Quinine-Induced Thrombotic Microangiopathy: A Report of 19 Patients

Page, Evaren E.; Little, Dustin J.; Vesely, Sara K.; George, James N.

doi:10.1053/j.ajkd.2017.05.023

Cited by 33 publications

(23 citation statements)

References 33 publications

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“…While there is no established direct causal relationship between the two, there are multiple case reports that document the occurrence of TMA in patients with malaria; P. vivax infection, in particular [25][26][27][28]. Alternatively, there have also been documented cases of renal impairment due to TMA caused by treatment with antimalarial agents such as mefloquine and quinine agents [25,29]. It has been suggested that quinine dependent antibodies reacting with platelets and other cells contribute to quinine induced TMA [29].…”

Section: Pathogenesis Of Malarial Akimentioning

confidence: 99%

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Malaria and acute kidney injury

et al. 2019

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Malaria is a parasitic infection transmitted by mosquitos, resulting in significant morbidity and mortality. It affects 212 million worldwide, causing death in up to 303,000 children annually. In the USA, up to 1700 people are affected yearly. Although the prevalence in developed countries is less than in developing countries, travelers from low transmission areas, and those from endemic areas who later return, are very susceptible to malaria and its complications. Severe malaria can cause significant multiorgan dysfunction including acute kidney injury (AKI). The pathogenesis is not clearly understood but proposed mechanisms include acute tubular necrosis (ATN) due to impediments in renal microcirculation, infection-triggered proinflammatory reactions within the kidney, and metabolic disturbances. Providers must consider malarial infection in cases of AKI in someone with a travel history, as early recognition and treatment are crucial to improving outcomes. This article will review malariainduced AKI in order to provide a better understanding of this infection's effect on the kidneys.

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Section: Pathogenesis Of Malarial Akimentioning

confidence: 99%

“…Alternatively, there have also been documented cases of renal impairment due to TMA caused by treatment with antimalarial agents such as mefloquine and quinine agents [25,29]. It has been suggested that quinine dependent antibodies reacting with platelets and other cells contribute to quinine induced TMA [29].…”

Section: Pathogenesis Of Malarial Akimentioning

confidence: 99%

Malaria and acute kidney injury

et al. 2019

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“…However, quinine itself is also known to affect the kidney through immune-mediated reactions including drug-induced TMA [ 13 ]. In one case series of 19 people with confirmed quinine-induced TMA, each person experienced AKI without pre-existing CKD, one individual died and 17 of the remaining 18 required dialysis, three of whom required RRT indefinitely [ 16 ]. Although this infrequent acute syndrome is unlikely to confer risk of AKI at a population level, the mechanism of a quinine-dependant antibody reaction could be considered.…”

Section: Discussionmentioning

confidence: 99%

“…Quinine-induced TMA is thought to be mediated by antibodies that, in the presence of quinine, target antigens on neutrophils and platelets [ 15 ]. Although TMA is an uncommon adverse drug reaction, quinine-induced TMA can be life-threatening with up to 90% of individuals requiring dialysis [ 16 ]. Despite leg cramps sharing a number of common risk factors with AKI, and quinine itself known to affect the kidney by rare immune-mediated reactions, the relationship between cramps, quinine and AKI at a population level is unclear.…”

Section: Introductionmentioning

confidence: 99%

Quinine exposure and the risk of acute kidney injury: a population-based observational study of older people

et al. 2020

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Objectives to establish and quantify any observable association between the exposure to community prescriptions for quinine and acute kidney injury (AKI) events in a population of older adults. Design two observational studies using the same dataset, a retrospective longitudinal cohort study and a self-controlled case series (SCCS). Setting NHS health board in Scotland. Participants older adults (60+ years) who received quinine prescriptions in Tayside, Scotland, between January 2004 and December 2015. The first study included 12,744 individuals. The SCCS cohort included 5,907 people with quinine exposure and more than or equal to one AKI event. Main outcome measured in the first study, multivariable logistic regression was used to calculate odds ratios (ORs) for AKI comparing between episodes with and without recent quinine exposure after adjustment for demographics, comorbidities and concomitant medications. The SCCS study divided follow-up for each individual into periods ‘on’ and ‘off’ quinine, calculating incidence rate ratios (IRRs) for AKI adjusting for age. Results during the study period, 273,596 prescriptions for quinine were dispensed in Tayside. A total of 13,616 AKI events occurred during follow-up (crude incidence 12.5 per 100 person-years). In the first study, exposure to quinine before an episode of care was significantly associated with an increased probability of AKI (adjusted OR = 1.27, 95% confidence interval (CI) 1.21–1.33). In the SCCS study, exposure to quinine was associated with an increased relative incidence of AKI compared to unexposed periods (IRR = 1.20, 95% CI 1.15–1.26), with the greatest risk observed within 30 days following quinine initiation (IRR = 1.48, 95% CI 1.35–1.61). Conclusion community prescriptions for quinine in an older adult population are associated with an increased risk of AKI.

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“…In typical immune-mediated DITMA, symptoms occur within 21 days of initiation of a drug taken daily, or within 24 hours of exposure to a drug administered intermittently. [ 4 , 18 ] Ticlopidine, an antiplatelet drug of the thienopyridine family, is a common cause of immune-mediated DITMA. However, the time from drug exposure to onset of symptoms could be as long as 2 months for ticlopidine.…”

Section: Discussionmentioning

confidence: 99%

Ticagrelor-induced thrombotic thrombocytopenic purpura

Wang

Zhang²,

Li³

et al. 2018

Medicine

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Rationale:Ticagrelor, a new type of P2Y12 receptor antagonist, has been highly recommended to be used in acute coronary syndrome by the latest guideline, but its side effects are not well-known. We seek to illustrate a potential fatal condition, thrombotic thrombocytopenic purpura (TTP), caused by ticagrelor.Patient concerns:An 87-year-old man who had been prescribed with ticagrelor for 2 months after ST-elevation myocardial infarction (STEMI), presented with severe thrombocytopenia, anemia, renal and liver dysfunction, heart failure and fever.Diagnoses:Peripheral blood smear showed schistocytosis, and a disintegrin and metalloproteinase with thrombospondin motifs 13 (ADAMTS13) activity is low, with normal initial coagulation tests, which were compatible with a diagnosis of TTP.Interventions:After cessation of ticagrelor and initiation of therapeutic plasma exchange, our patient recovered.Outcomes:Re-administration of ticagrelor aggravated TTP and led the patient to death.Lessons:Clinicians should be aware of the possibility of ticagrelor-induced TTP in patients with a history of recent myocardial infarction; It is of crucial significance to discontinue and never reuse ticagrelor as long as it is suspected to be implicated in TTP.

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Quinine-Induced Thrombotic Microangiopathy: A Report of 19 Patients

Cited by 33 publications

References 33 publications

Malaria and acute kidney injury

Malaria and acute kidney injury

Quinine exposure and the risk of acute kidney injury: a population-based observational study of older people

Ticagrelor-induced thrombotic thrombocytopenic purpura

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