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Tubular Necrosis (tubular + necrosis)

Distribution by Scientific Domains

Medical Sciences	88%

Distribution within Medical Sciences

Transplantation	42%
Hepatology	15%

Kinds of Tubular Necrosis

acute tubular necrosis

Selected Abstracts

MINIMAL CHANGE DISEASE AND ACUTE TUBULAR NECROSIS CAUSED BY DICLOFENAC

NEPHROLOGY, Issue 1 2008
KRESIMIR GALESIC
[source]

Can Renal Acute Tubular Necrosis Be Differentiated from Autolysis at Autopsy?,

JOURNAL OF FORENSIC SCIENCES, Issue 2 2009
Linda Kocovski B.Sc.
Abstract:, We investigate the morphological characteristics that may differentiate between ischemic acute tubular necrosis (ATN) and autolysis in postmortem samples. Renal tissue from 57 postmortem cases with an antemortem diagnosis of ATN and 57 age-/sex-matched control cases were examined for 10 morphological characteristics: epithelial proliferation (Ki-67 immunoperoxidase positivity), fibrin thrombi, tubular epithelial whorls, mitoses, casts, autolysis, tubulorrhexis, epithelial flattening, interstitial inflammation, and interstitial expansion. Tubular epithelial whorls were found in 16 ATN cases and were absent in controls. These findings suggest that specific morphological criteria may distinguish ischemic ATN from autolysis. Diagnoses of ATN may be confirmed using these combined criteria as contributing to cause of death and/or to ascertain previously undiagnosed cases of ATN postmortem. [source]

Acute kidney injury in cirrhosis,

HEPATOLOGY, Issue 6 2008
Guadalupe Garcia-Tsao
Acute renal failure (ARF), recently renamed acute kidney injury (AKI), is a relatively frequent problem, occurring in approximately 20% of hospitalized patients with cirrhosis. Although serum creatinine may underestimate the degree of renal dysfunction in cirrhosis, measures to diagnose and treat AKI should be made in patients in whom serum creatinine rises abruptly by 0.3 mg/dL or more (,26.4 ,mol/L) or increases by 150% or more (1.5-fold) from baseline. The most common causes of ARF (the term is used interchangeably with AKI) in cirrhosis are prerenal azotemia (volume-responsive prerenal AKI), acute tubular necrosis, and hepatorenal syndrome (HRS), a functional type of prerenal AKI exclusive of cirrhosis that does not respond to volume repletion. Because of the progressive vasodilatory state of cirrhosis that leads to relative hypovolemia and decreased renal blood flow, patients with decompensated cirrhosis are very susceptible to developing AKI with events associated with a decrease in effective arterial blood volume. HRS can occur spontaneously but is more frequently precipitated by events that worsen vasodilatation, such as spontaneous bacterial peritonitis. Conclusion: Specific therapies of AKI depend on the most likely cause and mechanism. Vasoconstrictors are useful bridging therapies in HRS. Ultimately, liver transplantation is indicated in otherwise reasonable candidates in whom AKI does not resolve with specific therapy. (HEPATOLOGY 2008;48:2064-2077.) [source]

Acute renal failure in patients with cirrhosis: Perspectives in the age of MELD

HEPATOLOGY, Issue 2 2003
Richard Moreau
In patients with cirrhosis, acute renal failure is mainly due to prerenal failure (caused by renal hypoperfusion) and tubular necrosis. The main causes of prerenal failure are "true hypovolemia" (induced by hemorrhage or gastrointestinal or renal fluid losses), sepsis, or type 1 hepatorenal syndrome (HRS). The frequency of prerenal failure due to the administration of nonsteroidal anti-inflammatory drugs or intravascular radiocontrast agents is unknown. Prerenal failure is rapidly reversible after restoration of renal blood flow. Treatment is directed to the cause of hypoperfusion, and fluid replacement is used to treat most cases of "non-HRS" prerenal failure. In patients with type 1 HRS with very low short-term survival rate, liver transplantation is the ideal treatment. Systemic vasoconstrictor therapy (with terlipressin, noradrenaline, or midodrine [combined with octreotide]) may improve renal function in patients with type 1 HRS waiting for liver transplantation. MARS (for molecular adsorbent recirculating system) and the transjugular intrahepatic portosystemic shunt may also improve renal function in these patients. In patients with cirrhosis, acute tubular necrosis is mainly due to an ischemic insult to the renal tubules. The most common condition leading to ischemic acute tubular necrosis is severe and sustained prerenal failure. Little is known about the natural course and treatment (i.e., renal replacement therapy) of cirrhosis-associated acute tubular necrosis. [source]

