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

This review concerns the present state of accomplishments in the study of SEM of human and experimental renal disease. Critical techniques of specimen preparation reviewed include perfusion fixation, razor tissue sectioning, alcohol cryofracture, microtome sectioning of paraffin or styrene embedded tissue, ultraplaning with glass knives of hard carbowax embedded tissues and glomerular isolation. Gold-palladium coating and heavy metal impregnation with osmium, uranium, and silver are discussed. A compendium of SEM observations of human glomerular, vascular and tubular disease is presented. Techniques for SEM of experimental renal disease are reviewed. These include latex vascular injection, freeze drying, x-ray microanalysis and use of backscattered electron imaging. Experimental models previously investigated by SEM are puromycin aminonucleoside nephrosis, daunomycin nephrosis, and N,N1-Diacetylbenzedine glomerulopathy, nephrotoxic serum nephritis, and protamine perfusion glomerulopathy. Reviewed are acute tubular necrosis caused either by angiotensin, hypotension, norepinephrine, glycerol, mercury, and unilateral renal artery occlusion, also potassium depletion nephropathy, alloxan diabetes and diphenylamine-induced polycystic disease.
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PMID:SEM of human and experimental renal disease. 52 33

Thirty-four renal transplant recipients received drip infusion urograms from 2-24 days post-transplantation. Twenty-two patients exhibited changes in renal function within 1-4 days of the urogram that were indistinguishable from allograft rejection: a tender, swollen kidney, elevation of serum creatinine, oliguria, decreased urine sodium concentration, weight gain, and hypertension. Two patients developed acute tubular necrosis and required hemodialysis, but renal function in the remaining 20 patients improved after therapy for "graft rejection" with i.v. methyprednisolone sodium succinnate. Kidneys from older-age donors that were functioning suboptimally and kidneys which exhibited subsequent clinical allograft rejection were more at risk for contrast media toxicity. This suggests that occult vascular lesions may have been present in the allograft which were exacerbated when exposed to the irritant vascular effects of contrast media, producing a mild, reversible toxic nephritis. However, several kidneys with normal function and several kidneys which never exhibited rejection activity were also adversely affected by exposure to contrast media. It appears these agents should be used cautiously, if at all, in the early post-transplant period.
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PMID:Adverse effects of meglumine diatrizoate on renal function in the early post-transplant period. 110 14

Between 1980 and 1988, 12 patients at the Cleveland Clinic had biopsy-proven acute tubulointerstitial nephritis. Etiologies of the disease included drugs, systemic illness, and idiopathic causes. Clinical features were nonspecific, and the diagnosis of acute tubulointerstitial nephritis was seldom entertained in these patients prior to biopsy. Seven patients had unrelated underlying renal disease. Treatment included discontinuation of the offending agent and/or a trial of steroids. All patients had final creatinine levels lower than at diagnosis. Because the condition is potentially reversible, this disease should be considered in all patients with new azotemia who do not exhibit prerenal factors, features typical of acute tubular necrosis, red blood cell casts heralding a glomerular process, or evidence of obstructive uropathy.
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PMID:Acute tubulointerstitial nephritis. 155 Dec 11

The purpose of this study was to characterize the spectrum of renal lesions associated with plasma cell dyscrasias from a population of patients who had renal disease identified by kidney biopsy. Thirty-six patients (2.6% of 1361 kidney specimens examined over 6 years) had evidence of monotypical light chain with or without concomitant heavy chain deposition. A variety of lesions was found, including (a) AL-amyloid and glomerular nonamyloid light chain deposition manifesting as nodular, membranoproliferative, mesangioproliferative, and "minimal-change" glomerulopathies; (b) fibrillary glomerulopathy; (c) tubulointerstitial lesions (cast nephropathy, acute tubular necrosis, and tubulointerstitial nephritis); and (d) vascular (arterioles and small and medium-sized arteries) lesions. AL-amyloid was the most common renal lesion (39%), nonamyloid deposition occurred second most commonly (33%), and cast nephropathy ("myeloma kidney") was third most frequent (14%). Clinical and laboratory manifestations of a plasma cell dyscrasia were frequently subtle. Immunoelectrophoresis of both serum and urine did not demonstrate a monotypical light chain or immunoglobulin in almost 35% of this population. Thus, the correct diagnosis was not considered in the majority of these patients before biopsy. Progressive deterioration of renal function was common with all of the lesions, except for proximal tubule injury, which tended to improve over the period of study. Renal biopsy with careful examination for monotypical light chain with or without associated heavy chain deposition using immunofluorescence or immunoelectron microscopy was crucial in identifying and characterizing the varied lesions associated with lymphoplasmacytic disorders.
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PMID:Spectrum of glomerular and tubulointerstitial renal lesions associated with monotypical immunoglobulin light chain deposition. 190 26

A woman with a history of drug allergy, renal impairment and carcinoma of the breast with pulmonary micrometastases developed haemolytic anaemia and Stevens-Johnson syndrome following the use of mefenamic acid, paracetamol (acetaminophen) and furosemide (frusemide). In addition there was severe cholestatic hepatitis in the absence of clinical evidence of sepsis, biliary obstruction or recurrent metastases. The rash resolved on steroid therapy but the patient eventually died from both renal and liver failure. Acute tubular necrosis with a background of chronic tubulointerstitial nephritis was also found at autopsy. Although in the presence of multiple drug therapy the causative agent cannot be identified with absolute certainty, the association of these severe idiosyncratic hepatic and dermatological reactions with haemolytic anaemia strongly suggests mefenamic acid as the most likely culprit.
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PMID:A case of Stevens-Johnson syndrome, cholestatic hepatitis and haemolytic anaemia associated with use of mefenamic acid. 206 63

