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

The effect of intravenously administered distilled water was examined alone and during alkalization in a patient with gross hematuria associated with the sickle cell trait. On each of 4 occasions hematuria ceased promptly after the infusion of distilled water. Bicarbonate therapy also consistently decreased hematuria. In vitro studies on erythrocytes from another patient with sickle cell trait and hematuria demonstrated that slight increases in urinary pH similar to those that occur in the urine during alkalization can reverse or prevent erythrocyte sickling in the sicle cell trait. If patients with the sickle cell trait are hydrated adequately and have a good rate of urine flow distilled water can be given intravenously with virtually no danger of acute tubular necrosis secondary to erythrocyte hemolysis.
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PMID:The effect of bicarbonate and distilled water on sickle cell trait hematuria and in vitro studies on the interaction of osmolality and pH on erythrocyte sickling in sickle cell trait. 2 9

The delayed onset of anuria/oliguria in acute tubular necrosis has been theorized to represent a complicating compartment syndrome, i.e., parenchymal swelling within an unyielding capsule. To test this proposition, 12 monkeys had suprarenal aortic cross-clamping, followed by unilateral renal decapsulation to create an experimental as well as a control kidney unit in the same animal. Histologic examination uniformly confirmed tubular necrosis at death or sacrifice. Subsequent split renal function studies (creatinine, urea, and free water clearances) indicated significantly greater maintenance of renal function by the decapsulated kidney than by its paired control. Clinical evaluation in 21 hemorrhagic shock patients, with the capsule of one kidney stripped, revealed on follow-up that 15 developed a renal failure consistent with acute tubular necrosis. Although three patients with polyuric failure died before split studies could be run and two others have been too recent for computer analysis to have been completed, nine of the remaining ten had significantly greater renal plasma flows (194 versus 121 ml/min M(2), p < .01) and significantly greater urine flows (.99 versus .18 ml/min M(2), p < .01) on the decapsulated side than on the control, as determined by differential renal scans. No significant difference in these same lateralized renal functions was noted in the tenth patient with renal failure and in the six survivors without renal failure. Renal decapsulation as prophylaxis reduced the anticipated incidence of oliguria/anuria from an expected 75% to 7% (p < .01) in these 21 shock patients. Such data suggest that delayed renal ischemia, possibly based on a compartment syndrome, may be the cause for a progression of acute tubular necrosis from polyuria to oliguria and then to anuria.
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PMID:Renal decapsulation in the prevention of post-ischemic oliguria. 40 54

Studies were undertaken to determine whether a hypotensive episode under variable conditions is capable of inducing experimental acute renal failure in rats. Animals were subjected to hypovolemic shock by withdrawing volumes of blood necessary to maintain a systolic pressure of 30-40 mm Hg for 105-110 min. The blood was then reinfused and the animal was allowed to recover for 48 h prior to sacrifice. In an attempt to increase the injury, a second group of animals was salt-depleted prior to injury, a third group was volume-depleted by being deprived of H2O for 72 h prior of injury, a fourth group received 7.5 mg/kg indomethacin 30 min prior to injury, and a fifth group had 30% of the blood which was removed to produce shock hemolyzed and returned following the injury. In all groups examined, light microscopy revealed a moderate to severe acute tubular necrosis localized mainly in the outer stripe of the outer zone as defined by Peter (1909). Tubular damage was confined to the medullary pars recta of the proximal tubule and only in the most severe cases did injury involve the cortical pars recta and pars convoluta. Casts were present in the distal tubules and collecting ducts. Despite these significant histologic alterations, BUN values from all experimental groups remained within control levels. These studies clearly show that extensive necrosis of the medullary pars recta can be dissociated from the development of acute renal failure.
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PMID:Hypovolemic models of acute tubular necrosis in the rat kidney. 41 58

