A case of renal necrosis and fibrosis in the immediate newborn period. Association with the twin-to-twin transfusion syndrome.
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Three young infants who had severe gastroenteritis developed radiological and histological features of renal tubular necrosis. Characteristically the excretion urogram showed renal enlargement with prolonged and heavy opacification of the renal parenchyma and a pronounced increase in density of the pyramids. Subsequent radiological studies showed extensive papillary necrosis. Though these infants are now apparently fit, renal damage has occurred and this may eventually give rise to features indistinguishable from chronic pyelonephritis.
INTRODUCTION: Subcapsular cortical damage (SCCD) is a characteristic pathological change, which is seen in renal allograft biopsy specimen obtained immediately after laparoscopic donor nephrectomy (LDN). In this study we evaluated the early and late histopathological effect of SCCD examining renal allograft biopsy specimens obtained after kidney transplantation. MATERIALS AND METHODS: Laparoscopic donor nephrectomy was performed on 250 donors between July 2000 and September 2004 in our institution. Allograft biopsy of all 250 kidneys was performed immediately after LDN (zero hour biopsy). Of 250 biopsy specimens, 105 were diagnosed as SCCD and the allograft biopsy specimens obtained from 105 recipients after transplantation were enrolled in this study. All specimens were routinely examined by using light microscopy and immunofluorescence. RESULTS: In 87 patients 256 allograft biopsy specimens did not show post-pathological changes of SCCD. Twenty biopsy specimens obtained from 18 recipients showed tubular necrosis and a partly tubular regeneration and patchy interstitial hemorrhage, which seemed to be caused by SCCD. Ten allograft biopsy specimens from nine recipients demonstrated residual pathologic changes in SCCD early after transplantation. The other 10 specimens from nine recipients had abnormal histopathologic changes including interstitial edema and fibrosis, tubular atrophy and glomerular sclerosis in the subcapsular cortex late after transplantation. CONCLUSION: The early change of SCCD after transplantation remained intact and partial regeneration and the late showed subcapsular fibrosis with glomerular sclerosis. The incidence of the subcapsular lesions due to SCCD after transplantation was 17% in 105 allografts.
Ischemia-reperfusion injury is often responsible for delayed graft function after transplantation. Trimetazidine (TMZ) is an antioxidant agent used to protect grafts from ischemia-reperfusion injury. The aim of the study was to examine the effect of TMZ on nucleotide profile in rat kidney with ischemia-reperfusion injury. The study was carried out on Wistar rats divided into two groups: animals treated with TMZ and control group receiving placebo. TMZ 10mg/kg/day was administrated for 30 days. Concentrations of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), adenosine (Ado), guanosine triphosphate (GTP), guanosine diphosphate (GDP), guanosine monophosphate (GMP), guanosine (Guo), inosine monophosphate (IMP), inosine (Ino), hypoxanthine (Hyp), xanthine (Xan), uric acid (UA), uridine (Urd), nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) were determined in kidney tissues after ischemia-reperfusion using HPLC. The total adenine nucleotide concentration (TAN) and adenylate energy charge (AEC) were also determined. Moreover the kidneys were evaluated histologically. Tissue concentrations of ATP, ADP, AMP, TAN and AEC were significantly increased in kidneys from rats treated with TMZ in comparison with rats receiving placebo. Concentrations of products of nucleotide degradation: inosine (Ino), guanosine (Guo) and uridine (Urd), as well as oxypurines: Hyp and Xan, were significantly decreased in rats treated with trimetazidine. Moreover, significantly less pronounced acute tubular necrosis was observed in kidneys of rats treated with TMZ. These results suggest that trimetazidine protects against dephosphorylation of nucleotides and ischemic damage.
Renal pathological changes were studied by renal biopsy in 31 patients bitten by tropical poisonous snakes which included seasnake (2 cases), cobra (11 cases), green-pit viper (8 cases) and Russell's viper (10 cases). Renal failure was present only in patients bitten by seasnake and Russell's viper. Glomerular mesangial proliferation was noted in the victims of cobra, green-pit viper and Russell's viper. There was deposition of IgM AND C3 in the glomerular mesangium with extension along the capillary walls. Fibrin deposition was seen in green-pit viper cases. By electron microscopy electron dense deposits were observed in the glomerular basement membrane-like matrix. Irregular thickening of the basement membrane was found in cobra cases. Vascular changes included arteritis of the interlobular artery with C3 deposition in the arterial walls in Russell's viper cases and thrombophlebitis in both green-pit viper's and Russell's viper's victims. Dense deposits of C3 in the arteriolar walls were noted in viper-bite and cobra-bite. Tubular necrosis was demonstrated in patients envenomated by green-pit viper and Russell's viper. Necrosis was severe in seasnake and Russell's viper poisoning, but was mild in green-pit viper cases.
Cadaver kidneys from donors with DIC appear to have an increased incidence of delayed function and primary nonfunction. These kidneys may be safely transplanted if cortical necrosis is ruled out. Heparin, antiplatelet therapy, and withholding of cyclosporin A therapy in the early post-transplantation period may improve renal function if there is evidence of glomerular capillary thrombosis.
