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PubMed1986

[Histopathology of drug and toxin induced kidney lesions].

An overview is presented of the morphologic patterns associated with drug or toxin induced renal lesions. Most prominent are the arteritis, glomerulonephritis, tubular necrosis, renal cortical necrosis, intratubular crystal deposition, acute and chronic interstitial fibrosis, interstitial granulomas and acute renal insufficiency with normal renal histology. Findings are correlated with the nature of the noxious substances. Sources of error arising from the insufficient specificity of the morphological findings and the differential diagnostic considerations are fully and critically presented. The review can serve to direct the recognition of etiologic relationships through the interpretation of morphological findings in the kidney.

Acute Kidney Injury↗
PubMed1969

Kidney lesions induced in rats by p-aminophenol.

Necrosis of the terminal third of the proximal convulated tubule develops in rats after a single intravenous injection of p-aminophenol hydrochloride. As the tubules regenerate a chronic inflammatory reaction occurs in the interstitial tissue, and this reaction extends beyond the original zone of injury. These findings are additional evidence that some aromatic compounds are selectively nephrotoxic and may be particularly relevant to the problem of renal damage associated with heavy and prolonged doses of analgesics.

Aniline Compounds↗
PubMed1987

Morphology of regressive changes in the kidney following experimental ischaemia.

Total or partial renal ischaemia was studied in rats and pigs in a series of experiments, after total devascularization (ligature of renal vessels and ureter); ligature of isolated renal artery; experimental embolization of renal artery by non-resorbable material; devascularization of a specific renal segment by deep, strangulating sutures. Morphological studies showed that the resulting necrotization is represented most frequently by coagulation necrosis, less frequently by colliquating necrosis. Occlusion of the renal artery by embolization or ligature leads only to partial necrotization or atrophy. Total devascularization of the renal hilus or total devascularization of a specific renal segment by strangulating sutures leads to total destruction of the devascularized (devitalized) tissues. Within 8-12 weeks, the whole organ changes into a small residue of connective tissue. The possibility of the use of the devascularization technique in the treatment of tumours is discussed.

Animals↗
PubMed2000

[Etiologies of chronic renal insufficiency in a adult internal medicine service in Dakar].

Chronic renal failure (CRF) sets public health problems both as its prevalence and its morbidity. The treatment is costly, that's why developing countries must engage in preventive strategies. In this view, a retrospective study was led in Le Dantec Hospital from January 1st, 1998 to December 31st 1993. As a preliminary to a countrywide survey, it is necessary to find out the causes of CRF clarify the causes of CRF in a hospital setting and sketch out a preventive strategy. The patients included in this study were those with CRF. The diagnosis of CRF were based on medical history data, anemia, but mainly biological and ultrasound imaging: creatininima more than 18 mg/l, and/or creatinine clearance less than 80 ml/mn, whose diagnosis was little sized kidney. Of the 5276 in patients, 384 had CRF representing 7% of sample. Only 261 cases were retained broken down into 119 females and 142 males (sex-ratio: 1.19). Age span ranges from 15 to 88 years with a mean of 44 years. Etiologies were dominated by unknown causes, 89 cases (34.23%). Nephroangiosclerosis was the most common known cause, 65 cases (25%) followed by diabetes nephropathy with 54 cases (20.69%) and chronic glomerulonephretic representing 41 cases (15.76%). Other causes were identified in various proportions: cortical necrosis (4 casesà, hereditary nephropathies (2 cases), interstitial nephropathy (1 case), nephroponophteois, kidney polykystosis, prostate adenoma and bilharziosis were all found in one case each. This study pointed out to a need for a nation-wide survey to define the aetiologies of CRF. The study also showed that an early diagnosis and adequate treatment of high blood pressure, diabetes and GNC should certainly constitute the principal axes of investigation for prevention.

Adolescent↗
PubMed2006

Acute renal failure in pregnancy in a developing country: twenty years of experience.

