FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2034006725> ?p ?o ?g. }

• W2034006725 endingPage "464" @default.
• W2034006725 startingPage "458" @default.
• W2034006725 abstract "Acute interstitial nephritis (AIN) is an important cause of acute kidney injury (AKI), and its prevalence in the elderly may be increasing. It is largely unknown whether AIN in the elderly is similar to that in younger adults; therefore, we investigated the causes and characteristics of AIN in 45 elderly patients (65 years and older) and in 88 younger adults (18–64 years old). Compared with younger patients, the elderly had significantly more drug-induced AIN (87 vs. 64%), proton pump inhibitor–induced AIN (18 vs. 6%), but significantly less AIN due to autoimmune or systemic causes (7 vs. 27%). The two most common culprit drugs in the elderly were penicillin and omeprazole. Compared with younger patients, the elderly had higher prevalence of baseline CKD, higher peak creatinine, and more need for dialysis, all of which were significant. Among the elderly, 86% showed partial or complete recovery within 6 months. Significantly shorter delays in initiation of steroids correlated with recovery at 6 months. Lack of early recovery tended to correlate with progressive CKD. Compared with antibiotic-induced AIN, proton pump inhibitor–induced AIN had less severe AKI, but a longer duration of drug exposure, and was less likely to recover by 6 months, all significant. Thus, the vast majority of AIN cases in the elderly are due to drugs, primarily owing to proton pump inhibitors and antibiotics, while AIN of autoimmune or systemic origin is uncommon. Acute interstitial nephritis (AIN) is an important cause of acute kidney injury (AKI), and its prevalence in the elderly may be increasing. It is largely unknown whether AIN in the elderly is similar to that in younger adults; therefore, we investigated the causes and characteristics of AIN in 45 elderly patients (65 years and older) and in 88 younger adults (18–64 years old). Compared with younger patients, the elderly had significantly more drug-induced AIN (87 vs. 64%), proton pump inhibitor–induced AIN (18 vs. 6%), but significantly less AIN due to autoimmune or systemic causes (7 vs. 27%). The two most common culprit drugs in the elderly were penicillin and omeprazole. Compared with younger patients, the elderly had higher prevalence of baseline CKD, higher peak creatinine, and more need for dialysis, all of which were significant. Among the elderly, 86% showed partial or complete recovery within 6 months. Significantly shorter delays in initiation of steroids correlated with recovery at 6 months. Lack of early recovery tended to correlate with progressive CKD. Compared with antibiotic-induced AIN, proton pump inhibitor–induced AIN had less severe AKI, but a longer duration of drug exposure, and was less likely to recover by 6 months, all significant. Thus, the vast majority of AIN cases in the elderly are due to drugs, primarily owing to proton pump inhibitors and antibiotics, while AIN of autoimmune or systemic origin is uncommon. Acute kidney injury (AKI) in the elderly is of particular interest, as this growing population has the highest incidence of AKI.1.Anderson S. Eldadah B. Halter J.B. et al.Acute kidney injury in older adults.J Am Soc Nephrol. 2011; 22: 28-38Crossref PubMed Scopus (142) Google Scholar,2.Stallone G. Infante B. Grandaliano G. Acute kidney injury in the elderly population.J Nephrol. 2012; 25: S58-S66Crossref PubMed Scopus (4) Google Scholar Furthermore, the elderly appear to have a higher risk of development of chronic kidney disease (CKD) or end-stage renal disease (ESRD) after an episode of AKI than younger patients, and they have the highest mortality risk when they develop AKI during hospitalization.1.Anderson S. Eldadah B. Halter J.B. et al.Acute kidney injury in older adults.J Am Soc Nephrol. 2011; 22: 28-38Crossref PubMed Scopus (142) Google Scholar, 2.Stallone G. Infante B. Grandaliano G. Acute kidney injury in the elderly population.J Nephrol. 2012; 25: S58-S66Crossref PubMed Scopus (4) Google Scholar, 3.Del Giudice A. Aucella F. Acute renal failure in the elderly: epidemiology and clinical features.J Nephrol. 2012; 25: S48-S57Crossref PubMed Scopus (20) Google Scholar, 4.Ishani A. Xue J.L. Himmelfarb J. et al.Acute kidney injury increases risk of ESRD among elderly.J Am Soc Nephrol. 