scholarly journals Drug-Induced Acute Kidney Injury: A Study from the French Medical Administrative and the French National Pharmacovigilance Databases Using Capture-Recapture Method

2021 ◽  
Vol 10 (2) ◽  
pp. 168
Author(s):  
Anne-Lise Rolland ◽  
Anne-Sophie Garnier ◽  
Katy Meunier ◽  
Guillaume Drablier ◽  
Marie Briet
Keyword(s):  
Acute Kidney Injury ◽  
Medical Information ◽  
Significant Proportion ◽  
Kidney Injury ◽  
International Classification Of Diseases ◽  
Administrative Databases ◽  
Health Concern ◽  
Medical Information System ◽  
Drug Induced ◽  
Capture Recapture

Background: Acute kidney injury (AKI) is a public health concern. Among the pathological situations leading to AKI, drugs are preventable factors but are still under-notified. We aimed to provide an overview of drug-induced AKI (DIAKI) using pharmacovigilance and medical administrative databases Methods: A query of the PMSI database (French Medical Information System Program) of adult inpatient hospital stays between 1 January 2017 and 31 December 2018 was performed using ICD-10 (International Classification of Diseases 10th revision) codes to identify AKI cases which were reviewed by a nephrologist and a pharmacovigilance expert to identify DIAKI cases. In parallel, DIAKIs notified in the French Pharmacovigilance Database (FPVDB) were collected. A capture-recapture method was performed to estimate the total number of DIAKIs. Results: The estimated total number of DIAKIs was 521 (95%CI 480; 563), representing 20.0% of all AKIs. The notification was at a rate of 12.9% (95%CI 10.0; 15.8). According to the KDIGO classification, 50.2% of the DIAKI cases were stage 1 and 49.8% stage 2 and 3. The mortality rate was 11.1% and 9.6% required hemodialysis. Conclusion: This study showed that drugs are involved in a significant proportion of patients developing AKI during a hospital stay and emphasizes the severity of DIAKI cases.

Serial Quantification of Urinary Protein Biomarkers to Predict Drug-induced Acute Kidney Injury

2019 ◽  
Vol 20 (8) ◽  
pp. 656-664 ◽  
Author(s):  
Yi Da ◽  
K. Akalya ◽  
Tanusya Murali ◽  
Anantharaman Vathsala ◽  
Chuen-Seng Tan ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cystatin C ◽  
Calcineurin Inhibitors ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Renal Tubular Dysfunction ◽  
Protein Biomarkers ◽  
Drug Induced ◽  
Beta 2 ◽  
Beta 2 Microglobulin

Background: : Drug-induced Acute Kidney Injury (AKI) develops in 10-15% of patients who receive nephrotoxic medications. Urinary biomarkers of renal tubular dysfunction may detect nephrotoxicity early and predict AKI. Methods:: We prospectively studied patients who received aminoglycosides, vancomycin, amphotericin, or calcineurin inhibitors, and collected their serial urine while on therapy. Patients who developed drug-induced AKI (fulfilling KDIGO criteria) were matched with non-AKI controls in a 1:2 ratio. Their urine samples were batch-analyzed at time-intervals leading up to AKI onset; the latter benchmarked against the final day of nephrotoxic therapy in non- AKI controls. Biomarkers examined include clusterin, beta-2-microglobulin, KIM1, MCP1, cystatin-C, trefoil-factor- 3, NGAL, interleukin-18, GST-Pi, calbindin, and osteopontin; biomarkers were normalized with corresponding urine creatinine. Results:: Nine of 84 (11%) patients developed drug-induced AKI. Biomarkers from 7 AKI cases with pre-AKI samples were compared with those from 14 non-AKI controls. Corresponding mean ages were 55(±17) and 52(±16) years; baseline eGFR were 99(±21) and 101(±24) mL/min/1.73m2 (all p=NS). Most biomarker levels peaked before the onset of AKI. Median levels of 5 biomarkers were significantly higher in AKI cases than controls at 1-3 days before AKI onset (all µg/mmol): clusterin [58(8-411) versus 7(3-17)], beta-2-microglobulin [1632(913-3823) versus 253(61-791)], KIM1 [0.16(0.13-0.76) versus 0.07(0.05-0.15)], MCP1 [0.40(0.16-1.90) versus 0.07(0.04-0.17)], and cystatin-C [33(27-2990) versus 11(7-19)], all p<0.05; their AUROC for AKI prediction were >0.80 (confidence intervals >0.50), with average accuracy highest for clusterin (86%), followed by beta-2-microglobulin, cystatin-C, MCP1, and KIM1 (57%) after cross-validation. Conclusion: : Serial surveillance of these biomarkers could improve the lead time for nephrotoxicity detection by days.

