Kosin Medical Journal

Original articles

Effects of cholecalciferol and omega-3 fatty acids on hepcidin levels in 5/6 nephrectomy rats: Yu In Jeong, Hyo Jin Jung, Mi Hwa Lee, Young Ki Son, Seong Eun Kim, Won Suk An, Su Mi Lee; Kosin Med J. 2024;39(1):35-43. Published online September 25, 2023; DOI: https://doi.org/10.7180/kmj.23.137

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Abstract PDF PubReader ePub: Background
Anemia is a common complication of chronic kidney disease (CKD). In patients with CKD-related anemia, an inverse relationship between vitamin D and hepcidin levels has been observed. Hepcidin is a key regulator of iron homeostasis, mediated via binding to ferroportin. The aim of this study was to investigate the effects of cholecalciferol and omega-3 fatty acids (FA) on hepcidin levels using 5/6 nephrectomized (Nx) rats.
Methods
Male Sprague-Dawley rats were divided into five groups: sham control, 5/6 Nx, 5/6 Nx treated with cholecalciferol, 5/6 Nx treated with omega-3 FA, and 5/6 Nx treated with both cholecalciferol and omega-3 FA. We measured the hepcidin and ferroportin levels in the kidney and liver by enzyme-linked immunosorbent assays and Western blots. We evaluated hepcidin expression in the kidney by immunohistochemical staining.
Results
Among the five groups, 5/6 Nx rats exhibited the worst kidney function. Compared with the sham controls, 5/6 Nx rats showed significantly increased serum hepcidin levels and decreased vitamin D levels. Supplementation with either omega-3 FA or cholecalciferol decreased hepcidin and increased vitamin D levels, with a concurrent improvement of anemia. Furthermore, 5/6 Nx rats treated with omega-3 FA/cholecalciferol showed decreased ferroportin and ferritin levels, while iron and total iron-binding capacity levels increased.
Conclusions
Treatment with a combination of cholecalciferol and omega-3 FA may improve anemia in a CKD rat model by decreasing hepcidin levels.

Omega-3 fatty acids upregulate Nrf2 expression and attenuate apoptosis, inflammation, and fibrosis in a rat model of cyclosporine-induced nephropathy: Ji Young Lee, Young Ki Son, Mi Hwa Lee, Su Mi Lee, Seong Eun Kim, Won Suk An; Kosin Med J. 2023;38(3):184-192. Published online July 26, 2023; DOI: https://doi.org/10.7180/kmj.23.112

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Background
Cyclosporine A (CsA)-induced kidney injury is characterized by renal impairment with inflammatory cell infiltrations, apoptosis, fibrosis, and hypoxic injury. It is not clear whether omega-3 fatty acids (O-3 FAs), which have anti-inflammatory and antioxidant roles, affect nuclear factor erythroid 2-related factor 2 (Nrf2) expression. The aim of this study was to investigate whether O-3 FAs affect Nrf2 expression and exert anti-inflammatory, anti-apoptotic, and anti-fibrotic effects in CsA-induced nephropathy.
Methods
Male Sprague-Dawley rats were divided into control, CsA-treated, and CsA-treated with O-3 FA groups. Nrf2 expression was measured by Western blots and immunohistochemical staining.
Results
Kidney function was impaired in the CsA-treated rats compared to the controls. Caspase-3 and caspase-7 were activated in the CsA-treated group, and the Bax/Bcl2 ratio was higher. O-3 FAs attenuated these apoptosis-related changes. ED-1 and inhibition of kappa B (IĸB) protein expression were significantly upregulated in the CsA-treated group. Compared to the control group, O-3 FA supplementation attenuated the increased expression of ED-1 and IĸB related to inflammation. Smad2/3, Smad4, and transforming growth factor-β1 were activated in the CsA group, and O-3 FA treatment prevented these changes related to renal fibrosis. The expression of Nrf2 was reduced in CsA-treated rats, but Nrf-2 was increased by O-3 FA treatment.
Conclusions
We suggest that Nrf2 is a potential mediator induced by O-3 FA supplementation and that it attenuates pro-inflammatory pathways, fibrotic processes, and apoptosis. Further studies are needed to elucidate the crosstalk between Nrf2 expression and signals related to O-3 FA treatment.