2009; 20: 223-228Crossref PubMed Scopus (886) Google Scholar, 5.Coca S.G. Acute kidney injury in elderly persons.Am J Kidney Dis. 2010; 56: 122-131Abstract Full Text Full Text PDF PubMed Scopus (145) Google Scholar In this population, AKI remains the most common indication for kidney biopsy,6.Haas M. Spargo B.H. Wit E.J. et al.Etiologies and outcome of acute renal insufficiency in older adults: a renal biopsy study of 259 cases.Am J Kidney Dis. 2000; 35: 433-447Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar, 7.Moutzouris D.A. Herlitz L. Appel G.B. et al.Renal biopsy in the very elderly.Clin J Am Soc Nephrol. 2009; 4: 1073-1082Crossref PubMed Scopus (109) Google Scholar, 8.Nair R. Bell J.M. Walker P.D. Renal biopsy in patients aged 80 years and older.Am J Kidney Dis. 2004; 44: 618-626Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar and studies have shown that the performance of biopsies in this population is both safe and as likely to yield useful findings as in younger patients.8.Nair R. Bell J.M. Walker P.D. Renal biopsy in patients aged 80 years and older.Am J Kidney Dis. 2004; 44: 618-626Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar,9.Kohli H.S. Jairam A. Bhat A. et al.Safety of kidney biopsy in elderly: a prospective study.Int Urol Nephrol. 2006; 38: 815-820Crossref PubMed Scopus (39) Google Scholar Acute interstitial nephritis (AIN) is an important and common cause of AKI. The prevalence of AIN has been found to occur in 15–27% of patients in whom kidney biopsy is performed for AKI.6.Haas M. Spargo B.H. Wit E.J. et al.Etiologies and outcome of acute renal insufficiency in older adults: a renal biopsy study of 259 cases.Am J Kidney Dis. 2000; 35: 433-447Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar,10.Farrington K. Levison D.A. Greenwood R.N. et al.Renal biopsy in patients with unexplained renal impairment and normal kidney size.Q J Med. 1989; 70: 221-233PubMed Google Scholar Since AIN from drugs was first described,11.More R.H. McMillan G.C. Duff G.L. The pathology of sulfonamide allergy in man.Am J Pathol. 1946; 22: 703-735Google Scholar,12.Baldwin D.S. Levine B.B. McCluskey R.T. et al.Renal failure and interstitial nephritis due to penicillin and methicillin.N Engl J Med. 1968; 279: 1245-1252Crossref PubMed Scopus (242) Google Scholar the prevalence of drug-induced AIN (DI-AIN) continues to rise, likely because of the widespread use of antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and other drugs.13.Praga M. Gonzalez E. Acute interstitial nephritis.Kidney Int. 2010; 77: 956-961Abstract Full Text Full Text PDF PubMed Scopus (280) Google Scholar The use of these drugs has increased especially in elderly patients (over 65 years of age),1.Anderson S. Eldadah B. Halter J.B. et al.Acute kidney injury in older adults.J Am Soc Nephrol. 2011; 22: 28-38Crossref PubMed Scopus (142) Google Scholar and the prevalence of AIN in this population has been reported to be higher than in younger patients.14.Davison A.M. Jones C.H. Acute interstitial nephritis in the elderly: a report from the UK MRC Glomerulonephritis Register and a review of the literature.Nephrol Dial Transplant. 1998; 13: 12-16Crossref PubMed Scopus (45) Google Scholar Furthermore, there appears to be a higher risk of AIN in elderly patients from certain drugs such as NSAIDs.15.Lamy P.P. Renal effects of nonsteroidal antiinflammatory drugs. Heightened risk to the elderly?.J Am Geriatr Soc. 1986; 34: 361-367Crossref PubMed Scopus (40) Google Scholar A recent Spanish biopsy registry study16.Goicoechea M. Rivera F. Lopez-Gomez J.M. Increased prevalence of acute tubulointerstitial nephritis.Nephrol Dial Transplant. 2012; 00: 1-4Google Scholar showed the prevalence of AIN to have increased about threefold in all patients from 1994 to 2009, but in elderly patients specifically this increase was a marked eightfold. This increase was postulated to be due to the increasing biopsy rate in the elderly, as well as increasing use of the drugs that are most commonly implicated in DI-AIN such as antibiotics and NSAIDs. A biopsy study of 259 elderly patients with AKI in 2000 by Haas et al. found a prevalence of AIN of 19%.6.Haas M. Spargo B.H. Wit E.J. et al.Etiologies and outcome of acute renal insufficiency in older adults: a renal biopsy study of 259 cases.Am J Kidney Dis. 2000; 35: 433-447Abstract Full Text Full Text PDF PubMed Scopus (192) Google Scholar Since the introduction of proton pump inhibitors (PPIs) in 1989,17.Brewster U.C. Perazella M.A. Proton pump inhibitors and the kidney: critical review.Clin Nephrol. 