UNLABELLED: Acute renal failure (ARF) has become a rare complication of pregnancy in developed countries. The aim of this study was to describe changing trends in pregnancy-related acute renal failure (PR-ARF) in two successive periods; 1982-1991 and 1992-2002. From July 1982 to December 2002, 190 cases of PR-ARF were observed in Eastern India (11.6% of total number of ARF needing dialysis). Obstetrical complications were causative factors for ARF in 15% (65/426) and 10% (125/1201) of patients in the two periods, respectively. The incidence of PR-ARF fell from 15% in 1982-1991 to 10% in 1992-2002, with respect to the total number of acute renal failure cases. Post-abortal ARF showed a declining trend, 9% in the 1980s to 7% in the 2000s, of the total number of ARF cases. Preeclampsia-eclampsia was the cause of obstetrical ARF in 23% (1982-1991) and 14.4% (1992-2002) of cases in these two periods. The percentage of total ARF due to eclampsia declined from 3.5% during the period 1982-1991 to 1.4% in 1992-2002. Puerperal sepsis contributed to 0.8% of total ARF in recent years, compared to 2.4% in the earlier period. The incidence of cortical necrosis decreased significantly (p < 0.001) from 17% in 1982-1991 to 2.4% in the 2000s. The maternal mortality reduced to 6.4% in 1992-2002 from initial high mortality of 20% in the period of 1982-1991. CONCLUSION: PR-ARF which remained high in the initial period has decreased in recent years. This is associated with a declining trend in

Abortion, Induced↗
PubMed1976

Experimental galactosamine-induced hepatitis. Effect of anticoagulant and antifibrinolytic agents on microclot formation.

An experimental hepatitis was induced in rabbits by intravenous infusion of 1 g galactosamine per kilogram of body weight. Galactosamine administration caused microclot formation in kidneys, liver, lungs, and spleen in a low percentage. If, however, animals were infused with the fibrinolysis inhibitor epsilon-aminocaproic acid in addition to galactosamine, microclots were generated in a high percentage. The microclots exhibited typical staining characteristics like those observed in the generalized Shwartzman reaction. Some animals developed bilateral renal cortical necrosis. Heparin treatment prevented the occurrence of microclot fromation after galactosamine administration, but it neither prolonged the survival time of the animals nor prevented or reduced liver cell damage. Increases in serum GPT and bilirubin levels were similar in heparin-treated and untreated rabbits. The experiments indicate that disseminated intravascular coagulation is involved in galactosamine-induced hepatitis but does not contribute to the severity of the liver injury.

Alanine Transaminase↗
PubMed1984

Autopsy findings in postoperative acute renal failure patients, collected from the annuals of pathological autopsy cases in Japan.

Autopsy findings in post-surgical acute renal failure cases were studied in 131 cases on diaysis collected from annuals of pathological Autopsy Cases in Japan (1958-1981). Fifty (38.2%) abdominal and 48 (36.6%) cardiovascular operative procedures were the origins of the 131 post-operative acute renal failure patients treated by dialysis. The incidence of acute tubular necrosis was 68.7 per cent. There were 13 non-obstetric cases (19.9%) of acute bilateral cortical necrosis. Direct causes of death in postsurgical acute renal failure patients were mainly infection (61.7%) and bleeding (21.0%) The incidence of patients with infectious disease complicating postsurgical acute renal failure was 60.3 per cent and the rate of those between 20 and 70 years of age was constant. The incidence of patients with bleeding was 45.0 per cent and no significant differences were seen in the 20-70 year age range.

Acute Kidney Injury↗
PubMed2003

Comparative responses to mode of oral administration and dose of ochratoxin A or nephrotoxic extract of Penicillium polonicum in rats.

Administration of Penicillium polonicum extract to male Sprague-Dawley rats (200 g), either mixed in feed or given daily by gavage, for 5 days, had no clinical effects. However, at necropsy on day 6 marked histopathological changes occurred in renal tubule epithelia, including mitotic figures, karyomegalic nuclei, and frequent apoptosis identified specifically by TUNEL methodology and confocal microscopy. Ochratoxin A given similarly to rats (daily, 1 mg or 0.2 mg) was also clinically asymptomatic except for the 1 mg dose given by gavage; rats in this group lost weight. Marked renal tubular necrosis, though even without any significant accompanying apoptosis, was evident only at this higher dose by gavage; it was associated also with the highest incidence of renal DNA adducts and a disproportionately high concentration of ochratoxin A in plasma on day 6. Significantly fewer renal DNA adducts were detected in rats given 1 mg ochratoxin A in feed. The study demonstrates the potential for exaggerated toxicological responses to ochratoxin A administered by gavage through predicted consequential surges in the circulating concentration of the mycotoxin.

Administration, Oral↗
PubMed1975

Disseminated intravascular coagulation induced by liquoid in the rat. I. Correlation of hematologic and complement abnormalities with renal lesions studied by light, fluorescence, and electron microscopy.

