Byoung Soo Cho

A High Glucose Concentration Stimulates the Expression of Monocyte Chemotactic Peptide 1 in Human Mesangial Cells

The mechanism of glomerular infiltration of monocytes remains unknown in diabetic nephropathy. We examined the effect of a high glucose concentration on monocyte chemotactic peptide 1 (MCP-1) expression in human mesangial cells (MCs) by using enzyme-linked immunosorbent assay and reverse transcription coupled with polymerase chain reaction (PCR). More than a 50% increase in the MCP-1 protein production was observed in MCs cultured in high-glucose medium (450 mg/dl) as compared to normal glucose (100 mg/dl; 1,496 ± 75 vs. 966 ± 15 pg/ml after 24 h, 1,910 ± 93 vs. 1,250 ± 55 pg/ml after 48 h). Semiquantitative PCR showed that phorbol myristate acetate (100 nM) increased the ratio of PCR products for MCP-1 to housekeeping gene glyceraldehyde-3-phosphate dehydrogenase on densitometric results at 24 h by 2.7-fold, which was prevented by calphostin C (200 nM) pretreatment. High glucose increased the ratio by 3-fold as compared to normal glucose at 24 h (0.72 ± 0.11 vs. 0.24 ± 0.01). This was also suppressed by calphostin C pretreatment. These findings demonstrate that high glucose can directly increase MCP-1 expression in MCs, which may contribute to monocyte infiltration in diabetic nephropathy, and this is regulated by protein kinase C.

Polymorphisms in Interleukin-1β and Interleukin-1 Receptor Antagonist Genes Are Associated with Kidney Failure in Korean Patients with Type 2 Diabetes mellitus

Background/Aim: Cytokines play an important role in the pathogenesis of kidney diseases. The aim of the study was to investigate the impact of interleukin (IL)-1 cluster genes on diabetic nephropathy in Korean patients with type 2 diabetes mellitus (DM). Methods: We investigated –511 C/T polymorphism of IL-1β and tandem repeat polymorphism in intron 2 of IL-1 receptor antagonist in type 2 DM patients with end-stage kidney failure as compared with patients without nephropathy. Results: The IL1B2 allele was found more frequently in patients with kidney failure than in controls (57.4 vs. 46.1%, p < 0.05). An excessive homozygous carriage of IL1B2 was found in patients with kidney failure when compared with controls (30.5 vs. 18.3%, p < 0.05). The allelic frequency of IL1RN*2 was also higher in cases than in controls without nephropathy (8.4 vs. 2.8 %, p < 0.05). The carriage rate of IL1RN*2 was significantly associated with an increased risk of kidney failure (15.8 vs. 5.6%; OR 3.19, 95% CI 1.24–8.17). The risk of kidney failure was highest in those carrying both IL1RN*2 and IL1B2 (OR 3.90, 95% CI 1.34–11.40). Conclusion: IL1B2 and IL1RN*2 genotypes of the IL-1 cluster genes are associated with diabetic nephropathy in Korean patients with type 2 DM.

Cataract and glaucoma in Korean children with chronic glomerulonephritis receiving systemic corticosteroid treatment

Editor, I n paediatric chronic glomerulonephritis, systemic corticosteroid treatment is administered for a long period of time. Therefore, there is a high probability of steroid-induced ocular complications such as cataracts and glaucoma. We examined the association of ocular complications with systemic corticosteroid treatment through clinical reports conducted on a large number of Korean children with chronic glomerulonephritis. We retrospectively analysed medical records of 238 Korean children with chronic glomerulonephritis who received systemic corticosteroid treatment between January 2000 and December 2006 in the Department of Pediatrics at Kyung-Hee University Medical Center. Systemic corticosteroid treatment is divided into methylprednisolone pulse treatment and long-term low-dose oral prednisolone treatment. The number of pulse treatment cycles given depended on the degree of proteinuria improvement. After pulse treatment, low-dose oral prednisolone was administered and slowly tapered. The duration of the corticosteroid administration was calculated at the time the intraocular complications developed. If the intraocular complications did not develop in the patients, the duration was calculated at the time of last observation. The total corticosteroid dose was calculated based on the sum of corticosteroid used for methylprednisolone pulse treatment and low-dose oral corticosteroid treatment during the entire treatment period. All patients were examined for the occurrence of cataracts and measurement of intraocular pressure (IOP) before and every 3–6 months after starting corticosteroid treatment. The association of cataract and glaucoma with dose and duration of corticosteroid treatment was analysed statistically by using the binary logistic regression analysis. Cataracts occurred in 74 patients, an incidence of 31%. In cataract cases, there was a statistically significant association with the frequency of intravenous methylprednisolone pulse treatment (Table 1). So exposure to high-dose corticosteroid may accelerate the onset of corticosteroid-induced cataract formation. Several reports especially have investigated the relationship between corticosteroid pulse treatment and cataracts. Nakamura et al. (2003) reported that in postrenal transplant, corticosteroid pulse treatment is considered to be a risk factor for developing steroid cataracts. Nerome et al. (2008) reported that in paediatric patients, frequency of intravenous methylprednisolone pulse treatment was a significant risk factor for inducing cataracts. But considering that total corticosteroid dose, total corticosteroid dose per weight was not associated with cataract formation, the duration of high-dose corticosteroid treatment may be a more significant risk factor for inducing cataract than high dose of corticosteroid. Pavlin et al. (1977) reported that in 62 recipients of renal transplants, a positive correlation was found between the development of cataracts and the number of days on which the dose exceeded 100 mg. Therefore, extensive high-dose