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)

Review of clinical and pathologic data from ten fatal cases of Rocky Mountain spotted fever (RMSF) revealed the importance of acute renal failure in the clinical course and of multifocal perivascular interstitial nephritis as the principal pathologic lesion. In nine cases, Rickettsia rickettsii were demonstrated by immunofluorescence in the areas of vasculitis. Evidence was lacking for the role of disseminated intravascular coagulation, glomerulonephritis, or myoglobinuria in the pathogenesis of acute renal failure in these cases. Rickettsia-induced vascular injury led to acute renal failure by several mechanisms. Hypovolemia early in the course resulted in reversible, prerenal azotemia. Transient hypotension in midcourse produced acute tubular necrosis. In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria. The interstitial nephritis could not be demonstrated conclusively to contribute to the acute renal failure.
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PMID:Acute renal failure in Rocky Mountain spotted fever. 43 98

The essential pathologic lesion in Rocky Mountain spotted fever (RMSF) is a vasculitis that may involve the kidneys as well as the heart, brain, skin, and subcutaneous tissues. Histopathologic information concerning the response of the kidneys in RMSF is rather limited, however. In this study renal tissue from 17 children who died of RMSF was examined by light, electron, and immunofluorescence microscopy. A lymphocytic or mixed inflammation, or both, involving vessels and interstitium of the kidney was found in all patients. In addition, 10 patients had histologic evidence of acute tubular necrosis, and another 3 had glomerular lesions consisting of focal segmental tuft necrosis or increased cellularity secondary to neutophilic infiltration, or both. Immunofluorescence- and electron-microscopic studies failed to demonstrate immune-complex deposition within glomeruli, a finding that suggests that immunoglobulin and classic immune complexes were not involved in the pathogenesis of the renal lesions at the time of death. These findings suggest the possibility that the pathogenesis of the renal lesion in RMSF may be due to a direct action of the organism (Rickettsia rickettsii) on the vessel wall.
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PMID:Kidney lesions in Rocky Mountain spotted fever: a light-, immunofluorescence-, and electron-microscopic study. 52 76

One hundred and seventy-five 67Ga-citrate scans were performed to detect suspected occult inflammatory processes. None of the patients had a known malignancy. Renal activity was noted in 12 patients (6.8%) on the 48-hr image. These patients had either pyelonephritis, acute tubular necrosis, vasculitis, or a renal abscess. Since delayed 67Ga uptake in the kidneys may be the first evidence of renal disease, further investigation, including either arteriography or biopsy, is necessary. In patients with a known malignancy, tumor involvement must be considered.
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PMID:Significance of delayed 67Ga localization in the kidneys. 96 53

Reports of acute tubular necrosis following envenomation by hornets are rare. A 38-year-old farmer presented with evidence of haemolysis and acute renal failure following multiple hornet stings (Vespa orientalis). Biopsy of skin from the site of the stings showed evidence of vasculitis. Renal biopsy showed characteristic changes of acute tubular necrosis. Intravascular haemolysis due to haemolytic properties of the hornet venom was considered to be chiefly responsible for the renal lesions in this patient.
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PMID:Acute renal failure following hornet stings. 127 11

Out of 152 cases of Acute renal failure (ARF) 32 patients (21%) were subjected to kidney biopsy. All patients had intrinsic ARF. Prerenal azotemia and obstructive uropathy were excluded. Histologic observations were: Crescentric glomerulonephritis in 7 (21.9%), acute endocapillary proliferative glomerulonephritis 5 (15.6%), acute interstitial nephritis 7 (21.9%), necrotizing vasculitis 4 (12.5%), acute tubular necrosis in 5 (15.6%) and membrano-proliferative GN with superimposed crescent in 2 (6.2%) while renal cortical necrosis was seen in 6.2% of cases. Prebiopsy diagnosis was correct in only 10 (31.25%) cases. The result of biopsy had altered clinical diagnosis in 22 (68.75%) patients and precise renal biopsy diagnosis resulted in therapeutic changes in 54.8% of patients with ARF.
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PMID:Clinical significance of kidney biopsy in acute renal failure (ARF). 129 67

There have been recent reports of rhabdomyolysis associated with cocaine abuse. The pathologic findings from these cases have not been described. Pathologic abnormalities in two fatalities with cocaine-associated rhabdomyolysis, including one with hyperpyrexia, acute renal failure, and disseminated intravascular coagulation, are discussed in detail. Skeletal muscle in both cases showed necrosis without evidence of vasculitis, polarizable foreign crystals, or other specific lesions. The individual with renal failure showed acute tubular necrosis with granular myoglobin casts in tubules. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Adulterants may also play a role. In unexplained cases of rhabdomyolysis, toxicologic evidence of cocaine should be sought. In those cases of rhabdomyolysis associated with acute renal failure, the presence of cocaine in blood may be prolonged because of impaired renal clearance.
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PMID:Rhabdomyolysis associated with cocaine abuse. 174 98