2007; 68: 65-72Crossref PubMed Google Scholar their high efficacy and low side effect profile has led to their becoming one of the most widely prescribed drugs in the world.18.Forgacs I. Loganayagam A. Overprescribing proton pump inhibitors.BMJ. 2008; 336: 2-3Crossref PubMed Scopus (387) Google Scholar PPIs are emerging as a significant cause of AIN, and elderly patients appear to have greater susceptibility to them.19.Simpson I.J. Marshall M.R. Pilmore H. et al.Proton pump inhibitors and acute interstitial nephritis: report and analysis of 15 cases.Nephrology (Carlton). 2006; 11: 381-385Crossref PubMed Scopus (106) Google Scholar, 20.Ray S. Delaney M. Muller A.F. Proton pump inhibitors and acute interstitial nephritis.BMJ. 2010; 341: c4412Crossref PubMed Scopus (32) Google Scholar, 21.Sierra F. Suarez M. Rey M. et al.Systematic review: proton pump inhibitor-associated acute interstitial nephritis.Aliment Pharmacol Ther. 2007; 26: 545-553Crossref PubMed Scopus (137) Google Scholar Although the high and increasing incidence and impact of AKI in the elderly has been well elucidated, as has the high incidence of AIN in this population,16.Goicoechea M. Rivera F. Lopez-Gomez J.M. Increased prevalence of acute tubulointerstitial nephritis.Nephrol Dial Transplant. 2012; 00: 1-4Google Scholar the causes of AIN in this population are not well described. The goal of this study is to describe the causes, clinical presentation, and outcome of AIN in the elderly and to compare this with younger patients. One hundred thirty-three adult Mayo patients with biopsy-proven AIN were identified from 1993 to 2011, 45 (34%) of whom were ≥65 years of age (Table 1). The total number of adult Mayo patients with native kidney biopsy during the same period was 7575, indicating that the prevalence of adult AIN in our medical center is 1.8%, which is comparable to prior studies that reported 1–3% prevalence.16.Goicoechea M. Rivera F. Lopez-Gomez J.M. Increased prevalence of acute tubulointerstitial nephritis.Nephrol Dial Transplant. 2012; 00: 1-4Google Scholar The median age of the elderly was 73 years and 49 years in those aged <65 years. The elderly patients were more likely to present with pyuria (P=0.04), but tended to be less likely to have fever (P=0.09). There was otherwise no difference in clinical symptoms (Table 1). In both groups, the AKI was predominantly nonoliguric in nature. The elderly patients had lower estimated glomerular filtration rate (eGFR) at baseline—55ml/min per 1.73m2 compared with 69ml/min per 1.73m2 in the younger patients (P=0.0018)—and they were more likely to have CKD at baseline—69% compared with 28% (P<0.0001). During the episode of AKI, the elderly patients had higher creatinine levels at the time of biopsy, 4.0 vs. 3.3mg/dl (P=0.021), and higher peak creatinine, 4.7 vs. 3.4mg/dl (P=0.012). Of the 45 elderly patients, 15 patients (33%) required dialysis during the episode of AKI compared with 14 (16%) non-elderly patients (P=0.0213). Younger patients had a lower prevalence of DI-AIN (64%) compared with the elderly (87%; P=0.0054). A majority of patients were treated with steroids: 93% in the elderly patients and 83% in the non-elderly patients (P=0.09). Histologically, the elderly had a higher percentage of sclerotic glomeruli (P=0.0004) and more interstitial fibrosis and tubular atrophy (P=0.01). No difference was found between the presence of moderate/severe interstitial fibrosis and tubular atrophy and progressive disease (P=0.39). There was no difference in the occurrence of granulomatous AIN on biopsy: 22% compared with 28% (P=0.44).Table 1Demographic, clinical, laboratory, treatment, and outcome characteristics of patients with AIN (N=133)Characteristics≥65 years (N=45)<65 years (N=88)P-valueAge, years73 (70,78.5)49 (35,58)<0.001Male sex20 (44)44 (50)0.54Race-White41/42 (98)80/84 (95)0.60Rash7/45 (16)15/88 (17)0.83Fever4/45 (9)18/88 (20)0.09Oliguria8/45 (16)11/88 (13)0.41Leukocytosis11 (24)27 (31)0.45Eosinophilia11/40 (28)11/80 (14)0.07Triad: fever+rash+eosinophilia2/40 (5)7/81 (9)0.47Pyuria26/44 (59)35/87 (40)0.04Hematuria13/44 (30)26/86 (30)0.94Eosinophiluria14/31 (45)14/51 (27)0.10Proteinuria41/44 (93)81/88 (92)0.82Nephrotic-range proteinuria7/44 (16)12/88 (14)0.73White cell casts2/44 (5)2/88 (2)0.47Baseline serum creatinine (mg/dl)1.1 (1.0,1.4)1.1 (0.9,1.2)0.27Baseline estimated GFR55 (47,65)69 (53,85)0.0018CKD at baseline29/42 (69)19/67 (28)<0.0001Serum creatinine at time of biopsy (mg/dl)4.0 (2.7,5.9)3.3 (1.9,5.1)0.021AKIN stage Stage 16/42 (14)15/64 (23)0.26 Stage 211/42 (26)17/64 (27)— Stage 325/42 (60)32/64 (50)—Peak serum creatinine (mg/dl)4.7 (3.2,8.6)3.4 (2.4,6.4)0.012Comorbid conditions41/44 (93)70/87 (80)0.056Drug-induced AIN39 (87)56 (64)0.0054Dialysis15 (33)14 (16)0.0213Interstitial fibrosis/tubular atrophy None7 (16)33 (37)— Mild29 (64)38 (43)— Moderate9 (20)12 (14)— Severe0 (0)5 (6)0.01% Globally sclerotic glomeruli18.0 (6.5,33)0 (0,17)0.0004Granuloma present10 (22)25 (28)0.44Recovery within 6 months0.36 Complete14/36 (39)33/63 (52)— Partial17/36 (47)21/63 (34)— None5/36 (14)9/63 (14)—Latest serum creatinine (mg/dl)1.6 (1.2,2.2)1.3 (1,2)0.15Ultimate outcome——0.21 Normal15/32 (47)33/57 (58)— Progressive CKD14/32 (44)23/57 (40)— ESRD3/32 (9)1/57 (2)—Abbreviation: AIN, acute interstitial nephritis; CKD, chronic kidney disease; ESRD, end-stage renal disease; GFR, glomerular filtration rate.Continuous variables are reported as median (interquartile range) and categorical as number (percentage). Open table in a new tab Abbreviation: AIN, acute interstitial nephritis; CKD, chronic kidney disease; ESRD, end-stage renal disease; GFR, glomerular filtration rate. Continuous variables are reported as median (interquartile range) and categorical as number (percentage). By the end of the first 6 months after the diagnostic biopsy, the majority of patients achieved either complete (CR) or partial recovery (PR) at 47 and 38%, respectively, with only 14% having a status of no recovery (NR); there was no difference between the elderly or non-elderly patients as regards this status (CR: 39%, PR: 47%, NR: 14% compared with CR: 52%, PR: 34%, NR: 14%; P=0.36). At the end of follow-up (median 73 months), four patients had ESRD, three of whom were elderly. Of all the 133 patients in the study, 95 had DI-AIN, of whom 39 patients (41%) were elderly and 56 (59%) were not (Table 2; Figure 1). The elderly patients were more likely to have drugs as the cause of AIN (87 vs. 64%, P=0.005), as detailed in Table 2, and they had more DI-AIN (87 vs. 64%, P=0.005), including more PPI–induced AIN (18 vs. 6%, P=0.03), and less AIN associated with autoimmune/systemic diseases (7 vs. 27%, P<0.01). In the younger patients, half of the cases of AIN associated with autoimmune/systemic diseases were due to sarcoidosis.Table 2Causes of AIN by age group (N=133)CauseNumber of patients (%)≥65 years (N=45)<65 years (N=88)Drug induced39 (87)56 (64) Antibiotics21 (47)26 (30) NSAIDs1 (2)9 (10) PPIs8 (18)5 (6) Other drugs3 (7)8 (9) Multiple drugs6 (13)8 (9)Autoimmune/systemic disorders3 (7)24 (27) Sarcoidosis1 (2.3)12 (13.6) Sjogren’s1 (2.3)5 (5.7) TINU0 (0)3 (3.4) IgG4 related0 (0)2 (2.3) Other—sweets, MCTD/CREST1 (2.3)2 (2.3)Infectious1 (2)4 (4.5) Bacterial1 (2)2 (2.3) Viral0 (0)1 (1.1) Fungal0 (0)1 (1.1)Other1 (2)4 (4.5) Reactive interstitial nephritis (Councilman’s disease)0 (0)2 (2.3) Malignancy1 (2)1 (1.1) CVID0 (0)1 (1.1)Unknown1 (2)0 (0)Abbreviations: AIN, acute interstitial nephritis; CVID, common variable immunodeficiency; CREST, calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly and telangiectasia; MCTD, mixed connective tissue disease; NSAIDs, nonsteroidal anti-inflammatory drugs; PPIs, proton pump inhibitors; TINU, tubulointerstitial nephritis and uveitis.Infectious causes included one Enterococcus, one Escherichia coli, one unidentified bacterium, one adenovirus, and one Candida. Malignancies included one chronic lymphoid leukemia and one mantle cell lymphoma. Open table in a new tab Abbreviations: AIN, acute interstitial nephritis; CVID, common variable immunodeficiency; CREST, calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly and telangiectasia; MCTD, mixed connective tissue disease; NSAIDs, nonsteroidal anti-inflammatory drugs; PPIs, proton pump inhibitors; TINU, tubulointerstitial nephritis and uveitis. Infectious causes included