions of Iysates of 232 x 10(6) rabbit leukocytes which had been incubated in cultures at 37 C for 24 hours produced disseminated intravascular coagulation and vasculitis involving the pulmonary arteries in normal rabbits. Intraaortic infusions of lysates of 230 x 10(6) similarly incubated leukocytes produced renal thrombosis and renal cortical necrosis in normal rabbits. These observations suggest that the procoagulant of granulocytic leukocytes could play a role in the generalized Shwartzman reaction and other syndromes of disseminated intravascular coagulation.
One case of renal cortical necrosis is reported. The results of ultrasound and angiographic imaging and the relevant literature are reviewed. The examinations, particularly selective angiography, are of great interest in the diagnostic and in the etiology of this disease.
Forty-nine out of 662 patients (7.4%) dialysed for acute renal failure were found to have bilateral renal cortical necrosis. Amongst 6061 autopsies carried out in our centre during the same period, the incidence of cortical necrosis was 0.7%. Obstetric causes were responsible for the renal lesion in 35 (71%) and non-obstetrical causes in 14 patients. In the obstetric group, cortical necrosis was observed in association with spontaneous or induced abortion in 39% and as a complication of late pregnancy in 33%. The non-obstetric causes included snake bite in 26 (12%), acute gastro-enteritis in 5 (10%), haemolytic uremic syndrome in 2 (4%) and G6PD deficiency with intravascular haemolysis in one patient (2%). Thirty-nine (80%) patients were anuric or severely oliguric throughout their illness but a steady rise in urinary output following a protracted phase of oligo-anuria was observed in ten patients. Forty-two (86%) patients died and seven survived. None of the survivors, however, achieved a normal renal function (Ccr 8 ml to 28 ml/min). The diagnosis of renal lesion was confirmed during life in 8 and after death in 41 patients. Morphological lesions were consistent with bilateral diffuse cortical necrosis in 39 (80%) and patchy lesions in 10 patients. Factors responsible for the high incidence of cortical necrosis amongst Indian patients have been high-lighted.