• 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.

• Journal of Veterinary Clinics
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• v.20 no.4
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• pp.449-457
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• 2003

To investigate the renal effects of enrofloxacin administration on rats induced with dehydration or hyperoxaluria, male rats were treated with enrofloxacin of 50 mg to 500 mg/kg b.w.. The microscopical observations of kidney and urine sediment were carried out in the experimental groups. The result obtained were as follows; The male rats deprived of water for 72 hours and administered with enrofloxacin. As enrofloxacin administration dose was increased, clinical signs such as loss of appetite, depression, weakness, and loss of urine output became more severe. In the histopathological findings, there were hyperemia and hemorrhage in renal cortex, vacuolation and necrosis of renal tubular epithelia, proteinous casts within renal tubules. The male rats were orally administered with sodium oxalate and injected with enrofloxacin for 7days. As enrofloxacin administration dose was increased, clinical signs such as the loss of appetite and water consumption, and weakness became more severe. In the histopathological findings, there are hemorrhage of glomeruli and cortical hyperemia, vacuolation and necrosis of tubular epithelia, proteinous casts in renal tubules. In the microscopical findings of urine sediment, there are calcium oxalate crystal (diamond-like type) and magnesium ammonium phosphate crystals (rhomboid). The male rats were intraperitoneally injected with sodium oxalate and administered with enrofloxacin for 7days. As enrofloxacin administration dose was increased, clinical signs such as the loss of appetite and water consumption, weakness were more severe. In the histopathological findings, there were hyperemia and hemorrhage in both glomeruli and renal cortex. Severe necrosis of renal tubular epithelia, bluish materials within renal tubules were also found. In the microscopical findings of urine sediment, there were many calcium oxalate crystals. The present results suggest that enrofloxacin has some injurious effects in rats having dehydration or hyperoxaluria, and clinically, we should consider these renal injury effects when we use enrofloxacin in patients accompanied renal disease, dehydration and hyperoxaluria conditions.

• Journal of Veterinary Clinics
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• v.24 no.1
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• pp.73-75
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• 2007

Heat stroke can lead multi-organ damage with hemorrhage and necrosis in the lungs, heart, liver, kidneys, brain and Ut. Heat stroke occurs when the elevation of core body temperatures induce a failure of thermoregulatory mechanism. A four-year-old male African Lion(Panthera leo) showed clinical signs such as panting, tachycardia, hyperthermia, unconsciousness and mydriasis under He hish humidity and hot weather. Clinical treatment and pouring cool water was unsuccessful. Grossly, congestion of lungs and pleura was observed. Yellowish discoloration was observed in the renal cortex. Microscopically, the coagulative necrosis in kidney and congestion of lungs and spleen were observed. In our knowledge, this case was closely associated with acute heat stroke.

• Korean Journal of Veterinary Research
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• v.54 no.4
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• pp.225-231
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• 2014

Klotho deficiency is an early event in acute kidney injury (AKI) that exacerbates acute kidney damage. The present study explored the expression of Klotho and inflammation related factors in cisplatin-induced AKI. Rats (n = 18) were treated with cisplatin intraperitoneal injection (5 mg/kg) or left untreated as controls (n = 6), then sacrificed at 5 (n = 6) and 10 days (n = 6) treatment. Five days after cisplatin injection, the serum kidney enzymes and kidney cell apoptosis were significantly increased. Moreover, the expression of Klotho was decreased when compared to the control group, especially in the cortex and outer medulla regions. In contrast, inflammation related signals including nuclear factor kappa B, tumor necrosis factor-${\alpha}$, and tumor necrosis factor-like weak inducer of apoptosis were enhanced. However, 10 days after cisplatin injection, Klotho expression was enhanced upon both IHC and Western blot analysis, with slightly recovered renal function and decreased apoptosis. Furthermore, inflammation related signals expression was decreased relative to the 5 days group. Overall, this study confirmed the opposite expression patterns between Klotho and inflammation related signals and their localization in cisplatin-induced AKI kidney.

