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)

A 42-year-old male was hemodialyzed for 2 years with excellent control of calcium-phosphate metabolism. He received a cadaveric renal transplant but experienced a prolonged episode of acute tubular necrosis during which he could not tolerate phosphate-binding antacids. His calcium X phosphate product became markedly elevated for 20 days. Following a brief period of function, the homograft was removed on the 45th post-transplant day after severe rejection and subsequent infection. Chest X-ray was normal. Six days after graft nephrectomy, he became acutely dyspneic and markedly hypoxemic. Diffuse, flocculent pulmonary infiltrates appeared on the chest film. The patient expired 1 day later. At postmortem examination, there was severe, diffuse pulmonary alveolar calcification demonstrated by chemical and histologic examination. Although unlikely, the prolonged post-transplant period characterized by elevated calcium X phosphate product may have played a pathogenetic role. Calciphylaxis may have occurred, with hyperparathyroidism as the sensitizing agent and any of several drugs acting as challenger.
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PMID:Sudden fatal pulmonary calcification following renal transplantation. 33 63

A 24-year-old male homosexual drug addict was admitted in coma and circulatory failure after a 10 g overdose of acebutolol. The usual resuscitative measures were undertaken, together with administration of adrenaline and gastric lavage. Six hours of external cardiac massage and pacing, and high catecholamine doses (36 mg.h-1 of adrenaline and 60 micrograms.kg-1 x min-1 of dobutamine) were required before the circulatory system became again spontaneously efficient. After this acute episode, the patient improved despite acute tubular necrosis. On the third day, bilateral alveolar and interstitial lesions were found on the chest film. Bronchoalveolar lavage and protected distal brushings were carried out. Both Aeromonas hydrophila and Staphylococcus aureus were found in the cultured brushings. Treatment with ceftriaxone, vancomycin and amikacin was introduced. This nosocomial pneumonia was very haemorrhagic, resulting in several bloody casts responsible for several episodes of atelectasis. The patient was definitely extubated on the 18th day, and left the ICU 23 days later without any sequela. His HIV status was negative. Four other infections with the same strain of Aeromonas hydrophila occurred at the same time as this patient's. The common source for this germ was found to be soft water. Several measures have since been undertaken: removal of a centralized water softener, filtration and higher chlorine content in the water circuit, and updating of intensive care protocols for disinfection of equipment.
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PMID:[Nosocomial Aeromonas hydrophila pneumonia complicating toxic coma]. 833 70

The effect of gentamicin on transport of pyroglutamylhistidine (pGlu-His) was examined in rabbit renal brush-border membrane vesicles (BBMV). Gentamicin, an aminoglycoside antibiotic, is limited in its usage because of nephrotoxicity characterized in part by transport defects in the proximal tubule. Since there is no information regarding the effects of gentamicin on renal peptide carriers, uptake of [3H]pGlu-His was measured in BBMV following either in vivo or in vitro exposure to the antibiotic. One hour after in vivo administration, the maximal rate (Vmax) for pGlu-His transport was significantly reduced in isolated membrane vesicles washed free of the drug, but the apparent Michaelis constant (Km) was unaltered. Coincubation of membranes with gentamicin during measurements of pGlu-His uptake had a similar effect, causing a significant decrease in the Vmax but not the Km of transport. The addition of 5 mM magnesium to the uptake medium prevented the in vitro but not the in vivo effect. The data indicate that high doses of gentamicin inhibit the capacity but not the affinity of dipeptide transport in the kidney, prior to morphological changes which typify acute tubular necrosis. The in vitro effect is rapid and involves a direct action of gentamicin on the brush-border membrane. The in vivo experiments show that toxicity may be prolonged and remains following removal of the drug from the renal brush border.
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PMID:Gentamicin inhibits carrier-mediated dipeptide transport in kidney. 878 Feb 57

Ex vivo NMR spectroscopy was used to investigate pH in 67 human kidney transplants. (1)H and (31)P spectra were recorded at 1.5 T during regular hypothermic storage in histidine-tryptophane-alpha-ketoglutarate (HTK) solution. Estimations of cytosolic pH from chemical shift differences between inorganic phosphate and phosphodiesters and of extracellular pH from the varepsilon1 and delta2 protons of histidine were based upon systematic titration studies. The possibility to predict acute tubular necrosis (ATN) by measuring pH was compared to results obtained with peak area ratios of phosphomonoesters (PME) and Pi and of the gamma-phosphorus of nucleoside 5'-triphosphate (gamma-NTP) and Pi. Cytosolic pH was 6.86+/-0.10 in kidneys showing immediate post-transplant function and 6.84+/-0.10 in those with ATN. Time-dependent studies demonstrated a monoexponential pH decay (velocity constant: 0.14+/-0.07 h(-1)). Extracellular pH varied between 7.40 and 7.15. Grafts with immediate function showed higher PME/Pi (2.24+/-0.57 vs. 1.77+/-0.50, p<0.05) and gamma-NTP/Pi (0.33+/-0.16 vs. 0.16+/-0.08, p<0.001). Intra- and extracellular pH can be monitored non-invasively during hypothermic transplant storage. The pH gradient between both compartments provides quantitative information about the buffer capacity of the preservation medium. Acidification is not a primary cause of ATN during regular HTK storage. The total nucleotide pool is a determinant of the reversibility of ischemic injury.
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PMID:Tissue pH in human kidney transplants during hypothermic ischemia. 1093 Jul 84