Biomarkers of drug-induced acute kidney injury in the adult

2015 ◽  
Vol 11 (11) ◽  
pp. 1683-1694 ◽  
Author(s):  
Glenda C Gobe ◽  
Jeff S Coombes ◽  
Robert G Fassett ◽  
Zoltan H Endre
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Drug Induced

Metabolomic profiling of urine-derived extracellular vesicles from rat model of drug-induced acute kidney injury

2021 ◽  
Vol 546 ◽  
pp. 103-110
Author(s):  
Masayoshi Saito ◽  
Satoshi Horie ◽  
Hidenori Yasuhara ◽  
Akane Kashimura ◽  
Eiji Sugiyama ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Extracellular Vesicles ◽  
Rat Model ◽  
Kidney Injury ◽  
Drug Induced ◽  
Metabolomic Profiling

Evaluation of the usefulness of novel biomarkers for drug-induced acute kidney injury in beagle dogs

2014 ◽  
Vol 280 (1) ◽  
pp. 30-35 ◽  
Author(s):  
Xiaobing Zhou ◽  
Ben Ma ◽  
Zhi Lin ◽  
Zhe Qu ◽  
Yan Huo ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Beagle Dogs ◽  
Drug Induced ◽  
Novel Biomarkers

Drug-induced acute kidney injury

2007 ◽  
Vol &NA; (245) ◽  
pp. 939-942
Author(s):  
Gayathri K Rajakaruna ◽  
Tehreem F Butt
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Drug Induced

scholarly journals Immunopathogenesis of Acute Kidney Injury

2018 ◽  
Vol 46 (8) ◽  
pp. 930-943 ◽  
Author(s):  
Zaher A. Radi
Keyword(s):  
Acute Kidney Injury ◽  
T Cells ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Drug Induced ◽  
Inflammatory Damage ◽  
Anti Inflammatory ◽  
Renal Tubular ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Pathophysiologically, the classification of acute kidney injury (AKI) can be divided into three categories: (1) prerenal, (2) intrinsic, and (3) postrenal. Emerging evidence supports the involvement of renal tubular epithelial cells and the innate and adaptive arms of the immune system in the pathogenesis of intrinsic AKI. Pro-inflammatory damage-associated molecular patterns, pathogen-associated molecular patterns, hypoxia inducible factors, toll-like receptors, complement system, oxidative stress, adhesion molecules, cell death, resident renal dendritic cells, neutrophils, T and B lymphocytes, macrophages, natural killer T cells, cytokines, and secreted chemokines contribute to the immunopathogenesis of AKI. However, other immune cells and pathways such as M2 macrophages, regulatory T cells, progranulin, and autophagy exhibit anti-inflammatory properties and facilitate kidney tissue repair after AKI. Thus, therapies for AKI include agents such as anti-inflammatory (e.g., recombinant alkaline phosphatase), antioxidants (iron chelators), and apoptosis inhibitors. In preclinical toxicity studies, drug-induced kidney injury can be seen after exposure to a nephrotoxicant test article due to immune mechanisms and dysregulation of innate, and/or adaptive cellular immunity. The focus of this review will be on intrinsic AKI, as it relates to the immune and renal systems cross talks focusing on the cellular and pathophysiologic mechanisms of AKI.

