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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We are reporting the first case, to our knowledge, of a venous embolus to a transplanted kidney. The embolus occurred five days after transplantation of a cadaver kidney in a 31-year-old woman who was receiving estrogen-progesterone therapy for menorrhagia. Five hours after acute onset of left flank pain and anuria, the embolus was identified at the anastomosis of the donor renal vein to the external iliac vein. The embolus was manipulated distally in the external iliac vein and excluded by proximal division of the vein. Recovery was eventually complete, despite two major postoperative complications, acute tubular necrosis and a perirenal hematoma secondary to heparin sodium therapy. Radionuclide scanning was critically important in establishing the diagnosis and in assessing the potential for the kidney to recover from acute tubular necrosis. On the basis of this experience, we believe that prompt surgical intervention is indicated for acute venous occlusion.
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PMID:Venous embolus to a transplanted kidney. Diagnosis and treatment. 78 79

Scanning with technetium-99m was used as a diagnostic aid in renal transplant patients with post-transplant oliguria. It is a safe and dependable method of determining whether the renal vasculature is still intact and can often be used to differentiate acute tubular necrosis from acute rejection.
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PMID:Dynamic scintiscanning with technetium-99m as a diagnostic aid in oliguria after renal transplant. 79 Jun 7

To date angiography has been the most precise diagnostic modality for the evaluation of a transplanted kidney. In the immediate postoperative period angiography can clearly demonstrate the integrity of the vascular anastomoses, and in most cases helps to differentiate between acute tubular necrosis and acute rejection. It is also helpful in the evaluation of the transplant kidney later in the postoperative period, since it can provide some estimate of the vascular effects of chronic rejection and distinguish between hypertension secondary to chronic rejection or renal artery stenosis. Serial isotope techniques may play a more important role in the evaluation of the transplanted kidney in the future, but at present angiography is the diagnostic modality of choice at the Cleveland Clinic.
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PMID:Selective renal angiography: its value in renal transplantation. 79 Jul 34

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

Scanning (SEM) and transmission (TEM) electron microscopy were used to elucidate morphological changes associated with acute tubular necrosis induced by high doses of mercuric chloride. Marked morphological changes were demonstrated in proximal tubules with TEM at one hour and with both SEM and TEM at six hours. These changes appeared earlier than reported in previous studies using any dose. The scanning microscopic provided a three-dimensional view of proximal cells showing changes in early injury with subsequent separation of the injured cells from the remaining cells. Certain of these residual cells change into low-lying cells with reline the proximal tubule. Variability was seen in the number of residual cells. However, once cell injury was initiated, necrosis proceeded in a reproducible manner.
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PMID:Scanning and transmission electron microscopy of mercuric chloride-induced acute tubular necrosis in rat kidney. 80 31

Djenkolic acid was extracted from djenkol beans with 70% ethanol and water and was quantitatively determined by paper chromatography. Djenkol beans contained 0.3-1.3 gm% djenkolic acid and about 93% of this acid occurred in the free state. The toxicity of djenkol beans was studied in 5 rhesus monkeys, 9 albino rats and 22 mice fed with 70% ethanol extracts. The total urinary output decreased. There was an increase in specific gravity of the urine during the period of feeding monkeys with djenkol beans. Urinary samples of the experimental animals were turbid and contained some red cells, white cells, epithelial cells, albumin and amorphous particles. One of 22 mice excreted sharp needle-shaped crystals in the urine on day 3 after feeding. Histological examination of kidneys of rats and mice showed mild to severe acute tubular necrosis with some glomerular cell necrosis.
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PMID:Studies on djenkol bean poisoning (djenkolism) in experimental animals. 82 79

We report a case of renal cortical microabscesses which presented as oliguric acute renal failure. Prior to the biopsy the patient was suspected of having acute pyelonephritis with acute tubular necrosis. Biopsy was performed to rule out rapidly progressive glomerulonephritis as a cause of his renal failure. To our surprise, we found multiple small microabscesses in the renal cortiex. Renal cortical microabscesses should be considered as a reversible acute renal failure.
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PMID:Renal cortical microabscesses as cause of reversible acute renal failure. 84 81

The pathologic changes induced by Cis-platinum (II) diamminedichloride (CPDD) therapy in the kidneys are described in 12 patients with solid tumors and malignant lymphomas. According to dosage of CPDD the patients were divided into two groups: 1) low-dose group--.0.5-2 mg/kg daily, for 1 to 6 days; and 2) high-dose group--single injection of 3 or more mg/kg with concommitant mannitol-induced diuresis. Pathologic changes in the kidneys were essentially similar in both groups and consisted of focal acute tubular necrosis, affecting primarily the distal convoluted tubules and collecting ducts, dilatation of convoluted tubules, and formation of casts. These changes persisted as long as 29 days post CPDD therapy. In addition, the collecting ducts exhibited significant epithelial atypia. BUN and serum creatinine levels were elevated in both groups. The mean BUN/serum creatinine values were 54/2.2 mg/100 ml and 32/2.0 mg/100 ml for low and high-dose groups, respectively. Since the nephrotoxicity of CPDD is known to be dose-related, our findings suggest that mannitol-induced diuresis has considerably decreased the renal toxic damage of CPDD therapy in these patients.
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PMID:The renal pathology in clinical trials of cis-platinum (II) diamminedichloride. 85 39

The increased nephrotoxicity of simultaneously administered kanamycin and low molecular weight dextran was studied in rats. The simultaneous administration of the two drugs showed an increase of nephrotoxicity, and caused pronounced vacuolation of the cytoplasm in the proximal tubular cells. The vacuoles were confirmed to be phagolysosomes by electron microscopic, histochemical and cell fractionation methods. The cell fractionation technique indicated that these phagolysosomes contained both kanamycin and dextran. The alteration of membrane was observed in the phagolysosomes, and these lysosomes of damaged renal tissue seemed to be more fragile than normal. The possible role played by lysosomes in the pathogenesis of acute tubular necrosis was discussed.
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PMID:Cytochemical studies of acute tubular necrosis caused by simultaneous administration of dextran and kanamycin. 85 38

Eleven out of a series of twenty-nine patients (37-9%) with acute copper sulphate poisoning developed acute renal failure. Intravascular haemolysis appeared to be the chief factor responsible for renal lesions in these patients. Histological lesions observed in the kidney varied from those of mild shock to well established acute tubular necrosis. In one case, granulomatous lesions were seen in response to tubulorrhexis. Renal failure was the chief indication for dialysis in ten patients, whereas one patient was dialysed primarily for removal of copper. Notwithstanding the adequate control of uraemia by dialysis, only six of the eleven patients recovered. Septicaemia was responsible for death in three, hepatic failure in one and methaemoglobinaemia in another. It is postulated that release of copper from haemolysed red cells during acute haemolytic episodes may initiate, or contribute to, the development of renal damage.
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PMID:Acute renal failure following copper sulphate intoxication. 87 9


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