Rationale:TAFRO syndrome is a systemic inflammatory disease characterized by a constellation of symptoms: Thrombocytopenia, Anasarca, MyeloFibrosis, Renal dysfunction, and Organomegaly. Progressive renal insufficiency is a predominant symptom; however, the mechanism of acute kidney injury (AKI) remains unclear, probably because severe thrombocytopenia prevents kidney biopsy. We report a rare case of TAFRO syndrome with histologically confirmed renal involvement.Patients concerns:A 70-year-old man developed fever, anasarca, AKI, thrombocytopenia, and hepatosplenomegaly.Diagnoses:Plasma vascular endothelial growth factor and serum interleukin-6 levels were significantly elevated. The diagnosis of TAFRO syndrome was made based on his clinical and laboratory findings. Kidney biopsy was performed for the evaluation of AKI and provided a diagnosis of membranoproliferative glomerulonephritis–like lesions due to endothelial injury. Glomerular capillary lumens were extremely narrowed or occluded by endothelial swelling, and marked widening of the subendothelial space by electron-lucent material resulted in mesangiolysis and a double-contoured glomerular basement membrane with no immune complex deposits.Interventions and Outcomes:The patient required temporary hemodialysis due to oliguric AKI, but steroid therapy rapidly improved renal function.Lessons:Typically, patients with progressive renal involvement in TAFRO syndrome rapidly develop oliguric or anuric AKI. This report suggests that the reduction of glomerular perfusion by glomerular endothelial injury might be a primary factor in the progressive AKI of TAFRO syndrome. Our case and the literature review indicate that steroid and/or biological therapies result in highly favorable renal outcomes in patients with progressive AKI in TAFRO syndrome.

Background Evidence on the associations of carotid intima‐media thickness and carotid plaque characteristics with stroke subtypes and coronary artery disease risks in Asians is limited. This study investigated these associations in the Japanese general population. Methods and Results Maximum intima‐media thicknesses of both the common carotid artery and internal carotid artery and carotid plaque characteristics were evaluated in 2943 Japanese subjects aged 40 to 75 years without history of cardiovascular disease. Subjects were followed up for a median of 15.1 years. Using a multivariate Cox proportional hazard model, we found that hazard ratios (HRs) and 95% CIs for the highest (≥1.07 mm) versus lowest (≤0.77 mm) quartiles of maximum intima‐media thicknesses of the common carotid artery were 1.97 (1.26–3.06) for total stroke, 1.52 (0.67–3.41) for hemorrhagic stroke, 2.45 (1.41–4.27) for ischemic stroke, 3.60 (1.64–7.91) for lacunar infarction, 1.53 (0.69–3.41) for nonlacunar cerebral infarction, 2.68 (1.24–5.76) for coronary artery disease, and 2.11 (1.44–3.12) for cardiovascular disease (similar results were found for maximum intima‐media thicknesses of the internal carotid artery). HRs(95% CIs) for heterogeneous plaque versus no plaque were 1.58 (1.09–2.30) for total stroke, 1.25 (0.58–2.70) for hemorrhagic stroke, 1.74 (1.13–2.67) for ischemic stroke, 1.84 (1.03–3.19) for lacunar infarction, 1.58 (0.80–3.11) for nonlacunar cerebral infarction, 2.11 (1.20–3.70) for coronary artery disease, and 1.71 (1.25–2.35) for cardiovascular disease. Conclusions Maximum intima‐media thicknesses of the common carotid artery, maximum intima‐media thicknesses of the internal carotid artery, and heterogeneous plaque were associated with the risks of stroke, lacunar infarction, coronary artery disease, and cardiovascular disease in Asians.

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.

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.