Under the proper experimental conditions, disseminated intravascular coagulation,"an intermediary mechanism of disease," results in the classic endotoxin-induced generalized Shwartzman reaction. Other substances, such as liquoid, a highly negatively charged anticoagulant, trigger a generalized Shwartzman reaction-like phenomenon in rabbits. We studied the effects of a single high intravenous dose of liquoid (12.5 mg.) upon the rat's coagulation and complement systems and their correlation with the kidney morphology by light, fluorescence, and electron microscopy. Thrombin time was prolonged; fibrinogen, plasminogen, and factors VIII and XII concentrations were markedly decreased, whereas fibrin degradation products were increased in the experimental animals when compared with the saline-injected controls (p greater than 0.001). Total hemolytic complement, hemolytic activity of terminal components (C3 to C9), and C3 protein concentration were significantly reduced (p greater than 0.001). The liquoid-injected rats developed cortical necrosis and manifested oliguria and anuria, with elevated blood urea nitrogen levels, when survival was longer than 3 hours. Histologically, thrombi of fibrin-like material filled the glomerular capillaries. Deposits of fibrin, and also of immunoglobulin G and C3, were readily identifiable by specific immunofluorescence, Linear or granular fluorescent deposits (or both) along the glomerular basement membranes and in the mesangium were observed. Electron microscopy demonstrated necrosis of glomeruli and abundant thrombi of fluffy, compact granular, or fibrillar electron-dense material. No typical fibrin periodicity was detected. These experiments support the concept of activation of the coagulation and the complement systems. We postulate that liquoid produced not only a consumptive coagulopathy in the rat but also a direct or perhaps anindirect activation of complement. Whether this latter has occurred through the classic or an alternate pathway remains to be elucidated.

Animals↗
PubMed1963

Antigen-antibody reaction in the pathogenesis of bilateral renal cortical necrosis.

In the presence of reticuloendothelial blockade, the intravenous injection of a protein antigen into specifically immunized rabbits or the infusion of soluble immune complexes into normal animals has been shown to result in the production of bilateral renal cortical necrosis. The similarity in the pathogenesis of this lesion and that seen in the classical generalized Shwartzman reaction produced by bacterial endotoxins is indicated by (a) the failure of both lesions to develop in animals pretreated with large doses of heparin, (b) by the finding of "heparin-precipitable fibrinogen" in the circulation, and (c) by the presence of massive fibrin deposits within the glomerular capillaries. These findings indicate that antigen-antibody reactions in vivo are capable of activating the blood coagulation system and that the mode of action of bacterial endotoxins may have an immunological basis.

Animals↗
PubMed1977

Pathogenesis of vascular injury in rejecting rat renal allografts.

Unmodified rejection of rat renal allografts was characterized by the early onset and rapid progression of endothelial damage in venules and capillaries which culminated in ischemic cortical necrosis. This pattern of endothelial injury correlated with lymphocyte accumulation in vascular lumens and could not be duplicated by renal perfusion with alloantibodies or prevented by C'3 depletion. In contrast, endothelial integrity and normal graft function were maintained over study intervals extending to 200 days when Brown Norway (BN) rat kidneys were transplanted into Lewis (Le) rat kidney recipients subjected to neonatal thymectomy or lymph drainage. Vascular lesions occurred when syngeneic thoracic duct lymphocytes were transfused into these recipients, but irreversible endothelial injury could be prevented by simultaneous injections of immune plasma. These findings indicate that the destruction of donor endothelium is mediated by thymus-dependent immune mechanisms which can be altered by thoracic duct drainage to promote indefinite survival of renal allografts across major histocompatibility loci.

Animals↗
PubMed2006

[A new method for standardized diagnosis following renal transplantation. Ultrasound with contrast enhancement].

Ultrasound (US) imaging is an important diagnostic tool following renal transplantation. Unfortunately, due to the heterogeneity of the recipients and their multimorbidity, imaging procedures in the early phase after kidney transplantation are difficult and of limited use. We performed a study to evaluate the use of a contrast enhancer for US examination as a standardized method in the follow-up of kidney transplant recipients.The study included 40 recipients: 32 were examined on the 5th to 7th day following transplantation and 8 patients at the time when clinically suspicious findings occurred (acute rejection, tumor, acute tubular necrosis). Following the intravenous application of the contrast medium, pictures were taken during the arterial and parenchymatous phase and compared with conventional B-mode and power Doppler pictures of the same visual plane. Three examiners assessed different parameters of the transplant organ (max. vascularized area, suspected hematomas, tumors, rejection, acute tubular necrosis). Findings were confirmed by histological results of a biopsy if rejection, tumor, or acute tubular necrosis were suspected. Application of ultrasound contrast medium significantly increased visualization of the vascularized kidney area. Also, US findings in the follow-up after acute rejection therapy corresponded with the clinical course; 19 hematomas could be detected with contrast medium compared to only 9 without. With contrast medium a perfusion deficit was detectable in three patients compared to one patient with power Doppler US. Also, US contrast medium helped to detect tumor vascularization in two patients in whom conventional sonography suspected no abnormality. Ultrasound contrast medium enhancement is a reproducible, reliable, and easy to apply method which is superior to conventional sonography in the follow-up after kidney transplantation. This method is also helpful to detect and control acute rejections and to better visualize hematomas, deficits of perfusion, and tumors.

