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)

Cefoxitin was administered by the intramuscular route to 102 patients who had infections of mild or moderate severity. The assessment of clinical and bacteriologic outcome was derived from data for 79 patients. Assessments of tolerance and safety were made for all patients who received 1 g of cefoxitin diluted in 1 ml of 0.5% or 1.0% lidocaine four times daily. Cure or improvement occurred in 45 of 47 patients with skin or soft tissue infections, in all of 16 patients with lower respiratory tract infections, and in 10 of 12 patients with urinary tract infections. One patient developed acute tubular necrosis. Eosinophilia was seen in 7% of patients treated with cefoxitin. The intramuscular preparation was not painful to 96% of the patients. Cefoxitin given by the intramuscular route can be used as an alternative to intravenous cefoxitin for treatment of mild or moderate infections, for continuation of treatment when the intravenous route is not appropriate, and for treatment of ulcers of polymicrobial etiology on ischemic extremities or on extremities of diabetic patients.
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PMID:Intramuscular cefoxitin. 40 Sep 34

The cephalosporin antibiotics cephaloridine and cephalothin are known to cause renal damage. Experience with newer congeners is not yet sufficient to predict their potential nephrotoxocity. The renal lesion produced by cephaloridine is primarily due to the intrinsic toxicity of this drug for the cells of the proximal renal tubule and depends upon its peculiar transport characteristics. In contrast, renal injury due to cephalothin resembles that seen with the penicillins. Thus, some instances of cephalothin nephropathy appear to be toxic in nature with a histologic picture of acute tubular necrosis, whereas others exhibit signs of hypersensitivity including rash, eosinophilia, and interstitial nephritis. Among the factors alleged to contribute to the nephrotoxicity of cephalosporins is their administration with aminoglycosides. Although the physician should be aware of the possibility of a potential adverse interaction between these groups of antibiotics, the evidence is not sufficiently conclusive to warrant avoidance of the combination when it appears to be therapeutically useful.
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PMID:The nephrotoxicity of cephalosporins: an overview. 65 5

Nephrotic syndrome was the commonest clinical presentation among 2827 consecutive adult Indian patients from whom adequate kidney biopsies were obtained for suspected renal disease. In 83 per cent of cases the nephrotic syndrome was due to minimal change disease, focal segmental glomerulosclerosis, mesangiocapillary glomerulonephritis, membranous usually secondary to tuberculosis or leprosy, was present in only 34 patients. Acute nephritis, the next most frequent clinical presentation, was due to diffuse endocapillary proliferative, crescentic or mesangial proliferative glomerulonephritis in 88 per cent of cases, almost half of whom had elevated serum streptococcal antibody titres. Eosinophilia showed a highly significant association with diffuse endocapillary proliferative and mesangiocapillary glomerulonephritis. Idiopathic IgA nephropathy was present in only 10, and antiglomerular basement membrane antibody disease in only one, of the 238 patients whose biopsies were studied by immunofluorescence. Complications of pregnancy accounted for 70 per cent of cases of cortical necrosis. Acute gastroenteritis, septicaemia, abortions, snake bite and allopathic and indigenous medicines were important causes of acute tubular necrosis.
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PMID:Renal disease in adult Indians: a clinicopathological study of 2,827 patients. 344 84

The relevance of eosinophilia in the physiopathology of transplant rejection has yet to be established. The appearance of eosinophilia has been occasionally associated with an adverse prognosis on graft rejection episodes. The aim of the present study was to evaluate the role and prognostic implications of blood and graft eosinophilia in kidney transplant rejection. We have examined the intrarenal infiltrate in 173 fine-needle aspiration biopsies from 36 consecutively transplant patients, and blood samples obtained simultaneously with fine-needle aspirations. Two different immunosuppressive regimens were administered: triple therapy (azathioprine + prednisone + antilymphocytic globulin) in patients with posttransplant acute tubular necrosis and cyclosporine A monotherapy in the rest of the patients. Comparing the two immunosuppressive groups, more elevated eosinophil values were observed in the monotherapy group during stable graft and also at the rejection episode. In the monotherapy group, a significant increase in the eosinophil values, in peripheral blood samples and in the intragraft infiltrates were noted at the rejection episode with respect to the stable situation. Following pulsed-steroid treatment an immediate disappearance of the eosinophils was evident. In contrast, no differences could be demonstrated between these two clinical situations in the TT group. Higher rates of eosinophils in the intrarenal infiltrate with respect to peripheral blood samples were observed during rejection episodes, suggesting some role of the eosinophils in the physiopathology of graft rejection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood and graft eosinophilia as a rejection index in kidney transplant. 824 97