Novel approaches to assessing renal function in cirrhotic liver disease

HEPATOLOGY RESEARCH, Issue 9 2007
Andrew J. Portal
Renal dysfunction is common in patients with end-stage liver disease. Etiological factors include conditions as diverse as acute tubular necrosis, immunoglobulin A nephropathy and hepatorenal syndrome. Current standard tests of renal function, such as measurement of serum urea and creatinine levels, are inaccurate as the synthesis of these markers is affected by the native liver pathology. This article reviews novel markers of renal function and their potential use in patients with liver disease. [source]

Long-term evolution of the acute tubular necrosis (ATN) induced by glycerol: role of myofibroblasts and macrophages

INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 4 2002
Telma J. Soares
Summary. Late structural changes such as interstitial fibrosis in the renal cortex and tubular atrophy have been detected after severe acute tubular necrosis (ATN). The aim of this study was to investigate the expression of fibronectin, ,-smooth muscle actin and macrophages during the evolution of the ATN induced by glycerol and their relationship with the late structural changes observed in the kidneys of these animals. Forty-nine male Wistar rats were injected with a 50% glycerol solution, 8 mL/kg (4 mL/kg applied i.m. to each hind leg) and 14 with 0.15 m NaCl solution. Before glycerol injection on day 1, water was removed for 17 h. Blood and urine samples were collected 1 day after the injection to quantify sodium and creatinine. The animals were killed 5, 30 and 60 days after the injections and the kidneys removed for histological and immunohistochemical studies. The results of the histological and immunohistochemical studies were scored according to the extent of lesion or staining in the cortical tubulointerstitium, respectively. The percentage of tubulointerstitial lesions was determined by morphometry. Glycerol-injected rats presented a transitory increase in plasma creatinine levels and in fractional sodium excretion. The immunohistochemical studies showed increased fibronectin, ,-smooth muscle actin (,-SM-actin), TGF-, and ED-1 (macrophages) staining in the renal cortex from rats killed 5, 30 and 60 days after glycerol injection (P < 0.05) compared to control. The animals killed on day 30 and 60 also presented chronic lesions (fibrosis, tubular dilatation and atrophy) in the renal cortex, despite the recovery of renal function. Macrophages, TGF-, and myofibroblasts may have contributed to the development of renal fibrosis in these rats. [source]

Can Renal Acute Tubular Necrosis Be Differentiated from Autolysis at Autopsy?,

Melatonin, a potent regulator of hemeoxygenase-1, reduces cardiopulmonary bypass-induced renal damage in rats

JOURNAL OF PINEAL RESEARCH, Issue 3 2009
Zhongqiu Wang
Abstract:, Acute renal dysfunction is a frequent complication after cardiac surgery with cardiopulmonary bypass (CPB). This study was designed to evaluate the potential protective effect of melatonin on CPB-induced renal damage in a rat model. Forty male Sprague,Dawley rats were randomly divided into four groups: sham, control (CPB + placebo), low dose of melatonin (CPB + 10 mg/kg melatonin) and high dose of melatonin (CPB + 20 mg/kg melatonin). Blood samples were collected at the beginning, at the end of CPB, and at 0.5, 1, 2, 3, and 24 hr postoperation. Serum creatinine and blood urea nitrogen levels were assayed. Rats were killed 24 hr after surgery, the histologic appearance of the kidney and malondialdehyde (MDA), myeloperoxidase (MPO), catalase (CAT) and superoxide dismutase (SOD) contents were determined. The expression levels of hemeoxygenase-1 (HO-1) protein and gene were determined using western blotting and real-time PCR, respectively. In the control group, CPB surgery significantly increased urea, creatinine levels in serum, MDA and MPO levels in tissues, while decreasing SOD and CAT activities in tissues. Histopathologic findings of the control group confirmed that there was renal impairment by cast formation and tubular necrosis in the tubular epithelium. These changes were markedly reversed in both low dose of melatonin and high dose of melatonin groups. Furthermore, HO-1 gene transcript and protein were significantly upregulated in the kidney tissues after melatonin treatment compared with the placebo treatment. Our findings show that melatonin was effective in preventing CPB-induced renal damage probably through its antioxidant function and upregulation of HO-1. [source]

Clinical features of acute renal failure associated with hepatitis A virus infection

