Time to Acute Kidney Injury in β-Lactam-Induced Acute Interstitial Nephritis.
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ABSTRACT:
SUBMITTER: Lazarus B
PROVIDER: S-EPMC7335949 | biostudies-literature | 2020 Jul
REPOSITORIES: biostudies-literature
Publications
Time to Acute Kidney Injury in β-Lactam-Induced Acute Interstitial Nephritis.
Lazarus Benjamin B Davies Matthew R P MRP Trubiano Jason A JA Pellicano Rebecca R
Kidney international reports 20200420 7
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Project description:Sarcoidosis affects multiple organs including lung, heart and kidney. Sarcoidosis causes hypercalcemia, hypergammaglobulinemia, and rarely, granulomatous interstitial nephritis, resulting in renal stromal damage. Granulomatous interstitial nephritis is characterized as interstitial nephritis with noncaseating epithelioid granulomas. Diagnosing granulomatous interstitial nephritis before patient's death is challenging; hence, only few cases proven by renal biopsy have been reported till date. We present a case of acute kidney injury caused by granulomatous interstitial nephritis as a renal manifestation of sarcoidosis proven by renal biopsy, which can be confirmed by 18F-fluorodeoxyglucose positron emission tomography/computed tomography. Glucocorticoid therapy was helpful for improving and maintaining her renal function over a 6-year period.
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Project description:WNT signaling mediates various physiological and pathological processes. We previously showed that WNT10A is a novel angio/stromagenic factor involved in such processes as tumor growth, wound healing and tissue fibrosis. In this study, we investigated the role of WNT10A in promoting the fibrosis that is central to the pathology of acute interstitial nephritis (AIN). We initially asked whether there is an association between kidney function (estimated glomerular filtration rate; eGFR) and WNT10A expression using kidney biopsies from 20 patients with AIN. Interestingly, patients with WNT10A expression had significantly lower eGFR than WNT10A-negative patients. However, changes in kidney function were not related to the level of expression of other WNT family members. Furthermore, there was positive correlation between WNT10A and α-SMA expression. We next investigated the involvement of WNT10A in kidney fibrosis processes using COS1 cells, a kidney fibroblast cell line. WNT10A overexpression increased the level of expression of fibronectin and peroxiredoxin 5. Furthermore, WNT10A overexpression renders cells resistant to apoptosis induced by hydrogen peroxide and high glucose. Collectively, WNT10A may induce kidney fibrosis and associate with kidney dysfunction in AIN.
| S-EPMC4108433 | biostudies-literature
Project description:IntroductionAcute interstitial nephritis (AIN) is a significant cause of acute kidney injury, with varying etiologies and outcomes. This study aimed to examine the causes, clinical characteristics, management, and kidney outcomes in patients with biopsy-confirmed AIN.MethodsA retrospective review was conducted on 166 patients diagnosed with AIN through kidney biopsy at Mayo Clinic between 2012 and 2023. Demographic, clinical, laboratory, and pathological data were collected. The primary outcome was kidney function recovery within the first 6 months. Statistical analyses included univariable and multivariable logistic regression, Kaplan-Meier survival analysis, and Cox proportional hazards modeling.ResultsMedications were the primary cause of AIN (67%), followed by autoimmune diseases (20%) and infections (6%). Within 6 months, 76% of patients achieved kidney recovery. Multivariable analysis indicated that moderate to severe interstitial fibrosis and tubular atrophy (IFTA) and dialysis requirement were associated with nonrecovery, whereas a prebiopsy diagnosis of AIN was positively associated with kidney recovery. Drug-related AIN had higher recovery rates compared to all other causes (81% vs. 66%, P = 0.04), and moderate to severe IFTA and dialysis need remained significant predictors of decreased recovery. Steroid therapy, used in 81% of patients, did not significantly influence kidney recovery in the overall cohort or in drug-induced AIN.ConclusionThis study provides insights into the characteristics and outcomes of biopsy-confirmed AIN. IFTA and dialysis requirement were significant factors associated with worse kidney outcomes. These findings may help inform clinical management and prognostication in patients with AIN.
| S-EPMC11652094 | biostudies-literature
Project description:This study aims to figure out the worldwide prevalence of anticancer therapy-associated acute kidney injury (AKI) and tubulointerstitial nephritis (TIN) and the relative risk of each cancer drug. We conducted an analysis of VigiBase, the World Health Organization pharmacovigilance database, 1967-2023 via disproportionate Bayesian reporting method. We further categorized the anticancer drugs into four groups: cytotoxic therapy, hormone therapy, immunotherapy, and targeted therapy. Reporting odds ratio (ROR) and information component (IC) compares observed and expected values to investigate the associations of each category of anticancer drugs with AKI and TIN. We identified 32,722 and 2056 reports (male, n = 17,829 and 1,293) of anticancer therapy-associated AKI and TIN, respectively, among 4,592,036 reports of all-drug caused AKI and TIN. There has been a significant increase in reports since 2010, primarily due to increased reports of targeted therapy and immunotherapy. Immunotherapy exhibited a significant association with both AKI (ROR: 8.92; IC0.25: 3.06) and TIN (21.74; 4.24), followed by cytotoxic therapy (7.14; 2.68), targeted therapy (5.83; 2.40), and hormone therapy (2.59; 1.24) for AKI, and by cytotoxic therapy (2.60; 1.21) and targeted therapy (1.54; 0.61) for TIN. AKI and TIN were more prevalent among individuals under 45 years of age, with a female preponderance for AKI and males for TIN. These events were reported in close temporal relationship after initiation of the respective drug (16.53 days for AKI and 27.97 days for TIN), and exhibited a high fatality rate, with 23.6% for AKI and 16.3% for TIN. These findings underscore that kidney-related adverse drug reactions are of prognostic significance and strategies to mitigate such side effects are required to optimize anticancer therapy.
