Pediatric Nephrology
Pediatr Nephrol (1992) 6 : 5 1 6 - 5 1 8 9 IPNA 1992
Original article Renal cortical and renal medullary necrosis in the first 3 months of life Gary R. Lernerl, Ruben Kurnetzl, 3, Jay Bernstein2, 4, Chung-Ho Chang2, Larry E. Fleischmann 1, and Alan B. Gruskinl Departments of I Pediatrics and 2 Pathology, Children's Hospital of Michigan and Wayne State University School of Medicine, Michigan, USA Departments of 3 Pediatrics and 4 Pathology, William Beaumont Hospital, Royal Oak, Michigan, USA Received January 7, 1992; received in revised form May 3, 1992; accepted May 15, 1992
Abstract. 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. Comp ~ s o n 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.
Key words: Renal cortical necrosis - Renal medullary necrosis - Radiocontrast medium - Congenital heart disease - Renal failure - Infant
Introduction Renal cortical (RCN), renal medullary (RMN), and combined renal cortical and medullary (RCN-RMN) necrosis in the newborn are uncommon disorders, seldom recognized during life. The clinical manifestations - hematuria, oliguria, and renal enlargement - are nondiagnostic and are associated with several more common neonatal renal abnormalities. RCN and RMN share the same clinical antecedents, namely asphyxia and anemia, which are believed to cause reduced renal blood flow and ischemic necrosis. The reason(s) for the localization of necrosis to either the cortex or the medulla is unexplained. This is the third series of patients with RCN and RMN reported from Children's Hospital of Michigan. The two prior series, reported in 1951 and 1961 respectively, each contained 11 cases [1, 2]. The present series contains 82 cases culled from a review of 1,638 autopsies performed in infants 3 months of age and younger during the years 1970 through 1989.
Materials and methods The autopsy files for the 20-year period 1970-1989 were reviewed to identify cases of RCN and RMN in 1,638 children 3 months and younger. The histopathological sections in each case were reexamined by two pathologists. Hospital charts were systematically reviewed in the 82 infants identified as having RCN, RMN, or RCN-RMN. Azotemia was defined as a blood urea nitrogen >20 mg/dl, acidemia as a serum pH
Pediatr Nephrol (1992) 6 : 5 1 6 - 5 1 8 9 IPNA 1992
Original article Renal cortical and renal medullary necrosis in the first 3 months of life Gary R. Lernerl, Ruben Kurnetzl, 3, Jay Bernstein2, 4, Chung-Ho Chang2, Larry E. Fleischmann 1, and Alan B. Gruskinl Departments of I Pediatrics and 2 Pathology, Children's Hospital of Michigan and Wayne State University School of Medicine, Michigan, USA Departments of 3 Pediatrics and 4 Pathology, William Beaumont Hospital, Royal Oak, Michigan, USA Received January 7, 1992; received in revised form May 3, 1992; accepted May 15, 1992
Abstract. 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. Comp ~ s o n 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.
Key words: Renal cortical necrosis - Renal medullary necrosis - Radiocontrast medium - Congenital heart disease - Renal failure - Infant
Introduction Renal cortical (RCN), renal medullary (RMN), and combined renal cortical and medullary (RCN-RMN) necrosis in the newborn are uncommon disorders, seldom recognized during life. The clinical manifestations - hematuria, oliguria, and renal enlargement - are nondiagnostic and are associated with several more common neonatal renal abnormalities. RCN and RMN share the same clinical antecedents, namely asphyxia and anemia, which are believed to cause reduced renal blood flow and ischemic necrosis. The reason(s) for the localization of necrosis to either the cortex or the medulla is unexplained. This is the third series of patients with RCN and RMN reported from Children's Hospital of Michigan. The two prior series, reported in 1951 and 1961 respectively, each contained 11 cases [1, 2]. The present series contains 82 cases culled from a review of 1,638 autopsies performed in infants 3 months of age and younger during the years 1970 through 1989.
Materials and methods The autopsy files for the 20-year period 1970-1989 were reviewed to identify cases of RCN and RMN in 1,638 children 3 months and younger. The histopathological sections in each case were reexamined by two pathologists. Hospital charts were systematically reviewed in the 82 infants identified as having RCN, RMN, or RCN-RMN. Azotemia was defined as a blood urea nitrogen >20 mg/dl, acidemia as a serum pH
