ACASE OF RENAL CORTICAL NECROSIS WITH DYSTROPHIC CALCIFICATION DEMONSTRATED AT THE POSTGRADUATE MEDICAL SCHOOL OF LONDON.
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Sequential changes in the kidney during the generalized Shwartzman reaction were studied electron microscopically. The first anatomical change was infiltration of neutrophils into the glomerular capillaries. Endothelial damage was not noticeable until the capillaries were filled with fibrin deposits. Fibrin appeared in the mesangium at almost the same time as in the capillary lumina, traversing through the endothelial fenestrae. Endothelial damage was more common in the mesangial portion than in the peripheral portion of the capillaries. Severe mesangiolysis developed after loss of endothelial cells had been followed by massive penetration of intracapillary contents. Later, signs of repair were evident in some parts of the damaged endothelium. The development of cortical necrosis coincided with the appearance of mesangiolysis and arteriolar thrombotic lesions.
Cefuroxime axetil has been associated with few reported adverse effects. We report a case of bilateral renal cortical necrosis in a female after receiving 7 doses over 4 treatment days. The patient presented with worsening symptoms consisting of arthralgias, pruritus, and abdominal pain. Laboratory data obtained was indicative of worsening renal failure and thrombocytopenia. The patient required hemodialysis by the third day. Kidney biopsy revealed cortical necrosis. The possible pathogenesis of cefuroxime axetil causing cortical necrosis in this case and a review of other reported cases of chemical induced renal cortical necrosis is discussed.
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The authors report a case of acute renal failure resulting from acute cortical necrosis. A selective renal angiogram defined a very unusual, abrupt termination of vascularity at the interlobular and arcuate levels. Nephro-angiography is an important tool in the diagnosis of acute cortical necrosis in the initial phase of acute renal failure.
A 34-year-old woman presented with postpartum renal cortical necrosis. Contrast-enhanced computerized tomography (CT) of her kidneys showed a narrow subcapsular band of increased density that was separated from the medulla by a distinct band of decreased density. This is analogous to the decreased cortical nephrogram seen on arteriography. The CT scan may be a useful, non-invasive diagnostic procedure in renal cortical necrosis.
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The authors report three cases in which echotomographic findings were suggestive of cortical necrosis in a grafted kidney (cortical hypoechogenic border). This proved to actually be the diagnosis in one case only.
Renal cortical necrosis, renal medullary necrosis, and combined renal cortical-medullary necrosis result from renal ischemia without vascular occlusion. Renal hypoperfusion and ischemic injury in infants have been ascribed to massive blood loss, hemolytic disease, septicemia, and severe hypoxemia. In a postmortem study we identified 82 cases among 1,638 autopsies during the 20 years between 1970 and 1989 in infants 3 months old or less at the time of death. The frequency of renal necrosis in autopsy cases increased significantly during the last 6 years of the study. The distribution of the renal lesion was cortical in 28, medullary in 23, and combined in 31. Forty infants carried diagnoses of congenital heart disease, 17 of asphyxial shock, 9 of sepsis, 3 of infectious myocarditis, 9 of major malformations, 4 of anemic shock, 1 of vascular malformation, and 1 of gastroenteritis and dehydration. A significantly higher proportion of babies with congenital heart disease had cortical involvement. Comparison of clinical characteristics revealed a significantly higher frequency of prematurity, respiratory distress syndrome, bleeding diathesis, and possibly sepsis in the children with congenital heart disease, suggesting that these factors are important in the pathogenesis of the renal lesion. Fourteen infants underwent cardiac catheterization; there was no demonstrable association between the renal lesions and the use of radiographic contrast medium. We conclude that severe congenital heart disease itself is a risk factor for life-threatening renal cortical and medullary necrosis.
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