Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following studies showing an association between helminth infections and protection from cerebral malaria, we compared 22 patients with malaria-associated acute renal failure with 157 patients with moderately severe malaria. Helminths were associated with protection from renal failure (adjusted odds ratio [AOR], 0.16 [0.03-0.85], P = 0.03). Helminth-infected controls were less likely to have jaundice (AOR, 0.39 [0.16-0.96], P = 0.04) or to have peripheral mature schizonts (AOR, 0.2 [0.07-0.62], P = 0.005) than controls without helminths. This suggested that preexisting helminth infections may have been protective by influencing sequestration and obstructive jaundice, 2 possible determinants of acute tubular necrosis.
Am J Trop Med Hyg 2001 Dec
PMID:Helminth infections are associated with protection from malaria-related acute renal failure and jaundice in Thailand. 1179 82

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.
Clin Transplant 2002 Dec
PMID:Factors contributing to long graft survival in non-heart-beating cadaveric renal transplantation in Japan: a single-center study at Kitasato University. 1243 17

Using the NAPRTCS database from January 1987 to January 2001, we examined 2687 adolescent (age 13-17 yr) index renal transplants to analyze differences in demographic treatment, and outcomes in adolescents with FSGS compared to other renal disease. 338 (12.6%) of adolescents had a primary diagnosis of FSGS. Adolescents with FSGS were more likely to be black and less likely to receive pre-emptive transplants (p < 0.001). No differences existed in HLA matching or immunosuppression regimens. Acute tubular necrosis occurred in more FSGS adolescents compared to non-FSGS adolescents following LD (11% vs. 4.7%) or CD (25.1% vs. 17.8%) transplants (p < 0.001). There were no significant differences in acute rejection rates between adolescents with FSGS and other adolescents. Graft survival was worse for LD FSGS adolescents (6 yr, 56%) compared to non-FSGS adolescents (77%) (p < 0.001) and was not significantly different from CD graft survival in FSGS (51%) or non-FSGS groups (61%). The relative risk (RR) of graft failure was greatest in LD transplant with FSGS (RR = 1.75; p < 0.001), compared to LD transplants without FSGS (RR = 1.0). Recurrent primary disease accounted for 15.2% of all graft failures in adolescents transplanted for FSGS with no difference between LD (17%) or CD (13.8%) grafts. Recurrent disease accounted for 3.2% of graft failures in adolescents without FSGS. Recurrent disease was the only cause of graft failure that differed between groups (p < 0.001). When compared to patients up to age 12 yr with FSGS, graft survival in both LD and CD transplants was worse in adolescents with FSGS (LD p = 0.035, CD p < 0.001). In conclusion, FSGS has a negative impact on graft survival in adolescents. Recurrence of FSGS results in a loss of the expected LD graft survival advantage in adolescents. Furthermore, adolescents with FSGS have decreased graft survival compared to younger children with FSGS. These data suggest that the rationale for LD transplantation in adolescents with FSGS should be based on factors other than the increased graft survival typically seen with LD transplantation.
Pediatr Transplant 2002 Dec
PMID:Outcome of renal transplantation in adolescents with focal segmental glomerulosclerosis. 1245 1

