• Journal of Veterinary Clinics
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• v.26 no.3
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• pp.306-310
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• 2009

Mass mortality was occurred in adult koi carp(Cyprinus carpio) at a private pond near Samchunpo city in the early November, 2007. Its water temperature was $11^{\circ}C$ and turbidity was very high. The fishes diseased were shown widely distributed hemorrhages, deep ulcerations on the whole body surface and severe erosions in the all fins. In necropsy, excess ascitic fluid was observed and spleen and kidney affected were enlarged. In microscopic observation, it was examined widely distributed severe dermal ulceration, multifocal gill lamella hyperplasia, severe fibrinous pericarditis, multifocal nephritis and hepatitis. The bacteria suspected were isolated using tryptone soya agar and identified as motile Aeromonas hydrophila as results of biochemical tests using API 20E and 20NE. According to previous reports, A. hydrophila infection were mainly occurred in fingerling at high temperature. However, this case exhibited that A. hydrophila infection can develop on adult koi carp even in the winter season.

• Korean Journal of Veterinary Research
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• v.39 no.6
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• pp.1126-1140
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• 1999

Renal failure is one of the main causes of economic impacts in the poultry industry and complex syndrome with different severity of clinical signs caused by multiple nephropathogenic factors such as infectious bronchitis viral infection and excess salt and calcium in diet. To evaluate the correlation between severity of renal failure and the causative nephropathogenic factors, one-day-old specific pathogen free chicks were treated with either single causative factor or multiple causative factors described as above. Each group was designed as control for non-treated control, IB for infectious bronchitis virus (IB virus) infection, IBHNa for IB virus infection with high diet salt, IBHCa for IB virus infection with high diet calcium, IBHNC for IB virus infection with high diet salt and calcium, HNa for high diet salt, HCa for high diet calcium and HNC for high diet salt and calcium. Chickens were inoculated with IB virus at 1-day-old and remained on their respective diets until 21 day of age. The high dietary salt feeding groups such as IBHNa, IBHNC, HNa, HNC increased water intake, watery diarrhea, general subcutaneous edema and the high dietary calcium feeding groups such as IBHCa and IBHNC showed severe visceral gout. Two more than treated groups caused high mortality in comparison with the single treated groups. IB virus exposure significantly increased urate deposition and lymphocytic interstitial nephritis. Especially urate deposition dramatically increased when excess diet calcium was combined together. In excess diet salt treated groups enlarged edematous kidneys were observed and hypertrophy of glomeruli were showed. These results suggest that IB virus enhanced the incidence and severity on chicken renal failure clearly related to the quantity of salt and calcium.

• Clinical and Experimental Pediatrics
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• v.55 no.4
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• pp.136-142
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• 2012

Purpose: Urinary excretion of N acetyl-beta-D glucosaminidase (NAG) and ${\beta}_2$-microglobulin (${\beta}_2$-M) was increased in the presence of proximal tubular damage. Based on these urinary materials, we investigated the ability of expecting renal function in chronic glomerular diseases. In this study, we evaluated the relationship between glomerular filtration rate (GFR) urinary NAG, and urinary ${\beta}_2$-M. Methods: We evaluated 52 children with chronic kidney disease at the Chung-Ang University Hospital between January 2003 and August 2009. We investigated the 24-hour urinalysis and hematologic values in all 52 patients. Serum creatinine, creatinine clearance (Ccr), serum cystatin C, urinary ${\beta}_2$-M and urinary NAG were measured. Results: Out of 52 patients, there were 13 children with minimal change in disease, 3 children with focal segmental glomerulosclerosis, 17 children with immunoglobulin A nephropathy, 15 children with Henoch-Sch$\ddot{o}$nlein purpua nephritis, 3 children with poststreptococcal glomerulonephritis, and 1 child with thin glomerular basement membrane disease. In these patients, there were significant correlation between the Ccr and urinary NAG (r=-0.817; $P$ <0.01), and between the GFR (as determined by Schwartz method) and urinary NAG (r=-0.821; $P$ <0.01). In addition, there was a significant correlation between the GFR (as determined by Bokencamp method) and urinary NAG (r=-0.858; $P$ <0.01). Conclusion: In our study, there was a significant correlation between the GFR and urinary NAG, but there was no correlation between the GFR and urinary ${\beta}_2$-M, suggesting that the GFR can be predicted by urinary NAG in patients with chronic glomerular disease.

• Childhood Kidney Diseases
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• v.10 no.1
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• pp.40-44
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• 2006

[ $Henoch-Sch{\"{o}}nlein$ ] purpura(HSP) is a systemic small vessel vasculitis characterized by cutaneous purpura, arthritis, abdominal pain and nephritis. The characteristic rash of HSP consists of palpable purpura on the buttocks and lower extremities. Bullous lesions often appear in adults with HSP, whereas they are very rare in children with HSP. In this case report, the patient presented with arthralgia and abdominal pain and had hemorrhagic bullae as a prominent manifestation of the disease. The skin biopsy of the patient revealed typical leukocytoclastic vasculitis of dermal vessels and prominent IgA and fibrinogen deposits on capillary walls by direct immunofluorescence. We confirmed the diagnosis of HSP and observed improvement of clinical symptoms and signs within a few days after corticosteroid treatment. We therefore report a case with a review of the literature.

