ABSTRACT
PURPOSE: This study was performed to demonstrate a correlation among urinary 15d-PGJ2, proinflammatory cytokines (i.e. IL-23, IL-6, and TGF-beta1), and CRP, and to determinate the contributors to prognostic score and proteinuria in IgAN patients. METHODS: Fifty-four patients with biopsy-proven IgAN were enrolled. For comparison with IgAN, five MCD patients were also enrolled. Immunohistochemical staining for PPAR-gamma in kidney tissue and measurements of urinary IL-6, IL-23, TGF-beta1, 15d-PGJ2 and serum CRP were performed RESULTS: There was no difference according to PPAR-gamma staining. 15d-PGJ2 was negatively correlated with urinary IL-23, TGF-beta1, and CRP. Among proinflammatory cytokines and CRP, there were positive relationships with each other except for IL-23 and CRP. TGF-beta1 in the group having proteinuria more than 3 g/day was statistically higher than that in the sole hematuria group. However, in multivariate regression analysis, not a single relation was found between TGF-beta1 and proteinuria. Prognostic score was correlated with IL-6, IL-23, TGF-beta1, CRP, 15d-PGJ2, and 24hr proteinuria. 24hr proteinuria was correlated with IL-6 and 15d-PGJ2. In multivariate regression analysis, CRP, 15d-PGJ2, and 24hr proteinuria contributed to prognostic score, and only 15d-PGJ2 contributed to 24hr proteinuria. Last, urinary 15d-PGJ2 in IgAN was higher than that in MCD. CONCLUSION: Endogenous 15d-PGJ2 was associated with inflammation and might be considered as a material which could delay the damage of kidney in IgAN. In the future, larger cohort and long-term follow-up studies are needed to demonstrate the role of 15d-PGJ2 as prognostic indicator or marker of kidney damage.
Subject(s)
Humans , Cohort Studies , Corneal Dystrophies, Hereditary , Cytokines , Follow-Up Studies , Glomerulonephritis, IGA , Hematuria , Immunoglobulin A , Inflammation , Interleukin-23 , Interleukin-6 , Kidney , Prostaglandin D2 , Proteinuria , Transforming Growth Factor beta1ABSTRACT
BACKGROUND: Chronic kidney disease has deleterious influences on pregnancy, both fetus and mother. To determine the pregnancy outcome and associated risk factors, we analyzed 36 pregnancies in 26 women with various chronic kidney diseases. METHODS: Retrospective analysis of 36 pregnancies was performed in women with chronic kidney disease who underwent antenatal care and delivery at Pusan National University Hospital from January 1993 to December 2002. RESULTS: The mean age of patients was 29.7 +/- 3.6 years. Underlying kidney disease was lupus nephritis in 10 patients (11 pregnancies), IgA nephropathy in 7 patients (8 pregnancies), focal segmental glomerulosclerosis in 4 patients (9 pregnancies), membranoproliferative glomerulonephritis in 4 patients (7 pregnancies), membranous glomerulonephritis in 1 patient (1 pregnancy). Of the 36 pregnancies, fetal loss occurred in 14 pregnancies (38.9%), premature delivery 7 pregnancies (19.4%) and normal delivery 15 pregnancies (41.7%). Deterioration of maternal renal function occurred in 10 pregnancies (27.8%), hypertension 18 pregnancies (50.0%) and aggravation of proteinuria 26 pregnancies (72.2%). Fetal loss and deterioration of maternal renal function were more frequent in patients with preconception serum creatinine value (SCr) >or=1.4 mg/dL than in those with SCr or=140/90 mmHg during pregnancy was associated with low birth weight (p=0.027, OR 0.034, 95% CI 0.002-0.682). Deterioration of maternal renal function during pregnancy was recovered in 40.0%, hypertension was recovered in 50.0% and proteinuria was recovered in 77.8% within 1 year after delivery. CONCLUSION: Preconceptional impairment of maternal renal function and uncontrolled hypertension during pregnancy seem to be an important factors associated with fetal loss and low birth weight, respectively.
Subject(s)
Female , Humans , Infant, Newborn , Pregnancy , Pregnancy , Creatinine , Fetus , Glomerulonephritis, IGA , Glomerulonephritis, Membranoproliferative , Glomerulonephritis, Membranous , Glomerulosclerosis, Focal Segmental , Hypertension , Infant, Low Birth Weight , Kidney Diseases , Lupus Nephritis , Mothers , Multivariate Analysis , Pregnancy Outcome , Proteinuria , Renal Insufficiency, Chronic , Retrospective Studies , Risk FactorsABSTRACT
BACKGROUND: It is known that non-steroidal antiinflammatory drugs (NSAIDs) reduce the amount of proteinuria in nephrotic syndrome. It is based on the facts that the NSAIDs block the production of prostaglandins. Therefore selective cyclooxygenase-2 (COX-2) inhibitor may be expected to play a role in reduction of the proteinuria in nephrotic syndrome. METHODS: Twenty-seven Sprague-Dawley rats were divided into 3 groups. After 3 to 5 days of adaptation, we gave puromycin aminonucleoside to groups A and B via intraperitoneal route. The third group C was a normal control group. Selective COX-2 inhibitor was orally given to group A for 2 weeks. Each group was divided again into 3 subgroups by the day of experiment: 1, 14 and 21-day subgroups. We checked the changes in the serum and urine creatinine, albumin concentrations, creatinine clearances, the amount of proteinuria and the pathologic findings. The differences between groups were tested by 2-way ANOVA and Dunnett T-test, and the changes of proteinuria were tested by Repeated measures ANOVA. RESULTS: The changes of 24-hour urine protein excretion were significantly different between three groups (p<0.01). Protein excretion of group A was significantly decreased, especially between 14 and 21 days (p<0.05). The changes of creatinine clearance were significantly different between three groups (p<0.05), between 1 and 21 days (p<0.05). Electron microscopy showed morphological recovery of foot processes after administration of selective COX-2 inhibitor in PAN nephropathy rats (group A). CONCLUSION: It is suggested that selective COX- 2 inhibitors may be effective in reducing proteinuria and protecting the renal function in nephrotic syndrome.