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)

In 54 patients with graft failure the changes of urine sodium concentration and of urinary enzyme activities (alanine aminopeptidase, AAP) were investigated. It was found that: (1) the kidneys with irreversible acute tubular necrosis are characterised by high urine sodium level, and low AAP activities. These changes correspond to the end stage of renal insufficiency. (2) Low concentration of sodium and extremely high AAP excretion are characteristic in grafts with severe rejection episodes. (3) If kidneys lost their function due to irreversible rejection, the biochemical variables showed the same changes as in the first group. We concluded that by continuous determination of sodium levels and enzyme activities in urine and by their correlation it is possible to detect the non-functioning grafts in the early posttransplantation period.
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PMID:[Biochemical parameters for determination of graft viability during the early postoperative period (author's transl)]. 36 May 49

Three patients having lepromatous leprosy developed acute renal failure. Two patients completely recovered and one was left with a moderate degree of renal insufficiency. Renal tissue obtained by percutaneous biopsy revealed acute tubular necrosis in two and diffuse crescentic glomerulonephritis in the third case.
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PMID:Acute renal failure in leprosy. 56 62

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

Two patients developed acute tubular necrosis, characterized clinically by acute oliguric renal failure, while they were receiving a combination of cephalothin sodium and gentamicin sulfate therapy. Patients who are given this drug regimen should be observed very carefully for early signs of nephrotoxicity. High doses of this antibiotic combination should be avoided especially in elderly patients. Patients with renal insufficiency should not be given this regimen.
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PMID:Nephrotoxicity of combined cephalothin-gentamicin regimen. 113 Sep 30

The hepatorenal syndrome following right hemiphepatectomy is reported in a previously healthy patient who sustained a shotgun wound in the abdomen. In spite of the development of severe oliguric renal insufficiency and the administration of massive amounts of volume expanders and furosemide, the urine sodium concentration remained very low, therby excluding the diagnosis of acute tubular necrosis. Although severe hyperbilirubinemia developed, the prothrombin time was only slightly abnormal and the liver doubled in size in the 2 weeks after surgery. The study of functional renal failure in patients with liver disease other than decompensated cirrhosis and with significant preservation of hepatic function may suggest that factors other than a circulating toxin participate in mediating the hepatorenal syndrome.
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PMID:Hepatorenal syndrome following hemihepatectomy. 126 Nov 3

The urinary sediment was examined by light microscopy in 65 consecutive inpatients with renal insufficiency (not due to pre- or postrenal factors) referred to a nephrology consult service for evaluation. In the 60 patients in whom a single diagnosis was reached, the sediments of 34 (57%) contained an easily recognized cell, which we have called the "bubble cell". These cells were bizarre, large cells with a single nucleus, which appeared to contain one or more fluid-filled vesicles. Bubble cells were most prevalent in the sediment of patients with acute tubular necrosis but were also seen a variety of other renal diseases. In most patients with acute tubular necrosis, the sediment also contained "normal"-appearing renal tubular cells, muddy brown casts, and oval fat bodies which were indistinguishable from those seen in the nephrotic syndrome. By electron microscopy, the bubble cells appeared to be vacuolated renal tubular epithelial cells, which had characteristics of viable cells. Most bubble cells excluded the vital dye Trypan blue, whereas the normal-appearing renal tubular cells were typically strongly positive. It was concluded that bubble cells, often accompanied by oval fat bodies, are commonly present in the sediment of patients with acute tubular necrosis as well as many other types of renal disease. Most cells which would be classified as "normal" renal tubular cells in these sediments are dead. In contrast, the findings suggest that the bubble cell represents an injured but viable renal tubular cell. The frequent finding of oval fat bodies in the same sediments suggests that the oval fat body is also produced by tubular cell injury.
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PMID:Bubble cells: renal tubular cells in the urinary sediment with characteristics of viability. 188 70