• Korean Journal of Veterinary Research
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• v.22 no.2
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• pp.221-232
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• 1982

This paper dealt with the pathological and clinical findings on the experimentally induced rodenticide (fluoroacetate, zinc phosphide, thallium sulfate, coumarin) and NaCN poisoning of ruminants (Holstein cattle and/or Korean native goat) for the purpose of the diagnosis in the accidental rodenticide poisoning of cattle. The results observed are summarized as follows: Fluoroacetate poisoning (cattle and goat): in the clinical signs, there were depression, convulsion, dyspnea, groan, grinding of the teeth, vomiting, opisthotonus and post-mortem tympany. In the macroscopical findings, the blood was more or less poor coagulative and dark red, bloody fluid with foam in the trachea, hyperemia and hemorrhage of tracheal mucosa and lung, cloudy swelling and hyperemia of kidney, epicardial hemorrhage(cattle), and hyperemia of abomasum, intestine and brain were observed. In the microscopical findings, there were pulmonary edema and hemorrhage, necrosis of convoluted tubular epithelium and interstitial hemorrhage of kidney, focal coagulative necrosis of myocardium, hemorrhage of pancreas and spleen, dilatation of Virchow-Robin space and hyperemia of brain, and necrosis with desquamation of mucosal epithelia of abomasum and upper small intestine. In the histological lesions of the liver, lobular peripheral hyperemia, centrilobular necrosis and cytoplasmic inclusion bodies of the hetatic cells were observed. The cytoplasmic inclusion body of the hepatic cells was not seen in the affected goat, but hydropic degeneration of the hepatic cells was marked. Zinc phosphide poisoning (cattle and goat): clinically, the affected animals died in recumbent position after ataxia, dyspnea and convulsion. In the macroscopical findings, hyperemia and hemorrhage of lung, cloudy swelling and hyperemia of liver and kidney, hemorrhage of spleen (cattle), and catarrh of abomasum and small intestine were observed. In the microscopical findings, necrosis of the convoluted tubular epithelium and hyperemia of kidney, hemorrhage of spleen, hyperemia of lung, hyperemia or hemorrhage of heart, cloudy. swelling and fatty changes of hepatic cells, dilatation of hepatic central vein, hyperemia of brain, and catarrh of abomasal and small intestinal mucosae were observed. Thallium sulfate poisoning (cattle): in the macroscopical findings dark red color of blood, hyperemia and hemorrhage of lung, bloody fluid with foam in the tracheal mucosa, petechiae of tracheal mucosa, cloudy swelling and hemorrhage of liver, necrotic lesions and hemorrhage of renal cortex and epicardial hemorrhage were observed. In the microscopical findings, severe hemorrhages of the lung, cloudy swelling and necrosis of hepatic cells, hyperemia and hemorrhage of liver, focal coagulative necrosis of mycordium, necrosis of the convoluted tubular epithelium and hyperemia of kidney, hyperemia and hemorrhage of spleen and dilatation of Virchow-Robin apace in brain were observed. Coumarin poisoning (goat): the poisoned animals died in the state of groan and depression. In the macroscopical findings, poor coagulation of blood, hemorrhage of lung, cloudy swelling and severe hemorrhages of liver, cloudy swelling and hemorrhage of kidney, abomasal hemorrhage, catarrh of small intestine, and hyperemia and hemorrhage of the other organs were observed, In the microscopical findings, hyperemia and hemorrhage of lung and kidney, cloudy swelling of the convoluted tubular epithelium of kidney, severe hepatic hyperemia, cloudy swelling and hydropic degeneration of heptatic cell, and hyperemia and hemorrhage of brain and spleen were observed. NaCN poisoning (cattle and goat): clinically, there were convulsion, severe dyspnea, paresis of hind limb, depression and then rigor of four limbs. In the macroscopical findings, bright red color of blood, hyperemia and bright and red tinge of lung cloudy swelling of kidney and liver, and hyperemia of abomasum were observed. In the microscopical findings, cloudy swelling and hydropic degeneration of hepatic cell, hyperemia and edema of lung, necrosis and degeneration of the convoluted tubular epithelium and hemorrhage in kidney, dilatation of Virchow-Robin space of brain and hemorrhage of spleen were observed.

• Korean Journal of Veterinary Research
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• v.45 no.1
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• pp.99-103
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• 2005

We report septicemic colibacillosis accompanied by white-spotted kidney in a 30-day old female Holstein-Friesian dairy calf. Grossly, there were numerous white spots sized average 0.5cm in diameter in both kidneys. When sectioned sagittally, there were radially oriented gray streaks extending outward and reaching the renal cortex. The renal papillae were ulcerated, white to gray in color and very friable. Histologically, there was extensive purulent inflammation characterized by severe neutrophilic cellular infiltrations in the tubular lumens and interstitia. In addition, massive coagulative necrosis were found in the apices of papillae. Numerous Gram-negative bacterial colonies were detected in both of the renal and lung tissues. Beta-hemolytic Escherichia coli (E. coli) was purely isolated from the renal parenchyma, peritoneal surface and pleural surface. Based on the above results, we suggest that the generalized septicemia with pyelonephritis may be oriented from the lower urinary tract infection with E. coli in this case.

