The incidence of acute kidney injury (AKI) in infective endocarditis (IE), its risk factors and consequences on patient and renal survival remain debated. Methods: Patients hospitalized for a first episode of IE (possible or definite according to modified Duke criteria) between 2013 and 2016 were included. The primary endpoint was to determine risk factors for early AKI (E-AKI) during the first week of management of IE. Results: A total of 276 patients were included: 220 (79.7%) had definite IE and 56 (20.3%) had possible IE. E-AKI occurred in 150 patients (53%). IE due to Staphylococcus aureus (OR 3.41; 95% CI 1.83-6.39; p < 0.01), history of diabetes (OR 2.34; 95% CI 1.25-4.37; p < 0.01), peripheral arterial disease (OR 2.59; 95% CI 1.07-6.23; p < 0.05), immunological manifestations (OR 3.11; 95% CI 1.31-7.39; p = 0.01), and use of norepinephrine (OR 3.44; 95% CI 1.72-7.02; p < 0.01) were associated with E-AKI. In subgroup analysis, infectious disease consultation was associated with a lower risk of AKI at day 7 (OR 0.41; 95% CI 0.16-0.88; p = 0.04). E-AKI was associated with 1-year mortality (OR 1.65; 95% CI 1.03-2.64; p = 0.04) and chronic kidney disease progression (OR 2.23; 95% CI 1.30-3.82; p < 0.01).Conclusions: E-AKI is common in IE and often associated with non-modifiable variables. Multidisciplinary management should be mandatory, and awareness of AKI diagnosis and etiological explorations should be raised.

<i>Pneumocystis jirovecii</i> pneumonia is an opportunistic disease usually prevented by trimethoprim-sulfamethoxazole. A 49-year-old HLA-sensitized male with successful late conversion from tacrolimus-based to belatacept-based immunosuppression developed <i>P. jirovecii</i> pneumonia for which he presented several risks factors: low lymphocyte count with no CD4+ T cells detected since 2 years, hypogammaglobulinemia, history of acute cellular rejection 3 years before, and immunosuppressive treatment (belatacept, everolimus). Because of respiratory gravity in the acute phase, the patient was given oxygen, corticosteroids, and trimethoprim-sulfamethoxazole. Thanks to the improvement of respiratory status, and because of the renal impairment, trimethoprim-sulfamethoxazole was converted to atovaquone for 21 days. Indeed, after 1 week on intensive treatment, the benefit-risk balance favored preserving renal function according to respiratory improvement status. <i>P. jirovecii</i> pneumonia prophylaxis for the next 6 months was monthly aerosol of pentamidine. Long-term safety studies or early/late conversion to belatacept did not report on <i>P. jirovecii</i> pneumonia. Four other cases of <i>P. jirovecii</i> pneumonia under belatacept therapy were previously described in patients having no <i>P. jirovecii</i> pneumonia prophylaxis. Studies on the reintroduction of <i>P. jirovecii</i>pneumonia prophylaxis after conversion to belatacept would be of interest. It could be useful to continue regular evaluation within the second-year post-transplantation regarding immunosuppression: T-cell subsets and immunoglobulin G levels.