There is a growing number of hospitalised patients who develop a drug-induced renal problem because increasing numbers of potent drugs have been added to the therapeutic arsenal in recent years. The 3 clinical syndromes that can be recognised in drug-induced nephropathy are acute renal failure, chronic interstitial nephritis and the nephrotic syndrome. The first can be caused by prerenal problems, acute interstitial nephritis, acute tubular necrosis and intratubular obstruction. The most important drugs that cause prerenal failure are NSAIDs, captopril and cyclosporin. NSAIDs inhibit the synthesis of prostaglandins, and consequently vasoconstriction of the afferent arteriole leads to lowering of the glomerular filtration rate (GFR); captopril blocks the formation of angiotensin II (which also leads to a lower GFR), and should be used with caution in patients with stenotic renal arteries; cyclosporin causes vasoconstriction of the afferent arteriole, which is probably mediated by the sympathetic system. Combinations of these drugs result in increased nephrotoxicity. The drugs most likely to cause acute interstitial nephritis are antibiotics and NSAIDs. Normally, signs of an allergic reaction are also present. Acute interstitial nephritis is usually self-limiting, but in some studies it is claimed that steroids may promote recovery. Four important causal agents of acute tubular necrosis are aminoglycosides, amphotericin B, radiocontrast agents and cyclosporin. Approximately half of the cases of drug-induced renal failure are related to the use of aminoglycosides: generally, 10 days after start of treatment a nonoliguric renal failure develops, with recovery after withdrawal of the drug in almost all cases. The aminoglycosides are particularly nephrotoxic when combined with other nephrotoxic drugs. 80% of amphotericin B-treated patients develop renal insufficiency, a percentage that increases as the cumulative dose exceeds 5g. It is because of its unique antifungal properties that there are still some indications for the use of this highly nephrotoxic drug; the high percentage of nephrotoxicity can probably be prevented in part by sodium loading. The nephrotoxicity of radiocontrast agents is largely dependent on renal function: from 0.6% in patients with normal renal function to 100% in patients with a serum creatinine above 400 mumol/L. Diabetes mellitus does not add greatly to the risk of radiocontrast nephrotoxicity. The nephrotoxicity of cyclosporin is dose-dependent and reversible, although there are some reports of irreversibility after long term use. Cyclosporin can also result in nephrotoxicity in combination therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Drug-induced nephrotoxicity. Aetiology, clinical features and management. 204 84

Thirty four patients with advanced renal insufficiency and after kidney transplantation have been prospectively studied using pulsed wave doppler. The doppler flows were evaluated using an index of resistance. The index of resistance varies proportionally with the peripheral resistances. This study showed in 14 patients without symptoms a mean index of resistance equal to 0.71 +/- 0.087. During acute rejection, the mean index of resistance increases to 0.91 +/- 0.12 (p less than 0.01). Seven patients with acute tubular necrosis and an index of resistance equal to 1 (p less than 0.01). There is no increase of the indices of resistance in patients with cytomegalovirus infection or with overdosed cyclosporin treatment. The pulsed wave doppler has a very good sensitivity to diagnose the acute rejection (90%) and acute tubular necrosis (100%) but cannot differentiate them. However, the repetition of systematic examinations allows the early diagnosis of acute rejection and the follow-up of the vascularization of anuric kidneys related to tubulopathy.
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PMID:[Diagnosis of early complications of the transplanted kidney by pulsed Doppler]. 206 79

Acute renal failure is a frequent and dramatic clinical syndrome, producing a wide variety of serious and potentially lethal disorders in infancy. Review of 30 cases of severe acute renal failure occurred from 1985 in our unit reveals that the major causes are: acute tubular necrosis (33%), hemolytic uremic syndrome (16%), post-streptococcal glomerulonephritis (16%). 16 patients aged from 7 days to 15 years weighing 2 to 59 kilos, underwent dialysis: 8 HD, 7 PD, 1 both. Functional recovery occurred in 13 patients (82%); 3 patients died for the condition that precipitated renal insufficiency.
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PMID:[Acute renal failure. 3 years' activity of a pediatric dialysis unit]. 238 22

The reversibility of the nematocide 1,2-dibromo-3-chloropropane (DBCP)-induced renal injury was studied in adult male F344 rats. After a single dose of 200 mg DBCP/kg body weight, rats were sacrificed at 1, 3, 6, 9, 14, 28, and 196 days. Twenty-four hours after DBCP treatment, the animals showed signs of acute renal insufficiency, which, based on serum chemistry and urinalysis results, was reversed by the 14th day. Morphologic findings consisted of severe acute tubular necrosis, which was localized to the juxtamedullary cortex. The lesion was recognizable at 24 hrs and fully developed at 3 days post-exposure. The proximal convoluted tubuli were primarily affected, but there were also spotty necroses in distal convoluted tubuli and loops of Henle. Beginning regeneration was evident at 3 days post-exposure. Multiple mitoses, some of them abnormal, were seen. Four weeks after treatment some mitotic activity was still present, but the regeneration of the tubular epithelium was largely completed. There were several dilated, distorted tubuli lined with abnormal epithelial cells with large, hyperchromatic nuclei. Interstitial fibrosis was mild and there was no interstitial inflammation. Twenty-eight weeks post-exposure the nuclear atypia persisted in the tubular epithelium. Glomerular findings were minimal and consisted of focal hyperplasia of the epithelial cells of the parietal layer of Bowman's capsule and shrinking of the glomerular tufts at 4 weeks post-exposure. At 28 weeks post exposure only rare foci of glomerulosclerosis were seen. Epithelial cells of the renal pelvis showed minimal nuclear and cytoplasmic swelling 24 hrs after DBCP exposure. Urothelial atypia was not present. The results indicate that a single dose of DBCP is capable of producing nuclear atypia that persists in the renal tubuli beyond the regenerative phase. Follow-up of patients that have been chronically exposed to DBCP with periodic examination of urinary cytology is suggested.
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PMID:1,2-Dibromo-3-chloropropane (DBCP)-induced nuclear atypia in rat kidney. 273 9


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