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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

Groups of ten male rats were treated with a high challenge dose of cephaloridine (CPH, 3750 mg kg-1), with methylprednisolone (MP, 100 mg kg-1) or with cephaloridine and methylprednisolone (CPH + MP) by single subcutaneous injection. A control group received the injection vehicles only. Urine was collected from all animals daily over 18-h collection periods, up to 96 h after treatment. Blood was collected at 24, 48, 72 and 96 h after treatment. At necropsy, kidneys were weighed, processed and examined histopathologically. Results show that methylprednisolone significantly ameliorated the nephrotoxicity of the challenge dose of cephaloridine. CPH-only treated rats had severe toxic nephrosis characterised by acute tubular necrosis, and elevated blood urea and creatinine. By contrast, the majority of CPH + MP treated rats had only a slight or moderate toxic nephrosis, and had lower blood urea and creatinine levels compared with rats treated with CPH only, indicating preservation of kidney function. Interestingly, rats treated with CPH + MP had higher urinary enzymes (alkaline phosphatase, lactate dehydrogenase, gamma glutamyltransferase and N-acetyl-beta-glucosaminidase) as well as protein and glucose, compared with rats treated with CPH only. This is taken to indicate that rats treated with CPH only had such marked kidney damage and necrosis that the population of cells able to produce these marker enzymes was significantly and rapidly depleted, but the protection afforded by methylprednisolone allowed CPH + MP treated rats to sustain urinary enzyme output. Effects on urinary glucose and other parameters such as body weight and kidney weight demonstrate interactions between glucocorticoid pharmacology and cephaloridine nephrotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucocorticoid amelioration of nephrotoxicity: a study of cephaloridine-methylprednisolone interaction in the rat. 757 15

Renal involvement in parasitic infections are polymorphic. Plasmodium malariae often leads to membranoproliferative glomerulonephritis whereas acute tubular necrosis or post-infectious acute glomerulonephritis are observed with Plasmodium falciparum. Urogenital taxis of Schistosoma haematobium is responsible for frequency of chronic tubular and interstitial nephritis. Without specific treatment, the renal function progressively deteriorates and urological complications appear. Schistosoma mansoni mainly leads to mesangial and membranoproliferative glomerulonephritis. Membranoproliferative and membranous glomerulonephritis are reported with loasis. Onchocerca volvulus also leads to membranoproliferative glomerulonephritis and lipoid nephrosis. Renal involvement with Wuchereria bancrofti is rare. With leishmaniosis, it is often mild but more serious observations are described: acute glomerulonephritis, nephrotic syndrome or acute interstitial nephritis. Renal hydatic cysts are diagnosed in two or three per cent of cases. Surgery is the only treatment. Immunosuppressive or antimalarial treatments seem to be ineffective in the outcome of chronic glomerulonephritis.
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PMID:[Important parasitic nephropathies: update from the recent literature]. 1022 26

Acute renal insufficiency is often called "lower nephron nephrosis." Its recognition, its prognostic significance, and its therapy by conservative measures are receiving increasing clinical emphasis. The mortality rate in this complicated syndrome still remains unduly high. One method of therapy of anuric patients whose lives are in jeopardy because of fulminating uremia or critical potassium intoxication is use of an artificial kidney to "purify" the blood stream by means of extracorporeal dialysis.The author describes clinical (and laboratory) experience with ten such dialyzed patients, eight of whom presented the classical picture of acute renal insufficiency. Four died, one from unrecognized coronary occlusion, another from antecedent, overwhelming peritonitis. Two other patients with chronic kidney disorders received no benefit from dialysis and died of renal disease. Good biochemical and clinical response was brought about in six cases of lower nephron nephrosis. Presumably, these six patients would have died had they not been subjected to artificial dialysis.
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PMID:The Kolff-Merrill artificial kidney; clinical application in acute renal insufficiency. 1436 83