Cortical necrosis is a rare complication of renal transplants, which requires urgent diagnosis and management to avoid unnecessary immunosuppression. Seven renal transplants with suspected cortical necrosis were evaluated by Doppler-US, 99mTc-DTPA-perfusion study and Gd-DTPA-enhanced dynamic MRI. In four transplants, cortical necrosis was confirmed by angiography and histology. In diagnosing cortical necrosis with preserved medullary perfusion (n = 2) dynamic MRI was superior to the other modalities. Totally necrotic renal transplants (n = 2) were reliably diagnosed by all imaging methods.
Previous studies have shown ocular haemorrhages in choline-deficient rats. The aim of this paper is to study further the relationship between ocular and renal lesions and biochemical alterations in rats fed a choline-deficient diet. Fifty one weanling male Wistar rats, were divided into two groups. Thirty one of them were fed a choline-deficient diet and the rest was fed a choline-supplemented diet ad libitum. Animals from both groups were killed between the fifth and the eighth day. Urea, creatinine and homocysteine concentrations in blood were determined. Eyes were used for light microscopy study; high resolution light microscopy and the study of the retina as "rétine a plat". Kidneys were studied by light microscopy. Choline-supplemented rats did not show ocular or renal lesion. Choline-deficient rats that showed renal lesions, tubular or cortical necrosis, did not always have ocular changes. There were no ocular changes in the only choline-deficient rat without renal lesion. The ocular changes consisted mainly in haemorrhage in both cameras and ciliary and vitreous bodies. Correlations between ocular and renal lesion (r = 0.72, p < 0.0001, CI 95%: 0.48-0.86); ocular lesion and creatinine (r = 0.86, p < 0.0001, Cl 95%: 0.72-0.93) and ocular lesion and urea (r = 0.70, p < 0.0001, Cl 95%: 0.44-0.85) were positive. Choline-deficiency induces ocular haemorrhagic lesions after the development of renal necrosis. The ocular pathology could be due to the immaturity of the ocular vasculature at this age. The hyaloid, choroid and retinal system are involved.
Renal cortical and medullary infarction are 2 of the severe complications of perinatal asphyxia and shock. The angiographic and ultrasonographic findings in these conditions have not been described previously. They demonstrate nephromegaly, a nonhomogeneous nephrogram, and internal echoes. Similar findings may be seen in renal vein thrombosis, hydronephrosis, and polycystic kidneys.
The acute unmodified rejection of (Lewis x Brown Norway) F(1) to Lewis renal allografts is characterized by an early and progressive lymphoid cell infiltrate, glomerular necrosis, necrotizing arteritis and ischemic cortical necrosis leading to graft destruction. A single low dose of enhancing antiserum given at the time of transplantation prolongs graft survival by abrogating the necrotizing lesions in glomeruli and arteries and the subsequent cortical necrosis. Passive enhancement in this model is interpreted as representing predominantly a block in the humoral antibody-mediated rejection response. It is suggested that the block is effected mainly, peripherally, ie, at the level of the transplanted kidney itself.
Electron microscopic examination of biopsy material from two patients with renal cortical necrosis following Russell's viper bite, showed extensive destruction of glomerular and tubular cells with haemorrhage into the glomerular urinary space and tubules. The non-selective cell destruction seen suggests an ischaemic aetiology and the presence of fibrin in the glomeruli indicates that the ischaemia may be due to intravascular coagulation.
A study was made of the acute and chronic (15 days) functional and morphologic effects on the rat kidney of warm ischemia and contralateral nephrectomy, in order to define a suitable animal model for testing renal transplant preservation techniques when warm ischemia is a contributing factor. Spontaneous recovery from 30-min warm ischemia was complete, and the model was consequently unsuitable; the high mortality from 90 min was unacceptable. Warm ischemia of 60 minutes produced severe renal tubular necrosis, an acceptable mortality, residual morphologic damage, and impairment of isolated kidney perfusion parameters at 15 days. Renal function in vivo was normal in many of these animals, despite appreciable residual morphologic changes, and it is evident that functional data alone are not sufficient for assessment of preservation regimens.
The nephrotoxicity of dimethylarsinic acid (cacodylic acid, DMA) was examined in male and female F344/DuCrj rats. DMA administered perorally at doses of 113, 85, and 57 mg/kg for 4 weeks produced dose-related decreases in body weight and survival rate in both sexes. Mortality was higher and appeared more quickly in females than in males. Histopathological findings in the kidney were proximal tubular degeneration and necrosis, as well as papillary necrosis, and hyperplasia of the epithelium covering the papillae. Since extensive proximal tubular necrosis was observed only in dead animals of both sexes, and not in survivors or the controls, it was therefore concluded that the main cause of death could be attributed to nephrotoxicity of DMA. The results thus show that DMA is nephrotoxic to both male and female rats.