To evaluate possible causes of the diminished prostaglandin production in advanced hepatorenal syndrome, prostaglandin endoperoxide synthase and prostacyclin synthase were localized and semiquantitated by immunofluorescence in postmortem, biopsy and nephrectomy renal tissues. In normal kidneys, antiprostacyclin synthase serum caused intense staining in peritubular capillaries, in the adjacent renal interstitial cells and in glomerular mesangial regions. Antiprostaglandin endoperoxide synthase serum caused staining of collecting duct epithelial cells, cells of the thin ascending limb and possibly glomerular mesangial cells. Prostacyclin synthase-positive staining was graded 5+ (scale of 0+ to 5+) in all kidney samples. Medullary collecting tubule prostaglandin endoperoxide synthase-positive staining was graded 4+ or 5+ in kidney samples from patients with acute tubular necrosis or acute tubulointerstitial nephritis and from patients with liver failure without the hepatorenal syndrome. However, prostaglandin endoperoxide synthase-positive staining was markedly diminished or absent (average 1+) in patients with the hepatorenal syndrome. These data suggest that loss of the medullary prostaglandin endoperoxide synthase is the cause of diminished urinary prostaglandin E2 excretion in the hepatorenal syndrome.
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PMID:Immunohistochemical distribution of renal prostaglandin endoperoxide synthase and prostacyclin synthase: diminished endoperoxide synthase in the hepatorenal syndrome. 311 64

Renal involvement in legionnaires' disease is a well-known, yet incompletely understood, complication. Manifestations of renal involvement include proteinuria, hematuria, pyuria, cylindruria, and azotemia. Previous cases of legionnaires' disease with renal involvement have shown pathophysiologic changes consistent with acute tubulointerstitial nephritis or acute tubular necrosis. A toxic metabolite produced by Legionella pneumophila has been theorized to produce a vasoconstrictive effect on the renal microvasculature, leading to ischemia and renal dysfunction. The case reported here is unique in that the patient presented with interstitial nephritis in the absence of pulmonary signs or symptoms.
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PMID:Interstitial nephritis in a patient with Legionnaires' disease. 380 71

Renal involvement is a well described complication of Legionnaires' disease and is often manifested as mild, transient azotemia, hematuria, proteinuria, pyuria or cylinduria. Acute renal failure complicating Legionnaires' disease has also been described, and some patients have required hemodialysis. Renal morphology has only been described in a few cases. We report two cases of Legionnaires' disease who developed acute renal failure. The serotype of the Legionella pneumophilia isolated from one of the patients had never been isolated from humans before. This patient expired and at autopsy the kidney revealed acute tubular necrosis, but there was no evidence for interstitial or glomerular disease. Renal morphology in six previously reported cases revealed acute tubulointerstitial nephritis in three cases and acute tubular necrosis in the other three. We conclude that acute renal failure may accompany severe Legionnaires' disease, and the development of the renal failure is not related to hemodynamic factors, while nephrotoxic antibiotics may be a contributing factor.
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PMID:Legionnaires' disease associated with acute renal failure: a report of two cases and review of the literature. 388 29

Eight hypertensive children with acute post-streptococcal glomerulonephritis were given intravenous frusemide, 2 mg/kg, and the results compared with 8 similar cases not given the diuretic. Mean urine flow increased from 0.24 ml/min/m2 before frusemide to 3.63 ml/min/m2 in the 6 hours afterwards and was still 0.72 ml/min/m2 48 hours later. In contrast mean urine flow remained unchanged over 48 hours in those not given frusemide. Despite similar initial blood pressures the duration of hypertension was much shorter (mean 4.7 days) after frusemide than in the controls (mean 11.0 days) and the edema-free weight was achieved more rapidly (6.8 days compared with 13.9 days). Plasma renin activity (PRA) did not rise after frusemide in the children with acute nephritis. This was in contrast to the rapid rise seen in normal humans thus indicating a dissociation between the diuretic and renin-releasing activities of frusemide in acute nephritis. Seven children with the hemolytic-uremic syndrome or acute tubular necrosis showed no significant change in either urine flow or PRA after frusemide. Frusemide is therefore effective treatment for both hypertension and oliguria in acute nephritis. Failure of PRA to rise indicates that renin release mechanisms are abnormal in renal failure and that PRA levels need to be interpreted with caution in this condition.
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PMID:Response to frusemide in acute renal failure: dissociation of renin and diuretic responses. 699 79

Tubulo-interstitial nephropathy or nephritis is suggested if renal function is deteriorated and urinary findings are slight. In most cases, the daily urinary protein excretion is less than 1 g and macrohematuria is not present. Urinary excretion of N- acetyl-beta-glucosaminidase and beta 2-microglobulin is a good indicator for tubulo-interstitial damage. Acute renal failure is caused either by acute tubulo-interstitial nephritis or acute tubular necrosis. In either case, renal biopsy is essential for diagnosis and to characterize the renal damage. In the interstitium, edema and fibrosis are seen and lymphocytes, plasma cells, polymorpholeukocytes, and/or eosinophils infiltrate. Tubular basement membrane is sometimes disrupted and lymphocytes have infiltrated inside (tubulitis).
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PMID:[Renal biopsy for diagnosis of interstitial nephritis]. 756 31


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