Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although unilateral clamping of the renal artery to induce chronic ischemia of the kidney tissue has been utilized in several animal species, the resultant morphologic, ultrastructural and immunologic changes have never been well characterized. Moreover, the pathogenesis of these changes, as well as their roles in causing or facilitating the development of chronic tubulointerstitial nephritis have not been known. To examine some of these issues, male Sprague-Dawley rats were subjected to unilateral stenosis of the left main renal artery for 28 days. Stenotic and contralateral kidneys of experimental animals and kidneys from sham-operated controls were subjected to: (1) light microscopic, electron microscopic and immunofluorescent studies; (2) morphometric quantitation of the structural changes; (3) staining for actin, epithelial membrane antigen, keratin, and vimentin by immunoperoxidase technique; (4) staining for complex glycoproteins by a panel of 13 lectins; and (5) phenotyping and quantitation of the interstitial inflammatory infiltrates by monoclonal antibodies, using immunoperoxidase technique. The results reveal that: (1) The ischemic kidney tissue displays marked tubulointerstitial damages including abundant interstitial chronic inflammatory infiltrates, with good preservation of glomerular structure, which is consistent with the standard criteria of chronic tubulointerstitial nephritis. (2) The antigenic profile of the ischemic tubular epithelium displayed marked alterations including a neo-expression of vimentin and keratin, as well as a loss of endogenous avidin binding activity, Ia antigen and several complex surface glycoproteins detectable by lectins. (3) Neither electron dense deposits nor immunoglobulins are detectable in the kidneys from experimental or control animals. (4) Tubulitis, defined as infiltration of tubular epithelium by inflammatory cells, was present in up to 42.2% of tubular cross sections of the ischemic kidneys. (5) The interstitial inflammatory infiltrates were composed of B lymphocytes, T helper lymphocytes, and macrophages whereas the T non-helper lymphocytes were scanty, a phenotypic pattern similar to that of several other experimental rat models of chronic tubulointerstitial nephritis. It is concluded that: (1) In the Sprague-Dawley rats, ischemia alone can cause a constellation of changes fulfilling the accepted features of chronic interstitial nephritis; (2) ischemia alters the antigenic profile of the tubular epithelium and thereby may initiate a cell mediated immune response, accounting for the observed tubulitis and interstitial inflammation; and (3) ischemia may well be the final common pathway for chronic tubulointerstitial nephritis of diverse etiologies.
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PMID:Experimental chronic renal ischemia: morphologic and immunologic studies. 138 Jan 4

Chronic pyelonephritis (c.p.) is by definition an infectious tubulo-interstitial nephritis. It has to be differentiated from other etiologic forms of tubulo-interstitial nephritis. Therefore strict morphological criteria are needed for diagnosis. The characteristic lesion is a large cortico-medullary scar overlying a dilated chronically inflammed calyx. The macroscopic aspect and the histologic survey picture are more important than histologic details. A diagnosis on renal biopsies is therefore not warranted. Vesico-renal reflux and papillary morphology play an important pathogenetic role. Beside the more common focal scar a diffuse form of scarring can be observed. A limited number of conditions only have to be considered in differential diagnosis. The Ask-Upmark kidney seems to be a special form of c.p. related to urinary tract infection and reflux in early infancy. Pelvi-calyceal lithiasis without superimposed infection causes a picture very similar to a pyelonephritic scar. A reliable differentiation between c.p. and analgesic nephropathy may cause problems in endstage kidneys with sloughed off papillae. Various mechanisms of renal damage such as bacterial infection, immunological mediated inflammation, leakage of urinary constituents into the interstitium especially Tamm-Horsfall-protein and ischemia have to be considered. Despite the frequency of urinary tract infections chronic progressive pyelonephritis is rare. Predisposing factors are needed for progression of the disease. These include congenital or acquired urinary tract obstruction, vesico-renal reflux and papillary damage with intrarenal obstruction to the urinary flow. Other important factors are focal and segmental glomerulosclerosis and hypertension.
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PMID:[Chronic pyelonephritis and its differential diagnosis. A disease changing with time]. 248 12

