The occurrence of preeclampsia before 20 weeks of gestation is rare and usually associated with trophoblastic diseases or antiphospholipid syndrome. Here, we report a case of preeclampsia before 20 weeks of gestation in the absence of the aforementioned disorders. A healthy 30-year-old nulliparous woman presented with new onset of hypertension and proteinuria at 18 weeks of gestation. Fetal ultrasound did not reveal any abnormalities. Empirical steroid treatment was initiated based on a tentative diagnosis of underlying renal disease. The clinical course of the disease was progressive despite steroid treatment and the fetus died in utero 8 days after the initiation of treatment. Following delivery, a renal biopsy was performed and provided a diagnosis of preeclampsia. All symptoms resolved postpartum. This report demonstrates that preeclampsia may occur before 20 weeks of gestation and should always be considered in the differential diagnosis of pregnant women with new onset of hypertension with proteinuria. Previous published cases are summarized briefly.
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.
Low birth weight (LBW) has been known to increase the susceptibility to renal injury in adulthood. A 26-year-old woman developed proteinuria in early pregnancy; she had been born with very LBW. The clinical course was progressive, and an emergency Caesarean section was performed at 36 weeks due to acute kidney injury. A renal biopsy provided a diagnosis of post-adaptive focal segmental glomerulosclerosis. Increased demand for glomerular filtration during early pregnancy appeared to have initiated the renal injury. This report highlights the fact that pregnancy might be a risk factor for renal injury in women born with LBW.
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.
Chronic granulomatous disease (CGD) is a rare immunodeficiency disorder with genetic defects in the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex in phagocytes, leading to recurrent severe infections and granuloma formation. Genitourinary involvement, including obstructive granulomas, infections, nephrotoxicity of anti-infective agents, and amyloidosis, is frequently observed in patients with CGD, whereas the clinical and pathological details of the less commonly reported glomerular disease remain obscure. Here, we report the case of a patient with CGD who developed rapidly progressive IgA vasculitis-associated nephritis (IgAVN) and review the literature on biopsy-proven glomerular diseases in patients with CGD. A 22-year-old male patient with CGD developed rapidly progressive glomerulonephritis (RPGN) following peripheral purpura and was diagnosed with crescentic IgAVN based on the renal biopsy evaluation. There was no evidence of active infections, and he received pulse intravenous methylprednisolone followed by oral prednisolone. His renal function returned to normal within 4 weeks, and his proteinuria and microhematuria finally resolved. The present case and literature review indicate that IgAVN and IgA nephropathy with RPGN are the most common causes of glomerular disease in patients with CGD. Clinicians should be aware of the possibility of these diseases as causes of RPGN in CGD, because delays in diagnosis and appropriate treatment may affect renal outcomes.
Keywords:lupus nephritis, anti-glomerular basement membrane antibody, kidney biopsy, IgG 〈Abstract〉 A 43-year old male was admitted to our hospital because of nephrotic syndrome and an acute kidney injury. He had a history of lupus nephritis type V 8 years ago, but had achieved complete remission after treatment. Serological tests showed elevated anti-glomerular basement membrane antibody levels. A kidney biopsy examination showed crescentic glomerulonephritis without IgG deposits. Thus, a diagnosis of lupus nephritis type IV+V was made. Steroid therapy was started, and plasma exchange was performed. Despite these therapies, the patient's renal function deteriorated, and hemodialysis was initiated. Intravenous cyclophosphamide pulse therapy was added, but the patient's renal function did not improve. A second kidney biopsy was performed on the 48th day. It showed the linear deposition of IgG along the capillary wall, which led to a diagnosis of anti-glomerular basement membrane disease. A further immunosuppressive regimen was considered to be ineffective. Therefore, the steroid therapy was tapered, and hemodialysis was continued. This case report demonstrates that anti-glomerular basement membrane disease can occur during the course of lupus nephritis.
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