Adolescent↗
PubMed1973

Interaction of angiotensin with disseminated intravascular coagulation: a possible mechanism in the genesis of acute renal failure.

Because of the importance of the renin-angiotensin system in renal homeostatic mechanisms, the effect of angiotensin administration upon disseminated intravascular coagulation has been studied in rabbits. An infusion of angiotensin II (0.1 mug/kg/min for 2 hours) produced neither histologic abnormalities in the kidneys nor an elevation of creatinine. After an infusion of thrombin (2.0 units/kg/min for 2 hours) only 3 of 10 rabbits, when sacrified 24 hours later, showed histologic lesions comprised of occasional fibrin thrombi and foci of tubular necrosis. Creatinine levels did not rise. In contrast, the combination of angiotensin and thrombin resulted in renal lesions in 12 of 14 animals. Four had frank cortical necrosis, while combinations of tubular necrosis, glomerular thrombosis and segmental glomerular infarction occurred in the others, together with elevated creatinine levels. Blockade of alpha-adrenoreceptors with phenoxybenzamine in 12 animals did not prevent either these histologic changes or creatinine elevation, showing that the effect of angiotensin was independent of alpha-adrenoreceptor stimulation. The synergistic interaction between angiotensin and disseminated intravascular coagulation was not explained by differences in the consumption of plasma fibrinogen but apparently was due to localization of fibrin thrombi within glomerular capillaries by the vasomotor actions of angiotensin, as has previously been shown to occur with alpha-adrenoreceptor simulation. Such a mechanism might contribute to renal glomerular deposition of fibrin in acute ischemic renal failure.

Acute Kidney Injury↗
PubMed2005

Management and outcome of living kidney grafts with multiple arteries.

PURPOSE: Kidney allografts with multiple renal arteries (MRAs) have been used with increasing frequency since the advent of laparoscopic live donor nephrectomy. To determine if MRA grafts affect the short- and long-term outcomes of grafts and patients, we analyzed 340 grafts procured by open nephrectomy. METHODS: We divided the graft recipients into five groups according to the methods used for vascular reconstruction. We compared patient and graft survival, serum creatinine levels, total (rewarm) ischemic times (TIT), incidence of acute tubular necrosis (ATN), need for antihypertensive drugs, incidence of acute rejection episodes, and vascular and urologic complications, between the MRA group and a control group of patients with single-artery renal grafts. RESULTS: In patients who underwent multiple anastomoses in situ, prolonged TIT resulted in an increased incidence of ATN, but there was no significant difference between the MRA groups and the control group (P = 0.45). The incidence of vascular complications was higher in the MRA groups (P < 0.01), but there were no significant differences in the other variables among the groups. CONCLUSION: Multiple renal artery grafts procured by open nephrectomy can be transplanted as successfully as those with single arteries, by using meticulous suturing techniques.

Adolescent↗
PubMed1977

Neonatal renal papillary and cortical necrosis.

Renal papillary and cortical necrosis (RPCN) in newborn infants has been generally fatal. This report describes three survivors of neonatal RPCN who have been followed up from 23 to 57 months. The cause of RPCN was hemorrhage and asphyxia neonatorum in two patients and hemorrhage and shock in one. The diagnosis was confirmed in one patient by an excretory urogram at 3 weeks of age and in another by renal biopsy at 5 weeks of age. In the third, diagnosis was made retrospectively. Findings from subsequent examination showed that creatinine clearance was normal in one patient, slightly reduced in another, and moderately reduced in the third. Maximum ability to concentrate urine was decreased in all. Follow-up excretory urograms in all three patients showed dilated bizarre-appearing calices and renal cortical atrophy. These radiologic findings are similar to those found in segmental hypoplasia or chronic (atrophic) pyelonephritis.

Biopsy↗
PubMed1982

Different functional characteristics of residual nephrons in infantile vs adult diffuse cortical necrosis.

