ABSTRACT
BACKGROUND: Acute tubulo-interstitial nephritis (TIN) is an important cause of acute renal failure, and is often caused by hypersensitivity to drugs. The aim of this study was to determine the aetiology of interstitial nephritis among an unselected cohort of patients, and to identify those drugs commonly implicated. METHODS: A single-centre retrospective analysis was carried out of renal biopsy results from 296 consecutive patients between 1995 and 1999. RESULTS: Acute TIN was identified in 24 (8.1%) biopsies. Eight out of 14 cases with presumed drug-related TIN could be attributed to the proton pump inhibitors omeprazole and lansoprazole. The two cases of lansoprazole-associated TIN are the first to be reported with this drug. The presentation and favourable response to treatment of these patients are described. CONCLUSION: Drugs are the most common cause of interstitial nephritis in the population studied. Those drugs most commonly associated with interstitial nephritis were the proton pump inhibitors omeprazole and lansoprazole.
Subject(s)
Enzyme Inhibitors/adverse effects , Nephritis, Interstitial/chemically induced , Omeprazole/analogs & derivatives , Omeprazole/adverse effects , Proton Pump Inhibitors , 2-Pyridinylmethylsulfinylbenzimidazoles , Adolescent , Adult , Aged , Creatinine/blood , Female , Humans , Lansoprazole , Male , Middle Aged , Nephritis, Interstitial/blood , Retrospective Studies , United KingdomABSTRACT
Hyperplasia of usual type (HUT) is part of the spectrum of benign proliferative disease in the breast and confers an increased risk of developing invasive cancer. Its role as a putative precursor of invasive ductal carcinomas in the breast is, however, controversial. HUT is occasionally seen bilaterally but it is not clear whether there is a genetic predisposition to the process. This study has analysed 14 cases of bilateral HUT in the breast (28 independent lesions) by comparative genomic hybridization (CGH) analysis to define DNA copy number changes and to investigate any commonality in these genetic alterations. The mean number of alterations seen was 1.6 (46/28) in all lesions, with common losses at chromosomes 1p, 16p, 17q, and 22q. Bilaterally, only five alterations were seen in common across both lesions in both breasts, but no single locus was altered preferentially. These data indicate that a proportion of HUT in the breast are indeed clonal, neoplastic proliferations which exhibit genetic alterations in common with invasive breast cancer, albeit at very low levels. The limited data from these experiments do not reveal a specific predisposition locus.