one Enterococcus, one Escherichia coli, one unidentified bacterium, one adenovirus, and one Candida. Malignancies included one chronic lymphoid leukemia and one mantle cell lymphoma. Overall, in elderly patients, antibiotics were the most common culprit (47%), followed by PPIs at 18%. In 13% of these patients, one specific drug could not be identified, and they were categorized as multidrug causes. NSAIDs caused only 2% of cases in the elderly. In the younger patients, antibiotics remained the main culprit at 30%, but the second commonest was NSAIDs in 10% with only 6% due to PPIs. As shown in Table 3, penicillins and fluoroquinolones were the commonest antibiotic causes. Omeprazole was the main PPI causing AIN in this study, implicated in 11 cases, 7 of whom were elderly. The three most common culprit drugs for AIN in the elderly were penicillin (21%), omeprazole (18%), and fluoroquinolones (13%), whereas in the younger age group these were penicillin (20%), fluoroquinolones (14%), and ibuprofen (8%).Table 3Causes of drug-induced AIN by age group (N=95)DrugsNumber of patients (%)≥65 years (N=39)<65 years (N=56)Antibiotics21 (54)26 (47) Penicillins8 (21)11 (20) Fluroquinolones5 (13)8 (14) Cephalosporins3 (7.5)2 (4) Vancomycin1 (2.5)3 (5) Sulfonamides1 (2.5)1 (2) Rifampin1 (2.5)1 (2) Imipenem2 (5)0 (0)PPIs8 (20.5)5 (9) Omeprazole7 (18)4 (7) Esomeprazole0 (0)1 (2) Rabeprazole1 (2.5)0 (0)NSAIDs1 (2.5)9 (16) Ibuprofen0 (0)5 (8) Nabumetone0 (0)1 (2) Salicylates0 (0)1 (2) Celecoxib0 (0)1 (2) Rofecoxib1 (2.5)0 (0) Combination of NSAIDs0 (0)1 (2)Other drugs3 (7.5)8 (14) Allopurinol1 (2.5)1 (2) Cimetidine0 (0)1 (2) Creatine supplement0 (0)1 (2) Hydrochlorothiazide1 (2.5)1 (2) Lisinopril0 (0)1 (2) Mesalamine0 (0)1 (2) Olmesartan0 (0)1 (2) Revlimid0 (0)1 (2) Risedronate1 (2.5)0 (0)Multidrugs6 (15.5)8 (14) Combinations of antibiotics and other drugs4 (10.5)5 (9) Combinations of other drugs2 (5)3 (5)Abbreviations: AIN, acute interstitial nephritis; NSAIDs, nonsteroidal anti-inflammatory drugs; PPIs, proton pump inhibitors.The category of Multidrugs includes patients who were on several medications at the time of developing acute kidney injury and no particular drug could be identified as the culprit drug. Most of these included a combination of antibiotics and other drugs such as PPIs, NSAIDs, and on one occasion allopurinol. Other drug combinations included NSAIDs, varenicline, and furosemide, as well as azathioprine. Open table in a new tab Abbreviations: AIN, acute interstitial nephritis; NSAIDs, nonsteroidal anti-inflammatory drugs; PPIs, proton pump inhibitors. The category of Multidrugs includes patients who were on several medications at the time of developing acute kidney injury and no particular drug could be identified as the culprit drug. Most of these included a combination of antibiotics and other drugs such as PPIs, NSAIDs, and on one occasion allopurinol. Other drug combinations included NSAIDs, varenicline, and furosemide, as well as azathioprine. Out of the 38 elderly patients with DI-AIN who were treated with steroids, 8 had less than 8 weeks of follow-up without CR and were excluded from the outcome analysis. A comparison between the three recovery groups (CR, PR, or NR) of the remaining 30 patients revealed that a majority of the elderly with DI-AIN who received steroids had some recovery by 6 months. Of note, neither baseline eGFR nor CKD status correlated with recovery status (P=0.38 and 0.38, respectively). Similar findings occurred with serum creatinine at the time of biopsy (P=0.39), AKIN stage (P=0.34), and peak serum creatinine (P=0.32). Histological findings also did not correlate with recovery. The duration of culprit drugs (P=0.15) or steroid therapy (P=0.40) did not show any relationship with recovery status. The median duration of steroids among these 38 elderly patients was 5 weeks, and the median initial steroid dose was 60mg of prednisone orally (range 20–80mg). Eight patients were initially treated with intravenous steroids. Those with NR at 6 months were more likely to have PPIs as the cause of AIN compared with CR or PR (29 vs. 7%, P=0.046). There was a correlation between delays from onset of AKI to initiation of steroid therapy with recovery (P=0.031). The median delay from onset of AKI and discontinuation of the culprit drug to initiation