RESUMO
(1) Background: Chronic kidney disease (CKD), as well as antimicrobial resistance (AMR) represent major global health problems, with important social and economic implications. It was reported that CKD is a risk factor for antimicrobial resistance, but evidence is scarce. In addition, CKD is recognized to be a risk factor for complicated urinary tract infections (UTIs). (2) Methods: We conducted an observational study on 564 adult in-hospital patients diagnosed with urinary tract infections. The aim of the study was to identify the risk factors for AMR, as well as multiple drug resistance (MDR) and the implicated resistance patterns. (3) Results: The mean age was 68.63 ± 17.2 years. The most frequently isolated uropathogens were Escherichia coli strains (68.3%) followed by Klebsiella species (spp. (11.2%). In 307 cases (54.4%)), the UTIs were determined by antibiotic-resistant bacteria (ARBs) and 169 cases (30%) were UTIs with MDR strains. Increased age (≥65) OR 2.156 (95% CI: 1.404−3.311), upper urinary tract obstruction OR 1.666 (1.083−2.564), indwelling urinary catheters OR 6.066 (3.919−9.390), chronic kidney disease OR 2.696 (1.832−3.969), chronic hemodialysis OR 4.955 (1.828−13.435) and active malignancies OR 1.962 (1.087−3.540) were independent risk factors for MDR UTIs. In a multivariate logistic regression model, only indwelling urinary catheters (OR 5.388, 95% CI: 3.294−8.814, p < 0.001), CKD (OR 1.779, 95% CI: 1.153−2.745, p = 0.009) and chronic hemodialysis (OR 4.068, 95% 1.413−11.715, p = 0.009) were risk factors for UTIs caused by MDR uropathogens. (4) Conclusions: CKD is an important risk factor for overall antimicrobial resistance, but also for multiple-drug resistance.
RESUMO
BACKGROUND: Kidney involvement is a frequent complication of systemic lupus erythematosus (SLE) and kidney biopsy is essential in differentiating lupus nephritis (LN) from thrombotic microangiopathy (TMA) secondary to antiphospholipid autoantibodies (aPL). Association between antiphospholipid syndrome (APS) and acquired hemophilia due to inhibitors was very rarely described in SLE patients. CASE PRESENTATION: We present the case of a 61-year-old male diagnosed with SLE who acquired deficiency of clotting factor VIII due to circulating inhibitors, admitted for acute kidney injury (AKI), microangiopathic hemolytic anemia, thrombocytopenia, and diplopia. Kidney biopsy showed TMA due to APS, but no signs of LN. Head computed tomography identified low dense areas in the white matter, suggesting small blood vessels' involvement. A diagnosis of probable catastrophic antiphospholipid syndrome (CAPS) was established and treatment with low molecular weight heparin, intravenous methylprednisolone, plasmapheresis, and rituximab was initiated, followed by resolution of AKI, diplopia, and TMA with complete depletion of CD19+B-lymphocytes (CD19+B-Ly) after one month. We further review the current knowledge regarding pathogenesis and management of CAPS in SLE patients. CONCLUSIONS: Targeted therapy was possible after kidney biopsy, improving renal and general prognosis. CD19+B-Ly repopulation preceded biological relapse, so monitoring of CD19+B-Ly may serve as a tool to predict relapses and guide rituximab therapy.