The resistive index (RI), calculated from the duplex Doppler waveform, was compared with clinical and laboratory findings and the results of renal biopsy in 41 patients with nonobstructive (medical) renal disease. Kidneys with active disease in the tubulointerstitial compartment had a mean RI of 0.75 +/- 0.07. This was statistically significantly different (p less than .01) from the RI in kidneys with disease limited to the glomeruli (mean RI of 0.58 +/- 0.05). Acute tubular necrosis resulted in an elevated RI (mean RI = 0.78 +/- 0.03) as did vasculitis/vasculopathy (mean RI = 0.82 +/- 0.05). Patients with hypertension, proteinuria, or hematuria did not have kidneys with a significantly higher RI than did patients without these clinical factors. Kidneys found to be abnormally echogenic did not have an RI significantly different from kidneys of normal echogenicity. There was a weak correlation between creatinine level and RI value, reflected by a linear correlation coefficient of 0.34. In patients with normal renal RIs, the mean creatinine level was 1.7 +/- 1.7, whereas in those with abnormal RI values (greater than or equal to 0.70), the mean creatinine level was 3.7 +/- 3.6. We conclude that some forms of nonobstructive renal disease can produce changes in the Doppler waveform detectable by RI measurement. The production of Doppler waveform changes is strongly influenced by the site of the main disease within the kidneys. Active disease within the tubulointerstitial compartment (acute tubular necrosis, interstitial nephritis) or vasculitis/vasculopathy generally resulted in an elevated RI, whereas disease limited to the glomeruli, no matter how severe, did not significantly elevate the RI. Degree of renal dysfunction as indicated by serum creatinine level probably affects the Doppler waveform to some degree, but the relationship is weak.
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PMID:Intrarenal arterial Doppler sonography in patients with nonobstructive renal disease: correlation of resistive index with biopsy findings. 211 Jul 32

A patient developed serum sickness and acute renal failure following therapy with streptokinase for myocardial ischaemia. There was a previous history of a cellulitic infection of the leg, and antibodies to streptokinase were measurable in a serum sample taken from the patient before therapy. A cryoglobulin was detected at the time of presentation with serum sickness. This contained polyclonal IgG (with anti-streptokinase activity), streptokinase, and C3. Circulating immune complexes were demonstrated by C1q-binding assay. Deposition of C3 was observed in skin and renal biopsies, and bound to erythrocytes. Renal histology, however, showed acute tubular necrosis, with no vasculitis or inflammatory cell infiltrate. This case provides an unusual example of the characterization of an immune complex comprising a specific antibody and an exogenous antigen, and has clinical implications for the use of streptokinase.
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PMID:Serum sickness and acute renal failure after streptokinase therapy for myocardial infarction. 232 3

In the past 15 years, there has been an explosion in the number of nonsteroidal anti-inflammatory drugs on the market. Along with this explosion have come increasing reports of the physiologic and pathologic changes seen in the kidneys. This report reviews the effects of prostaglandins on the kidney and the physiologic changes that result when prostaglandin synthesis is blocked. The world literature on renal complications of nonsteroidal anti-inflammatory drugs is reviewed and 274 cases of acute renal disease associated with their use are reported. The following cases are described: nephrotic syndrome (34); acute interstitial nephritis (51); acute tubular necrosis (29); papillary necrosis (53); poor perfusion with renal failure (40); acute glomerulitis or vasculitis (13); and unspecified renal failure (102). Fenoprofen appeared to be more nephrotoxic than other nonsteroidal anti-inflammatory drugs and resulted in multiple renal lesions in the same patient.
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PMID:Effects of nonsteroidal anti-inflammatory drugs on prostaglandins and renal function. 286 41

Indirect immunoperoxidase analysis using monoclonal antibodies (Mo Ab) was performed in 33 renal biopsies with interstitial cellular infiltration obtained from non-transplanted patients. We reviewed four acute interstitial nephritis (IN), three chronic IN, four granulomatous IN, four acute tubular necrosis, four vasculitis, seven primary glomerulonephritis and seven active lupus nephritis (LN). We used Mo Ab recognizing T and B cell markers [OKT3, OKT8, T4, B1, IOT14 (IL2 receptor)], HLA-DR related antigen (I2) and monocytes/macrophages (LeuM3). In all cases the interstitial cellular infiltrates were predominantly T cells, whereas the B cell population accounted for less than 20% of the infiltrate. LeuM3+ cells were present in 28 of 32 cases, usually in a lesser proportion than T cells. IOT14+ cells were exceptional. T4+/T8+ cells were clearly greater than one in three acute IN, three granulomatous IN, two LN and two vasculitis. The T8+ cell population predominated in one case of chronic IN related to a non-steroidal anti-inflammatory drug. In all the remaining cases T4+ and T8+ cells were equally present. Aberrant strong HLA-DR expression within tubular cells was noted in nine cases (4 LN) irrespective of the presence of tubular lesions. On the basis of the phenotypic analysis, our data do not support a specific pattern of the infiltrate in regard to a given etiology and thus cannot be used as a diagnostic tool. However, such analysis may aid in understanding the mechanisms of tissue injury.
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PMID:Characterization of mononuclear cell subsets in renal cellular interstitial infiltrates. 352 2


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