of steroids was 11 and 7 days, respectively. Three patients, all of whom were under the age of 65 years, received mycophenolate. In two of these patients, this was in conjunction with steroids after an initial poor response to steroids only. The third patient received intravenous steroids for a few days, and then mycophenolate. Two patients achieved complete recovery, and the other patient achieved PR. Recovery status at the end of 6 months correlated with long-term recovery (median time 108 months), with 40% of those in the NR group ultimately developing ESRD compared with none in the CR/PR group (P=0.0185). We compared antibiotic-caused AIN (antibiotic-AIN) with PPI-caused AIN (PPI-AIN), as shown in Table 4. As only one patient in this category had NSAIDs as the cause, this group was excluded. Those with antibiotic-AIN tended to be more likely to present with rash than PPI-AIN (P=0.09) and more likely to be inpatients at the time of diagnosis, 76 vs. 25% (P=0.011), and to present with proteinuria (P=0.003). Although baseline serum creatinine and CKD did not differ, those with antibiotic-AIN had more severe AKI, with higher serum creatinine at biopsy (5.4 vs. 2.6mg/dl, P=0.0018), higher AKIN stage (P=0.0003), as well as higher peak serum creatinine (P=0.0012) and higher likelihood of dialysis (P=0.0159). Those with PPI-AIN tended to have more interstitial fibrosis and tubular atrophy (P=0.09), which may have been due to the much longer duration of exposure to the culprit drug they had compared to antibiotic-AIN (median 234 vs. 15 days, P=0.011). This long duration of exposure may have been related to the lower suspicion AIN before biopsy (25 vs. 88%, P=0.0022) on the part of treating clinicians. There were longer delays from onset of AKI to performing biopsy, as well as treating with steroids in those with PPI-AIN (P=0.0013 and P=0.0034, respectively). There were also longer delays in starting steroids from the time of drug withdrawal (P=0.0008).Table 4Comparison of antibiotic-induced AIN and PPI-induced AIN in elderly patients (N=29)CharacteristicsAntibiotics (N=21)PPIs (N=8)P-valueAge, years73 (68,79)73 (71,77)0.83Male sex10 (48)4 (50)0.91Race-White20/20 (100)6/7 (86)0.085Rash6 (29)0 (0)0.09Fever3 (14)0 (0)0.26Triad: fever+rash+eosinophilia2/20 (10)0/5 (0)0.46Pyuria12 (57)5/8 (63)0.79Hematuria8 (38)5/13 (38)0.98Eosinophiluria9/17 (53)2/5 (40)0.61Oliguria5 (24)0 (0)0.13Proteinuria21 (100)5 (63)0.003Amount of proteinuria, ratio1.4 (0.7,3.7)0.5 (0.1,1.1)0.038Nephrotic-range proteinuria5 (24)0 (0)0.13Baseline serum creatinine (mg/dl)1.0 (0.9,1.1)1.0 (1,1.3)0.70Baseline estimated GFR55 (53,70)56 (54,70)0.99CKD at baseline11/19 (58)5/8 (63)0.82Serum creatinine at biopsy (mg/dl)5.4 (3.6,9.9)2.6 (1.9,2.8)0.0018AKIN stage Stage 10/19 (0)3/8 (37.5)— Stage 23/19 (16)4/8 (50)— Stage 316/19 (84)1/8 (12.5)0.0003Interstitial fibrosis/tubular atrophy None5 (24)0 (0)— Mild14 (67)6 (75)— Moderate2 (9)2 (25)0.23 Severe0 (0)0 (0)—Peak serum creatinine (mg/dl)6.4 (3.9,11.4)2.7 (2.3,3.3)0.0012Comorbid conditions18/20 (90)8/8 (100)0.35Pre-biopsy diagnosis of AIN14/16 (88)2/8 (25)0.0022Dialysis10 (48)0 (0)0.0159Duration of culprit drug, days15 (5,42)234 (33,266)0.011Steroid therapy20/21 (95)8/8 (100)0.53Recovery within 6 months Complete6/14 (43)2/7 (28.5)— Partial7/14 (50)3/7 (43)— None1/14 (7)2/7 (28.5)0.43Recovered by 6 months13/14 (93)5/7 (71)0.046Latest serum creatinine (mg/dl)1.6 (1.2,2.6)1.6 (1.0,2.0)0.54Ultimate outcome Normal5/12 (42)4/7 (57)— Progressive CKD5/12 (42)3/7 (43)— ESRD2/12 (16)0/7 (0)0.50Abbreviations: AIN, acute interstitial nephritis; CKD, chronic kidney disease; ESRD, end-stage renal disease; GFR, glomerular filtration rate; PPIs, proton pump inhibitors.Continuous variables are reported as median (interquartile range) and categorical as number (percentage). Open table in a new tab Abbreviations: AIN, acute interstitial nephritis; CKD, chronic kidney disease; ESRD, end-stage renal disease; GFR, glomerular filtration rate; PPIs, proton pump inhibitors. Continuous variables are reported as median (interquartile range) and categorical as number (percentage). Those with antibiotic-AIN were more likely than those with PPI-AIN to have achieved some degree of recovery (CR/PR) by 6 months (93 vs. 71%, P=0.046). Over the long term, there was no difference in outcomes (P=0.50), in the 19 patients in whom this information was available. AIN was first described by Councilman in 189822.Councilman W.T. Acute interstitial nephritis.J Exp Med. 1898; 3: 393-420Crossref PubMed Scopus (106) Google Scholar as an acute inflammatory disease associated with scarlet fever and diphtheria. Over time, although infectious causes were the most common causes, this has been superseded by drugs, which are responsible for 60–70% of all cases. Virtually all classes of drugs have been implicated in causation of AIN.23.Michel D.M. Kelly C.J. Acute interstitial nephritis.J Am Soc Nephrol. 