JOURNAL OF VIRAL HEPATITIS, Issue 9 2010
Y. J. Jung
Summary., Acute hepatitis A (AHA) is one of the most common infectious diseases; it is usually a self-limiting disease affecting the liver. Although extrahepatic manifestations are not common, some cases have been reported associated with acute renal failure. We reviewed the clinical features of patients with AHA complicated by acute renal failure (ARF group) and compared them with patients with noncomplicated AHA (non-ARF group). The medical records of 208 consecutive patients with AHA who were diagnosed between January 2003 and October 2008 were reviewed. We identified 15 patients (7.2%) with ARF associated with AHA. There were no differences between the ARF and non-ARF group with regard to gender and age. The peak value of alanine aminotransferase (ALT) (median: 6060 IU/L vs 1792 IU/L, P < 0.001), prothrombin time (PT) (International normalized ratio, median 1.72 vs 1.10, P < 0.001), and total bilirubin level (median: 9.6 mg/dL vs 6.3 mg/dL, P = 0.04) were significantly higher in the ARF than in the non-ARF group. Twelve patients (80%) recovered completely with haemodialysis (seven patients, 46.7%) or only conservative management (five patients, 33.3%), while one patient underwent liver transplantation because of fulminant hepatic failure, and two patients died because of fulminant hepatic failure. There were no deaths among patients with noncomplicated AHA in the non-ARF group. Five patients underwent kidney biopsy; two patients were diagnosed with acute tubular necrosis, two patients with acute interstitial nephritis with IgA nephropathy and one patient with acute tubulointerstitial nephritis. All patients in the ARF group had microscopic haematuria and proteinuria (100%vs 31.1%, P < 0.001). Urine sodium levels were more than 10 mEq/L in 10 patients. The findings of high urinary sodium concentrations, microscopic haematuria and proteinuria did not support the diagnosis of hepatorenal syndrome (HRS). Patients with AHA with ARF had higher ALT levels, more prolonged PTs, and higher total bilirubin levels. The prognosis for these patients was poorer than for those without ARF. However, the patients with ARF and nonfulminant AHA had recovered with proper treatment and should not be confused with patients that have HRS. [source]

Experiences with acute kidney injury complicating non-fulminant hepatitis A

NEPHROLOGY, Issue 6 2008
HYUN W KIM
SUMMARY: Aim: To describe the clinical features and to identify factors related to development of acute kidney injury in acute hepatitis A patients. Methods: The study and control groups consisted of 21 and 425 patients who did or did not develop acute kidney injury, respectively, after acute hepatitis A from January 1997 to May 2007. Results: There were 13 men and eight women; their mean age at diagnosis was 28.8 ± 8.2 years in the study group. Peak values for renal and liver function impairment consisted of a median serum creatinine of 4.6 mg/dL (range, 1.5,15.3 mg/dL) on day 6 (range, days 1,20) and a median total bilirubin of 10.7 mg/dL (range, 2.6,57.5 mg/dL) on day 8 (range, day 1,19). Serum creatinine concentrations returned to baseline level by a median of 16 days and total bilirubin levels returned to normal by a median of 62 days. Six of 21 (29%) patient underwent haemodialysis. Renal biopsies performed in two patients showed acute tubular necrosis and interstitial nephritis, respectively. Logistic regression analysis showed that a lower haematocrit, the presence of coagulopathy and high C-reactive protein concentration on admission, and higher peak bilirubin value during the illness were associated with development of acute kidney injury. Conclusion: Acute hepatitis A should be considered in the differential diagnosis of patients with acute kidney injury, even without fulminant hepatic failure. A lower haematocrit, the presence of coagulopathy and high C-reactive protein level at presentation, and higher peak bilirubin level during the illness were associated with development of acute kidney injury in acute hepatitis A patients. [source]

Paraquat-induced Fanconi syndrome

NEPHROLOGY, Issue 5 2005
HYO W GIL
SUMMARY: The ingestion of paraquat, a non-selective herbicide, can be fatal in humans. Paraquat is toxic to multiple organs, including the kidney, heart, gastrointestinal tract and central nervous system. Although paraquat has been established as one cause of acute tubular necrosis, Fanconi syndrome presenting as severe hypophosphataemia after paraquat intoxication has not been reported. Here, we report the case of a 44-year-old Korean woman who presented with generalized proximal tubular dysfunction including aminoaciduria, phosphaturia and glycosuria after paraquat intoxication. We found that severe hypophosphataemia induces deep drowsiness. Renal biopsy findings indicated the presence of acute tubular necrosis that may be reversible. [source]

Loss of Solute Carriers in T Cell-Mediated Rejection in Mouse and Human Kidneys: An Active Epithelial Injury,Repair Response

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 10 2010
G. Einecke
T cell-mediated rejection of kidney allografts causes epithelial deterioration, manifested by tubulitis, but the mechanism remains unclear. We hypothesized that interstitial inflammation triggers a stereotyped epithelial response similar to that triggered by other types of injury such as ischemia-reperfusion. We identified solute carrier transcripts with decreased expression in mouse allografts, and compared their behavior in T cell-mediated rejection to native kidneys with ischemic acute tubular necrosis (ATN). Average loss of solute carrier expression was similar in ATN (77%) and T cell-mediated rejection (75%) with high correlation of individual transcripts. Immunostaining of SLC6A19 confirmed loss of proteins. Analysis of human kidney transplant biopsies confirmed that T cell-mediated rejection and ATN showed similar loss of solute carrier mRNAs. The loss of solute carrier expression was weakly correlated with interstitial inflammation, but kidneys with ATN showed decreased solute carriers despite minimal inflammation. Loss of renal function correlated better with decreased solute carrier expression than with histologic lesions (r = 0.396, p < 0.001). Thus the loss of epithelial transcripts in rejection is not a unique consequence of T cell-mediated rejection but an active injury,repair response of epithelium, triggered by rejection but also by other injury mechanisms. [source]

