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

Twelve Rhesus monkeys were inoculated intravenously with about 500 000 malaria parasites, Plasmodium knowlesi. Acute hemolysis occurred 5 days later, and all animals died on the 6th or 7th day after inoculation. All organs were gray-green to gray-brown because of deposition of hemoglobin and malaria pigments. This deposition was particularly striking in the lung, brain, abdominal fat and serous surfaces. Microscopic changes indicative of acute hypoxia were found in the liver (centrilobular necrosis) and kidneys (acute tubular necrosis). Terminal intravascular coagulopathy was evidenced by widely distributed, recently formed, fibrin thrombi.
 ...
PMID:Plasmodium knowlesi malaria in the Rhesus monkey. 41 5

Acute renal failure (ARF) is a serious complication in clients who have undergone bone marrow transplantation (BMT). The majority of cases develop as a result of intrarenal damage. Renal ischemia or nephrotoxic drugs, free hemoglobin, and free myoglobin contribute to acute tubular necrosis (ATN), which is the most likely cause of ARF in BMT clients. Nursing care of hospitalized BMT clients is directed toward the prevention of ARF by identifying clients who are at risk, the early diagnosis of renal impairment, and the administration of comprehensive treatment. Nurses play a vital role in the early diagnosis of renal impairment by assessing the client's fluid status, serum and urine electrolyte levels, and daily weights. The nursing role in managing clients with ARF includes preventing drug nephrotoxicity, maintaining fluid and electrolyte balance, preventing infection, and providing emotional support.
 ...
PMID:Acute renal failure in bone marrow transplantation. 143 67

Acute renal failure is divided into its classic parts: prerenal azotemia, postrenal azotemia (obstruction), and renal azotemia (including acute tubular necrosis). The division of acute tubular necrosis into the ischemic and toxic varieties is supplemented by an analysis of toxic varieties into those caused by antibiotics, radiologic contrast agents, chemotherapeutic-immunosuppressive agents, heavy metals, organic solvents, etc. Acute tubular necrosis caused by hemoglobin and myoglobin is described in detail. The importance of urinalysis and the urinary indices in distinguishing prerenal azotemia from acute tubular necrosis is stressed. Finally, current prognosis and treatment are reviewed.
 ...
PMID:Acute renal failure. 333 29

A 31-year-old patient was admitted to the hospital because of dark red urine which on examination was found to be due to extracellular hemoglobin. The cause of the hemoglobinuria was exposure to arsine gas from a cylinder thought to be empty. The worker's exposure time was approximately one to two minutes. The degree of hemolytic anemia required only one unit of packed red cells. The patient was hydrated intravenously to avoid acute tubular necrosis. The arsenic content in the urine taken was 0.72 mg/L on the day of admission and dropped to 0.1 mg/L on the fourth day of hospitalization. The patient was discharged eight days after admission, when clinical and hematological status had improved sufficiently. Occupational history revealed that protective procedures employed in the handling of the cylinders containing the arsine gas were inadequate. It was found that the valve on one of the cylinders was half-opened and leaking and that the dust caps, which were attached to the outside of the valves of the cylinders, were present on some and not on others and, where present, had been hand-tightened and not wrench-tightened. Moreover, the cylinders although specified to be empty, were not, according to regulations requiring pressure to be less than 25 pounds gauge or 45 absolute.
 ...
PMID:Arsine poisoning. 721 60