The evaluation and management of acute renal failure in the ICU patient remains a formidable task because of the complexity of this condition. Clinical and physiologic assessment and complementing laboratory and imaging tests are currently insufficient to differ between true renal parenchymal damage (acute tubular necrosis; it is important to realize that this term does not necessarily imply widespread injury, because whole organ dysfunction in humans has often been associated with very limited parenchymal cellular necrosis) and prerenal azotemia (decreased renal blood flow with altered glomerular hemodynamics and subsequently diminished glomerular filtration, without significant epithelial cell injury). Moreover, tubular damage and altered glomerular hemodynamics may coexist or lead to each other, and their relative contribution to the evolving renal dysfunction has not been unequivocally established. The limited data regarding the renal pathology of such patients and the scant information about human morphologic and functional correlates further undermine our knowledge about diagnostic and therapeutic approaches to these patients. Advanced techniques are critically needed to establish noninvasively the dynamic status of renal parenchymal microcirculation and the distribution of intrarenal oxygenation and to identify evolving cellular energy depletion and tubular cell damage. A few technologies are potentially promising, such as blood oxygen level dependent magnetic resonance imaging, positron emission tomography, and kidney injury molecule-1 detection in patients' urine. Because of the difficulties in analyzing the pathophysiology in humans, clinicians continue to rely largely on animal models to guide understanding and rationale for the identification of therapeutic targets. Data from such animal studies are complemented by studies in isolated perfused kidneys, isolated tubules, and tubular epithelial cell cultures. In this report, we summarize some concepts of acute tubular necrosis that have evolved as a result of these studies, evaluate available animal models, and underscore controversies regarding experimental acute tubular necrosis.
Curr Opin Crit Care 2002 Dec
PMID:Animal models of acute tubular necrosis. 1245 37

Pretransplant renal failure is a well-known risk factor which adversely affects the prognosis after liver transplantation. We report a case with pretransplant renal failure and discuss the perioperative management of such patient. The patient was 62 year-old-woman who was diagnosed with end-stage liver disease due to primary biliary cirrhosis, for which living donor liver transplantation (LDLT) was indicated. Her pretransplant serum creatinine was 9.4 mg/dl due to combination of drug-induced (antibiotics) acute tubular necrosis and hepatorenal syndrome. The management of renal failure consisted of the avoidance of calcineurin inhibitor as an induction immunosuppression and the use of perioperative continuous hemodiafiltration (CHDF). The postoperative course of the patient was complicated with CMV pneumonia and acute rejection, however she recovered and discharged on 94 POD with well-preserved graft function and normal renal function without any adverse sequela. LDLT for patients with renal failure can be performed successfully by careful management.
Fukuoka Igaku Zasshi 2002 Dec
PMID:[Living donor liver transplantation for a patient with renal failure]. 1263 31

In this study we have analyzed incidence, causes and clinical course of ARF due to primary intrarenal disease other than acute tubular necrosis. Thousand hundred and twenty two cases of ARF of diverse etiology were studied over a period of 16 years; July 1984 to Dec, 1999. Surgical ARF 231 (20.6%) were not included in the present study. Intrinsic renal diseases were responsible for ARF in 891 (79.4%) of cases. The most common intrinsic renal diseases 705 (79.4%) causing ARF were ischemic/toxic acute tubular necrosis, but not included in this study. Acute renal failure was related to acute glomerulonephritis (9.3%), acute interstitial nephritis (7%), and renal cortical necrosis in (4.6%) of cases. Therefore intrinsic renal diseases other than ATN were the causative factor for acute renal failure in 186 (20.8%) patients in our study. Crescentic (51.8%) and endocapillary proliferative glomerulonephritis (34.9%), were the main glomerular diseases responsible for ARF and 75.9% of GN was related to infectious etiology. Fifty three percent of acute interstitial nephritis was drug induced and in 25 (40%) patients it was related to an infectious etiology. Renal cortical necrosis due to HUS was observed in 16 (39%) children and majority (76.47%) of the cases had a diarrhoeal prodrome. Obstetrical complications were the main causes (61%) of cortical necrosis in adults with acute renal failure. Thus, intrinsic renal diseases other than ATN were responsible for ARF in 186 (20.8%) cases. Post-infectious glomerulonephritis, acute interstitial nephritis and renal cortical necrosis (complicating HUS in children and obstetrical complications in adult) are the main causes of acute renal failure in our study. Both acute GN and interstitial nephritis had excellent prognosis, however renal cortical necrosis was associated with a very high mortality.
 ...
PMID:Acute renal failure due to intrinsic renal diseases: review of 1122 cases. 1273 29