Drug-Induced Kidney Disease Associated With Selected Antibiotics

2020 ◽  
Vol 35 (5) ◽  
pp. 225-229
Author(s):  
Alexia S. Alvarez ◽  
Oluseyi Oyerinde ◽  
Justin P. Reinert
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Older People ◽  
Hospital Costs ◽  
Kidney Injury ◽  
Clear Understanding ◽  
First Line ◽  
Drug Induced ◽  
Improved Outcomes ◽  
Hospital Stays

Structural and functional degeneration of the kidneys occur as the human body ages, making oler people especially susceptible to the consequences of acute kidney injury. Furthermore, the use of nephrotoxic agents, combined with the increased incidence of acute kidney injury and likelihood of an intensive-care unit admission, makes geriatric patients prone to develop drug-induced kidney disease. Vancomycin is routinely used as the first-line treatment for methicillin-resistant Staphylococcus aureus, but is known to be nephrotoxic; studies have shown that an early switch from vancomycin to alternatives does not necessarily prevent renal insult. Therefore, we aim to discuss the mechanisms of drug-induced kidney disease with regard to vancomycin, daptomycin, and ceftaroline and to provide insight as to their safety profiles with regard to older people. A clear understanding of this topic will aid clinicians in selecting drug therapy and may lead to shortened hospital stays, lower hospital costs, and improved outcomes of critically ill older people.

scholarly journals Acute Kidney Injury and In-Hospital Mortality: A Retrospective Analysis of a Nationwide Administrative Database of Elderly Subjects in Italy

2019 ◽  
Vol 8 (9) ◽  
pp. 1371 ◽  
Author(s):  
Fabbian ◽  
Savriè ◽  
De Giorgi ◽  
Cappadona ◽  
Di Simone ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Hospital Mortality ◽  
Kidney Injury ◽  
International Classification Of Diseases ◽  
Administrative Database ◽  
Elderly Subjects ◽  
Dialysis Treatment ◽  
The Third ◽  
Classification Of Diseases

Background: The aim of this study was to investigate the association between acute kidney injury (AKI) and in-hospital mortality (IHM) in a large nationwide cohort of elderly subjects in Italy. Methods: We analyzed the hospitalization data of all patients aged ≥65 years, who were discharged with a diagnosis of AKI, which was identified by the presence of the International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM), and extracted from the Italian Health Ministry database (January 2000 to December 2015). Data regarding age, gender, dialysis treatment, and comorbidity, including the development of sepsis, were also collected. Results: We evaluated 760,664 hospitalizations, the mean age was 80.5 ± 7.8 years, males represented 52.2% of the population, and 9% underwent dialysis treatment. IHM was 27.7% (210,661 admissions): Deceased patients were more likely to be older, undergoing dialysis treatment, and to be sicker than the survivors. The population was classified on the basis of tertiles of comorbidity score (the first group 7.48 ± 1.99, the second 13.67 ± 2,04, and third 22.12 ± 4.13). IHM was higher in the third tertile, whilst dialysis-dependent AKI was highest in the first. Dialysis-dependent AKI was associated with an odds ratios (OR) of 2.721; 95% confidence interval (CI) 2.676–2.766; p < 0.001, development of sepsis was associated with an OR of 1.990; 95% CI 1.948–2.033; p < 0.001, the second tertile of comorbidity was associated with an OR of 1.750; 95% CI 1.726–1.774; p < 0.001, and the third tertile of comorbidity was associated with an OR of 2.522; 95% CI 2.486–2.559; p < 0.001. Conclusions: In elderly subjects with AKI discharge codes, IHM is a frequent complication affecting more than a quarter of the investigated population. The increasing burden of comorbidity, dialysis-dependent AKI, and sepsis are the major risk factors.

