• Childhood Kidney Diseases
• /
• 제17권2호
• /
• pp.86-91
• /
• 2013

목적: 본 연구는 가와사키 질환의 신장 침범에 대하여 비교적 덜 침습적이며, 특이도와 민감도가 높은 검사인 Technetium-99m dimercaptosuccinic acid scintigraphy (DMSA renal SPECT)을 통하여 밝혀보고자 한다. 방법: 2011년 3월부터 10월까지 국민건강보험 일산병원에서 가와사키로 진단된 15명의 환아들을 대상으로 진행하였다. 15명의 환아 모두 가와사키의 급성기에 DMSA renal SPECT를 시행하였다. 또한 신장 세뇨관 손상 지표인 요중 ${\beta}2$-microglobulin (${\beta}2$-MG)을 측정하여 이를 통한 가와사키 환아에서 신장 손상의 조기 진단 가능 여부를 연구해보았다. 결과: 환아 15명 모두의 신기능 검사는 정상이었다. 소변 검사상 현미경적 혈뇨와 농뇨가 각각 13%, 33%에서 관찰되었다. 요중 ${\beta}2$-MG는 46%에서 증가된 소견을 보였다. 또한 환아들을 요중 ${\beta}2$MG를 기준으로 증가되어 있는 군과 증가되지 않은 군으로 나누어 비교, 분석해 보았으며, 두군간에 임상 증상, 임상 검사, 초음파 검사 및 심초음파 검사에서 유의한 차이를 보이지 않았다. 모든 환아에서 DMSA renal SPECT는 정상 소견을 보였다. 결론: 본 연구에서 가와사키 질환의 신장 침범은 경한 소변 검사 이상 및 일부 환아에서의 요중 ${\beta}2$-MG의 상승 소견을 보였으며, DMSA renal SPECT에서 관찰될 정도의 신장 침범은 보이지 않았다.

• 한국식품영양과학회지
• /
• 제34권7호
• /
• pp.968-972
• /
• 2005

기능성 식품소재로서 이미 많이 알려진 키토산이 신장과 관련하여 식품이나 의료용 소재로서 활용이 가능한 지를 알아보기 위하여 신장 기능과 민감하게 관련이 있는 효소인 RDPase, Udpase의 활성을 체내$\cdot$체외 실험을 통하여 관찰하였다. 체외 실험에서 글리세롤에 의해 유도된 RDPase의 유리$\cdot$활성 감소를 다시 회복시키는 것을 관찰하였다. 체내실험에서 글리세롤 투여에 의하여 손상된 신장의 근위세뇨관에서 급격히 증가한 RDPase의 활성을 키토산이 확실하게 감소시키는 것을 관찰할 수 있었다. 키토산을 공급한 쥐의 소변에서의 Udpase의 활성이 증가하는 것을 관찰하였다.

• 한국산업보건학회지
• /
• 제11권2호
• /
• pp.153-160
• /
• 2001

Objectives : The authors evaluated the effects on renal function of workers chronically exposed to low-level organic solvent mixtures. Methods : The authors measured the level of urine ${\beta}2$-microglobulin(${\beta}2$-MG) and microalbumin as biochemical markers of renal function and damage in 29 male workers exposed to organic solvents for more than five years and compared their results with those of 30 male office clerks as a reference group. Results : 1. The mean values of hemoglobin, hematocrit, SGOT, SGPT, ${\gamma}$-GTP were all within normal limits and there was no significant difference, except for hemoglobin(p<0.01), between exposed and reference group. 2. The values of BUN and serum creatinine were within reference limits and there was no significant difference between exposed and reference group. 3. The difference of mean values of urine microalbumin corrected by urine creatinine were statistically significant (p<0.01), but those of urine ${\beta}2$-MG was not. 4. There were no correlation of urine hippuric acids with BUN, serum creatinine, urine microalbumin and ${\beta}2$-MG. 5. There were no significant difference of BUN, serum creatinine, urine microalbumin and ${\beta}2$-MG upon work duration. Conclusions: It is assumed that chronic low-level organic solvent exposure in these workers shows early renal dysfunction, glomerular changes. The result corresponds to previous studies showing the relationship between hydrocarbon exposure and glomerulonephritis. For evaluation of impairment on kidney tubules, we need further study using more precise markers and long-term follow-up.

• Kidney Research and Clinical Practice
• /
• 제37권4호
• /
• pp.315-322
• /
• 2018

The high mortality rates associated with acute kidney injury are mainly due to extra-renal complications that occur following distant-organ involvement. Damage to these organs, which is commonly referred to as multiple organ dysfunction syndrome, has more severe and persistent effects. The brain and its sub-structures, such as the hippocampus, are vulnerable organs that can be adversely affected. Acute kidney injury may be associated with numerous brain and hippocampal complications, as it may alter the permeability of the blood-brain barrier. Although the pathogenesis of acute uremic encephalopathy is poorly understood, some of the underlying mechanisms that may contribute to hippocampal involvement include the release of multiple inflammatory mediators that coincide with hippocampus inflammation and cytotoxicity, neurotransmitter derangement, transcriptional dysregulation, and changes in the expression of apoptotic genes. Impairment of brain function, especially of a structure that has vital activity in learning and memory and is very sensitive to renal ischemic injury, can ultimately lead to cognitive and functional complications in patients with acute kidney injury. The objective of this review was to assess these complications in the brain following acute kidney injury, with a focus on the hippocampus as a critical region for learning and memory.

