scholarly journals Amoxicillin‐induced crystal nephropathy: A nationwide French pharmacovigilance databases study

2020 ◽  
Vol 86 (11) ◽  
pp. 2256-2265 ◽  
Author(s):  
Laure Thomas ◽  
Christine Le Beller ◽  
Thierry Trenque ◽  
Joëlle Michot ◽  
Marie Zenut ◽  
...  
Keyword(s):  
Crystal Nephropathy

scholarly journals Only Hyperuricemia with Crystalluria, but not Asymptomatic Hyperuricemia, Drives Progression of Chronic Kidney Disease

2020 ◽  
Vol 31 (12) ◽  
pp. 2773-2792
Author(s):  
Markus Sellmayr ◽  
Moritz Roman Hernandez Petzsche ◽  
Qiuyue Ma ◽  
Nils Krüger ◽  
Helen Liapis ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Aristolochic Acid ◽  
Interstitial Fibrosis ◽  
Ckd Progression ◽  
Fticr Mass Spectrometry ◽  
Progressive Decline ◽  
Granulomatous Interstitial Nephritis ◽  
Crystal Nephropathy ◽  
Aristolochic Acid I

BackgroundThe roles of asymptomatic hyperuricemia or uric acid (UA) crystals in CKD progression are unknown. Hypotheses to explain links between UA deposition and progression of CKD include that (1) asymptomatic hyperuricemia does not promote CKD progression unless UA crystallizes in the kidney; (2) UA crystal granulomas may form due to pre-existing CKD; and (3) proinflammatory granuloma-related M1-like macrophages may drive UA crystal-induced CKD progression.MethodsMALDI-FTICR mass spectrometry, immunohistochemistry, 3D confocal microscopy, and flow cytometry were used to characterize a novel mouse model of hyperuricemia and chronic UA crystal nephropathy with granulomatous nephritis. Interventional studies probed the role of crystal-induced inflammation and macrophages in the pathology of progressive CKD.ResultsAsymptomatic hyperuricemia alone did not cause CKD or drive the progression of aristolochic acid I-induced CKD. Only hyperuricemia with UA crystalluria due to urinary acidification caused tubular obstruction, inflammation, and interstitial fibrosis. UA crystal granulomas surrounded by proinflammatory M1-like macrophages developed late in this process of chronic UA crystal nephropathy and contributed to the progression of pre-existing CKD. Suppressing M1-like macrophages with adenosine attenuated granulomatous nephritis and the progressive decline in GFR. In contrast, inhibiting the JAK/STAT inflammatory pathway with tofacitinib was not renoprotective.ConclusionsAsymptomatic hyperuricemia does not affect CKD progression unless UA crystallizes in the kidney. UA crystal granulomas develop late in chronic UA crystal nephropathy and contribute to CKD progression because UA crystals trigger M1-like macrophage-related interstitial inflammation and fibrosis. Targeting proinflammatory macrophages, but not JAK/STAT signaling, can attenuate granulomatous interstitial nephritis.

Acute Methotrexate-Induced Crystal Nephropathy

2015 ◽  
Vol 373 (27) ◽  
pp. 2691-2693 ◽  
Author(s):  
Alexandre P. Garneau ◽  
Julie Riopel ◽  
Paul Isenring
Keyword(s):  
Crystal Nephropathy

Crystal nephropathy and amoxicillin: insights from international spontaneous reporting systems

2021 ◽  
Author(s):  
Milo Gatti ◽  
Michele Fusaroli ◽  
Emanuel Raschi ◽  
Irene Capelli ◽  
Elisabetta Poluzzi ◽  
...  
Keyword(s):  
Spontaneous Reporting ◽  
Crystal Nephropathy ◽  
Reporting Systems

Acute sulfamethoxazole-induced crystal nephropathy

2018 ◽  
Vol 44 (9) ◽  
pp. 1575-1576 ◽  
Author(s):  
Nina de Montmollin ◽  
Emmanuel Letavernier ◽  
Muriel Fartoukh ◽  
Vincent Labbe
Keyword(s):  
Crystal Nephropathy

scholarly journals High Incidence of Amoxicillin-Induced Crystal Nephropathy in Patients Receiving High Dose of Intravenous Amoxicillin

2020 ◽  
Vol 9 (7) ◽  
pp. 2022 ◽  
Author(s):  
Anne-Sophie Garnier ◽  
Juliette Dellamaggiore ◽  
Benoit Brilland ◽  
Laurence Lagarce ◽  
Pierre Abgueguen ◽  
...  
Keyword(s):  
Rare Complication ◽  
Kidney Injury ◽  
Female Gender ◽  
Primary Objective ◽  
University Hospital ◽  
High Dose ◽  
Medical Reason ◽  
Crystal Nephropathy ◽  
Increased Risk ◽  
High Incidence