In this report we study the functional characteristics of residual nephrons in a 37 year-old woman, 7 months after diffuse bilateral cortical necrosis (CN) of unknown etiology, and in two infants, aged 13 and 15 months, who suffered CN in early infancy after surgical shock and acute dehydration, respectively. In the three cases CN was proven histologically by renal biopsy but undamaged nephrons were only present in the juxtamedullary area in the adult patient whereas in the two infants they were located in the outer part of the cortex. At the time of the study all patients presented a similar degree of renal insufficiency (creatinine clearance: 17-23 ml/min/1.37 m2). The adult patient showed a partly conserved ability to concentrate the urine, a marked free water formation in relation to the degree of distal sodium delivery and an unimpaired capacity to acidify the urine after an acid load. Both infants, by the contrary, were unable to concentrate the urine, had lower free water formation at similar rates of distal sodium delivery and presented a clear incapacity to acidify the urine. These results confirm previous finding indicating the sparing of juxtamedullary nephrons after CN in the adult subject but favor the existence of a surviving population of superficial nephron when CN occurs in early infancy. These differences are probably in relation with associated damage of deep cortex and medulla infancy due to the specific characteristics of blood flow distribution present at that age.

Acute Kidney Injury↗
PubMed2006

Renal parenchymal oxygenation and hypoxia adaptation in acute kidney injury.

The pathogenesis of acute kidney injury (AKI), formally termed acute tubular necrosis, is complex and, phenotypically, may range from functional dysregulation without overt morphological features to literal tubular destruction. Hypoxia results from imbalanced oxygen supply and consumption. Increasing evidence supports the view that regional renal hypoxia occurs in AKI irrespective of the underlying condition, even under circumstances basically believed to reflect 'direct' tubulotoxicity. However, at present, it is remains unclear whether hypoxia per se or, rather, re-oxygenation (possibly through reactive oxygen species) causes AKI. Data regarding renal hypoxia in the clinical situation of AKI are lacking and our current concepts regarding renal oxygenation during acute renal failure are presumptive and largely derived from experimental studies. There is robust experimental evidence that AKI is often associated with altered intrarenal microcirculation and oxygenation. Furthermore, renal parenchymal oxygen deprivation seems to participate in the pathogenesis of experimental AKI, induced by exogenous nephrotoxins (such as contrast media, non-steroidal anti-inflammatory drugs or amphotericin), sepsis, pigment and obstructive nephropathies. Sub-lethal cellular hypoxia engenders adaptational responses through hypoxia-inducible factors (HIF). Forthcoming technologies to modulate the HIF system form a novel potential therapeutic approach for AKI.

Adaptation, Physiological↗
PubMed2006

Anti-inflammatory and antinecrotic effects of the volatile anesthetic sevoflurane in kidney proximal tubule cells.

Renal ischemia-reperfusion (IR) injury is a major clinical problem without effective therapy. We recently reported that volatile anesthetics protect against renal IR injury, in part, via their anti-inflammatory properties. In this study, we demonstrate the anti-inflammatory and antinecrotic effects of sevoflurane in cultured kidney proximal tubule cells and probed the mechanisms of sevoflurane-induced renal cellular protection. To mimic inflammation, human kidney proximal tubule (HK-2) cells were treated with tumor necrosis factor-alpha (TNF-alpha; 25 ng/ml) in the presence or absence of sevoflurane. In addition, we studied the effects of sevoflurane pretreatment on hydrogen peroxide (H2O2)-induced necrotic cell death in HK-2 or porcine proximal tubule (LLC-PK1) cells. We demonstrate that sevoflurane suppressed proinflammatory effects of TNF-alpha evidenced by attenuated upregulation of proinflammatory cytokine mRNA (TNF-alpha, MCP-1) and ICAM-1 protein and reduced nuclear translocation of the proinflammatory transcription factors NF-kappaB and AP-1. Sevoflurane reduced necrotic cell death induced with H2O2 in HK-2 cells as well as in LLC-PK1 cells. Sevoflurane treatment resulted in phosphorylation of prosurvival kinases, ERK and Akt, and increased de novo HSP-70 protein synthesis without affecting the synthesis of HSP-27 or HSP-32. We conclude that sevoflurane has direct anti-inflammatory and antinecrotic effects in vitro in a renal cell type particularly sensitive to injury following IR injury. These mechanisms may, in part, account for volatile anesthetics' protective effects against renal IR injury.

Anesthetics, Inhalation↗