A statistical analysis was made of 2,000 consecutive cases in which prostatic operations were done in the period 1947-1957 at the Southern Pacific General Hospital. The operations included transurethral resections as well as perineal, retropubic and suprapubic prostatectomy. The mortality rates were lowest for transurethral resection and highest for retropubic prostatectomy. Coronary artery disease and pulmonary embolism were the chief causes of death. It was generally felt that preliminary partial vasectomy previous to transurethral resection added very little to successful convalescence. Although distilled water was used routinely for irrigation during transurethral resection, there was no incidence of lower nephron nephrosis. The incidence of recurrence of prostatic obstruction was highest by far after transurethral resection.
Calif Med 1959 Dec
PMID:Prostatectomy: a survey of 2,000 cases. 1383 45

Acute renal failure (ARF) is an uncommon but alarming complication of idiopathic nephrotic syndrome. The renal failure could be secondary to causes evident from the history and evaluation, such as severe intravascular volume depletion, acute tubular necrosis, allergic interstitial nephritis, bilateral renal vein thrombosis, acute pyelonephritis, or rapid progression of the original glomerular disease. It may be termed idiopathic if the underlying cause is undetermined. We present three children with idiopathic nephrotic syndrome who were admitted with acute renal failure. One case was due to drug-induced allergic interstitial nephritis. The other two were idiopathic in nature. Improvement in renal function occurred in the three patients over a variable period of 10 days to 4 weeks. After careful exclusion of well-known causes of acute renal failure, idiopathic acute renal failure (IARF) should be considered as a diagnostic possibility in these patients. The exact pathophysiology of IARF is not understood. Possible proposed explanations include interstitial edema, tubular obstruction, altered glomerular permeability, and unrecognized hypovolemia.
Pediatr Nephrol 2003 Dec
PMID:Acute renal failure in children with idiopathic nephrotic syndrome. 1457 39

A 66-year old man called for an ambulance from his home because of acute chest pain. When the crew arrived he was unresponsive and hypotensive. Sublingual nitroglycerine was given and subsequently the patient collapsed into circulatory failure and respiratory arrest. He was intubated and transported to the nearest hospital. The severe hypotension was combated with fluids and norepinephrine. During the next few hours his skin gradually turned intensely yellow, as did the urine. Acute myocardial infarction also occurred and renal failure developed. The cause of the neon-yellow colour was a complete mystery until a police patrol sent to his apartment found several empty packages of dipyridamole (Persantin Depot) corresponding to 34 g, an overdose seven times higher than any previous case reported in the literature. This drug has a distinct yellowish colour. The patient's condition gradually improved and he could be extubated within a week. Haemodialysis was needed for two weeks because of acute tubular necrosis after the prolonged period of hypotension, but thereafter he recovered.
Lakartidningen 2003 Dec 11
PMID:[A case report. Unconscious patient with neon yellow skin was intoxicated with dipyridamole]. 1471 9

Since December 1995, pediatric renal transplant recipients in our unit have received a DMSA scan as soon as possible post-transplant in order to provide a baseline for comparison in the event of subsequent complications. We retrospectively reviewed the case notes and DMSA scans of the 45 patients who underwent a scan within 9 wk of their transplant to see if pre or peri-transplant factors or post-transplant complications were associated with defects on scanning. Forty percentage of scans had defects. The presence of defects was not associated with potential predisposing factors such as patient or donor age, cadaveric or live donation, cold ischemia time, multiple donor vessels, the use of non-heart beating donors, the mean time to scan, the serum creatinine, or the presence of structural renal tract anomalies predisposing to UTI. However, 87% of patients had complications before the scan, including UTI, rejection, acute tubular necrosis, transplant biopsy and drug toxicity. Children with no clinical complications had a significantly reduced risk of a defect (p = 0.035), while biopsy was associated with the presence of defects (p = 0.0034). Twenty patients had one or more follow up DMSA scans: one patient developed a new focal defect. In conclusion, renal transplant defects are frequently found on DMSA scanning even early after transplantation and are non-specifically associated with many different complications.
Pediatr Transplant 2003 Dec
PMID:The significance of a defect on DMSA scan in children with renal transplants. 1487 Aug 90


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