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| S-EPMC7335961 | biostudies-literature
Project description:Glucagon-like peptide 1 receptor agonists (GLP-1RAs) are being investigated to slow the decline of kidney function in type 2 diabetics with chronic kidney disease (CKD). These agents have proven benefits on cardiac outcomes and all-cause mortality as well as in reducing the incidence of macroalbuminuria. Ours is a case of drug-associated acute interstitial nephritis requiring hemodialysis temporally related to a semaglutide dose increase. This case is unique as the index patient had no underlying CKD. Limited cases of acute kidney injury, superimposed on underlying CKD, in patients taking the GLP-1RA semaglutide have been reported. To our knowledge, there are no existing case reports in the literature of GLP-1RA-associated acute interstitial nephritis in a patient with baseline normal kidney function. Because our prescription of these agents is increasing and is anticipated to increase further with growing scientific evidence for their benefit, we sought to highlight this possible, important serious adverse effect of semaglutide.
| S-EPMC9719074 | biostudies-literature
Project description:BACKGROUND:Injured patients are at risk of developing acute kidney injury (AKI), which is associated with increased morbidity and mortality. The aim of this study is to describe the incidence, timing, and severity of AKI in a large trauma population, identify risk factors for AKI, and report mortality outcomes. METHODS:A prospective observational study of injured adults, who met local criteria for trauma team activation, and were admitted to a UK Major Trauma Centre. AKI was defined by the Kidney Disease Improving Global Outcomes (KDIGO) criteria. Multivariable logistic regression and Cox proportional hazard modelling was used to analyse parameters associated with AKI and mortality. RESULTS:Of the 1410 patients enrolled in the study, 178 (12.6%) developed AKI. Age; injury severity score (ISS); admission systolic blood pressure, lactate and serum creatinine; units of Packed Red Blood Cells transfused in first 24 hours and administration of nephrotoxic therapy were identified as independent risk factors for the development of AKI. Patients that developed AKI had significantly higher mortality than those with normal renal function (47/178 [26.4%] versus 128/1232 [10.4%]; OR 3.09 [2.12 to 4.53]; p<0.0001). After adjusting for other clinical prognostic factors, AKI was an independent risk factor for mortality. CONCLUSIONS:AKI is a frequent complication following trauma and is associated with prolonged hospital length of stay and increased mortality. Future research is needed to improve our ability to rapidly identify those at risk of AKI, and develop resuscitation strategies that preserve renal function in trauma patients.
| S-EPMC6347290 | biostudies-literature
Project description:Recently, the usefulness of serum uromodulin (sUmod) as a novel renal biomarker has been attracting attention. Clinical evidence regarding sUmod measurements has been accumulated by analyzing cross-sectional data. However, little is known about the longitudinal data on sUmod. Therefore, we decided to investigate the variability of sUmod in patients with acute kidney injury due to different causes. High concentrations of sUmod have been observed in patients with acute tubular injury (ATI) and/or acute interstitial nephritis (AIN). sUmod could be used as an auxiliary diagnostic tool for ATI and AIN.
| S-EPMC9743145 | biostudies-literature
Project description:IntroductionColistin is used to treat severe antibiotic-resistant Gram-negative infections (GNIs). With the rise of antibiotic resistance, colistin has been used increasingly as a 'last-line' therapy for multidrug-resistant GNIs. We evaluated the incidence of acute kidney injury (AKI) and mortality among patients receiving colistin or one of the new β-lactam/β-lactamase inhibitors (βL + βLI) (ceftazidime/avibactam, ceftolozane/tazobactam, or meropenem/vaborbactam).MethodsThis retrospective cohort study used data from the Premier Healthcare Database. The cohort included propensity score-matched adults with an inpatient stay between January 2016 and December 2018. Patients given both colistin and BL + BLI as treatment for ≥ 72 h were excluded. AKI was defined as acute renal failure or dialysis during hospitalization with antibiotic administration. Propensity score matching was used to control for selection bias and confounding. Logistic regression evaluated associations between treatment, AKI, and in-hospital mortality.ResultsThe total number of patients in the matched cohorts were 256 in each. Overall, 23.8% and 13.3% of patients receiving colistin or new βL + βLI agents, respectively, experienced AKI during hospitalization (p = 0.002); odds of AKI for colistin were 3.0 (95% CI 1.71, 5.21). Following propensity score-matching, patients without baseline renal disease experienced AKI during hospitalization to a higher degree in the colistin group compared to the βL + βLI group (17.1% vs. 6.8%); colistin use was associated with 3.7 times higher odds (95% CI 1.84, 7.42) of AKI compared to βL + βLI agents. The odds of mortality in patients on colistin developing AKI were more than three times that of patients receiving a BL + BLI agent who developed AKI. Among patients receiving colistin, incident AKI was associated with 6.1 times higher odds (95% CI 2.53, 14.71) of mortality.ConclusionsPatients receiving colistin for GNIs had significantly higher odds of AKI and mortality than those receiving βL + βLI.
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