• Korean Journal of Veterinary Research
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• v.38 no.4
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• pp.918-928
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• 1998

The present study was done with two aims. First, to evaluate the radiographic measurements of liver volumes in normal and hepatomegaly dogs induced by carbon tetrachloride. Second, to investigate quantitative tissue echo pattern by ultrasonography. Gray level histogram of the normal liver and the kidney were estimated with carbon tetra-chloride intoxication. In normal, r-square for liver volume to body weight was 0.93372, and this showed direct linear regression. Gray level histograms of the normal liver and the kidney were $19.150{\pm}2.490$(mean${\pm}$SD) and $13.175{\pm}2.686$(mean${\pm}$SD) respectively(p < 0.01). Liver parenchymal echogenicity was more hyperechogenic than kidney cortex echogenicity. Liver/Kidney ratio was $1.504{\pm}0.313$ and it can be used relative comparison of liver and kidney parenchymal echogenicity. In carbon-tetrachloride($CCl_4$) intoxication, changes of liver volume appeared to increase up to 24 hours after administration (p < 0.05), and decreased gradually to normal level after 2~5 days. Gray level histogram of liver parenchyma decreased up to 24hours (p < 0.01) after intoxication and then gradually increased to normal level. But that of kidney cortex had no significant change. Liver/Kidney ratio also decreased by 2 days(p < 0.01) and then gradually increased to normal level. On histopathologic features of hepatic tissues in carbon tetrachloride intoxication, both coagulative necrosis of hepatic cell and hemorrhage of centrilobular & midzonal area were identified. Conclusively, plain radiography is a useful diagnostic method for evaluating liver volume in mild hepatomegaly. Especially, it is considered that an adequate numerical processing of the liver length, depth and thoracic width and depth measurement would be helpful. Using gray level histogram, ultrasonographic evaluation was useful objective methods in early diagnosis of diffuse hepatic disease.

• Journal of Veterinary Clinics
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• v.22 no.4
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• pp.439-443
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• 2005

Rejection is one of the life-threatening complications after organ transplantation. An eight-month-old, intact male, mixed breed dog was presented with acute rejection after renal allograft. The heterotopic renal transplantation with bilateral nephrectomy was performed in the dog. The triple drug protocol for immunosuppression was applied for prevention of the acute rejection. Postoperative care was done according to the transplantation protocol of VMTH, Kangwon National University. The dog was euthanized when the serum creatinine concentration exceeded 5 mg/dL followed by tile signs of illness. The transplanted kidney was enlarged. The renal cortex lesions were characterized by necrosis of the renal tubules and the glomeruli. Interstitial lesions were characterized by hemorrhage and severe infiltration of lymphoid cells. Intrarenal arteries showed necrosis of the walls and infiltration of perivascular lymphoid cells. In immunohistochemical (IHC) findings, infiltration of the CD4 and the CD8 positive T lymphocytes was examined. In this case, acute rejection was shown by humoral and cellular immunity on the basis of histopathologic and IHC evaluation.

• Korean Journal of Veterinary Pathology
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• v.3 no.2
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• pp.95-97
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• 1999

A case of renal candidiasis is reported in a 4-year-old male Masked Palm civet (Paguma larvata) On necropsy, the kidneys were bilaterally swollen, pale and had numerous 1 to 3 mm diameter white foci throughout the parenchyma on cut section. The urinary bladder was filled with opaque and milky exudate. Histologically, severe infiltration of neutrophils and macrophages and necrosis were noted in the interstitial areas of both cortex and medulla and in the lumens of renal tubules and collecting duct often resulting in cystic dilation of the tubules. PAS-positive fungal yeasts or pseudohyphae were often associated with the lesion. Candida albicans was isolated from the kidney and urinary bladder.

• Korean Journal of Veterinary Service
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• v.35 no.1
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• pp.59-62
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• 2012

A 3-year-old Jeju native black sow with sudden death was requested to the Jeju Self-Governing Provincial Veterinary Research Institute for diagnosis in July 2009. Because the pig died suddenly, we could not find any clinical signs. Gross lesions such as pulmonary edema, redness of heart, liver, kidney and lymph nodes were observed at necropsy. Histopathologically, there were severe eosinophilic meningoencephalitis, atrophy, degeneration and necrosis of laminar neurons, and neovascularization in cerebral cortex. Based on histopathological findings and history taking about temporal suspension of water supply, this case was diagnosed as salt poisoning of a Jeju native sow. In our best knowledge, this is the first report for salt poisoning of sow in Korea, especially in Jeju native pig.