Occasionally, over-anticoagulation with warfarin induces acute kidney injury (AKI) characterized by glomerular hemorrhage with tubular obstruction by red blood cell casts, which is widely acknowledged as warfarin-related nephropathy. Owing to extensive use of direct oral anticoagulants, similar AKI cases have been reported among patients treated with dabigatran. Dabigatran is primarily excreted by the kidneys; thus, renal impairment is one of the risk factors for dabigatran-induced bleeding complications. Nevertheless, risk factors for dabigatran-induced anticoagulant-related nephropathy (ARN) remain partially clarified. Here, we report a histologically established case of dabigatran-induced ARN with undiagnosed IgA nephropathy in a patient with normal baseline renal function. In addition, we summarize previously published cases of biopsyproven, dabigatran-related ARN. A 67-year-old female with normal preexisting renal function developed macrohematuria and AKI. She had been treated with dabigatran for deep vein thrombosis. A renal biopsy diagnosed ARN with inactive IgA nephropathy. After dabigatran withdrawal, her macrohematuria and renal function improved. This report demonstrates that ARN could occur in patients with normal baseline renal function. Our case and prior reports suggest that IgA nephropathy could be a risk factor for dabigatran-induced ARN.
MYH9-related disease is a rare genetic disorder characterized by macrothrombocytopenia, with frequent proteinuric nephropathy, hearing loss, and cataract. Although proteinuric nephropathy usually progresses to renal failure, there is no established treatment for the nephropathy. We herein describe the case of a 19-year-old man carrying an E1841K MYH9 mutation, who developed persistent proteinuria. The patient was diagnosed with early-stage MYH9-related nephropathy based on the histological examination of a kidney biopsy specimen. The patient was treated with enalapril, which significantly reduced the proteinuria with no decline in his renal function. The early administration of renin-angiotensin system blockade therapy may have beneficial effects on MYH9-related nephropathy in patients with E1841K mutations. We also briefly summarize previously published cases of MYH9-related nephropathy treated with renin-angiotensin system (RAS) blockade therapy.
Mass vaccination is the most important strategy to terminate the coronavirus disease 2019 (COVID-19) pandemic. Reports suggest the potential risk of the development of new-onset or relapse of minimal change disease (MCD) following COVID-19 vaccination; however, details on vaccine-associated MCD remain unclear. A 43-year-old man with MCD, who had been in remission for 29 years, developed nephrotic syndrome 4 days after receiving the third dose of the Pfizer-BioNTech vaccine. His kidney biopsy revealed relapsing MCD. Intravenous methylprednisolone pulse therapy followed by oral prednisolone therapy was administered, and his proteinuria resolved within 3 weeks. This report highlights the importance of careful monitoring of proteinuria after COVID-19 vaccination in patients with MCD, even if the disease is stable and no adverse events occurred during previous vaccinations. Our case report and literature review of COVID-19 vaccine-associated MCD indicated that MCD relapse tends to occur later after vaccination and slightly more often following the second and subsequent vaccine doses than new-onset MCD.
Background: Septic pulmonary embolism (SPE) is an uncommon but serious complication resulting from infection of the blood. Gram-positive cocci, including methicillin-susceptible Staphylococcus aureus and methicillin-resistant Staphylococcus aureus, are the most common causative organisms of SPE. Few case reports have been published on SPE caused by Pseudomonas aeruginosa (P. aeruginosa), and thus, the consensus treatment of SPE caused by P. aeruginosa infections remains undetermined. Management of P. aeruginosa infection can be challenging due to its poor prognosis and antimicrobial resistance. Here, we report a case of successful combination antibiotic therapy for SPE associated with infective endocarditis (IE) caused by P. aeruginosa in a hemodialysis patient, with a review of the literature. Case presentation: A 62-year-old man receiving maintenance hemodialysis as treatment for end-stage renal disease due to IgA nephropathy was admitted to our hospital with high fever and chills lasting 10 days. Chest computed tomography revealed multiple nodular shadows, and gram-negative rods were confirmed by blood culture obtained on admission. We suspected SPE and initiated meropenem (MEPM) treatment. P. aeruginosa was identified in blood cultures, and transesophageal echocardiography demonstrated vegetation on the tricuspid valve. Therefore, a diagnosis of SPE associated with IE caused by P. aeruginosa was made. P. aeruginosa isolates showed good susceptibility to MEPM, but no symptomatic improvement was observed. Thus, antibiotics were changed from MEPM to a combination of ceftazidime and tobramycin (TOB). The patient exhibited a favorable response to the combination therapy, although we discontinued TOB on day 23 because of tinnitus symptoms. Conclusions: We report a rare case of SPE associated with IE caused by P. aeruginosa in a hemodialysis patient. Combination antibiotic therapy may be effective in this situation.
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