We report a 55-year-old male with a diagnosis of intravascular lymphoma and hemophagocytosis. He initially presented with hemolytic anemia and splenomegaly and was successfully treated with oral steroids. His clinical course was later complicated by fever, cytopenias, hypoalbuminemia, disseminated intravascular coagulation, gastrointestinal bleeding and acute tubular necrosis. Results of an extensive investigation for fever of unknown origin were negative. Although the patient was treated aggressively with antimicrobials, transfusion support and dialysis, he expired 3 weeks after hospitalization. Post-mortem analysis revealed large CD30- and CD45-positive lymphoma cells in an intravascular distribution in most of the organs studied. Histopathology of the spleen and bone marrow was significant for fulminant hemophagocytosis.
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PMID:Intravascular lymphoma associated with hemophagocytic syndrome: a rare but aggressive clinical entity. 1465 9

In most severe cases of strychnine poisoning, the patient dies before reaching the hospital. This report describes the treatment and successful outcome of a patient who had taken a dose of strychnine that would normally be fatal. A 28-y-old man was admitted 2 h after ingestion of 1 to 1.5 g of strychnine. He had a Glasgow Coma Score of 14/15 and was severely agitated and in mild respiratory distress; blood pressure was 90/60 mmHg, pulse 110/min, and peripheral pulses weak. He had generalized hyperactive reflexes and had several generalized tonic-clonic convulsions in the emergency department. Treatment consisted of gastric lavage with water, oral administration of activated charcoal and sorbitol solution, continuous intravenous administration of midazolam and then sodium thiopental, furosemide, sodium bicarbonate and hemodialysis for acute renal failure. His clinical course included respiratory distress, agitation, generalized tonic-clonic convulsions, hyperactivity, oliguria and acute tubular necrosis prior to recovery in 23 days. This patient ingested what would normally be a fatal amount of strychnine, had signs and symptoms of severe toxicity and recovered, suggesting that with aggressive supportive care patients may have favorable outcomes.
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PMID:A case of acute strychnine poisoning. 1508 Feb 7

To clarify the pathophysiological mechanism underlying acute renal injury caused by acute exposure to arsenic, we subcutaneously injected both BALB/c and C57BL/6 mice with sodium arsenite (NaAs; 13.5 mg/kg). BALB/c mice exhibited exaggerated elevation of serum blood urea nitrogen (BUN) and creatinine (CRE) levels, compared with C57BL/6 mice. Moreover, half of BALB/c mice died by 24 h, whereas all C57BL/6 mice survived. Histopathological examination on kidney revealed severe hemorrhages, acute tubular necrosis, neutrophil infiltration, cast formation, and disappearance of PAS-positive brush borders in BALB/c mice, later than 10 h. These pathological changes were remarkably attenuated in C57BL/6 mice, accompanied with lower intrarenal arsenic concentrations, compared with BALB/c mice. Among heavy metal inducible proteins including multidrug resistance-associated protein (MRP)-1, multidrug resistance gene (MDR)-1, metallothionein (MT)-1, and arsenite inducible, cysteine- and histidine-rich RNA-associated protein (AIRAP), intrarenal MDR-1, MT-1, and AIRAP gene expression was enhanced to a similar extent in both strains, whereas NaAs challenge augmented intrarenal MRP-1 mRNA and protein expression levels in C57BL/6 but not BALB/c mice. Moreover, the administration of a specific inhibitor of MRP-1, MK-571, significantly exaggerated acute renal injury in C57BL/6 mice. Thus, MRP-1 is crucially involved in arsenic efflux and eventually prevention of acute renal injury upon acute exposure to NaAs.
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PMID:MRP-1 expression levels determine strain-specific susceptibility to sodium arsenic-induced renal injury between C57BL/6 and BALB/c mice. 1569 64

We describe a patient with previously undiagnosed hypothyroidism who developed rhabdomyolysis while taking a statin. He had no other precipitating factors. The statin was stopped, intravenous fluids were started immediately and L-thyroxin was given after confirming the diagnosis of hypothyroidism. His symptoms improved over a few days. Because rhabdomyolysis is a rare but potentially life threatening disorder when complicated by acute tubular necrosis and renal failure, physicians must pay special attention when starting statins in patients with hyperlipidemia.
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PMID:Rhabdomyolysis due to the additive effect of statin therapy and hypothyroidism: a case report. 1799 11

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.
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PMID:Successful management of eviscerated renal allograft with preservation of function. 1832 80

An 11-year-old male developed systemic calciphylaxis during induction therapy for acute lymphoblastic leukemia. His predisposing conditions were hypercalcemia, supplements for pamidronate-induced hypocalcemia and hypophosphatemia and renal insufficiency. He died of cardiorespiratory arrest on the 20th day of induction treatment. Autopsy revealed extensive calcium deposits in the heart, lungs and kidneys. He had diffused alveolar damage, acute tubular necrosis, chronic pancreatitis and marked hepatic steatosis. Systemic calcium deposition may progress rapidly in children with hypercalcemia of malignancy. Since pamidronate reduces mineral resorption from tissues, calcium and phosphate replacements increase systemic mineral deposits. Thus, mineral supplements should be considered only to combat symptoms.
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PMID:Systemic calciphylaxis. 1849 73


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