• Bulletin of Food Technology
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• v.24 no.1
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• pp.53-61
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• 2011

• The Journal of Internal Korean Medicine
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• v.23 no.2
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• pp.222-227
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• 2002

Although there are a few reports concerning the side effects and toxicity of herbal medicines, there has not yet been any report concerning their causes, mechanisms or prevention. We investigated the internal reports concerning the side effects and toxicity of herbal medicines. In the findings, liver disorder (hepatic injury) was found in 7 cases, kidney disorders (nephropathy) were found in 12 cases, heart disorders were found in 4 cases and mineral-caused diseases were found in 2 cases. Besides, we found the major cause of the side effects and toxicity was drug abuse, such as over-dosage and long term medication. So, we hope this report brings more attention to the safety and toxicity of herbal medicines.

• Journal of Genetic Medicine
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• v.10 no.1
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• pp.7-12
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• 2013

Familial Juvenile hyperuricemic nephropathy (FJHN) is a rare autosomal dominant disorder, characterized by early onset of hyperuricemia, gout and progressive kidney disease. Hyperuricemia prior to renal impairment and decreased fractional excretion of uric acid are hallmarks of FJHN. Renal dysfunction gradually appears early in life and results in end-stage renal disease usually between the ages of 20 and 70 years. FJHN is mostly caused by mutations in the uromodulin gene located at 16p12. The course of FJHN is highly variable. Treatment includes management for hyperuricemia, gout and progressive kidney disease. Individuals with gout have been usually treated with allopurinol. But controversy exists as to whether uric acid lowering therapy prevents the progression of chronic kidney disease.

• Childhood Kidney Diseases
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• v.3 no.1
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• pp.95-99
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• 1999

Idiopathic membranous nephropathy is one of the most common causes of nephrotic syndromes in adults but rare in childhood. The occurrence of crescentic glomerulonephritis and membranous nephropathy in a patient is rare. This report describes a patient who initially was diagnosed as a membranous glomerulonephropathy at age 12 years and subsequently developed a crescentic, rapidly progressive glomerulonephritis at age 19 years. The patient responded to methylprednisolone pulse therapy and he maintained with partial remission and normal renal function with residual proteinuria.

• Journal of Korean Foot and Ankle Society
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• v.13 no.1
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• pp.109-112
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• 2009

Calciphylaxis is a rare disease that appear in patients with secondary hyper-parathyroidism or chronic renal failure or that show defect in calcium phosphate metabolism which is characterized by fibrin deposit or calcification of medial wall of vessels causing gradual ischemic skin necrosis. Calciphylaxis is a disease with poor prognosis as skin necrosis can progress rapidly. If left untreated, calciphylaxis will progress to sepsis with high mortality. The treatment is controversial but kidney transplantation or parathyroidectomy is suggested to recover calcium-phosphate metabolism. The authors have experienced calciphylaxis in a patient with chronic renal failure caused by DM nephropathy with characteristic skin lesion and rapid skin necrosis. We describe this case with documentary reviews.

• Korean Journal of Veterinary Research
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• v.46 no.1
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• pp.77-81
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• 2006

A 1-year and 6-month-old, intact male, Shih-tzu dog was referred to the Konkuk University Veterinary Teaching Hospital, due to ascite, melena, severe anemia, and polyuria/polydipsia. Complete blood count showed moderate leukocytosis, lymphocytosis, monocytosis, and microcytic hypochromic nonregenerative anemia. On serum biochemistry profiles, hypoalbuminemia and hypoproteinemia were observed, and proteinuria was detected on urinalysis. Pleural effusion and mild ascites were noted in radiological findings, and bilateral nephromegaly was noted on ultrasonography. Babesia gibsoni was detected by PCR. Babesiosis and glomerular disease was treated at a time with prednisolone and buparvaquone. This therapeutic regime was very efficacious and clinical sings were rapidly improved. Proteinuria and severe anemia were disappeared following therapy.

• Molecules and Cells
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• v.38 no.4
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• pp.285-296
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• 2015

Oxidative stress has been linked to the pathogenesis of diabetic nephropathy, the complication of diabetes in the kidney. NADPH oxidases of the Nox family, and in particular the homologue Nox4, are a major source of reactive oxygen species in the diabetic kidney and are critical mediators of redox signaling in glomerular and tubulointerstitial cells exposed to the diabetic milieu. Here, we present an overview of the current knowledge related to the understanding of the role of Nox enzymes in the processes that control mesangial cell, podocyte and tubulointerstitial cell injury induced by hyperglycemia and other predominant factors enhanced in the diabetic milieu, including the renin-angiotensin system and transforming growth factor-${\beta}$. The nature of the upstream modulators of Nox enzymes as well as the downstream targets of the Nox NADPH oxidases implicated in the propagation of the redox processes that alter renal biology in diabetes will be highlighted.

• Applied Microscopy
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• v.28 no.4
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• pp.577-590
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• 1998

Puromycin aminonucleoside (PAN) nephropathy was induced in a group of Sprague-Dawley rat by a single dose of intraperitoneal Injection to study an ultrastructural change of glomerulus. The experimental rats developed proteinuria three days after PAN injection. Electron microscopic studies of glomeruli showed the loss of epithelial foot processes, formation of cytoplasmic vacuoles, microvillous formation and increased numbers of lysosomes in the cytoplasm of podocytes. It is strongly suggested that proteinuria in PAN nephrosis may be primarily due to a glomerular epithelial lesion, leading to focal disarray of anionic sites or focal defects in the epithelial covering of the basement membrane. The loss of anionic sites in the basement membrane nay be caused by the foot process fusion and the epithelial detachment from the basement membrane.

• Childhood Kidney Diseases
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• v.26 no.2
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• pp.91-96
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• 2022

The messenger RNA-based vaccine for the coronavirus disease 2019 (COVID-19) may induce glomerulonephritis, including immunoglobulin A nephropathy (IgAN). New-onset IgAN triggered by vaccination against COVID-19 has been reported rarely, especially in children. Herein, we report a pediatric case of newly diagnosed IgAN after administration of the Pfizer vaccine for COVID-19. A 12-year-old girl was referred to our hospital for evaluation of gross hematuria after inoculation with the second dose of Pfizer's COVID-19 vaccine; she had no adverse effects after the first dose. At the time of admission, she showed heavy proteinuria and persistent hematuria. Kidney biopsy revealed an IgAN, and she was treated with an oral steroid and an angiotensin-converting enzyme inhibitor. Four months after discharge, the proteinuria and hematuria resolved completely.

• Childhood Kidney Diseases
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• v.27 no.2
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• pp.133-138
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• 2023

Nutcracker syndrome (NCS) is a disease caused by compression of the left renal vein between the superior mesenteric artery and the abdominal aorta. Immunoglobulin A (IgA) nephropathy (IgAN) is characterized by the predominance of IgA deposits in the glomerular mesangial area. Hematuria and proteinuria can be present in both diseases, and some patients can be concurrently diagnosed with NCS and IgAN; however, a causal relationship between the two diseases has not yet been clarified. Here, we report two pediatric cases of NCS combined with IgAN. The first patient presenting with microscopic hematuria and proteinuria was diagnosed with NCS at the initial visit, and the second patient was later diagnosed with NCS when proteinuria worsened. Both patients were diagnosed with IgAN based on kidney biopsy findings and treated with angiotensin-converting enzyme inhibitors and immunosuppressants. A high index of suspicion and timely imaging or biopsy are essential for the proper management of NCS combined with glomerulopathy.