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)

Growth arrest-specific gene 6 (Gas6) and its receptors Rse, Axl and Mer have recently been found to be involved in a rat model of chronic allograft nephropathy (CAN). Thus, in this study we investigated the function of Gas6 and its receptors in human renal allograft dysfunction. Expression of Gas6 and its receptors was detected by immunohistochemical staining. Gas6 and its receptors were widely expressed in glomeruli, tubules and vessels of renal allografts. Gas6 expression was detected in normal-functioning allografts and was increased in acute rejection ( P<0.05), acute tubular necrosis ( P<0.05) and CAN ( P<0.01). Gas6 receptors were not upregulated in any of the allograft groups, except for the Axl receptor, which increased only in acute tubular necrosis ( P<0.01). Gas6 expression was also found to correspond with the expression of alpha-smooth muscle actin, a general marker of CAN ( r(2)=0.21, P<0.01). These findings suggest that Gas6, acting as a growth factor, is increased in the process of kidney allograft dysfunction and in CAN.
Transpl Int 2003 Sep
PMID:Expression of growth arrest-specific gene 6 and its receptors in dysfunctional human renal allografts. 1276 29

Measurement of vascular resistive index (RI) by duplex Doppler sonography (DDS) has been proposed as a non-invasive technique to detect the presence of acute rejection in renal allograft recipients. Our aim was to evaluate the clinical utility of this technique. From 107 patients we reviewed 159 biopsies that were performed from 1993 to 2001 for the investigation of acute allograft dysfunction. Histological findings were correlated with RI measurements by contemporaneously performed DDS. The majority of biopsies were carried out within the first 3 months post-transplantation (111/159). Sixty-eight biopsies showed acute rejection, 91 biopsies had findings other than rejection (acute tubular necrosis, CyA toxicity, recurrent GN). Using a threshold mean RI value of 0.9, the test had a specificity for acute rejection of 89%, but a sensitivity of just 6%. If the threshold was lowered the sensitivity rose, but specificity declined sharply. Average RI in the rejection group was not higher than in controls (0.73+/-0.11 vs 0.74+/-0.11, respectively). We conclude that measurement of RI by DDS does not contribute to the diagnosis of acute allograft dysfunction.
Transpl Int 2003 Sep
PMID:Role of duplex Doppler sonography in diagnosis of acute allograft dysfunction-time to stop measuring the resistive index? 1276 33

Recurrence of focal segmental glomerulosclerosis (FSGS) in an allograft is a challenging clinical situation because it frequently results in graft loss. We report our experience with early use of plasmapheresis in recurrent FSGS. Of the 18 (33%) children with biopsy-proven FSGS (in their native kidneys) transplanted at our institution, 6 had recurrence (elevated urine protein/creatinine ratios) post transplant and were treated with plasmapheresis. Patients who received treatment within 1 day of the recurrence (4/6) went into remission after 5-13 plasmapheresis treatments, within 5-27 days of starting treatment. Patients who did not respond to plasmapheresis (2/6) were treated 7 and 17 days after onset of proteinuria; 1 of these had acute tubular necrosis and acute rejection leading to graft loss and the other developed acute rejections, ongoing proteinuria, and subsequent graft loss. All 4 patients who went into remission have maintained good graft function, 22-53 months post transplant. In our experience early institution of plasmapheresis for recurrent post-transplant proteinuria in FSGS is effective.
Pediatr Nephrol 2003 Sep
PMID:Early use of plasmapheresis for recurrent post-transplant FSGS. 1283 97

Fatty acids constitute a major source of metabolic fuel for energy production in kidney tissue. During acute renal failure (ARF) injury to the proximal tubule and medullary thick ascending limb leads to structural and functional alterations that result in reduced expression and activity of mitochondrial and peroxisomal fatty acid oxidation (FAO) enzymes. Reduced DNA binding activity of peroxisome proliferator activated receptor-alpha (PPARalpha) to its target genes and decreased expression of its tissue-specific coactivator PPAR-gamma-coactivator-1 (PGC-1) in the mouse proximal tubule and the medullary thick ascending limb, represent 2 potential mechanisms that account for the observed alterations of FAO during ARF. Pretreatment with PPARalpha ligands restores the expression and activity of renal FAO enzymes, and this metabolic alteration leads to amelioration of acute tubular necrosis caused by ischemia/reperfusion or cisplatin-induced ARF. More studies are needed to examine further the cellular mechanisms of substrate inhibition, and to determine if metabolic pathways, in addition to the recovery of FAO, account for the protective effect (s) of PPARalpha ligands during acute renal failure.
Semin Nephrol 2003 Sep
PMID:Energy metabolism and cytotoxicity. 1368 May 32