• The Korean Journal of Physiology and Pharmacology
• /
• 제22권6호
• /
• pp.661-670
• /
• 2018

Fimasartan, a new angiotensin II receptor antagonist, reduces myocyte damage and stabilizes atherosclerotic plaque through its anti-inflammatory effect in animal studies. We investigated the protective effects of pretreatment with fimasartan on ischemia-reperfusion injury (IRI) in a mouse model of ischemic renal damage. C57BL/6 mice were pretreated with or without 5 (IR-F5) or 10 (IR-F10) mg/kg/day fimasartan for 3 days. Renal ischemia was induced by clamping bilateral renal vascular pedicles for 30 min. Histology, pro-inflammatory cytokines, and apoptosis assays were evaluated 24 h after IRI. Compared to the untreated group, blood urea nitrogen and serum creatinine levels were significantly lower in the IR-F10 group. IR-F10 kidneys showed less tubular necrosis and interstitial fibrosis than untreated kidneys. The expression of F4/80, a macrophage infiltration marker, and tumor necrosis factor $(TNF)-{\alpha}$, decreased in the IR-F10 group. High-dose fimasartan treatment attenuated the upregulation of $TNF-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 in ischemic kidneys. Fewer TUNEL positive cells were observed in IR-F10 compared to control mice. Fimasartan caused a significant decrease in caspase-3 activity and the level of Bax, and increased the Bcl-2 level. Fimasartan preserved renal function and tubular architecture from IRI in a mouse ischemic renal injury model. Fimasartan also attenuated upregulation of inflammatory cytokines and decreased apoptosis of renal tubular cells. Our results suggest that fimasartan inhibited the process of tubular injury by preventing apoptosis induced by the inflammatory pathway.

• 한국임상수의학회지
• /
• 제26권1호
• /
• pp.29-35
• /
• 2009

본 연구의 목적은 돼지의 신장 자가이식에서 항산화제에 의한 허혈 및 재관류 손상의 감소에 대하여 ascorbic acid와 alpha-tocopherol이 미치는 영향을 평가하는 데 있다. 6두의 어린 돼지에 자가 신장 이식을 실시하였으며, 처치군에서는 수술 2일전 비타민 C와 E를 이틀 동안 전처치 하고, 그 뒤에 수술 중 비타민 C와 heparin이 첨가된 생리식염수를 절제되어 자가 이식할 신장에 관주하였다. 대조군에서는 수술 중 heparin이 첨가된 생리 식염수만을 절제되어 자가 이식할 신장에 관주하였다. 신장 기능을 평가하기 위하여 혈액 샘플을 채취하였으며, 수술 전, 수술 후 1, 3, 7, 14일에 혈청 creatinine과 BUN을 측정하였다. 그리고 병리조직 검사를 위해 14일 후 신장을 적출 보관하였다. 신장의 기능 검사에서 대조군과 처치군 사이에서 전체적인 유의성은 없었지만, 1일째, 3일째 또는 5일째에 두 그룹간의 유의적인 차이가 인정되었다 (p<0.05). 병리조직 검사 결과 처치군이 대조군 보다 더 적은 조직 손상의 정도를 보였다. 이러한 결과는, 비타민 C와 heparin을 이용한 신장의 관주 및 흡인의 과정이 신장의 허혈 및 재관류 손상을 감소시키는 데에 효과가 있었음을 시사하며, 이는 돼지의 신장 자가 이식에서 허혈 및 재관류의 손상을 감소시키며 신기능의 회복에 효과가 있음을 시사하는 바이다.

• Childhood Kidney Diseases
• /
• 제26권1호
• /
• pp.63-67
• /
• 2022

Nephrocalcinosis often occurs in infants and is caused by excessive calcium or vitamin D supplementation, neonatal primary hyperparathyroidism, and genetic disorders. Idiopathic infantile hypercalcemia (IIH), a rare cause of nephrocalcinosis, results from genetic defects in CYP24A1 or SLC34A1. Mutations in CYP24A1, which encodes 25-hydroxyvitamin D 24-hydroxylase, disrupt active vitamin D degradation. IIH clinically manifests as failure to thrive and hypercalcemia within the first year of life and usually remits spontaneously. Herein, we present a case of IIH wih CYP24A1 mutations. An 11-month-old girl visited our hospital with incidental hypercalcemia. She showed failure to thrive, and her oral intake had decreased over time since the age of 6 months. Her initial serum parathyroid hormone level was low, 25-OH vitamin D and 1,25(OH)₂ vitamin D levels were normal, and renal ultrasonography showed bilateral nephrocalcinosis. Whole-exome sequencing revealed compound heterozygous variants in CYP24A1 (NM_000782.4:c.376C>T [p.Pro126Ser] and c.1310C>A [p.Pro437His]). Although her hypercalcemia and poor oral intake spontaneously resolved in approximately 8 months, we suggested that her nephrocalcinosis and renal function be regularly checked in consideration of potential asymptomatic renal damage. Hypercalcemia caused by IIH should be suspected in infants with severe nephrocalcinosis, especially when presenting with failure to thrive.