Background: Amoxicillin (AMX)-induced crystal nephropathy (AICN) is considered as a rare complication of high dose intravenous (IV) AMX administration. However, recently, its incidence seems to be increasing based on French pharmacovigilance centers. Occurrence of AICN has been observed mainly with IV administration of AMX and mostly under doses over 8 g/day. Given that pharmacovigilance data are based on declaration, the real incidence of AICN may be underestimated. Thus, the primary objective of the present study was to determine the incidence of AICN in the current practice. Materials and Methods: We conducted a retrospective study between 1 January 2015 and 31 December 2017 in Angers University Hospital. Inclusion criteria were age over 18 years-old and IV AMX administration of at least 8 g/day for more than 24 h. Patients admitted directly into the intensive care units were excluded. Medical records of patients that developed Kidney Disease:Improving Global Outcome (KDIGO) stage 2–3 acute kidney injury (AKI) were reviewed by a nephrologist and a specialist in pharmacovigilance. AICN was retained if temporality analysis was conclusive, after exclusion of other causes of AKI, in absence of other nephrotoxic drug administration. Results: A total of 1303 patients received IV AMX for at least 24 h. Among them, 358 (27.5%) were exposed to AMX doses of at least 8 g/day and were included. Patients were predominantly males (68.2%) with a mean age of 69.1 years-old. AMX was administered for a medical reason in 78.5% of cases. Patients received a median dose of AMX of 12 g/day (152.0 mg/kg/day). Seventy-three patients (20.4%) developed AKI, 42 (56.8%) of which were KDIGO stage 2 or 3. Among the latter, AICN diagnosis was retained in 16 (38.1%) patients, representing an incidence of 4.47% of total patients exposed to high IV AMX doses. Only female gender was associated with an increased risk of AICN. AMX dose was not significantly associated with AICN development. Conclusion: This study suggests a high incidence of AICN in patients receiving high IV AMX doses, representing one third of AKI causes in our study. Female gender appeared as the sole risk factor for AICN in this study.

Drug-induced crystal nephropathy: an update

2008 ◽  
Vol 7 (2) ◽  
pp. 147-158 ◽  
Author(s):  
Sri G Yarlagadda ◽  
Mark A Perazella
Keyword(s):  
Drug Induced ◽  
Crystal Nephropathy

scholarly journals Intravenous hydroxocobalamin and crystal nephropathy

2017 ◽  
Vol 13 (9) ◽  
pp. 593-593 ◽  
Author(s):  
Matthieu Legrand ◽  
Vincent Mallet
Keyword(s):  
Crystal Nephropathy

scholarly journals A rare case of acute kidney injury due to levofloxacin-induced crystal nephropathy

2019 ◽  
Vol 29 (6) ◽  
pp. 424 ◽  
Author(s):  
SreeBhushan Raju ◽  
FaizanAhmed Ansari ◽  
Sonu Manuel ◽  
Rohan Dwivedi ◽  
ShashikiranKabbare Boraiah ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Rare Case ◽  
Kidney Injury ◽  
Crystal Nephropathy

Antiviral Drugs and Acute Kidney Injury (AKI)

2019 ◽  
Vol 19 (4) ◽  
pp. 375-382 ◽  
Author(s):  
Wattana Leowattana
Keyword(s):  
Acute Kidney Injury ◽  
Antiviral Drug ◽  
Kidney Injury ◽  
Rapid Onset ◽  
Antiviral Drugs ◽  
Drug Induced ◽  
Common Cause ◽  
True Prevalence ◽  
Tubular Necrosis ◽  
Crystal Nephropathy

The introduction of more efficient antiviral drugs are common cause drug-induced acute kidney injury (AKI). The true prevalence of antiviral drugs induced nephrotoxicity is hardly determined. It causes AKI by many mechanisms including acute tubular necrosis (ATN), allergic interstitial nephritis (AIN), and crystal nephropathy. ATN has been described with a few kinds of antiviral drugs such as cidofovir, adefovir and tenofovir with unique effects on transporter defects, apoptosis, and mitochondrial injury. AIN from atazanavir is a rapid onset of AKI and usually nonoliguric but dialytic therapy are needed because of severity. Additionally, crystal nephropathy from acyclovir, indinavir, and foscarnet can cause AKI due to intratubular obstruction. In this article, the mechanisms of antiviral drug-induced AKI were reviewed and strategies for preventing AKI were mentioned.

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