A 28-year-old woman experienced gross hematuria after the administration of the second dose of an mRNA vaccine (BNT162b2). She was diagnosed with IgA nephropathy (IgAN) by a renal biopsy two weeks after vaccination, which revealed a mild increase in mesangial cells and a matrix with co-depositions of galactose-deficient IgA1 and C3 in the mesangial region. The gross hematuria and proteinuria gradually improved without any medication, suggesting that immune activation by the mRNA vaccine may not elicit continuous disease progression of IgAN. Thus, further studies investigating the relationship between mRNA vaccines against COVID-19 and the progression of IgAN should be conducted.
Background Nephronophthisis (NPHP) is a chronic tubular interstitial disorder that exhibits an autosomal recessive genetic form and causes progressive renal failure in children. Patients with NPHP rarely show urinary abnormalities, edema, or hypertension. Thus, NPHP is often detected only when renal failure becomes advanced. NPHP can be divided into three types based on the age of end-stage renal failure, i.e., infant type (approximately 5 years old), juvenile type (approximately 13–14 years old), and adolescent type (approximately 19 years old). Here, we report a case of NPHP diagnosed by genetic analysis at 26 years of age with atypical histological abnormalities. Case presentation A 26-year-old woman showed no growth disorders or urinary abnormalities in annual school physical examinations. However, at a check-up at 26 years old, she exhibited renal dysfunction (eGFR 26 mL/min/1.73 m2). Urine tests indicated low specific gravity of urine, but not proteinuria or microscopic hematuria. Urinary β2-microglobulin was high (805 μg/L), and renal biopsy was performed for definitive diagnosis. Histological findings showed no significant findings in glomeruli. However, moderate fibrosis was observed in the interstitial area, and moderate atrophy was observed in the tubules. There were no significant findings in immunofluorescence analysis, and no electron dense deposits were detected by electron microscopy. Although cyst-like expansion of the tubules was unclear, tubular atrophy was dominantly found in the distal tubule by cytokeratin 7 staining. Genetic analysis of the NPHP1 gene showed complete deletion of this gene, leading to a definitive diagnosis of NPHP. Conclusions NPHP is not merely a pediatric disease and is relatively high incidence in patients with adult onset end-stage of renal disease. In this case, typical histological abnormalities, such as cyst-like expansion of the tubular lesion, were not observed, and diagnosis was achieved by genetic analysis of the NPHP1 gene, which is responsible for the onset of NPHP. In patients with renal failure with tubular interstitial disease dominantly in the distal tubules, it is necessary to discriminate NPHP, even in adult cases.
Hypertriglyceridemia and chronic kidney disease (CKD) are known risk factors for cardiovascular disease. However, treatment with statins, which control low-density lipoprotein cholesterol levels, increases the risk of estimated glomerular filtration rate (eGFR) reduction. Although conventional fibrates, such as bezafibrate (Beza-F) and fenofibrate (Feno-F), are the mainstay for hypertriglyceridemia treatment, they may be associated with a risk of increased serum creatinine level and renal dysfunction. Pemafibrate (Pema) is pharmacologically defined as a selective peroxisomal proliferator-activated receptor α modulator which is excreted in bile and not likely to cause renal dysfunction. We evaluated the efficacy and safety of switching from Beza-F or Feno-F to Pema in CKD patients with hypertriglyceridemia. We recruited 47 CKD patients with hypertriglyceridemia who were receiving Beza-F, Feno-F, or eicosapentaenoic acid (EPA) but were switched to Pema from 2018 to 2021. A retrospective analysis of renal function and lipid profiles was performed before and 24 weeks after switching. CKD patients switching from EPA to Pema were used as study control. The effect of Pema on hypertriglyceridemia was equivalent to that of Beza-F or Feno-F. However, after switching to Pema, eGFR showed a marked average improvement of 10.2 mL/min/1.73 m2 (P < .001). Improvement in eGFR and levels of n-acetyl-β-d-glucosaminidase and β-2-microglobulin was observed only in cases of switching from Beza-F or Feno-F but not from EPA. Although Beza-F and Feno-F are useful medications for the treatment of hypertriglyceridemia, these are associated with a high risk of renal dysfunction. We also found that the deterioration in eGFR due to Beza-F or Feno-F is reversible with drug withdrawal and may not increase the risk for long-term renal dysfunction. We suggest that Pema may be an effective and safe treatment for hypertriglyceridemia in CKD patients.
Here we report a case of TAFRO syndrome developed after the COVID-19 mRNA vaccination. Universal vaccination is important, however, the possibility of various complications after COVID-19 vaccination, including TAFRO syndrome, should be considered.
During the course of treatment for rheumatoid arthritis, anti-DNA antibody was detected, and systemic lupus erythematosus was diagnosed, who was subsequently treated with abatacept-and remission was achieved. Rebound of elevated anti-DNA antibody and urinary abnormalities were noted with MPO-ANCA positivity. Renal biopsy revealed lupus nephritis; followed by the development of rapidly progressive glomerulonephritis, which required apheresis (double filtration plasmapheresis) therapy, although no response was achieved. However, plasma exchange therapy was highly effective. These results suggest that MPO-ANCA-positive lupus nephritis can become severe and require intensive treatment in accordance with the treatment for severe vasculitis.
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