A prospective analysis of the value of urinary diagnostic indices in ascertaining the cause of acute renal failure was undertaken. Our results show that in the setting of acute oliguria a diagnosis of potentially reversible prerenal azotemia is likely with urine osmolality greater than 500 mosm/kg H2O, urine sodium concentration less than 20 meq/litre, urine/plasma urea nitrogen ratio greater than 8, and urine/plasma creatinine ratio greater than 40. Conversely, a urine osmolality less than 350 mosm/kg, urine sodium concentration greater than 40 meq/liter, urine/plasma urea nitrogen ratio less than 3, and urine/plasma creatinine ratio less than 20 suggest acute tubular necrosis. A significant number of oliguric patients will not have urinary indices that fall within these guidelines. In this setting, urine sodium concentration divided by the urine-to-plasma creatinine ratio (the renal failure index) and the fractional excretion of filtered sodium provide a reliable means of differentiating reversible prerenal azotemia from acute tubular necrosis.
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PMID:Urinary diagnostic indices in acute renal failure: a prospective study. 66 84

A case of spontaneous renal allograft rupture is described. Typically, this infrequent transplant complication occurred in the early post-transplant period in an oliguric setting with progressive pain, tenderness and swelling at the transplant site associated with hypotension and a decreasing hematocrit. Prompt surgical exploration and repair of the defect in the convex border of the renal allograft controlled hemorrhage and resulted in graft survival, and a normal blood urea nitrogen and creatinine 10 months after transplantation. There have been no rejection episodes and the renal biopsy demonstrated no evidence of rejection or acute tubular necrosis. Ice preservation for 24 hours and changes secondary thereto may have made the kidney susceptible to rupture when the position of acute flexion was assumed.
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PMID:Spontaneous renal allograft rupture without rejection: a case report. 78 13

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

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

Renal tubular function was evaluated in vitro by kidney slice uptakes of p-aminohippurate (PAH) and tetraethylammonium (TEA) at 24 and 48 h in water-drinking rats and at 24 h in chronic saline-loaded rats after induction of acute tubular necrosis (ATN) by HgCl2 and glycerol injection. Significant correlations between decrease tubular uptake of PAH and TEA and elevated serum creatinine levels were noted in both models of ATN in water- and saline-drinking rats. However, with the same degree of impairment of PAH and TEA uptakes the creatinine was significantly lower in saline-loaded rats than in water-drinking rats in both forms of ATN. The correlation between impaired tubular function and elevated creatinine suggests that tubular damage and glomerular filtration reduction might be pathophysiologically related in ATN.
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PMID:The role of tubular necrosis in the pathophysiology of acute renal failure. 94 Jun 26

Renal function was evaluated in 40 patients with fulminant hepatic failure, They were divided into two groups on the basis of glomerular filtration rates greater than 40 ml/min or less than 25 ml/min. A number of patients in group 1 had markedly abnormal renal retention of sodium together with a reduced free water clearance and low potassium excretion which could be explained by increased proximal tubular reabsorption of sodium. The patients in group 2 had evidence that renal tubular integrity was maintained when the glomerular filtration rate was greater than or equal ml/min (functional renal failure), but evidence of tubular damage was present when this was less than 3 ml/min (acute tubular necrosis).
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PMID:Abnormalities of sodium excretion and other disorders of renal function in fulminant hepatic failure. 96 82

Five cases of acute lead poisoning resulted from the self-injection of lead and opium pills which were crushed, heated and suspended in water. Two of the five patients died of illnesses in which hepatic failure and reversible acute tubular necrosis were prominent features. One of these two had a severe neuropathy, with flaccid quadriplegia and respiratory paralysis. The other three patients had relatively minor symptoms but unequivocal biochemical evidence of lead toxicity. Autopsy changes included hepatic degeneration with inclusion bodies, regenerating renal tubular epithelium and wasting of skeletal muscle. Hepatic lead content was extremely high in one case. Chelation therapy in the other fatal case resulted in a fall in blood lead to within normal limits and a clinical improvement, which was terminated by massive haemorrhage from a ruptured innominate artery.
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PMID:Acute lead poisoning: Five cases resulting from self-injection of lead and opium. 117 12


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