Alternative Macrophage Activation-Associated Transcripts in T-Cell-Mediated Rejection of Mouse Kidney Allografts

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 3 2010
K. S. Famulski
Macrophages display two activation states that are considered mutually exclusive: classical macrophage activation (CMA), inducible by IFNG, and alternative macrophage activation (AMA), inducible by IL4 and IL13. CMA is prominent in allograft rejection and AMA is associated with tissue remodeling after injury. We studied expression of AMA markers in mouse kidney allografts and in kidneys with acute tubular necrosis (ATN). In rejecting allografts, unlike interferon gamma (IFNG) effects and T-cell infiltration that developed rapidly and plateaued by day 7, AMA transcripts (Arg1, Mrc1, Mmp12 and Ear1) rose progressively as tubulitis and parenchymal deterioration developed at days 21 and 42, despite persistent IFNG effects. AMA in allografts was associated with transcripts for AMA inducers IL4, IL13 and inhibin A, but also occurred when hosts lacked IL4/IL13 receptors, suggesting a role for inhibin A. Kidneys with ATN injured by ischemia/reperfusion also had increased expression of AMA markers and inhibin A. Thus kidneys undergoing T-cell-mediated rejection progressively acquire macrophages with alternative activation phenotype despite strong local IFNG effects, independent of IL4 and IL13. Although the mechanisms and causal relationships remain to be determined, high AMA transcript levels in rejecting allografts are strongly associated with and may be a consequence of parenchymal deterioration similar to ATN. [source]

Successful Management of Eviscerated Renal Allograft with Preservation of Function

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 5 2008
H. Jeon
Although most wound complications after renal transplantation are minor, the renal allograft, in its superficial and extraperitoneal location, is vulnerable to exposure if there is wound breakdown resulting in loss of overlying tissue. We describe a 66-year-old man who received a renal allograft from a deceased donor for end-stage renal disease (ESRD) secondary to polycystic kidney disease. His immediate posttransplant course was complicated by delayed graft function from acute tubular necrosis, reexploration for perigraft hematoma and subsequent wound dehiscence. After unsuccessful conservative wound care, the renal allograft became completely eviscerated due to fascial retraction of the dehisced wound. While the allograft was initially covered with a pedicled rectus femoris muscle flap, several local tissue rearrangements were required for definitive coverage. The allograft function was recovered after initial flap coverage and was subsequently maintained; follow-up more than 2 years after transplantation has demonstrated not only continued stable graft function but also complete healing of the dehiscent wound. [source]

Peritubular Capillary Damage in Acute Humoral Rejection: An Ultrastructural Study on Human Renal Allografts

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 12 2005
P. Lipták
The ultrastructural features of peritubular capillary (PC) damage was studied in 12 kidney allografts with acute humoral rejection (AHR). AHR manifested in diffuse linear PC staining for C4d, and histology consistent with Banff grade III in 7 recipients and Banff grade II in 5. Allografts with acute tubular necrosis served as controls. First biopsies (post-transplantation day 16.2 ± 2.2): The intra-capillary exudate comprised monocytes (59%), polymorphonuclears (14%), lymphocytes (12%) and not otherwise specified mononuclears (15%). Three patterns of focal PC endothelial injury were observed: lysis, an increased rate of apoptosis and fragmentation. No correlation was found between the respective damage types and the inflammatory cell types or the Banff grades. Controls revealed endothelial swelling, detachment from basement membrane and fragmentation. Follow-up biopsies: Monocytes transformed into macrophages intra-luminally. The reparative changes comprised endothelial cytoplasmic protrusions, binucleated endothelial cells and capillary sprouts. Early transplant capillaropathy and transplant glomerulopathy were noted in 2 recipients. Literature data indicate that lysis is mediated by anti-HLA alloantibodies; apoptosis, demonstrated first in the present study, may be induced by non-HLA-type anti-endothelial antibodies. Fragmentation is caused by ischemia. Ongoing endothelial injury leads to transplant capillaropathy and transplant glomerulopathy, the characteristic lesions of chronic rejection. [source]

Early Presence of Calcium Oxalate Deposition in Kidney Graft Biopsies is Associated with Poor Long-Term Graft Survival

