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In this article, we present a case of Plasmodium falciparum malaria in a male patient who developed acute kidney injury during antimalarial treatment. A 38-years-old Turkish male patient was admitted to the emergency department with the complaints of fever and chills. The patient stated that he had no chronic illness, his complaints had started four days ago, and he had returned from Guinea 10 days ago. Multiple ring-shaped P. falciparum trophozoites were observed in Giemsa-stained thin blood smears, which were evaluated with a preliminary diagnosis of malaria due to travel history and clinical findings. Artemeter + Lumefantrine supplied by the provincial health directorate on the same night was administered according to the manufacturer's recommended dose posology. On the third day of clinical follow-up, clinical, vital and peripheric smear findings continued to improve, while laboratory tests showed an acute increase in creatinine values, which is a signs of acute kidney injury. The patient's creatinine values returned to normal on the sixth day with appropriate intravenous hydration. Keeping in mind that acute kidney injury can develop not only prior to treatment but also during the treatment period when patients receive antimalarial treatment, therefore, proper hydration and close monitoring of kidney functions during treatment are also important. [ABSTRACT FROM AUTHOR]

Background: Because of their similar modes of transmission, the simultaneous infection of viral hepatitis and human immunodeficiency virus are increasingly seen as a big problem related to human health. Aims: To determine the drug mutations in hepatitis B virus and/ or hepatitis C virus co-infected human immunodeficiency virus-1 patients in Turkey. Study Design: Retrospective cross-sectional study. Methods: The present study was conducted between 2010 and 2017. HBsAg, anti-hepatitis C virus, and anti-human immunodeficiency virus were tested with ELISA. All anti-human immunodeficiency virus positive results by ELISA were verified for anti-human immunodeficiency virus positivity by a Western blot test, and Antihuman immunodeficiency virus positive patients with HBsAg and/or anti-hepatitis C virus positivity were included in the study. Subtyping and genotypic resistance analyses were performed by population sequencing of the viral protease and reverse transcriptase regions of the human immunodeficiency virus-1 pol gene. Results: We detected 3896 human immunodeficiency virus-1 positive patients whose sera were sent from numerous hospitals across the country to our polymerase chain reaction unit for detection of drug resistance mutations and whose molecular laboratory tests were completed. Viral hepatitis co-infections were detected in 4.3% (n=170) of patients. Hepatitis B virus and hepatitis C virus co-infection were observed in 3.2% and 0.5% of all human immunodeficiency virus-1 infected patients, respectively. The major human immunodeficiency virus-1 subtype detected was group M, subtype B (62.9%). However, 13.5% of drug resistance mutation motifs were found in human immunodeficiency virus-1 genomes of patients included in the study. Conclusion: Due to similar transmission routes, HIV1 patients are at risk of hepatitis B and C virus co-infection. However, antiretroviral drug resistance mutation model is similar to patients with hepatitis negative. [ABSTRACT FROM AUTHOR]

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