1998; 9: 506-515PubMed Google Scholar, 24.Schwarz A. Krause P.H. Kunzendorf U. et al.The outcome of acute interstitial nephritis: risk factors for the transition from acute to chronic interstitial nephritis.Clin Nephrol. 2000; 54: 179-190PubMed Google Scholar, 25.Clarkson M.R. Giblin L. O'Connell F.P. et al.Acute interstitial nephritis: clinical features and response to corticosteroid therapy.Nephrol Dial Transplant. 2004; 19: 2778-2783Crossref PubMed Scopus (244) Google Scholar Autoimmune/systemic disorders are another important cause of AIN.26.Neilson E.G. Pathogenesis and therapy of interstitial nephritis.Kidney Int. 1989; 35: 1257-1270Abstract Full Text PDF PubMed Scopus (193) Google Scholar The prevalence of AIN in unselected biopsies has been reported to be 2–6%, and 13–25% in biopsies performed for AKI.14.Davison A.M. Jones C.H. Acute interstitial nephritis in the elderly: a report from the UK MRC Glomerulonephritis Register and a review of the literature.Nephrol Dial Transplant. 1998; 13: 12-16Crossref PubMed Scopus (45) Google Scholar,16.Goicoechea M. Rivera F. Lopez-Gomez J.M. Increased prevalence of acute tubulointerstitial nephritis.Nephrol Dial Transplant. 2012; 00: 1-4Google Scholar,27.Abdel-Kader K. Palevsky P.M. Acute kidney injury in the elderly.Clin Geriatr Med. 2009; 25: 331-358Abstract Full Text Full Text PDF PubMed Scopus (96) Google Scholar In patients over 60 years of age, the prevalence has been reported to be higher than those under the age of 60 years.14.Davison A.M. Jones C.H. Acute interstitial nephritis in the elderly: a report from the UK MRC Glomerulonephritis Register and a review of the literature.Nephrol Dial Transplant. 1998; 13: 12-16Crossref PubMed Scopus (45) Google Scholar It has been postulated that this may be because of an increased susceptibility in the aging kidney.14.Davison A.M. Jones C.H. Acute interstitial nephritis in the elderly: a report from the UK MRC Glomerulonephritis Register and a review of the literature.Nephrol Dial Transplant. 1998; 13: 12-16Crossref PubMed Scopus (45) Google Scholar,27.Abdel-Kader K. Palevsky P.M. Acute kidney injury in the elderly.Clin Geriatr Med. 2009; 25: 331-358Abstract Full Text Full Text PDF PubMed Scopus (96) Google Scholar A recent European biopsy register study16.Goicoechea M. Rivera F. Lopez-Gomez J.M. Increased prevalence of acute tubulointerstitial nephritis.Nephrol Dial Transplant. 2012; 00: 1-4Google Scholar showed the prevalence of AIN to have increased over the 16 years of follow-up, with the increase in patients over 65 years of age being the most significant. This finding may have been related to an increase in performance of biopsy in older patients, but it may also reflect a true increase in AIN incidence, perhaps fueled by higher intake of medications in these patients. In our study of 133 patients with biopsy-proven AIN over 19 years, 45 (34%) were ≥65 years of age. The prevalence of AIN among unselected native biopsies of adults was 1.8%. Although there were few differences in the clinical presentation of these patients compared with the younger group, the elderly did have a higher prevalence of CKD at baseline and lower b" @default.
• W2034006725 created "2016-06-24" @default.
• W2034006725 creator A5008779206 @default.
• W2034006725 creator A5016853434 @default.
• W2034006725 creator A5022179123 @default.
• W2034006725 creator A5046194391 @default.
• W2034006725 creator A5069001339 @default.
• W2034006725 creator A5070946918 @default.
• W2034006725 creator A5084355410 @default.
• W2034006725 date "2015-02-01" @default.
• W2034006725 modified "2023-10-14" @default.
• W2034006725 title "Clinical characteristics, causes and outcomes of acute interstitial nephritis in the elderly" @default.