Renal changes that occur with aging mainly consist of impairment in the ability to concentrate urine and to conserve sodium and water. These physiological changes increase the risk of volume depletion and the prerenal type of acute renal failure (ARF) in elderly people. Bladder outlet obstruction caused by benign prostatic hypertrophy is a common cause of ARF in elderly men. Another frequent cause of ARF in the elderly is drug-induced nephropathy. Nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics are most often implicated in the development of ARF in the elderly. However, considering the high usage of these drugs, the incidence of drug-induced nephropathy is relatively small. NSAIDs are more likely to cause ARF in patients with congestive heart failure, chronic renal disease (including diabetic nephropathy) or chronic liver disease than in otherwise healthy individuals. NSAID-induced ARF is often of the prerenal type, but may be caused by acute interstitial nephritis (AIN). The presence of heavy proteinuria or nephrotic syndrome differentiates NSAID-induced AIN from AIN caused by other drugs. Antibiotics, especially semisynthetic penicillins, more commonly give rise to AIN associated with peripheral blood eosinophilia and eosinophiluria than NSAIDs. Ciprofloxacin is increasingly reported to cause AIN. Fever commonly accompanies AIN, especially when induced by antibiotics. Aminoglycosides produce ARF by inducing acute tubular necrosis (ATN), which results from the excessive accumulation of myeloid bodies in the tubules. In all cases of ARF it is essential to obtain a good history, to perform a through physical examination, with particular attention to skin turgor, and to measure blood pressure, pulse rate (supine and upright), urinary electrolyte and creatinine levels. Fractional excretion of sodium and the urine:plasma creatinine ratio are reliable indices that distinguish prerenal ARF from ATN. A prompt response to fluid challenge, with an increase in urine output and urinary sodium excretion, and a rapid decrease in blood urea nitrogen, constitutes strong evidence for prerenal ARF. However, these indices are unreliable when prerenal ARF has progressed to ATN or when ARF has an obstructive pattern to begin with. In all cases of ARF, especially in elderly men, urinary tract obstruction should be suspected unless the history is otherwise clear cut. Ultrasound of the kidneys and bladder is a simple, non-invasive and meaningful test that can be used to rule out obstructive causes of ARF. If obstruction is the cause of ARF, ultrasound will be positive; in contrast, urinary obstruction is very unlikely if ultrasound findings are normal in a patient who has been oliguric or anuric for 48 hours or more. Similarly, acute glomerulonephritis, including rapidly progressive glomerulonephritis, should be suspected when ARF is associated with heavy proteinuria. In such instances, percutaneous renal biopsy is essential to document the diagnosis. It is of utmost importance to establish whether ARF is of prerenal or postrenal type, both of which are potentially fully reversible. In contrast, patients with ATN or rapidly progressive glomerulonephritis may not recover, or may only partially recover, their renal function. Haemodialysis and nutritional support are common measures for patients with severe ATN and a highly catabolic state. Corticosteroids and immunosuppressive therapy should be instituted for rapidly progressive glomerulonephritis, in addition to haemodialysis. haemodiafiltration instead of haemodialysis is recommended for patients who are haemodynamically unstable [i.e., with a persistently low blood pressure (systolic < or = 100 mm Hg)]. Haemodiafiltration has been shown to improve acid-base balance and uraemia better than standard haemodialysis. However, despite dialysis, mortality in patients with ARF associated with ischaemic ATN remains high.
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PMID:Management of acute renal failure in the elderly. Treatment options. 889 22

Drug-induced acute interstitial nephritis (AIN) is a relatively common cause of hospital-acquired acute kidney injury (AKI). While prerenal AKI and acute tubular necrosis (ATN) are the most common forms of AKI in the hospital, AIN is likely the next most common. Clinicians must differentiate the various causes of hospital-induced AKI; however, it is often difficult to distinguish AIN from ATN in such patients. While standardized criteria are now used to classify AKI into stages of severity, they do not permit differentiation of the various types of AKI. This is not a minor point, as these different AKI types often require different therapeutic interventions. Clinicians assess and differentiate AIN from these other AKI causes by utilizing clinical assessment, various imaging tests, and certain laboratory data. Gallium scintigraphy has been employed with mixed results. While a few serum tests, such as eosinophilia may be helpful, examination of the urine with tests such as dipstick urinalysis, urine chemistries, urine eosinophils, and urine microscopy are primarily utilized. Unfortunately, these tools are not always sufficient to definitively clinch the diagnosis, making it a challenging task for the clinician. As a result, kidney biopsy is often required to accurately diagnose AIN and guide management.
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PMID:Diagnosing drug-induced AIN in the hospitalized patient: a challenge for the clinician. 2469 Oct 17

Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is a rare and potentially fatal condition characterized by skin rash, fever, eosinophilia, and multiorgan involvement. Various drugs may be associated with this syndrome including carbamazepine, allopurinol, and sulfasalazine. Renal involvement in DRESS syndrome most commonly presents as acute kidney injury due to interstitial nephritis. An 11-year-old boy was referred to the Children's Hospital of Pusan National University because of persistent fever, rash, abdominal distension, generalized edema, lymphadenopathy, and eosinophilia. He previously received vancomycin and ceftriaxone for 10 days at another hospital. He developed acute kidney injury with nephrotic range proteinuria and hypocomplementemia. A subsequent renal biopsy indicated the presence of acute tubular necrosis (ATN) and late exudative phase of postinfectious glomerulonephritis (PIGN). Systemic symptoms and renal function improved with corticosteroid therapy after the discontinuation of vancomycin. Here, we describe a biopsy-proven case of severe ATN that manifested as a part of vancomycin-induced DRESS syndrome with coincident PIGN. It is important for clinicians to be aware of this syndrome due to its severity and potentially fatal nature.
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PMID:Acute tubular necrosis as a part of vancomycin induced drug rash with eosinophilia and systemic symptoms syndrome with coincident postinfectious glomerulonephritis. 2718 22