Fifty-five cases of primary (that is, without urinary tract abnormalities), acute pyelonephritis (PN) were studied by computed tomodensitometry (CT). There were 48 women and 7 men. All were febrile and 16 had positive blood cultures. In 7 cases, (4 diabetics and 3 malnourished alcoholics) PN was painless, diagnosis was delayed and lesions were severe. Two diabetics underwent emergency nephrectomy for sepsis. Conventional radiological techniques (IVP and ultrasonography) were poorly informative. In contrast, initial CT abnormalities were visible in 44 patients. They consisted of triangular or round hypodense images, diffuse hypodensity in a grossly swollen kidney, and/or abscesses. Hypodense images were presumably due to acute focal ischemia. Renal histology was available in five patients. It showed acute interstitial nephritis with leukocyte infiltrates, edema and hemorrhagic streaks. Pyelonephritis was due to E. coli in 48 cases (87.5%). In 27 cases E. coli isolates were studied by genotypic assays which detect the three most frequent (pap, afa and sfa) of the four operons known to encode adhesin. In all cases, at least one of these genotypic markers of uropathogenicity was found. In 27 cases, repeat CT was done shortly after treatment. It showed healing in only 12. Early cortical scar formation was visible in 2. Final evaluation in 27 cases with adequate follow-up showed that (in addition to the 2 patients who had been nephrectomized), in only 17 of 27 (63%) had the kidneys recovered a normal appearance. In two cases one kidney had undergone atrophy; renal biopsy showed subacute-chronic interstitial nephritis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Frequency of development of early cortical scarring in acute primary pyelonephritis. 265 59

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

Based on the clinico-laboratory and intravital morphological examination of 104 patients and the reported data the authors recognize 6 versions of chronic tubulo-interstitial nephritis (TIN): idiopathic, drug-induced, dysplastic, dysmetabolic, secondary TIN associated with primary glomerulopathies and vasorenal hypertension, secondary TIN in the presence of a long-term ischemia. Discuss the features of each form, diagnostic criteria, a possible importance of TIN for the development of arterial hypertension. Emphasize the importance of recognizing TIN in patients with primary glomerulopathies to early specify the causes of the deterioration of the disease course. Discuss the problems of therapy.
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PMID:[Chronic tubulointerstitial nephritis (structure, pathogenesis, clinical picture and morphology)]. 407 8

NSAIDs pose little threat of renal insult in normal, healthy persons at therapeutic dosages. However, NSAID administration to susceptible persons may cause decrements in renal plasma flow and glomerular filtration rate within hours. Such acute noxious renal effects are mediated by products of arachidonic acid metabolism. Precipitous decrements in glomerular filtration and renal ischemia, manifested by increased serum creatinine and urea nitrogen, are possible. However, these effects are usually fully reversible with prompt discontinuation of the offending NSAID. Risk factors for the development of these acute renal effects are known. Acute interstitial nephritis with or without nephrotic syndrome is a rare form of renal toxicity that typically occurs between 2-18 months of use. Renal impairment may be so severe as to require temporary hemodialysis; however, renal function usually returns to normal upon discontinuation of the NSAID. The mechanism of acute interstitial nephritis is presumed to be of allergic origin but could also be caused by a reactive metabolite. Fenoprofen use appears to be associated with a much higher risk for its development. In contrast to the acute effects of NSAIDs, irreversible, analgesic-associated nephropathy manifested by papillary necrosis and chronic interstitial nephritis may occur following months to years of high doses of analgesic mixtures. The mechanism by which combination analgesics produce this form of renal injury is unknown and could be either a result of medullary ischemia or a direct effect of a reactive metabolite. An important issue to be resolved is the relationship between the acute, reversible, prostaglandin-mediated renal effects of the NSAIDs and chronic, irreversible destruction, if such a relationship exists. Theoretically, continual or repeated decrements in renal function in patients with predisposing risk factors could cause or contribute to progressive deterioration in renal function. Elevations in blood pressure or interference with the effects of antihypertensive medications could theoretically also contribute to long-term renal deterioration. In addition to renal syndromes caused by NSAIDs that result in renal impairment, other transient effects on electrolyte and water metabolism may also occur. Reduced secretion of sodium may result in formation of edema, exacerbation of heart failure, or increased blood pressure. Hyporeninemic-hypoaldosteronism may produce hyperkalemia. Finally, reduced excretion of water has rarely caused hyponatremia. It has been suggested that NSAIDs may be renoprotective in patients with nephrotic syndrome. Others have suggested that sulindac is "renal-sparing" because of a unique metabolic pathway that supposedly limits the exposure of the kidney to the active sulfide metabolite.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal toxicity of the nonsteroidal anti-inflammatory drugs. 849 47