• Childhood Kidney Diseases
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• v.20 no.1
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• pp.23-28
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• 2016

Purpose: We investigated whether serum levels of insulin growth factor-1 (IGF-1) and insulin growth factor binding protein-3 (IGFBP-3) are valuable in predicting clinical outcomes or are correlated with other laboratory findings in children with Henoch-$Sch{\ddot{o}}nlein$ purpura (HSP). Methods: We examined 27 children who were consecutively admitted to our hospital with HSP between January 2011 and February 2012. Blood tests (C-reactive protein, white blood cell count, platelet count, erythrocyte sedimentation rate, albumin, immunoglobulin A, complement C3, antineutrophil cytoplasmic antibody, IGF-1, IGFBP-3) and urine tests were performed upon admission. IGF-1 and IGFBP-3 were resampled in the recovery phase. Controls included 473 children whose IGF-1 and IGFBP-3 were sampled for evaluating their growth, at the outpatient department of pediatric endocrinology in our hospital. IGF-1 and IGFBP-3 were compared between the HSP children and controls, and between the acute and recovery phases in HSP children. The ability of these values to predict clinical outcomes including renal involvement was analyzed using bivariate logistic regression analysis (BLRA). Results: IGF-1 and IGFBP-3 were not different between the HSP children and controls ($148.7{\pm}117.6$ vs. $69.2{\pm}96.9$, P=0.290: $3465.9{\pm}1290.9$ vs. $3597.2{\pm}1,127.6$, P=0.560, respectively). There was no significant difference in IGF-1 or IGFBP-3 between acute and recovery phases. Based on the BLRA, no variable, including IGF-1 and IGFBP-3, could predict clinical outcomes including the presence of nephritis Conclusion: We concluded that IGF-1 and IGFBP-3 do not predict clinical outcomes of HSP, including renal involvement, in this study.

• Childhood Kidney Diseases
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• v.24 no.2
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• pp.107-114
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• 2020

Purpose: The purpose of this study was to evaluate the prevalence, clinical characteristics, and long-term clinical effects of hypertension in Korean childhood-onset systemic lupus erythematous (SLE) patients. Methods: The medical records of SLE patients, diagnosed by 2019 SLE European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria, who visited Samsung Medical Center from January 2009 to May 2019 were reviewed. Disease activity and long-term damage were evaluated using the Modified Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) and the Pediatric Systemic Lupus International Collaborating Clinics/ACR Damage Index (Ped-SDI), respectively. The sex-, age- and height-blood pressure standards recommended by the American Academy of Pediatrics 2017 guideline was used to define hypertension. Results: A total of 32 patients were enrolled in this study. The median follow-up duration was 7.3 years and females were predominant. The median ages at SLE and hypertension diagnoses were 14.2 and 14.3 years, respectively. The biopsy-proven lupus nephritis was detected in 90.6% and 37.5% were class IV. During the follow-up, 12 patients (37.5%) had hypertension. Among them, 2 patients had 3 episodes of posterior reversible encephalopathy syndrome and 5 patients had left ventricular hypertrophy (LVH). Univariate analysis showed baseline hypertension was significantly correlated with a lower estimated glomerular filtration rate, higher body mass index and SLEDAI at baseline. The development of hypertension during the follow-up was significantly correlated with obesity, LVH, and higher Ped-SDI. Conclusion: Our study revealed that hypertension in pediatric SLE is associated with obesity and renal function at SLE diagnosis and could affect long-term damage.

• Journal of Yeungnam Medical Science
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• v.22 no.2
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• pp.253-258
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• 2005

Generalized edema and hypoalbuminemia are relatively common presenting manifestations in many clinical situations. The differential diagnosis of hypoalbuminemia include: Kwashiorkor, synthetic dysfunction of the liver, and excessive protein loss as in nephrotic syndrome. In systemic lupus erythematosus (SLE), hypoalbuminemia and generalized edema are most commonly due to protein loss associated with lupus nephritis; gastrointestinal involvement is uncommon, and therefore protein loss through the gastrointestinal tract is quite rare. We report a case of a protein losing enteropathy (PLE) associated with SLE. The patient was referred to our hospital for generalized edema, arthralgia and facial rash. After clinical evaluation, the patient met the criteria for the SLE diagnosis; hypoalbuminemia with general edema was consistent with a protein losing enteropathy. After two weeks of therapy with parenteral high dose glucocorticoid, the patients was improved in laboratory findings as well as clinical symptoms.