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 2 2005
Hélady Sanders Pinheiro
Accumulated oxalate will be excreted after renal transplantation, creating an increased risk of tubular precipitation, especially in the presence of allograft dysfunction. We evaluated calcium oxalate (CaOx) deposition in renal allograft biopsies with early dysfunction, its association with acute tubular necrosis (ATN) and graft survival. We studied 97 renal transplant patients, submitted to a graft biopsy within 3 months post-transplant, and reanalyzed them after 10 years. We analyzed renal tissue under polarized light and quantified CaOx deposits. CaOx deposits were detected in 52.6% of the patients; 26.8% were of mild and 25.8% of moderate intensity. The deposits were more frequent in biopsies performed within 3 weeks post-transplant (82.4 vs. 63.0%, p < 0.05) and in allografts with more severe renal dysfunction (creatinine 5.6 mg/dL vs. 3.4 mg/dL, p < 0.001). ATN incidence was also higher in patients with CaOx deposits (47% vs. 24%, p < 0.001). Twelve-year graft survival was strikingly worse in patients with CaOx deposits compared to those free of deposits (49.7 vs. 74.1%, p = 0.013). Our study shows a high incidence of CaOx deposits in kidney allografts with early dysfunction, implying an additional risk for acute tubular injury, with a negative impact on graft survival. [source]

Efficacies of caspofungin and a combination of caspofungin and meropenem in the treatment of murine disseminated candidiasis,

APMIS, Issue 12 2006
SEMA KECELI OZCAN
Disseminated candidiasis is relatively common in immunocompromised patients. The treatment protocol of these patients usually includes broad-spectrum antibiotics and also emprical antifungals initiated due to unresponsiveness to antibiotics. In this study the efficacies of caspofungin and meropenem , separately and together , in mice with disseminated candidiasis were studied. Immunocompetent mice were infected intravenously with 2×106 CFU of Candida albicans. At 24 h postinfection, intraperitoneal therapy was initiated and was continued for 7 days. Therapy groups included those given caspofungin (0.5, 1.25, 5 mg/kg/day), meropenem (20 mg/kg/day), and a combination of the two drugs. The outcome of therapy was evaluated by kidney tissue burden studies and histologic examination. In vitro, drug susceptibilities were tested by checkerboard analysis. Kidney CFU counts showed that mice that had received both drugs had lower residual burdens. Caspofungin was effective at doses of 0.5, 1.25, 5 mg/kg compared to infected untreated controls. In vitro, MICs of caspofungin and meropenem were <0.075 ,g/ml and >64 ,g/ml, respectively. Synergism was observed with the combination. Histopathology showed that the degree of inflammation was 25% less and tubular necrosis was more restricted in combined therapy than monotherapy. The results indicate that concurrent caspofungin and meropenem therapy may be beneficial [source]

Lycopene, a Carotenoid, Attenuates Cyclosporine-Induced Renal Dysfunction and Oxidative Stress in Rats

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 6 2007
Ahmet Ate, ahin
Adult male Sprague-Dawley rats were randomly divided into four groups. The control group received physiological saline; animals in the lycopene group received only lycopene (10 mg/kg); animals in the cyclosporine A group received only cyclosporine A (15 mg/kg) and animals in cyclosporine plus lycopene group received cyclosporine and lycopene for 21 days. The effects of lycopene on cyclosporine A-induced nephrotoxicity were evaluated by plasma creatinine, urea, sodium and calcium concentrations; kidney tissue thiobarbituric acid reactive species, reduced glutathione (GSH), glutathione peroxidase (GSH-Px) and catalase activities and histopatological examinations. Administration of cyclosporine A to rats induced a marked renal failure, characterized with a significant increase in plasma creatinine and urea concentrations. Cyclosporine A also induced oxidative stress as indicated by increased kidney tissue concentrations of thiobarbituric acid reactive species and GSH, and reduced activities of GSH-Px and catalase. Moreover, the kidneys of cyclosporine A-treated rats showed tubular necrosis, degeneration, dilatation, thickened basement membranes, luminal cast formation and inter-tubular fibrosis. Lycopene markedly reduced elevated plasma creatinine, urea levels and counteracted the deleterious effects of cyclosporine A on oxidative stress markers. In addition, lycopene ameliorated cyclosporine A-induced pathological changes including tubular necrosis, degeneration, thickened basement membranes and inter-tubular fibrosis when compared to the alone cyclosporine A group. These data indicate that the natural antioxidant lycopene might have protective effect against cyclosporine-induced nephrotoxicity and oxidative stress in rat. [source]

Protective Effect of Ebselen, a Selenoorganic Drug, against Gentamicin-Induced Renal Damage in Rats

