Cognitive Function and Quality of Life in Patients with Chronic Renal Failure on Hemodialysis / 대한신장학회잡지

BACKGROUND: Nowadays it is considered that increment of hematocrit in chronic renal failure patients improves quality of life and cognitive function. But previous studies cannot exclude the practice effect and suggestion because they were accessed in the same ways before and after the erythropoietin treatment. This study was designed into two groups by hematocrit levels to know if patients with higher hematocrit levels have better quality of life and neurocognitive function. METHODS: Fifty-two chronic renal failure patients during hemodialysis received neurocognitive function test by physician before checking several self rating scales about quality of life. RESULTS: Patients with higher hematocrit levels had better scores in neurocognitive function tests and there was a relationship between the age and cognitive function. But patients with higher hematocrit levels didn't have better quality of life than those with lower ones. Instead there was strong correlation between the Beck Depression Inventory score and quality of life. CONCLUSION: These findings suggest that higher hematocrit levels improve cognitive function in chronic renal failure patients on hemodialysis, but increased hematocrit level does not always mean the better quality of life. Other psychological managements for depressive moods are recommended for better quality of life.

Cognitive Function and Quality of Life in Patients with Chronic Renal Failure on Hemodialysis / 대한신장학회잡지

BACKGROUND: Nowadays it is considered that increment of hematocrit in chronic renal failure patients improves quality of life and cognitive function. But previous studies cannot exclude the practice effect and suggestion because they were accessed in the same ways before and after the erythropoietin treatment. This study was designed into two groups by hematocrit levels to know if patients with higher hematocrit levels have better quality of life and neurocognitive function. METHODS: Fifty-two chronic renal failure patients during hemodialysis received neurocognitive function test by physician before checking several self rating scales about quality of life. RESULTS: Patients with higher hematocrit levels had better scores in neurocognitive function tests and there was a relationship between the age and cognitive function. But patients with higher hematocrit levels didn't have better quality of life than those with lower ones. Instead there was strong correlation between the Beck Depression Inventory score and quality of life. CONCLUSION: These findings suggest that higher hematocrit levels improve cognitive function in chronic renal failure patients on hemodialysis, but increased hematocrit level does not always mean the better quality of life. Other psychological managements for depressive moods are recommended for better quality of life.

Effect of High Glucose, Angiotensin ll and Aniotenisn Converting Enzyme Inhibitor on the Expression of PC alpha1(IV) mRNA in Cultured Human Mesangial Cells / 대한신장학회잡지

OBJECTIVE: Diverse glomerular disorders leadsing to progressive glomerulosclerosis share the common features of increased mRNA expression for extra- cellular matrix protein and growth factors. The precise role of angiotensin II in contributing to these disturbances is currently unknown. ACE inhibitors have been proved to be beneficial in protecting against glomerular injury in animal models and many of human glomerular diseases. Type IV collagen is a main component of extracellular matrix in the mesangium : its increased accumulation is a common pathologic finding in the glomerulosclerosis. There are some evidences that the beneficial effect of ACE inhibitor does not solely depend on the hemodynamic effect, but may be mediated by other effect. The purpose of this study is to evaluate the effects of high glucose, angiotensin II and angiotensin converting enzyme inhibitor on the expression of PC alpha1(lV) in mesansial cells(MCs). METHODS: Human mesangial cells were cultured with standard method. To investigate the effect of each drug and high glucose condition, MCs were cultured in the normal-glucose medium(100mg/dl) and high-glucose medium(450mg/dl), respectively. An- giotensin II and angiotensin converting enzyme inhibitor(captopril) were added to culture medium at final concentration of 10 M which is the physiologic dose in vivo. MCs were cultured in each condition for 3days, when the maximal effect of high glucose on MCs, and harvested for mesurement of the expression of PC alpha1(IV) mRNA. To quantitate the PC alpha(1V) mRNA levels in each condition, semiquantitatine RT-PCR was done with co-amplification of house keeping gene. RESULTS: PCa1(IV) mRNA expression was significantly increased in high-glucose medium(30mM) compared to normal-glucose medium(5.5mM)(2.28+/-0.34 vs 0.96+/-0.08, p(IV) mRNA expression to 4.64+/-0.28(p<0.05). Angiotensin II in the normal-glucose medium increased the PC alpha1(lV) mHNA expression as 2.69+/-0.23 control(p<0.05). Addition of angiotensin converting enzyme inhibitor(Capopril, 10(-6)M) in high- glucose culture medium significantly suppressed the PC alpha1(IV) mRNA expression as 0.690.11(p<0.05). CONCLUSION: High glucose concentration in culture medium significantly increases the mRNA expression of procollagen alphal(IV) than normal glucose concentration. Angiotensin II increases the collagen mRNA expression directly and this effect was significantly prevented by ACE inhibitor. This result suggests that hyperglycemia in diabetic millieu can directly increase collagen production, and ACE inhibitor may inhibit progressive glomerulosclerosis by decreasing collagen production as well as reducing intraglomerular pressure.

The Effects of High Glucose, Angiotensin II and ACE Inhibitor on the Expression of TGFbeta mRNA in Cultured Human Mesangial Cells / 대한신장학회잡지

OBJECTIVE: Diabetic nephropathy is an important cause of end stage renal disease in Korea and associated with major morbidity and mortality. The precise pathogenic mechanism of this disease is still controversial, but it has been considered that multiple factors are contribute to the development and progression of diabetic nephropathy. One of these factors, renin-angiotensin system has been proven to be a major mediator of this disease via activation of angiotensin II, which has multiple functions such as induction of production of extracellular matrix protein and various intraglomerular cells, tubulointerstital component and increment of intraglomerular pressure. Transforming growth factor(TGFbeta) is a multifunctional cytokine with major profibrotic character, which stimulates the production of extracellular matrx(ECM) protein, inhibit the degradation of ECM and induce the interaction of mesangial cells with ECM via integrin receptors. This study was done to evaluate the role of angiotensin II and angiotensin converting enzyme inhibitor in expression of TGFbeta mRNA which is a main mediator in the pathogenesis of diabetic nephropathy. METHODS: Human mesangial cells(MCs) were cultured by standard culture techniqne. For this study, cells in the 5th to 7th passage were used. To make a different glucose concentration in culture medium, normal(100mg/dl) or high glucose(450mg/dl) concentrations of D-glucose were added, and cultured in 17% heat inactivated fetal bovine serum. Angiotensin II and ACE inhibitor(captopril) were administered to the culture medium at final concentration of 10-6M. After 72 hours, MCs were harvested to measure the expression of TGFbeta mRNA. To measure the mRNA expression of TGFbeta in each condition, semi quantitative PCR was done and all results were corrected by beta-actin gene. RESULTS: mRNA expression of TGFbeta was significantly increased in the high glucose medium(30 mM) compared to normal glucose medium(5.5mM) (3.82+/-0.465 vs 2.27+/-0.13, p<0.05). Administration of angiotensinII(10-6M) in high glucose medium induced a further increase in the TGFbeta expression to 4.29+/-0.476(p<0.05). AngiotensinII(10-6M) in normal glucose medium also showed a significant increase in TGFbeta expression as 3.40+/-1.88(p<0.05). Administration of ACE inhibitor(Captopril, 10-6M) in high glucose medium prevented the increse of TGFbeta expression(1.20+/-0.18 vs 3.82+/-0.465, p<0.05). CONCLUSION: From these findings, it suggest that angiotensinII is an important mediator in the pathogenesis of diabetic nephropathy. ACE inhibitor may have a role in the progress of this disease via direct suppression of TGFbeta system as well as beneficial intraglomerular hemodynamic effect.