Seon-Ho Ahn

Human CD36 overexpression in renal tubules accelerates the progression of renal diseases in a mouse model of folic acid-induced acute kidney injury

Background Acute kidney injury (AKI) is a risk factor for progression to chronic kidney disease, with even subclinical AKI episodes progressing to chronic kidney disease. Several risk factors such as preexisting kidney disease, hyperglycemia, and hypertension may aggravate renal disease after AKI. However, mechanisms underlying the progression of AKI are still unclear. This study identified the effect of human cluster of differentiation 36 (CD36) overexpression on the progression of folic acid-induced AKI. Methods Pax8–rtTA/tetracycline response element–human CD36 transgenic mice were used to elucidate the effect of human CD36 overexpression in the proximal tubules on folic acid-induced AKI. Results Results of histological analysis showed severely dilated tubules with casts and albuminuria in folic acid-treated transgenic mice overexpressing human CD36 compared with folic acid-treated wild-type mice. In addition, analysis of mRNA expression showed a significant increase in the collagen 3a1 gene in folic acid-treated transgenic mice overexpressing human CD 36 compared with folic acid-treated wild type mice. Conclusion Human CD36-overexpressing transgenic mice showed severe pathological changes and albuminuria compared with wild-type mice. Moreover, mRNA expression of the collagen 3a1 gene increased in folic acid-treated transgenic mice. These results suggest that human CD36 overexpression is a risk factor of AKI and its progression to chronic kidney disease.

Minimal Change Disease Associated with Ingestion of Poison Sumac

https://doi.org/10.4068/cmj.2018.54.3.201 C Chonnam Medical Journal, 2018 Chonnam Med J 2018;54:201-202 Corresponding Author: Jong Hwan Jung Division of Nephrology, Department of Internal Medicine, Wonkwang University Hospital, Wonkwang University School of Medicine, 895 Muwang-ro, Iksan 54538, Korea Tel: +82-63-859-2623, Fax: +82-63-855-2025, E-mail: chjh0502@gmail.com Article History: Received August 13, 2018 Revised August 23, 2018 Accepted August 27, 2018 FIG. 1. Light microscopic finding shows normal glomerulus except slightly increased mesangial matrix (Hematoxylin and Eosin stain, ×400) (A). Electron microscopic finding shows glomerular basement membrane with normal thickness and smooth contours without electrondense deposits. However, the foot processes of epithelial cells were prominently effaced (B). Minimal Change Disease Associated with Ingestion of Poison Sumac

Staphylococcal infection-associated crescentic immunoglobulin A nephropathy

ease presented to our hospital with acute fever, dyspnea, and oliguria. His vital signs were: blood pressure 100/60 mmHg, heart rate 120 beats per minute, and body temperature 38.5°C. Laboratory findings were: serum creatinine 2.99 mg/dL, leukocytes 21,230 × 10/μL, hemoglobin 7.6 g/dL, platelets 60,000/μL, and C-reactive protein 183.46 mg/L. Additionally, perinuclear anti-neutrophil cytoplasmic antibody (ANCA) and cytoplasmic ANCA were elevated, and C3 was decreased. However, there were no indications of vasculitis. Computed tomography revealed multifocal pneumonic infiltration along with bilateral cavitary lung lesions and a perirenal hematoma. We initiated empirical antibiotics. Blood cultures revealed methicillin-resistant Staphylococcus aureus, and the patient exhibited signs of uremia, for which he underwent emergency hemodialysis. Echocardiography revealed a tricuspid valve vegetation measuring 2.0 × 0.79 cm. While his renal function and pneumonic infiltration improved after 4 weeks, proteinuria persisted. A renal biopsy showed endocapillary proliferation and increased mesangial immunoglobulin A (IgA) accumulation acStaphylococcal infection-associated crescentic immunoglobulin A nephropathy