• 한국어병학회지
• /
• 제36권2호
• /
• pp.415-422
• /
• 2023

In veterinary medicine for mammals, studies are being conducted to confirm the effects of antioxidants using pathological toxicity model studies, and are also used to confirm the effect of mitigating liver or kidney toxicity of specific substances. It was considered necessary to study such a toxicity model for domestic farmed fish, so thioacetamide (TAA), a toxic substance that causes tissue damage by mitochondrial dysfunction, was injected into rainbow trout (Oncorhynchus mykiss), a major farmed freshwater fish species in Korea. The experiment was conducted with 40 rainbow trout (Oncorhynchus mykiss) weighting 53 ± 0.6 g divided into two groups. Thioacetamide(TAA) 300mg/kg of body weight was intraperitoneally injected into rainbow trout and samples were taken 1, 3, 5, 7 days after peritoneal injection. As a result, in serum biochemical analysis, AST levels related to liver function decreased 3 and 5 days after intraperitoneal injection and increased after 7 days, and ALT levels also increased after 7 days. In addition, creatinine related to renal malfunction increased 3 and 5 days after TAA injection. In histopathological analysis, pericholangitis and local lymphocyte infiltration were observed in the liver from 1 day after intraperitoneal injection of TAA, and hepatic parenchymal cell necrosis was also observed from 3 days after intraperitoneal injection. Hyaline droplet in renal tubular epithelial cell was observed from 1 day after TAA injection, and acute tubular damage such as tubular epithelial cell necrosis appeared from 3 days after TAA injection. Accordingly, it is thought that it will be able to contribute to studies that require a toxicity model.

• Journal of Acupuncture Research
• /
• 제18권2호
• /
• pp.111-122
• /
• 2001

Objectives ; This study was undertaken to determine if Salviae Radix herb-acupuncture (SRA) exerts protective effect against alterations in membrane transport function in rabbits with mercury chloride (Hg)-induced acute renal failure. Methods and Results ; The administration of Hg at a subcutaneous single dose of 10mg/kg caused a reduction in GFR to 9.4% of the basal value and an increase in fractional Na+ excretion to 10-fold, indicating generation of acute renal failure. When animals were acupunctured with $0.5m{\ell}$ of SRA extract (0.1%) in both sides of Shinsu(BL23) for 7 days prod to Hg administration, such changes were significantly attenuated. The fractional excretion of glucose and phosphate was increased to approximately 132-fold and 7-fold, respectively, in rabbits treated with Hg alone, but the fractional excretion of glucose was increased to 26-fold and that of phosphate was not different from the basal value in SRA-pretreated rabbits. Uptakes of glucose and phosphate in purified isolated brush-border membrane and $Na^+-K^+$-ATPase activity in microsomal fraction were inhibited in rabbits treated with Hg alone, suggesting that impairment in proximal reabsorption of glucose and phosphate is resulted from a direct damage of membrane transport carriers and disruption of the normal $Na^+$ gradient. Conclusions ; Such changes were prevented by SRA. Uptakes of organic ions, PAH and TEA, in renal cortical slices were inhibited by the administration of Hg, which was prevented by SRA. Pretreatment of an antioxidant DPPD attenuated the increase in the fractional excretion of glucose and phosphate induced by the administration of Hg.

• Toxicological Research
• /
• 제29권1호
• /
• pp.61-67
• /
• 2013

Development of a therapy providing protection from, or reversing gentamicin-sulfate (GS)-induced oxidative stress and nephrotoxicity would be of great clinical significance. The present study was designed to investigate the protective effects of Houttuynia cordata Thunb. (HC) against gentamicin sulfate-induced renal damage in rats. Twenty-eight Sprague-Dawley rats were divided into 4 equal groups as follows: group 1, control; group 2, GS 100 mg/kg/d, intraperitoneal (i.p.) injection; group 3, GS 100 mg/kg/d, i.p. + HC 500 mg/kg/d, oral; and group 4, GS 100 mg/kg/d i.p. + HC 1000 mg/kg/d, oral administration). Treatments were administered once daily for 12 d. After 12 d, biochemical and histopathological analyses were conducted to evaluate oxidative stress and renal nephrotoxicity. Serum levels of creatinine, malondialdehyde (MDA), and blood urea nitrogen (BUN), together with renal levels of MDA, glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) were quantified to evaluate antioxidant activity. Animals treated with GS alone showed a significant increase in serum levels of creatinine, BUN, and MDA, with decreased renal levels of GSH, SOD, and CAT. Treatment of rats with HC showed significant improvement in renal function, presumably as a result of decreased biochemical indices and oxidative stress parameters associated with GS-induced nephrotoxicity. Histopathological examination of the rat kidneys confirmed these observations. Therefore, the novel natural antioxidant HC may protect against GSinduced nephrotoxicity and oxidative stress in rats.