A 46-year-old morbidly obese man was admitted to the medical intensive care unit with respiratory failure. He required pressure-control ventilation and high levels of sedation with continuous-infusion lorazepam. He developed Stenotrophomonas maltophilia pneumonia; treatment included scheduled intravenous trimethoprim-sulfamethoxazole. Each of these drugs contain several hundred milligrams/milliliter of propylene glycol. On day 17 of his hospital course, 3 days after starting the trimethoprim-sulfamethoxazole, the patient developed acute renal failure consistent with acute tubular necrosis. Propylene glycol toxicity was suspected; therefore, all drugs containing propylene glycol were discontinued, and laboratory data were collected. A marked osmol gap, metabolic acidosis, and renal toxicity were attributed to both continuous and large intermittent doses of intravenous propylene glycol. Particular attention should be paid to the total amount of propylene glycol provided to patients from administered drugs. Patients in the intensive care setting who require high doses of intravenous lorazepam for sedation, as well as antimicrobial therapy with trimethoprim-sulfamethoxazole for treatment of either Stenotrophomonas maltophilia or Pneumocystis carinii pneumonia, may be at increased risk for propylene glycol toxicity and should be monitored closely.
Pharmacotherapy 2003 Sep
PMID:Acute tubular necrosis associated with propylene glycol from concomitant administration of intravenous lorazepam and trimethoprim-sulfamethoxazole. 1452 39

Strong evidence suggests that replicative senescence is involved in vivo because senescent cells have been detected in human tissues associated with physiological and pathological aging processes. Chronic allograft nephropathy (CAN) appears to be a major determinant of long-term survival in kidney transplantation. Several mechanisms are potentially involved; the aim of this study was to assess the impact of replicative senescence in CAN. Replicative senescent cells were detected on renal tissue cryosection using expression of a specific marker, senescence-associated beta-galactosidase (SA-beta-Gal) at pH 6. A total of 80 frozen renal samples (67 cases of CAN and 13 controls) were studied. To validate this marker, we measured in situ telomere length in cells expressing or not expressing SA-beta-Gal using a validated quantitative fluorescence in situ hybridization technique. The presence of senescent cells was correlated with clinicopathologic data. Telomere length was significantly lower in cells expressing SA-beta-Gal than in cells that did not. Replicative senescence was present in 45 out of 67 (67%) biopsy specimens and was significantly associated with the severity of CAN. No correlation with the notion of a previous episode of acute tubular necrosis, acute rejection, extrarenal epuration, duration of cold ischemia, and the delay between transplantation and biopsy was observed. However, the age of the donor, but not that of the recipient, was correlated with the occurrence of senescent cells. These results suggest that replicative senescence is a mechanism that might be involved in the development of CAN. The age of the donor appears to be the major determinant factor in replicative senescence.
Hum Pathol 2003 Sep
PMID:The role of replicative senescence in chronic allograft nephropathy. 1456 89

Although previous reports have attributed acute renal failure (ARF) following cardiovascular surgery to acute tubular necrosis (ATN), little emphasis has been placed on renal failure due to congestive heart failure (CARF). Of 100 cases of ARF studied prospectively over an 18-month period, 36 occurred after open-heart surgery. Nineteen of these cases were associated with heart failure. The remaining 17 had ATN as manifested by high urinary sodium, low urine/plasma creatinine, and abnormal urinary sediment. At the onset of CARF, intravascular volume expansion was universally present, and oliguria with pulmonary edema was common. Urinary chemistries were (mean +/- SD): sodium (mEq/L) 8 +/- 7, U/P creatinine 72 +/- 45, and FENa (%) 0.1 +/- 0.1. Therapy consisted of digoxin, furosemide (F), vasopressors (V), and, when indicated, intraaortic balloon counterpulsation. Survivors of CARF responded more frequently to F and required less V. Ultimately, survival depended upon improvement in cardiac performance. All oliguric ATN patients failed to respond to F. Mortality for the CARF group was 52%. In contrast, 82% of the oliguric ATN group expired, whereas overall ATN mortality was 60%. Cardiogenic acute renal failure is a frequent cause of ARF after open-heart surgery in our institution. It is characterized by prerenal urinary chemistries, has a high mortality, and may be reversible.
Cardiovasc Dis 1979 Sep
PMID:CARDIOGENIC ACUTE RENAL FAILURE (CARF) FOLLOWING OPEN-HEART SURGERY. 1521 6

