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PubMed1994

Contrast-enhanced computed tomography for demonstration of bilateral renal cortical necrosis.

Bilateral renal cortical necrosis as a rare form of acute renal failure was encountered in two patients with sepsis and acute renal failure. In both cases contrast-enhanced computed tomography showed characteristic findings: absent specification of the renal cortex and enhancement of subcapsular and juxtamedullary areas and of the medulla without excretion of contrast medium. Establishing an early diagnosis and visualizing the extent of renal cortical necrosis by means of contrast-enhanced computed tomography allow a prognostic evaluation of renal function and further planning of therapy.

Adult↗
PubMed1985

The role of p-aminophenol in acetaminophen-induced nephrotoxicity: effect of bis(p-nitrophenyl) phosphate on acetaminophen and p-aminophenol nephrotoxicity and metabolism in Fischer 344 rats.

Acetaminophen (APAP) produces proximal tubular necrosis in Fischer 344 (F344) rats. Recently, p-aminophenol (PAP), a known potent nephrotoxicant, was identified as a metabolite of APAP in F344 rats. The purpose of this study was to determine if PAP formation is a requisite step in APAP-induced nephrotoxicity. Therefore, the effect of bis(p-nitrophenyl) phosphate (BNPP), an acylamidase inhibitor, on APAP and PAP nephrotoxicity and metabolism was determined. BNPP (1 to 8 mM) reduced APAP deacetylation and covalent binding in F344 renal cortical homogenates in a concentration-dependent manner. Pretreatment of animals with BNPP prior to APAP or PAP administration resulted in marked reduction of APAP (900 mg/kg) nephrotoxicity but not PAP nephrotoxicity. This result was not due to altered disposition of either APAP or acetylated metabolites in plasma or renal cortical and hepatic tissue. Rather, BNPP pretreatment reduced the fraction of APAP excreted as PAP by 64 and 75% after APAP doses of 750 and 900 mg/kg. BNPP did not alter the excretion of APAP or any of its non-deacetylated metabolites nor did BNPP alter excretion of PAP or its metabolites after PAP doses of 150 and 300 mg/kg. Therefore, the BNPP-induced reduction in APAP-induced nephrotoxicity appears to be due to inhibition of APAP deacetylation. It is concluded that PAP formation, in vivo, accounts, at least in part, for APAP-induced renal tubular necrosis.

Acetaminophen↗
PubMed1979

Cyproterone acetate-promoted prevention of renal cortical necrosis following testosterone and vasopressin administration.

Bilateral focal renal cortical necrosis was observed after vasopressin administration in rats pretreated for 10 days with testosterone phenyl propionate. When the androgen-receptor blocking-agent cyproterone acetate was administered together with the testosterone, the subsequent vasopressin treatment did not cause renal cortical necrosis. The results suggest the role of the androgen receptors in the kidney in the induction of the phenomenon.

Animals↗
PubMed1987

Histochemical and ultrastructural study of renal cortical necrosis in rats treated with oestrone + vasopressin, and its prevention with a vasopressin antagonist.

Renal cortical necrosis was induced by the administration of vasopressin to oestrogen-pretreated rats. Histochemical (succinic dehydrogenase, trichrome, perjod acid Schiff) and electronmicroscopic methods were applied to examine how the vasopressin antagonist d(CH2)5Tyr(Met)AVP influences the development of this renal cortical necrosis. The experiments revealed that vasopressin did not induce hypoxia or necrosis in the renal tubules if the antagonist was administered simultaneously, even after oestrogen pretreatment. The conclusion is drawn that this pressor antagonist may be of value for the prevention of renal cortical necrosis in rats or in human beings.

Animals↗
PubMed1996

Renal cortical necrosis in pregnancy-related acute renal failure.

Of 63 patients of obstetrical acute renal failure, 15 cases (23.8%) had biopsy proven bilateral renal cortical necrosis. Remaining 48 patients (76.2%) had acute tubular necrosis. Eight of 39 cases in early pregnancy had cortical necrosis (postabortum) and 7 of 24 patients in late pregnancy revealed cortical necrosis. Diffuse and patchy cortical necroses were seen in 12 and 3 patients respectively. The incidence of cortical necrosis was almost equal in both early as well as late pregnancies. The high incidence (20.5%) of cortical necrosis following septic abortion remains the interesting feature of the present study in contrast to very low incidence (1.5%) of cortical necrosis in postabortum group in developed countries. The death occurred in most patients (14 ie, 93.3%) of cortical necrosis because of uraemic complications and sepsis.

Abortion, Septic↗
PubMed1985

Renal cortical necrosis following Bothrops jararaca and B. jararacussu snake bite.

Out of 22 patients admitted to the Intensive Care Unit of the Hospital das Clínicas, Federal University of Minas Gerais, with acute renal failure following Bothrops snake bite, 7 had renal cortical necrosis. This complication was suspected when the oligoanuric phase ranged from 21 to 28 days or when the patient, in spite of having a polyuric phase, maintained elevated blood levels of urea and creatinine after the interruption of the dialysis program, and was confirmed by a kidney biopsy. Three patients died and in two of them renal cortical necrosis was found at necropsy. Four patients were discharged from the hospital and follow-up was possible in two of them who showed recovery of renal function. Vasospasm, direct nephrotoxicity of Bothrops venom and/or disseminated intravascular coagulation leading to vascular occlusion and renal ischemia are the proposed pathogenetic mechanisms to explain renal cortical necrosis following Bothrops snake bite.

Acute Kidney Injury↗
PubMed1982

[Postpartum renal cortical necrosis].

The authors report two cases of post-partum cortical renal necrosis. The diagnosis was made on clinical and biological criteria (severe, prolonged oliguria, the signs of intra-vascular coagulation defects, a rise in L.D.H. and anaemia with micro-angiopathy. It is confirmed by selective renal arteriography and renal punch-biopsy. There is a threefold method of treatment: --of the kidney condition by repeated haemodialysis and diuretics; --antihypertensive treatment; --treatment aimed at the aetiological pathology (heparin, anti-platelet aggregation and fresh plasma). Functional recovery of the kidney was obtained in both cases (after an interval of 1 year and an interval of 1 1/2 year). The authors review the diagnostic, physiopathological, morphological and therapeutic elements in the condition of cortical renal necrosis.

Adult↗