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)

Mannitol may be useful clinically both as a diuretic and as an obligate extracellular solute. As a diuretic it can be used to treat patients with intractable edema states, to increase urine flow and flush out debris from the renal tubules in patients with acute tubular necrosis, and to increase toxin excretion in patients with barbiturate, salicylate or bromide intoxication. As an obligate extracellular solute it may be useful to ameliorate symptoms of the dialysis disequilibrium syndrome, to decrease cerebral edema following trauma or cerebrovascular accident, and to prevent cell swelling related to renal ischemia following cross-clamping of the aorta. Largely unexplored uses for mannitol include its use as an osmotic agent in place of dextrose in peritoneal dialysis solutions, its use to maintain urine output in patients newly begun on hemodialysis, and its use to limit infarct size following acute myocardial infarction.
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PMID:Mannitol. 38 67

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

Treatment with thromboxane (Tx) synthase inhibitors or free radical scavengers has been shown to afford protection from renal ischemia. Since free radicals are closely associated with thromboxane (Tx) synthesis, this study examines the thesis that free radical scavengers inhibit formation of Tx. Anesthetized rats (n = 42) underwent right nephrectomy. By random choice, before 45 min of left renal pedicle clamping, rats received: 0.5 ml dextrose placebo IV (n = 6); the hydroxyl radical scavenger dimethyl-thiourea (DMTU), 500 mg/kg IV (n = 10); or the superoxide scavenger superoxide dismutase (SOD), 24,000 Sigma Units (SU)/kg IV (n = 12). This dose of SOD was repeated before release of the clamp. Treatment with DMTU and SOD decreased plasma TxB2 levels following 5 min of reperfusion from 2,480 pg/ml in dextrose treated controls to 1,155 pg/ml (p less than 0.01) and 1,419 pg/ml (p less than 0.03), respectively. At 24 hr, DMTU and SOD therapy decreased creatinine from 3.0 mg/dl in controls to 1.6 mg/dl (p less than 0.01) and 2.1 mg/dl (p less than 0.05), respectively. At 24 hr, DMTU but not SOD decreased left renal weight from 113 to 94% (p less than 0.0003) of the weight of the previously removed right kidney, and histologically prevented acute tubular necrosis (p less than 0.05). In nephrectomized but nonischemic sham control rats (n = 7) plasma TxB2 and 6-keto-PGF1 alpha concentrations were 757 pg/ml and 82 pg/ml, creatinine level 0.9 mg/dl and kidney weight 94% of the previously removed right kidney.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of thromboxane (Tx) synthesis by free radical scavengers. 312 99

Of 48 patients with fulminant hepatic failure who progressed to grade III or IV encephalopathy 38 showed evidence of renal impairment. In 32 of these patients the underlying cause could be placed initially into one of three categories-prerenal uraemia (4 patients), acute tubular necrosis (16), and "functional renal failure" (12). The latter differed in several respects from that seen with liver failure secondary to cirrhosis. The frequency and type of renal impairment was the same in those patients in whom the fulminant hepatic failure had resulted from an overdose of paracetamol as in the other aetiological groups.Abnormalities in plasma electrolytes were common-in particular hypernatraemia occurred in 11 patients from an osmotic diuresis precipitated by hypertonic dextrose or fructose given intravenously, and from the sodium in the fresh frozen plasma used to correct the coagulation disturbance when renal excretion of this ion was inappropriately low.
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PMID:Frequency and type of renal and electrolyte disorders in fulminant hepatic failure. 481 48

The value of contrast dye to the planning and evaluation of cardiovascular disease cannot be overestimated. However, adverse renal sequellae may cause the surgeon to hesitate in obtaining an arteriogram, especially in patients with compromised renal function. The purpose of this study was to evaluate the incidence of renal dysfunction in patients requiring angiography. Standard contrast angiography for cerebral or peripheral vascular disease was administered to 150 consecutive patients (89 men and 61 women), with an average age of 63.3 years (range 49 to 89 years). All patients received 100 to 150 ml of dye, with a concentration of approximately 50% iodine. Patients were hydrated with 0.5 N saline/5% dextrose, intravenously, for 8 hours before the procedure (1 to 3 ml/kg/hr). In 31 patients (11 women and 20 men) the serum BUN and/or creatinine levels were elevated (mean BUN value of 48 +/- 9 mg/dl; mean creatinine level of 2.8 +/- 0.6 mg/dl). The patients with abnormal renal function received an additional 300 to 500 ml of intravenous fluid, plus 20 to 40 mg intravenous furosemide, 1 hour before roentgenography to establish a diuresis. All patients were hydrated for 6 hours after angiography with the same solution at the same rate (1 to 3 ml/kg/hr). There were no episodes of compromised renal or cardiopulmonary dysfunction because of contrast angiography. In no patient did the BUN or creatinine level rise, nor was there evidence of acute tubular necrosis, as documented by oliguria and abnormal cells in the urine. Angiography is a safe procedure, even with patients who may have compromised renal function, if appropriate prehydration/posthydration and diuretic measures are undertaken.
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PMID:Value of periangiography hydration. 649 79

One of the controversies in the nutritional therapy of patients with renal failure is the respective role of either the essential amino acids alone or both essential and nonessential amino acids in the treatment of these patients. During a period when essential amino acids were unavailable, a large number of patients with acute renal failure was treated with a modified solution consisting of both essential and nonessential amino acids. The solution consisted of 3.8 grams of nitrogen in 46 per cent dextrose in units of 750 milliliters. A mean of 2,322 +/- 151 calories was administered to this group of patients. Over-all, the survival rate was 9 per cent as opposed to 75 per cent in the previous group treated with essential amino acids only and hypertonic dextrose, 40 per cent, in the group of historical controls treated with hypertonic dextrose. The groups are not strictly comparable because the group treated with both essential and nonessential amino acids may not have been strictly comparable, particularly with a slightly longer duration of renal failure, higher initial blood urea nitrogen level and lower urine volume than either of the other two groups previously treated. While adequate stabilization, but not a decrease in the blood urea nitrogen level, may be achieved from the use of both essential and nonessential amino acids, the excessive mortality seen may be related to differential effects of essential amino acids in supporting host resistance, while nonessential amino acids do not. The results of this study suggest that, until the safety and efficacy of a mixture of essential and nonessential amino acids in renal failure can be demonstrated, essential amino acids remain the treatment of choice as the nutritional support of patients with acute tubular necrosis.
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PMID:Comparative study of parenteral nutrition in renal failure using essential and nonessential amino acid containing solutions. 677 42