This investigation was carried out on 851 consecutive judicial autopsies of drug addicts who died mostly of heroin overdose from 1977 to 1996. Research of anti-HIV/HBV/HCV antibodies was performed, and histologic sections were retrospectively reviewed. More than 65% were HBV/HCV-positive and about 17% HIV-positive; females were HIV-positive more often than males. Intracranial microhemorrhages were frequently found; cerebral infectious diseases were rare. Inflammatory heart lesions, myocardial fibrosis, and acute ischemia were common. Interstitial nephritis (found in about 8%) was more frequent in females, in older patients, and in those carrying HIV infection; glomerular sclerosis was detected in about 12%. Acute bronchitis and/or pneumonia was demonstrated in 12%, without significant association with HIV infection; pulmonary hemorrhages, foreign body granulomas, and food aspiration were also commonly seen; hyperplasia of pulmonary perivascular lymphatic tissue was rather characteristic. Liver was carrying steatosis in 66.3% and/or hepatitis in 64.5%; acute hepatitis was more frequent in females, chronic hepatitis in older subjects and in those proven positive for hepatotropic viruses; cirrhosis occurred more often in older patients, in those carrying virus infection, and in consumers of nonnarcotics drugs such as ethanol. No pathologic finding was clearly related to drug abuse; therefore, during autopsy, drug addiction can be suspected, but anamnestic and circumstantial data are needed to lead pathologists to request toxicologic analysis to ascertain the cause of death. The present investigation emphasizes that, in addition to the risk of death by overdose, the high incidence of acute and chronic diseases could seriously undermine the health status of heroin and/or other drug consumers.
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PMID:Histopathological findings in 851 autopsies of drug addicts, with toxicologic and virologic correlations. 1589 41

The objective of this study is to design a fluorescent imaging agent with R-Gel, one of the recombinant polymers (RCP), for renal inflammation. The R-Gel based on human type I collagen has multiple Arg-Gly-Asp (RGD) motifs which are ligands for some types of integrin receptors on the cell surface. After intravenous administration of R-Gel labeled by Cy7 of a fluorescent dye to three animal models of nephritis mousse, interstitial nephritis (by using UUO model mice), glomerulonephritis (HIGA mice), and ischemia-reperfusion injured kidney (I/R mice), the extent of fluorescent imaging at the renal inflammation was assessed. The Cy7-labeled R-Gel was accumulated in the inflammation site to a significantly greater extent than in the normal one at 24h after administration. The renal pattern of fluorescent imaging was similar to that of administration anti-Mac1 antibody. Taken together, it is conceivable that the R-Gel was targeted to macrophages infiltrated into the inflammation site of kidney.
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PMID:A new fluorescent imaging of renal inflammation with RCP. 2084 94

Cocaine, a natural alkaloid derived from the coca plant, is one of the most commonly used illicit drugs. Cocaine abuse causes systemic adverse effects like stroke, myocardic infarction, arterial dissection, vascular thrombosis and rhabdomyolysis. Cocaine use is, also, associated with renal complications such as acute kidney injury, vasculitis, acute interstitial nephritis, chronic kidney disease, malignant hypertension with thrombotic microangiopathy. Acute kidney injury may or may be not associated to rhabdomyolysis. Rhabdomyolysis caused by cocaine abuse is multifactorial, involving tissue ischemia secondary to vasoconstriction and cellular damage caused by the drug. We report a 50-year-old man with history of chronic hepatitis C and substance abuse admitted to our unit with severe rhabdomyolysis and acute kidney failure after nasal insufflation of cocaine overdose. Renal function recovered after several treatments of dialysis. We conclude that cocaine adversely impacts kidney function ; in addition cocaine and rhabdomyolysis are the double danger for acute kidney injury. Medical management of cocaine toxicity requires a multisystem approach, with close monitoring cardiac, neurological and renal function.
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PMID:[Acute kidney injury and rhabdomyolysis after cocaine overdose: case report and literature review]. 2958 60

Severe eating disorders characterized by repetitive episodes of purging and vomiting can occasionally trigger acute kidney injury. However, interstitial nephritis induced by episodes of repeated vomiting has rarely been reported, and the pathophysiology of this entity remains unknown. A 26-year-old man was admitted to our hospital because of known hypokalemia. His serum electrolyte profile showed: sodium 133 mEq/L, potassium 2.6 mEq/L, chloride 72 mEq/L, total carbon dioxide 50 mEq/L, blood urea nitrogen/creatinine ratio (BUN/Cr) 21.9/1.98 mg/dL, and magnesium 2.0 mg/dL. Arterial blood gas analysis showed: pH 7.557, partial pressure of carbon dioxide 65.8 mmHg, and bicarbonate 58.5 mEq/L. His urinary potassium concentration was 73.2 mEq/L, and Cr was 111 mg/dL. Renal biopsy revealed acute tubular necrosis and tubulointerstitial nephritis with a few shrunken glomeruli. Repeated psychogenic vomiting may precipitate acute kidney injury and interstitial nephritis secondary to volume depletion and hypokalemia. Serum electrolyte levels and renal function should be carefully monitored in patients diagnosed with eating disorders to prevent tubular ischemia and interstitial nephritis.
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PMID:Interstitial Nephritis Caused by Anorexia Nervosa in Young Male; A Case Report and Literature Review. 3004 30


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