• Kidney Research and Clinical Practice
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• v.37 no.4
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• pp.347-355
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• 2018

Background: Nephrotic syndrome (NS) is the most common glomerulopathy in children. Acute kidney injury (AKI) is a common complication of NS, caused by severe intravascular volume depletion, acute tubular necrosis, interstitial nephritis, or progression of NS. However, the incidence and risk factors of childhood-onset NS in Korea are unclear. Therefore, we studied the incidence, causes, and risk factors of AKI in hospitalized Korean patients with childhood-onset NS. Methods: We conducted a retrospective review of patients with childhood-onset NS who were admitted to our center from January 2015 to July 2017. Patients with decreased renal function or hereditary/secondary NS, as well as those admitted for management of other conditions unrelated to NS, were excluded. Results: During the study period, 65 patients with idiopathic, childhood-onset NS were hospitalized 90 times for management of NS or its complications. Of these 90 cases, 29 met the Kidney Disease Improving Global Outcomes criteria for AKI (32.2%). They developed AKI in association with infection (n = 12), NS aggravation (n = 11), dehydration (n = 3), and intravenous methylprednisolone administration (n = 3). Age ${\geq}9$ years at admission and combined use of cyclosporine and renin-angiotensin system inhibitors were risk factors for AKI. Conclusion: AKI occurred in one-third of the total hospitalizations related to childhood-onset NS, owing to infection, aggravation of NS, dehydration, and possibly high-dose methylprednisolone treatment. Age at admission and use of nephrotoxic agents were associated with AKI. As the AKI incidence is high, AKI should be considered during management of high-risk patients.

• Clinical and Experimental Pediatrics
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• v.62 no.5
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• pp.193-197
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• 2019

Alport syndrome (ATS) is an inherited glomerular disease caused by mutations in one of the type IV collagen novel chains (${\alpha}3$, ${\alpha}4$, and ${\alpha}5$). ATS is characterized by persistent microscopic hematuria that starts during infancy, eventually leading to either progressive nephritis or end-stage renal disease. There are 3 known genetic forms of ATS, namely X-linked ATS, autosomal recessive ATS, and autosomal dominant ATS. About 80% of patients with ATS have X-linked ATS, which is caused by mutations in the type IV collagen ${\alpha}5$ chain gene, COL4A5. Although an 80% mutation detection rate is observed in men with X-linked ATS, some difficulties do exist in the genetic diagnosis of ATS. Most mutations are point mutations without hotspots in the COL4A3, COL4A4, and COL4A5 genes. Further, there are insufficient data on the detection of COL4A3 and COL4A4 mutations for their comparison between patients with autosomal recessive or dominant ATS. Therefore, diagnosis of ATS in female patients with no apparent family history can be challenging. Therefore, in this study, we used whole-exome sequencing (WES) to identify mutations in type IV collagen in 2 girls with glomerular basement membrane structural changes suspected to be associated with ATS; these patients had no relevant family history. Our results revealed de novo c.4688G>A (p.Arg1563Gln) and c.2714G>A (p.Gly905Asp) mutations in COL4A5. Therefore, we suggest that WES is an effective approach to obtain genetic information in ATS, particularly in female patients without a relevant family history, to detect unexpected DNA variations.

• Childhood Kidney Diseases
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• v.23 no.1
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• pp.53-57
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• 2019

Renal cortical necrosis (RCN) is patchy or diffuse ischemic destruction of the renal cortex caused by significantly reduced renal arterial perfusion. It is a rare cause of acute kidney injury (AKI) and is associated with high mortality. Here, we review the case of RCN in a 15-year-old boy who developed AKI. A 15-year-old boy was referred to our hospital from a local hospital due to a sharp decrease in his renal function. He presented with acute flank pain, nausea with vomiting, and oliguria for the past two days. He had taken a single dose of antihistamine for nasal congestion. At our hospital, his peak blood pressure was 148/83 mmHg and he had a high body mass index of $32.9kg/m^2$. The laboratory data showed a blood urea nitrogen (BUN) of 28.4 mg/dL, a creatinine of 4.26 mg/dL, and a glomerular filtration rate estimated from the serum cystatin C of $20.2mL/min/1.73m^2$. Proteinuria (spot urine protein to creatinine ratio 1.66) with pyuria was observed. Kidney sonography showed parenchymal swelling and increased renal echogenicity. Due to rapidly progressing nephritis, steroid pulse therapy (750 mg/IV) was done on the second day of his admission and the patient showed complete recovery with normal renal function. However, the kidney biopsy findings revealed renal cortical hemorrhagic necrosis. Multifocal, relatively well-circumscribed, hemorrhagic necrotic areas (about 25%) were detected in the tubulointerstitium. Although RCN is an unusual cause of AKI, especially in children, pediatricians should consider the possibility of RCN when evaluating patients with rapidly decreasing renal function.