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)

Although haematuria is a relatively common symptom of hemophilia A and B, renal disease seemed to be a rarity and it has usually been held that this symptom was benign in nature. However detailed studies of renal function in a series of such patients using radiological and biochemical tests of renal function show significant differences compared to normal. These abnormalities seem to be associated with recurrent haematuria but do not appear to be related directly to replacement therapy with plasma concentrate and do not occur more frequently in patients who have received long term fibrinolytic inhibitors. Other rare renal disorders associated with haemophilia include nephrotic syndrome, trauma, acute tubular necrosis, analgesic nephropathy and chronic pyelonephritis.
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PMID:Renal disorders in haemophilia A and B. 26 97

Proteinuria was studied in ten renal allograft recipients; it was defined as: (a) glomerular--characterized by predominant albumin excretion; (b) tubular--significant excretion of both albumin and low molecular weight (LMW) proteins; and (c) glomerulo-tubular or mixed type, a combination of the two. LMW protein and albumin were quantitated by polyacrylamide gel electrophoresis with sodium dodecyl sulfate. In the immediate posttransplant period, LMW protein and albumin excretion, expressed as a percentage of creatinine clearance, were high, revealing a mixed pattern, and excretion of both protein classes was higher than during both acute tubular necrosis and acute rejection crisis. Tubular proteinuria was observed in acute tubular necrosis; a glomerulo-tubular or mixed pattern of protein excretion in acute rejection crises.
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PMID:Proteinuria following renal transplantation. 32 83

The accumulation of 99mtechnetium sulfur colloid (99mTcSC) was evaluated in 47 studies performed on 19 renal transplant patients by comparing its transplant activity to its bone marrow accumulation. There was a diagnosis of rejection of 21 of 22 studies (96.5%) in which marked transplant accumulation was noted. In 11 studies of patients with a clinical diagnosis of post-transplant acute tubular necrosis (ATN), the transplant activity varied from none to moderate. Rejection developed in 5 of 6 studies with minimal to moderate accumulation. Normally functioning renal transplant patients, or those with ATN and no superimposed rejection, do not show evidence of 99mTcSC accumulation.
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PMID:Clinical significance of 99mtechnetium sulfur colloid accumulation in renal transplant patients. 32 50

Ten patients received kidneys from living, related donors, the transplants having multiple renal arteries; a retrospective analysis of the postoperative Hippuran renograms is presented. All seven kidneys that had the large artery reopened before anastomosis of the smaller, developed scintigram findings suggestive of acute tubular necrosis (ATN) in the region with the more prolonged ischemia. Three similar kidneys with simultaneous recanalization of both renal arteries had normal Hippuran scintiphotos. Electron photomicrographs from upper- and lower-pole biopsies--in one case undergoing sequential revascularization--confirm the development of ischemic changes consistent with ATN in the half of the kidney developing scan findings of ATN.
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PMID:Segmental acute tubular necrosis in kidneys with multiple renal arteries transplanted from living related donors. 33 16

An adult renal transplant recipient was complicated with cryptococcal lung granuloma and meningitis. Treatment with the antifungal agents, 5-fluorocytocin and clotrimazole had to be discontinued due to side effects. Whereas, the intrathecal administration of amphotericin B proved effective for meningitis but intravenously it induced acute tubular necrosis to the transplanted kidney. In order to cure the persistant fungal lung granulomas in renal transplant patients early surgical excision seems to be essential.
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PMID:A case of renal transplant recipient complicated with cryptococcosis and amphotericin B induced acute tubular necrosis. 33 2

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

Renal allograft blood flow (RBF) was measured at operation by electromagnetic flow meter and probes in 45 patients (34 cadaver donors and 11 living related donors). Mean RBF in 26 patients without acute tubular necrosis (ATN), was 412 +/- 80 ml/min and in 19 patients with ATN, 270 +/- 100 ml/min (p less than .001). Only two of 24 transplants (8%) with RBF greater than 350 ml/min had ATN; whereas, 17 of 21 transplants (81 per cent) with RBF less than 350 ml/min had ATN (p less than .001). In cadaver donor transplants, RBF did not correlate with duration of ATN, warm ischemia time, total ischemia time, pulsatile perfusion time or renal vascular resistance during perfusion. Measurement of renal allograft blood flow can predict presence or absence of postoperative ATN in 87% of patients.
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PMID:Human renal allograft blood flow and early renal function. 33 86

In cirrhosis and fulminant hepatic failure acute renal failure may occur both without ("functional renal failure") and with tubular necrosis, the two probably being the ends of a spectrum. The underlying pathophysiological change is an intense renal and intra-renal vasoconstriction. Evidence is presented that this is due to systemic endotoxaemia resulting from failure of the liver to filter endotoxins absorbed from the gastrointestinal tract. Acute renal failure complicating obstructive jaundic has also been related to endotoxaemia, but in contrast to cirrhosis and fulminant hepatic failure this is usually due to an associated gram-negative infection and the renal failure almost invariably has the features of acute tubular necrosis. Endotoxins have two major effects on the kidney: (i) renal vasoconstriction, and (ii) glomerular and peritubular fibrin deposition. The nature of the renal failure depends on the balance between these variables which may be profoundly altered by the underlying liver disease.
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PMID:[Renal failure during liver disease--The significance of endotoxins (author's transl)]. 33 83

One hundred machine-preserved cadaver kidneys were transplanted irrespective of their flow rates on the preservation machine. Twenty-five per cent had flows of below 100 ml/min and 11 per cent had flows of below 80 ml/min. There was no correlation between the flow rate and function at 1, 3 or 12 months. There was no difference in the flow rate between those kidneys which functioned immediately and those which never functioned. A fall in flow rate was associated with acute tubular necrosis of longer duration but eventual function was not impaired. There was a higher incidence of early aggressive rejection in kidneys which functioned immediately. Preservation failure per se is a rare cause of primary non-function. Adherence to a policy of ignoring the flow characteristics of machine-preserved kidneys could make up to 25 per cent more kidneys available for transplantation.
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PMID:Flow and function in machine-preserved kidneys. 34 39

A case is reported of Fanconi syndrome and nonliquric renal failure, following a brief course of cephalothin and gentamicin, in a patient with diffuse histiocytic lymphoma. These drugs, especially when used in combination, have been associated with nephrotoxicity manifested as acute tubular necrosis and altered proximal tubular function, but biochemical evidence for generalized proximal tubular dysfunction has not been accurately defined. Thus far, only two other antibiotics, degraded tetracycline and streptozotocin, have been implicated in producing an acquired Fanconi syndrome.
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PMID:Fanconi syndrome associated with cephalothin and gentamicin therapy. 34 14


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