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2006
R. Dhanarajan
However, its clinical use is limited by its nephrotoxicity. Oxidative stress and nitrosative stress are reported to play important role in gentamicin nephrotoxicity. In the present study we investigated whether ebselen, an inhibitor of oxidative stress and nitrosative stress prevents or reduces gentamicin-induced renal damage in the rat. For this purpose male Wistar rats were divided into five groups and treated as follows. Group 1 (control group): dimethyl sulphoxide, intraperitoneally, Group 2: Gentamicin 100 mg/kg b.wt. subcutaneously, Group 3: 5 mg/g b.wt. ebselen intraperitoneally, Group 4: 2.5 mg/kg b.wt. ebselen followed by 100 mg/kg b.wt. gentamicin subcutaneously one hour later, and Group 5: 5 mg/kg b.wt. of ebselen followed by 100 mg/kg b.wt. gentamicin one hour later for four consecutive days. Nephrotoxicity was evaluated histopathologically by light microscopy, and biochemically by the measurement of the plasma creatinine and urea levels. Parameters of oxidative stress such as reduced glutathione, malondialdehyde, and activities of superoxide dismutase and glutathione peroxidase were measured in the kidney. Serum nitrite and nitrate were measured as indicators of nitrosative stress. Treatment of rats with gentamicin resulted in statistically significant reduction in reduced glutathione levels (51%) and the activities of antioxidant enzymes superoxide dismutase (56%) and glutathione peroxidase (39%) as compared with the controls in the kidneys. Renal malondialdehyde level was increased significantly (43%) as compared with the controls. Plasma creatinine levels, urea levels and nitrite levels were significantly increased (4, 4.5 and 160% times respectively) as compared with the controls. Histologically, damage to the renal cortex and medulla was observed moderate to severe tubular necrosis and glomerular congestion. Pretreatment with 2.5 mg/kg b.wt. ebselen prevented gentamicin induced damage to medulla; however, renal cortex showed mild damage and biochemically indicators of oxidative stress and nitrosative stress were significantly reduced. Pretreatment with 5 mg/kg b.wt. ebselen prevented gentamicin-induced oxidative damage and nitrosative damage and renal damage almost completely in 78% of the rats, in the other 22% of the rats, ebselen pretreatment reduced gentamicin-induced renal damage. The results of the present study suggest that ebselen may be useful as a nephroprotective agent. [source]

Renal autotransplantation for managing a short upper ureter or after ex vivo complex renovascular reconstruction

BJU INTERNATIONAL, Issue 6 2005
J. Christopher Webster
Several topics related to the upper urinary tract are covered this month. Renal autotransplantation for managing a short upper ureter or after ex vivo complex renovascular reconstruction is described by authors from Florida. Percutaneous nephrolithotomy and various technical aspects associated with it are presented by authors from Germany and India. OBJECTIVE To report our contemporary experience with renal autotransplantation (AT), an established treatment for managing patients with a shortened ureter or renovascular disease, as despite its historical importance, AT remains an underused technique by urologists. PATIENTS AND METHODS All patients undergoing AT between 1997 and 2002 for a short ureter after ureteric injury and for renovascular disease were assessed by creatinine level and blood pressure before and after surgery, and antihypertensive drug use and complications. RESULTS Eleven patients had AT for renovascular disease and four for ureteric injury. There was no statistical difference in creatinine levels or blood pressure before and after surgery in either group. Eight patients treated with AT for renovascular disease required less antihypertensive medication after surgery. Minor complications occurred in both groups and included a suture abscess, chronic wound pain, and transient acute tubular necrosis. One patient in the ureteric injury group required a transplant nephrectomy after renal vein thrombosis, and one in the renovascular group died from multi-organ system failure. CONCLUSION AT remains a treatment option for patients with a short ureter after ureteric injury and in those with renovascular disease. Patients had stable renal function and blood pressure after surgery. Most patients treated for renovascular disease required less medication after AT. The procedure is associated with both minor and major complications, which must be considered before surgery. [source]