Intrarenal microlymphatic filling was observed during a microangiographic and histologic study of unmodified canine allograft rejection. The extent of lymphatic visualization was correlated with the pathophysiologic state of the allograft. An example of renal lymphatic visualization following arterial perfusion of a human specimen is also presented. During early rejection, as microvascular and histologic alteration became more severe, there was prominent visualization of lymphatics. However, in late rejection, as cortical necrosis developed, lymphatic filling was less evident. Lymphatic visualization following arterial perfusion during rejection depends on progressive loss of microvascular integrity, contrast extravasation and subsequent filling of lymphatics which are acting as an alternate route of drainage for the excess interstitial edema present due to immune injury.
The accuracy of color Doppler US (CDUS) for the detection of main renal transplant artery stenoses is excellent (Se 92%; SP 99%). Whereas the sensitivity of CDUS is still unsatisfactory for the detection of arterial branch stenosis (Se 70%), it has become higher than previously reported because of the ability of color flow images to identify hemodynamic changes at the site of stenosis and focal downstream repercussions in the case of tight stenosis. Color Doppler US is a valuable method in the detection of segmental infarction or large areas of cortical necrosis. However, small superficial cortical perfusion defects are usually undetectable by color Doppler. Contrast-enhanced MRI appears to be more accurate than color Doppler US; it is useful in confirming the diagnosis of infarction and detecting small infarcts missed by color Doppler US, and provides an accurate evaluation of the extent of the infarct; Spectral features (reflux during the whole diastole) obtained from renal arteries in case of acute renal vein thrombosis are suggestive but not specific since they can be observed in the case of severe acute rejection with cortical necrosis. Such findings associated with a lack of venous Doppler signals in the whole kidney are highly suggestive of renal transplant vein thrombosis. Post-biopsy arteriovenous fistulas and false arterial aneurysms are accurately detected by color Doppler Imaging. Color Doppler appears to be the primary Imaging modality for early detection of renal allograft vascular complications.(ABSTRACT TRUNCATED AT 250 WORDS)
The clinical detection of evolving acute tubular necrosis (ATN) and differentiating it from other causes of renal failure are currently limited. The maintenance of the corticomedullary sodium gradient, an indicator of normal kidney function, is presumably lost early in the course of ATN. Herein, sodium magnetic resonance imaging (23Na MRI) was applied to study the early alteration in renal sodium distribution in rat kidneys 6 h after the induction of ATN. Three-dimensional gradient echo sodium images were recorded at 4.7 T with high spatial resolution. ATN was produced by the administration of radiologic contrast medium, combined with inhibition of nitric oxide and prostaglandin synthesis. The sodium images revealed that the sham-controlled kidney exhibited a linear increase in sodium concentration along the corticomedullary axis of 30+/-2 mmol/l/mm, resulting in an inner medulla to cortex sodium ratio of 4.3+/-0.3 (n=5). In the ATN kidney, however, the cortico-outer medullary sodium gradient was reduced by 21% (P<0.01, n=7) and the inner medulla to cortex sodium ratio was decreased by 40% (P<0.001, n=7). Small, though significant, increments in plasma creatinine at this time inversely correlated with the decline in the corticomedullary sodium gradient. Histological findings demonstrated outer medullary ATN involving 4% of medullary thick ascending limbs. Hence, 23Na MRI non-invasively quantified changes in the corticomedullary sodium gradient in the ATN kidney when morphologic tubular injury was still focal and very limited. MRI detection of corticomedullary sodium gradient abnormalities may serve to identify evolving ATN at its early phases.
In 21 recipients of renal transplants suspected of allograft necrosis, the authors correlated the results of imaging to pathologic and histologic data in order to describe the magnetic resonance (MR) imaging and color Doppler ultrasonographic (US) characteristics of infarction. All patients underwent MR imaging performed with and without gadolinium tetraazacyclododecanetetraacetic acid (DOTA) and color Doppler US. Nonenhanced T1-weighted images showed no obvious changes, whereas nonenhanced T2-weighted images demonstrated a slight increase in signal intensity in areas of ischemic necrosis and low or heterogeneous signal intensity in areas of hemorrhagic necrosis. Gd-DOTA-enhanced MR images showed no contrast material uptake in infarcted areas. Color Doppler US characteristics of infarction included absence of Doppler signal and alteration of the cortical echogenic structure, particularly in cases of ischemic necrosis. Color Doppler US allows measurement of vascular resistance and assessment of intrarenal vasculature and the renal pedicle. Gd-DOTA-enhanced MR imaging is useful in confirming the diagnosis of infarction and provides an accurate evaluation of the extent of the infarct.
Diffuse renal cortical necrosis from any cause is rare in the Western World. Over the last 5 decades, there have been isolated case reports of acute cortical necrosis as a consequence of acute pancreatitis, but the long-term outcome of these patients has not previously been reported. Here, we report 3 young men, aged 16-21 years, who have presented over the past 19 years with severe acute pancreatitis associated with oliguric acute renal failure. They were all found to have diffuse renal cortical necrosis and consequently made no renal recovery. Despite the appreciable mortality associated with acute pancreatitis complicated by acute renal failure, they all survived the initial illness and all have successfully undergone renal transplantation. We present a detailed account of each patient including diagnostic strategies and discuss the possible factors contributing to a favorable outcome in these patients.