Toxic nephropathy is an important cause of reversible renal injury. This article focuses on the nephrotoxicity of several new therapeutic compounds. Selective cyclooxygenase-2 inhibitor is associated with sodium retention, hypertension, ankle edema, and acute renal failure. The incidence of renal complication is similar to conventional nonsteroidal anti-inflammatory drugs. Bisphosphonates, especially when used in high dose for prolonged duration, can cause toxic acute tubular necrosis and renal failure. Pamidronate is also associated with a specific form of collapsing focal segmental glomerulosclerosis similar to one found in patients with human immunodeficiency virus (HIV) infection. Acyclic nucleoside phosphonate, a new group of antiviral agents, can cause Fanconi-like syndrome and progressive renal impairment. On the other hand, indinavir, a potent protease inhibitor for the treatment of HIV infection, can cause crystalluria, renal stone, acute tubular obstruction and chronic interstitial nephritis. Intravenous immune globulin and hydroxyethyl starch, a new plasma expander, are associated with acute renal failure with characteristic renal histology known as osmotic nephrosis. In short, physicians should be cautious about possible renal toxicity during the use of any new therapeutic agents.
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PMID:Nephrotoxicity related to new therapeutic compounds. 1595 51

A 59-year-old diabetic man was admitted for severe acute renal failure. Clinical signs were compatible with an acute tubular necrosis but no etiology was found. Kidney biopsy showed an osmotic nephrosis. Resumption of interrogatoire reveals consumption of Artemisia herba-alba accused in very few experimental studies to cause a lesion indicative of osmotic nephrosis.
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PMID:An exceptional case of acute renal failure: is there a renal toxicity of Artemisia herba-alba? 2072 71

A 38-year-old male was admitted with fever, progressive jaundice, cervical lymphadenopathy, hepatomegaly and acute oliguric renal failure. Epstein-Barr virus (EBV) infection was diagnosed by detection of EBV-DNA in plasma and confirmed by EBV seroconversion. Kidney biopsy revealed acute tubular necrosis and abundant casts, consisting of bilirubin pigment. With conservative treatment, the patient fully recovered from cholemic nephrosis, an uncommon condition, not described after EBV infection before.
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PMID:A case of mononucleosis infectiosa presenting with cholemic nephrosis. 2598 48

Hepatitis A is usually a benign self-limiting disease with few or no extrahepatic manifestations. Acute hepatitis A causing severe renal dysfunction is not very common, although described. Patients developing renal dysfunction post hepatitis A infection usually have prerenal acute kidney injury (AKI) or acute tubular necrosis due to vomiting, diarrhea, and poor fluid replacement. However, if renal dysfunction persists, other causes need to be evaluated. The term cholemic nephrosis or more specifically bile cast nephropathy has been described in the setting of cholestatic jaundice and decompensated liver failure where bilirubin levels reach above 20 mg/dL. Herein, we describe the clinical course of a patient who developed acute hepatitis A with severe liver dysfunction and subsequently AKI which persisted for six weeks. Renal biopsy showed the evidence of bile cast nephropathy. After six weeks of hemodialysis, urine output improved. He slowly recovered both hepatic and renal functions.
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PMID:Bile cast nephropathy causing acute kidney injury in a patient with nonfulminant acute hepatitis A. 3058 86

Cisplatin and ifosfamide are well-known nephrotoxic agents that can cause acute and chronic glomerular and/or tubular toxicity. We examined 2 adolescent patients who were receiving cisplatin and ifosfamide treatments. Pathological findings of patient 1 showed acute tubular necrosis-like patchy injury. Tubulointerstitial nephrosis and glomerular sclerosing were revealed in patient 2. These findings were consistent with the known damages induced by cisplatin and ifosfamide. Proteinuria and mild decline of eGFR were noticed after more than 10 months after the completion of the treatment. It is important to monitor such consequences in long-term follow up. Adult based medical services are required for childhood and adolescent cancer survivors.
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PMID:[Pathological Findings of Chronic Effects Observed in the Kidneys Exposed to Antineoplastic Agents in Two Adolescent Patients]. 3266 68