ABO-incompatible renal transplantation in Epstein syndrome

CLINICAL TRANSPLANTATION, Issue 2010
Masao Ogura
Ogura M, Kikuchi E, Kaito H, Kamei K, Matsuoka K, Tanaka H, Kuroda T, Sekine T, Ito S. ABO-incompatible renal transplantation in Epstein syndrome. Clin Transplant 2010: 24 (Suppl. 22): 31,34. © 2010 John Wiley & Sons A/S. Abstract:, Epstein syndrome (ES) is an autosomal dominant hereditary disease characterized by hereditary nephritis, sensory deafness, and thrombocytopenia. We herein report the case of a 20-yr-old man with ES who underwent ABO blood type-incompatible living-donor kidney transplantation from his mother. He was given platelet transfusion, and his pre-operative number of platelets were 108 × 103/,L. After transplantation, urine output and the decrease in serum creatinine (sCr) were within the acceptable ranges. On the seventh post-operative day (POD), sCr had risen and urine output decreased. Anti-type A antibody rapidly elevated from <2 times (×2) just before transplantation to 64 times (×64), and the patient required hemodialysis again. Resistance index (RI) by ultrasound increased from an average of 0.5 , 0.6 on POD 1 to an average of 0.7 , 0.8 on POD 7. However, several biopsies (POD 4, 7, and 10) showed no obvious findings of acute rejection except for intense C4d deposition. Because acute antibody-mediated rejection was not completely ruled out, he was treated with methyl-prednisolone pulse therapy, plasma exchange, cyclophosphamide, and immunoglobulin. Regardless, his titer of anti-type A antibody was still high, and he still presented oliguria. We performed an emergent splenectomy. Consequently, the levels of anti-type A antibody decreased, the RI also dropped to an average of 0.6. However, on POD 19 and 25 (platelets were 27 × 103/,L and 36 × 103/,L), he developed a massive intraperitoneal hematoma around the graft and region of the removed spleen, which pushed the graft out and caused acute tubular necrosis, resulting in anuria. The RI rose to an average of 0.8 , 1.0 after these episodes. He also experienced bleeding from a duodenal ulcer on POD 21. However, his renal function has fully recovered after acute hemodialysis for 35 d. The latest sCr was 1.5 mg/dL with a recovery in RI to 0.6. Although his platelet count was maintained at a minimum of 50 × 103/,L, he had several severe bleeding episodes, concluding that sufficient platelets are necessary after transplantation in ES. [source]

Progressive interstitial fibrosis of kidney allograft early after transplantation from a non-heart beating donor: possible role of persistent ischemic injury

CLINICAL TRANSPLANTATION, Issue 2010
Kohsuke Masutani
Masutani K, Kitada H, Yamada S, Tsuchimoto A, Noguchi H, Tsuruya K, Katafuchi R, Tanaka M, Iida M. Progressive interstitial fibrosis of kidney allograft early after transplantation from a non-heart beating donor: Possible role of persistent ischemic injury. Clin Transplant 2010: 24 (Suppl. 22): 70,74. © 2010 John Wiley & Sons A/S. Abstract:, The donor was 63-yr-old woman with subarachnoid hemorrhage. As she developed severe hypotension for more than four h before cardiac arrest, we biopsied the grafts and decided to transplant those kidneys. Recipient 1 was a 23-yr-old man on 13-yr dialysis program. After 19 d of delayed graft function (DGF), we discontinued hemodialysis (HD). However, the decrease in serum creatinine (sCr) was poor. The minimum sCr was 4.3 mg/dL on post-operative day (POD) 40, and increased to 6.5 mg/dL. The contralateral graft was transplanted to a 61-yr-old man (recipient 2) with 18-yr HD. After 15 d of DGF period, sCr decreased gradually and has been stable at 1.9 mg/dL. In recipient 1, graft biopsies performed on POD 15, 69, and 110, revealed progressive interstitial fibrosis and tubular atrophy (IF/TA) without evidences of acute rejection, tacrolimus associated injury, reflux nephropathy, or viral nephropathy. The second biopsy on POD 69 showed typical findings of acute tubular necrosis. We compared the clinical courses of the two recipients because certain features of recipient 1, such as age, duration of HD, total ischemic time, and body size were advantageous, whereas graft function was poorer than that in recipient 2. Recipient 1 developed severe anemia following the dissociation of graft function from recipient 2. In this case, posttransplant anemia and lower blood pressure might promote IF/TA through persistent ischemic tubular damage, and positive CMV antigenemia and its treatment could promote anemia. Especially in the kidney allograft from a marginal donor, we should consider various factors to obtain a better graft outcome. [source]

Risk factors for rising creatinine in renal allografts with 1 and 3 yr survival

CLINICAL TRANSPLANTATION, Issue 6 2006
Steven Paraskevas
Abstract:, Background:, Determining factors associated with negative slope of inverse creatinine vs. time (1/Cr vs. t) may help prevent a decline in renal allograft function. Methods:, A total of 1389 adult recipients of primary renal transplants were divided into quartiles based on the slope of 1/Cr vs. t calculated from 6 and 12 months post transplant. A multivariate analysis of risk factors for being in the worst vs. best quartile employed these variables: donor source, HLA mismatch, recipient age, donor age, panel-reactive antibody (PRA), acute rejection (AR), 3-month cyclosporin A (CsA) level, 1-yr CsA level and acute tubular necrosis. Two separate analyses compared risk factors in patients with 1 and 3 yr survival, respectively. Results:, In recipients with ,1 yr graft survival, high PRA and AR were associated with negative slopes of 1/Cr vs. t. For those with ,3 yr graft survival, both AR and 3-month CsA level >150 ng/mL were significant risk factors, using both 6- and 12-month slopes. Stratification of AR showed 1 AR episode ,6 months and multiple AR episodes carried significant risk for negative slopes. Conclusion:, Optimization of allograft function invokes a conundrum between the needs to avoid both AR and high early CsA levels. We support a policy of carefully balancing these two risks. [source]