Acute tubular necrosis (ATN) ranges from minimal histologic changes to overt necrotic tubules. Although histologic changes on routine stained sections can be seen in many ATN cases, they may be subtle in some cases. In some cases, electron microscopy may reveal more reliable findings to support a diagnosis of ATN. Thus, a molecular marker to confirm acute tubular damage and to differentiate mild from moderate tubular injury could provide more reliable detection of ATN at the light microscopic level. In this study, sections from native and transplant renal biopsies with the diagnosis of ATN were stained immunohistochemically for p53, an upstream marker for DNA damage, and compared with donor baseline biopsies as controls. The transplant and native ATN kidney groups had significantly higher numbers of p53 nuclear staining in renal tubular epithelium (transplant ATN: 4.58 +/- 1.51/mm2, n = 18, and native ATN: 6.12 +/- 1.99/mm2, n = 13) than the donor baseline group (1.09 +/- 0.51/mm2, n = 16) or controls-normal renal parenchyma away from tumors (0.029 +/- 0.017). Cases with moderate ATN changes showed significantly increased p53 tubular staining (transplant ATN: 9.20 +/- 2.59/mm2, n = 8, and native ATN: 14.3 +/- 1.88/mm2, n = 5) when compared with the mild ATN cases (transplant ATN: 0.87 +/- 0.30/mm2, n = 10, and native ATN: 1.01 +/- 0.39/mm2; n = 8). In summary, there was direct correlation between nuclear p53 staining and morphologic changes seen microscopically and ultrastructurally, suggesting that p53 can be used as a reliable marker of cellular damage to aid in the diagnosis of ATN.
Appl Immunohistochem Mol Morphol 2004 Sep
PMID:P53 protein is a reliable marker in identification of renal tubular injury. 1555 35

A 7-year-old boy suffered from jellyfish contact dermatitis and acute renal failure following a jellyfish sting. Three days before being admitted, he accidentally contacted a jellyfish on the left forearm, left thigh and trunk while wading at Pattaya beach, Eastern Thailand. Investigation revealed hemoglobinuria. Histologic findings of a renal biopsy indicated that acute tubular necrosis had caused acute renal failure in the present patient. Supportive treatments improved the dermatitis and renal function of this patient.
J Med Assoc Thai 2004 Sep
PMID:Acute renal failure in a child with jellyfish contact dermatitis. 1608 5

Activated leukocytes are implicated in development of ischemia/reperfusion (I/R)-induced organ injuries. Phosphodiesterase 3 inhibitors have anti-inflammatory effects by preventing cyclic adenosine monophosphate (cAMP) degradation. We examined the effects of olprinone, a specific phosphodiesterase 3 inhibitor, on I/R-induced acute renal injury model in rats. Forty-five minute renal I/R was induced in uni-nephrectomized rats. Rats were divided into a vehicle group, an olprinone group, and a dibutyril (DB) cAMP group. Olprinone (0.2 microg/kg/minute) infusion began 30 min after reperfusion and continued for 3 h. DBcAMP (5 mg/kg), a stable analog of cAMP, was intraperitoneally administered 5 min after reperfusion to clarify the effect of cAMP in our model. Olprinone reduced the I/R-induced increases in serum levels of blood urea nitrogen and creatinine, and improved histological changes, including acute tubular necrosis in the outer medulla. Hemodynamic status was not affected by olprinone. I/R-induced a decrease in renal tissue blood flow, an increase in renal vascular permeability, and an enhancement of leukocyte activation, reflected by renal tissue levels of myeloperoxidase activity, and the tissue levels of cytokine-induced neutrophil chemoattractant (an equivalent of human interleukin 8) and tumor necrosis factor-alpha were all significantly decreased by olprinone. Olprinone also increased the renal tissue and plasma levels of cAMP in rats subjected to renal I/R. DBcAMP showed similar effects. Our results indicated that olprinone reduced the I/R-induced acute renal injury, probably by inhibiting leukocyte activation. The effects of olprinone could be explained through its action on cAMP levels.
Shock 2005 Sep
PMID:Olprinone reduces ischemia/reperfusion-induced acute renal injury in rats through enhancement of cAMP. 1613 69


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