Heme proteins transport oxygen and facilitate redox reactions. Heme, however, may be dangerous, especially when free in biologic systems. For example, iron released from hemoglobin-derived heme can catalyze oxidative injury to neuronal cell membranes and may be a factor in post-traumatic damage to the central nervous system. We have shown that heme catalyzes the oxidation of low density lipoproteins which can damage vascular endothelial cells. The endothelium is susceptible to damage by oxidants generated by activated phagocytes, and this has been invoked as an important mechanism in a number of pathologies including the Adulte Respiratory Distress Syndrome (ARDS), acute tubular necrosis, reperfusion injury and atherosclerosis. Because of its highly hydrophobic nature, heme readily intercalates into endothelial membranes and potentiates oxidant-mediated damage. This injury is dependent on the iron content of heme and is completely blocked when concomitant hemopexin is added. Ferrohemoglobin, when added to cultured endothelial cells, is without deleterious effects, but if oxidized to ferrihemoglobin (methemoglobin), it greatly amplifies oxidant damage. Methemoglobin, but not ferrohemoglobin, releases its hemes which can then be incorporated into endothelial cells. Cultured endothelial cells, when exposed to methemoglobin but not ferrohemoglobin, cytochrome c or metmyoglobin, potentiate this oxidant injury. Stabilization of the methemoglobin by cyanide, haptoglobin or capture of the heme by hemopexin abrogates this effect. Paradoxically, more prolonged exposure of endothelium to heme or methemoglobin renders them remarkably resistant to oxidant challenge. Endothelium defends itself from heme by induction of the heme degrading enzyme heme oxygenase and the concomitant production of large amounts of the iron binding protein ferritin.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Heme and the vasculature: an oxidative hazard that induces antioxidant defenses in the endothelium. 808 43

The significance of poor medullary reperfusion in the etiology of acute tubular necrosis during renal transplantation is poorly understood. Our objective was to determine the kinetics of renal hemoglobin oxygenation using near-infrared spectroscopy during renal transplantation, to provide a framework against which the timing of mitochondrial dysfunction could be considered. New Zealand White rabbit kidneys were flushed with hypertonic citrate solution (0-2 degrees C and autografted immediately (group 1) or stored at 0-2 degrees C for 72 hours before autografting (group 2). Changes in oxyhemoglobin (HbO2) and deoxyhemoglobin (Hb) were monitored by near-infrared spectroscopy for 3 hours of reperfusion. Intrarenal perfusion was evaluated separately by barium sulfate angiography. Reperfusion resulted in rapid increases in HbO2 within 1 minute in both groups. Group 1 HbO2 fell sharply to a minimum at 3 minutes but recovered by 20 minutes; group 2 changes were similar, but there was no recovery (P<0.05 by 10 minutes). Hb increased rapidly in both groups upon reperfusion but in group 2 was significantly greater after 10 minutes (P<0.05). Total hemoglobin levels were similar in both groups. Renal hemoglobin saturation was 69% at 1 minute in both groups; there was no significant change in group 1 but a profound desaturation in group 2 to 25% at 10 minute (P<0.005) and no recovery thereafter. Barium sulfate distribution was normal in all group 1 kidneys; cortical distribution was normal in all group 2 kidneys, but medullary perfusion was poor for the first 60 minutes. Renal hemoglobin oxygenation kinetics as determined here do not correlate with the timing of mitochondrial dysfunction previously reported (Thorniley et al., Kidney International, 1994; 45: 1489). We conclude that secondary ischemia during reflow is not the only mechanism leading to acute tubular necrosis.
 ...
PMID:Hemoglobin oxygenation kinetics and secondary ischemia in renal transplantation. 860 68

Anemia negatively impacts cardiovascular comorbidity and hospitalization. In animals, recombinant erythropoietin (RhuEPO) leads to faster recovery after acute tubular necrosis. This study evaluates the effect of RhuEPO (Recormon, Hoffman-La Roche, Basel, Switzerland) on the correction of anemia and kidney function after renal transplantation. Patients receiving a renal transplant were randomized to receive or not receive RhuEPO 100 U/kg three times per week if the hemoglobin (Hb) level was less than 12.5 g/dL. The time to reach an Hb level greater than 12.5 g/dL was 66.5+/-14.5 days versus 52.6+/-23.7 days in the non-EPO and EPO groups, respectively (P=0.05). After 3 months, Hb levels were not different between the non-EPO and EPO groups (12.6+/-1.5 g/dL vs. 12.0+/-1.5 g/dL, respectively), although there was a higher increase in the EPO group (4.1+/-1.1 g/dL vs. 3.2+/-1.1 g/dL, P=0.02). In a Cox regression analysis, EPO use (relative risk 7.2, P=0.004) and dose (relative risk=0.63, P=0.04) were retained as independent variables predicting the time to reach an Hb level greater than 12.5 g/dL. In the EPO group, 14 of 22 patients reached the target Hb level of more than 12.5 g/dL versus 12 of 18 patients in the non-EPO group (P=not significant). Serum creatinine levels were not different between groups. RhuEPO in the immediate posttransplantation period seems to have no relevant clinical impact on the correction of anemia. There was no difference in the evolution of serum creatinine levels. In view of the cost, the use of RhuEpo in the posttransplantation period should be limited to high-risk patients.
 ...
PMID:Efficacy of erythropoietin administration in the treatment of anemia immediately after renal transplantation. 1569 72