The long-term outcome of tacrolimus in cadaveric kidney transplantation from non-heart beating donors

CLINICAL TRANSPLANTATION, Issue 2 2005
Nobuyuki Fukuhara
Abstract:, Tacrolimus (Tac), developed in 1990, has been applied as an immunosuppressive agent for liver, heart, and kidney transplantation and is known to have more powerful immunosuppressive effects than cyclosporine (CyA). To evaluate the efficacy of Tac in cadaveric kidney transplants from non-heart beating donors, we present the long-term outcome of patients receiving kidneys with ischemic damage, and compared it with that of CyA. Between July 1990 and December 2000, 55 patients with end-stage renal disease received kidneys from non-heart beating donors (Maastrichy category 3) and were treated with Tac and steroid immunosuppressive therapy. During the same period, we also performed 137 non-heart beating cadaveric renal transplants treated with CyA-based immunosuppressive therapy. The patient survival rate was 98% at 1 yr and 96% at 3,10 yr in the Tac group, and 97% at 1,3 yr, 93% at 5 yr and 85% at 10 yr in the CyA group. The graft survival rate was 91% at 1 yr, 80% at 3 yr, 63% at 5 yr and 34% at 10 yr in the Tac group, and 88% at 1 yr, 75% at 3 yr, 63% at 5 yr and 49% at 10 yr in the CyA group. There was no significant difference in either patient or graft survival rates between the two groups. Acute early rejection in the Tac group was less than that in the CyA group but acute tubular necrosis was the same in both groups. This indicates that Tac is available for cadaveric kidney transplants from non-heart beating donors. In conclusion, Tac is available as an immunosuppressive agent even for kidney transplants from non-heart beating donors. [source]

Factors contributing to long graft survival in non-heart-beating cadaveric renal transplantation in Japan: a single-center study at Kitasato University

CLINICAL TRANSPLANTATION, Issue 6 2002
Kazunari Yoshida
Yoshida K, Endo T, Saito T, Iwamura M, Ikeda M, Kamata K, Sato K, Baba S. Factors contributing to long graft survival in non-heart-beating cadaveric renal transplantation in Japan: a single-center study at Kitasato University. Clin Transplant 2002: 16: 397,404. © Blackwell Munksgaard, 2002 A total of 107 cadaveric kidneys from non-heart-beating donors (NHBDs) have been transplanted between 1974 and 2000 at Kitasato University Hospital, Sagamihara, Japan. The patient survival of the 107 recipients of cadaveric renal transplants at 1, 5 and 10 yr was 0.857, 0.770 and 0.746, respectively. The 50% graft survival was 3.8 yr. The 5 and 10-yr graft survival was 0.457 and 0.337, respectively. Twenty of the 107 recipients of non-heart-beating cadaveric renal transplantation had graft survival longer than 10 yr. Of these 20 patients, 14 survivors still maintain functioning renal grafts and two died with functioning graft, although the remaining four reverted to dialysis because of chronic rejection and nephropathy. The average graft survival of these 20 patients at the time of study was 13.3 yr and the longest was 21.4 yr. The average serum creatinine level at 10 yr after transplantation was 1.63 mg/dL, almost identical to that at 5 yr post-transplant. The donors aged on average 40.2 yr; 13 were male and seven were female. The youngest donor was 9-yr-old and the oldest was 66. The graft survival was significantly better in the group with donor age younger than 55 yr (Log-rank: p=0.007). The average weight of the renal graft was not different between the long and shorter graft survival groups. The average warm ischemic time and total ischemic time were 9.7 and 539.7 min, respectively. The duration of post-transplant acute tubular necrosis averaged 9.2 days. These parameters tended to be shorter than those in recipients with graft survival >10 yr, but with no statistical significance. The mean numbers of acute rejection (AR) episode within 3 months after transplantation were 0.25 ± 0.66 and 0.92 ± 0.90 (p=0.020) in long survival and shorter survival groups, respectively. Long survivors had a significantly lower incidence of AR. Two of 20 cases received conventional immunosuppression with prednisolone, azathioprine and mizoribin, and 18 had prednisolone and calcineurin inhibitor (CNI). Kaplan,Meier analysis showed a significant contribution of CNI to graft survival (p=0.036). However, the graft survival reduction rate after 1 yr post-transplant did not differ between conventional and CNI immunosuppression. These data suggest that renal grafts retrieved with proper organ procurement procedures from NHBDs may survive long-term and help to overcome donor shortage. [source]