• W2034006725 cites W1508489738 @default.
• W2034006725 cites W1567093751 @default.
• W2034006725 cites W1863187267 @default.
• W2034006725 cites W1922117259 @default.
• W2034006725 cites W1965491136 @default.
• W2034006725 cites W1967300023 @default.
• W2034006725 cites W1981665521 @default.
• W2034006725 cites W1983854969 @default.
• W2034006725 cites W1984850666 @default.
• W2034006725 cites W1991668710 @default.
• W2034006725 cites W1996207478 @default.
• W2034006725 cites W2019371023 @default.
• W2034006725 cites W2021690806 @default.
• W2034006725 cites W2026294611 @default.
• W2034006725 cites W2032603652 @default.
• W2034006725 cites W2047621580 @default.
• W2034006725 cites W2076073035 @default.
• W2034006725 cites W2084162564 @default.
• W2034006725 cites W2091234866 @default.
• W2034006725 cites W2096760252 @default.
• W2034006725 cites W2109654391 @default.
• W2034006725 cites W2122627234 @default.
• W2034006725 cites W2135329620 @default.
• W2034006725 cites W2143757728 @default.
• W2034006725 cites W2146905590 @default.
• W2034006725 cites W2151756973 @default.
• W2034006725 cites W2163900716 @default.
• W2034006725 cites W2332475916 @default.
• W2034006725 cites W2339612342 @default.
• W2034006725 cites W2409098454 @default.
• W2034006725 cites W4249861865 @default.
• W2034006725 doi "https://doi.org/10.1038/ki.2014.294" @default.
• W2034006725 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25185078" @default.
• W2034006725 hasPublicationYear "2015" @default.
• W2034006725 type Work @default.
• W2034006725 sameAs 2034006725 @default.
• W2034006725 citedByCount "86" @default.
• W2034006725 countsByYear W20340067252014 @default.
• W2034006725 countsByYear W20340067252015 @default.
• W2034006725 countsByYear W20340067252016 @default.
• W2034006725 countsByYear W20340067252017 @default.
• W2034006725 countsByYear W20340067252018 @default.
• W2034006725 countsByYear W20340067252019 @default.
• W2034006725 countsByYear W20340067252020 @default.
• W2034006725 countsByYear W20340067252021 @default.
• W2034006725 countsByYear W20340067252022 @default.
• W2034006725 countsByYear W20340067252023 @default.
• W2034006725 crossrefType "journal-article" @default.
• W2034006725 hasAuthorship W2034006725A5008779206 @default.
• W2034006725 hasAuthorship W2034006725A5016853434 @default.
• W2034006725 hasAuthorship W2034006725A5022179123 @default.
• W2034006725 hasAuthorship W2034006725A5046194391 @default.
• W2034006725 hasAuthorship W2034006725A5069001339 @default.
• W2034006725 hasAuthorship W2034006725A5070946918 @default.
• W2034006725 hasAuthorship W2034006725A5084355410 @default.
• W2034006725 hasBestOaLocation W20340067251 @default.
• W2034006725 hasConcept C126322002 @default.
• W2034006725 hasConcept C177713679 @default.
• W2034006725 hasConcept C2777058396 @default.
• W2034006725 hasConcept C2780091579 @default.
• W2034006725 hasConcept C2780888721 @default.
• W2034006725 hasConcept C71924100 @default.
• W2034006725 hasConceptScore W2034006725C126322002 @default.
• W2034006725 hasConceptScore W2034006725C177713679 @default.
• W2034006725 hasConceptScore W2034006725C2777058396 @default.
• W2034006725 hasConceptScore W2034006725C2780091579 @default.
• W2034006725 hasConceptScore W2034006725C2780888721 @default.
• W2034006725 hasConceptScore W2034006725C71924100 @default.
• W2034006725 hasIssue "2" @default.
• W2034006725 hasLocation W20340067251 @default.
• W2034006725 hasLocation W20340067252 @default.
• W2034006725 hasOpenAccess W2034006725 @default.
• W2034006725 hasPrimaryLocation W20340067251 @default.
• W2034006725 hasRelatedWork W1008668110 @default.
• W2034006725 hasRelatedWork W183968875 @default.
• W2034006725 hasRelatedWork W1977436855 @default.
• W2034006725 hasRelatedWork W2187941038 @default.
• W2034006725 hasRelatedWork W2241230181 @default.
• W2034006725 hasRelatedWork W2418393170 @default.
• W2034006725 hasRelatedWork W2440391015 @default.
• W2034006725 hasRelatedWork W2799731539 @default.
• W2034006725 hasRelatedWork W4236587169 @default.
• W2034006725 hasRelatedWork W83233002 @default.
• W2034006725 hasVolume "87" @default.
• W2034006725 isParatext "false" @default.
• W2034006725 isRetracted "false" @default.

• next