scholarly journals Drug-induced acute kidney injury

2019 ◽  
Vol 25 (6) ◽  
pp. 550-557 ◽  
Author(s):  
Mark A. Perazella
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Drug Induced

scholarly journals P0475CRESCENTIC GLOMERULONEPHRITIS FOLLOWING HCV TREATMENT WITH DAAS, THE NON-CLASSIC TALE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Mohamed Elrggal ◽  
Mariam Emam ◽  
Wesam Ismail
Keyword(s):  
Acute Kidney Injury ◽  
Serum Creatinine ◽  
Sustained Viral Response ◽  
Kidney Injury ◽  
Small Vessel ◽  
Small Vessel Vasculitis ◽  
Hcv Treatment ◽  
Drug Induced ◽  
First Case ◽  
Necrotizing Glomerulonephritis

Abstract Background and Aims Observational studies suggest that acute kidney injury may occur in up to 15% of patients treated with sofosbuvir based regimens. Histological findings show features of acute interstitial nephritis (AIN) or acute tubular necrosis (ATN). Here, we report the first case of small vessel vasculitis following sofosbuvir treatment. Method A 65-year-old female with controlled T2DM was recently diagnosed with HCV. She attained sustained viral response (SVR) after a three-month course of (sofosbuvir + daclatasvir + ribavirin). Kidney functions were normal pre and post treatment. Three months later, she presented with puffiness, bilateral lower extremities edema (no rash) and vomiting. Labs showed acute kidney injury (AKI), nephrotic proteinuria and haematuria (table 1). Immunological investigations (C3, C4, ANA, ANCA and anti-GBM), paraproteinemia workup and cryoglobulins were all negative. Renal US was also normal. Kidney biopsy revealed focal necrotizing glomerulonephritis with 70% crescents (figure 3,4). No chronic changes were detected in the glomeruli, interstitium or tubules. The patient received pulse methylprednisolone 0.5 gm for 3 days followed by oral prednisolone 60 mg/day. Oral cyclophosphamide was initiated at 150 mg after biopsy result was obtained. Our patient showed clinical and laboratory improvement (figure 1,2), however, she developed bone marrow suppression that required cessation of cyclophosphamide. Valsartan initiated to control proteinuria with slight increase in serum creatinine to 1.4 mg/dl. The patient is still under close follow up every two weeks, with a plan to introduce rituximab if serum creatinine continued to increase. Results AKI following HCV treatment with DAA has been reported. Explanation includes AIN, ATN and cryoglobulinemic vasculitis (CV). AIN and ATN usually occur during the treatment course, which is not the case in our patient as she developed AKI three months following the end of the treatment, and the biopsy did not show signs of either ATN or AIN. New onset CV has been reported previously in 3 case reports following SVR after DAA treatment. Previous reports explained that HCV can induce B-cell clonal proliferation that may persist independent of viral eradication and produce IgM kappa which will result in cryoglobulinemic GN, again this is not true in our case. Our patient did not have a rash, her serum cryoglobulin was negative and complement levels (C3 and C4) were normal and biopsy did not show evidence of CV. As far as we know, this is the first case with suspected sofosbuvir associated small vessel vasculitis to be reported. Despite the patient had a negative serum ANCA levels, we suspect that this is a case of drug induced vasculitis. Drug induced vasculitis has been reported with hydralazine, propylthiouracil and cocaine, none of these drugs were used in our case. Also, there is no reported case of vasculitis associated with ribavirin or daclatasvir. Thus, we suspect Sofosbuvir is the cause of drug induced vasculitis in this patient. Conclusion Crescentic GN following HCV treatment using DAA is a serious complication that should be promptly diagnosed and managed. Physicians treating HCV infected patients should be aware of this possible complication and monitor for kidney function even after achieving SVR.

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