A 60-year-old man, who had been diagnosed as having paroxysmal nocturnal hemoglobinuria(PNH) in 1994, was admitted to our hospital with general fatigue, and dark urine after a common-cold in January 2001. In the peripheral blood, the red blood cell count was 136 x 10(4)/microl, hemoglobin 4.0 g/dl and hematocrit 12.4%. The serum creatinine level was 9.9 mg/dl. Kidney biopsy revealed focal and segmental proliferation of mesangial cells, mesangial matrix expansion, acute tubular necrosis, interstitial fibrosis and hemosiderine deposits in the tubular epithelial cells confirmed by Berlin-blue staining. Immunofluorescence microscopy showed IgA and C3 deposition in the mesangium. Electron microscopy revealed electron dense deposits in the mesangial area and heavy electron-dense hemosiderin pigments in proximal tubular epithelial cells. After the transfusion of six units of washed red blood cells and two sessions of hemodialysis, the renal function returned to the levels before admission.
 ...
PMID:[Case of paroxysmal nocturnal hemoglobinuria complicated with IgA nephropathy who developed acute renal failure induced by hemolytic crisis]. 1613 Apr 10

There are no multifactorial studies of complications after renal transplant in the Hispanic population. The objective of this study was to identify which factors are associated with the development of complications after renal transplantation. This retrospective study was performed on all patients transplanted in the Puerto Rico Transplant Program during 2002. Independent variables included preoperative albumin, white blood cell (WBC) count, hemoglobin, creatinine, weight, height, body mass index (BMI), type of dialysis, time on dialysis, and urine production after transplant. Dependent parameters included posttransplant diuresis, wound infection, wound dehiscence, lymphoceles, acute tubular necrosis, length of stay, postoperative weight, graft survival, and patient survival. Data were analyzed with parametric and nonparametric techniques using STAT 200 software. Sixty-four patients were included in the study: 37 male, 27 female. No significant differences in complication rate or length of stay were found with age, preoperative albumin, WBC count, hemoglobin, creatinine, weight, height, dialysis modality, and donor type. Significant factors included type of dialysis, time on dialysis, and BMI. Preoperative albumin if > 3 was not a prognostic indicator for the development of surgical complications following renal transplantation. Only preoperative weight, BMI, and dialysis duration were significant factors in the development of postoperative complications and prolonged hospital stay in this sample Hispanic transplant population. These data are important in formulating selection, education, and transplant management policy.
 ...
PMID:Study of factors that affect complications after renal transplantation. 1664 7

Worldwide use of herbal therapy has increased dramatically in recent years. Most herbal therapies were not regulated as medicines, and their adverse effects often were underreported. We report a patient who developed acute renal failure, acute hepatic failure, autoimmune hemolytic anemia, and thrombocytopenia after oral intake of hot-water extract of Cupressus funebris Endl (Mourning Cypress), which is rich in flavonoids. Her renal biopsy showed acute tubular necrosis, interstitial nephritis, and hemoglobin casts. The clinical course and pathological findings were consistent with flavonoid-induced acute nephropathy. We emphasize that flavonoids are not harmless and may induce acute life-threatening renal damage.
 ...
PMID:Flavonoid-induced acute nephropathy by Cupressus funebris Endl (Mourning Cypress). 1705 87


1 2 Next >>