Citations

Citations to this article as recorded by

Omega-3 fatty acids: promising therapeutic agents for combating kidney injuries
Hee-Jae Cha
Kosin Medical Journal.2023; 38(3): 157. CrossRef

Dietary education may reduce blood cadmium and mercury levels in chronic kidney disease patients with higher blood cadmium and mercury levels: Su Mi Lee, Young-Seoub Hong, Byoung-Gwon Kim, Jung-Yeon Kwon, Yongsoon Park, Seong Eun Kim, Won Suk An; Kosin Med J. 2023;38(2):107-116. Published online May 24, 2023; DOI: https://doi.org/10.7180/kmj.23.101

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Abstract PDF Supplementary Material PubReader ePub

Background
Exposure to cadmium and mercury is associated with renal dysfunction. This study aimed to investigate the possible ability of dietary education to decrease blood cadmium and mercury levels in patients with chronic kidney disease (CKD).
Methods
Twenty-seven patients with CKD were enrolled in this prospective, single-arm pilot study. Patients with blood cadmium levels ≥1.4 μg/L were instructed to reduce their intake of shellfish, while those with blood mercury levels ≥5.0 μg/L were asked to reduce their intake of externally blue-colored fish.
Results
Seven dialysis patients and 15 pre-dialysis patients completed the study. Compared with baseline, the blood cadmium (2.0±0.7 μg/L vs. 1.8±0.7 μg/L, p=0.031) and mercury levels (4.4±2.6 μg/L vs. 3.5±1.9 μg/L, p=0.005) after 1 year significantly decreased, although the dietary intake was not significantly different in patients with blood cadmium levels ≥1.4 μg/L and blood mercury levels ≥5.0 μg/L. In pre-dialysis patients, kidney function worsened after 1 year compared with that at baseline despite the reduction in blood cadmium and mercury levels.
Conclusions
Reduction of food intake containing cadmium and mercury may lower the blood cadmium and mercury levels in CKD patients with higher cadmium and mercury levels. Higher blood cadmium levels may cause renal disease progression in pre-dialysis patients, and further studies are necessary to determine the underlying mechanisms.

Citations

Citations to this article as recorded by

Impact of dietary education on blood cadmium and mercury levels in chronic kidney disease: a path to renal health improvement
Ho Sik Shin
Kosin Medical Journal.2023; 38(2): 73. CrossRef

Case reports

A Case of Steroid Resistant Minimal Change Disease Associated with Portal Vein Thrombosis Treated by Combined Immunosuppressive Agents: Hyo Jin Jung, Su Mi Lee, Seo Hee Rha, Seong Eun Kim, Young Ki Son, Ki Seung Kim, Won Suk An; Kosin Med J. 2017;32(1):90-98. Published online June 30, 2017; DOI: https://doi.org/10.7180/kmj.2017.32.1.90

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Abstract PDF PubReader ePub: Minimal change disease (MCD) is a common cause of nephrotic syndrome and relatively well responds with steroid treatment. However, nearly half of patients with MCD experience recurrence of nephrotic syndrome. Thromboembolic events including renal vein thrombosis may occur in patients with MCD, but portal vein thrombosis rarely occurs. We experienced a case of frequent relapse/steroid dependent MCD with nephrotic syndrome progressed to steroid resistance associated with portal vein thrombosis. This patient showed complete remission of MCD and resolution of portal vein thrombosis after treatment with corticosteroid, cyclosporine, mycophenolate mofetil, and anticoagulant.

A Case of Lactate Containing Peritoneal Dialysis Solution Induced Lactic Acidosis Corrected by Changing to Hemodialysis: Eun Bin Kim, Ki Seung Kim, Su Mi Lee, Young Ki Son, Seong Eun Kim, Won Suk An; Kosin Med J. 2017;32(1):105-110. Published online June 30, 2017; DOI: https://doi.org/10.7180/kmj.2017.32.1.105

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Abstract PDF PubReader ePub: Elevated lactate levels are associated with acute illnesses, and the mortality is high. Here, we report a case of lactate-containing peritoneal dialysis (PD) solution inducing lactic acidosis corrected by changing to hemodialysis (HD). This 70-year-old female patient was treated with PD 8 months previously for end-stage renal disease caused by diabetes mellitus. She was admitted complaining of general weakness. Initial lactate level was 22.1 mg/dL and increased to 62.4 mg/dL showing high anion gap metabolic acidosis and compensatory hyperventilation. There are no definite causes of lactic acidosis besides the use of PD solutions containing a lactate component. The patient's lactate level was decreased after temporarily changing the dialysis modality to HD. Her lactate level was increased again after restarting PD, and decreased to normal after restarting HD. We report this case because physicians should consider lactate-containing PD solution as a possible cause of lactic acidosis.

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