No abstract available.
Glomerulonephritis*

OBJECTIVES: lschemic acute renal failure(ARF) is characterized by an abrupt and sustained decline in GFR within minutes to days after renal ischemia and not immediately reversed on restoration of renal blood flow. The typical delay of a few days to a few weeks suggests reversible parenchymal damage awaiting cell regeneration for functional recovery. Many potentially cell damaging factors, such as ATP depletion, plasma membrane phospholipid degradatian and superoxide-induced membrane damage, play a central part in ischemic injury. More recently, much attention has been focused on the role of calcium, especially ischemic cell injury and the possible therapeutic role of calcium channel blockers emerged from studies conducted several years ago. In the past, it was thought that activation of renin-angiotensin system plays a role in the pathogenesis of ARF. Now the role of angiotensin in human renal ischemia also appears to be controversial. The following study was done in order to investigate the effect of a calcium channel blocker, nifedipine, on gene expression of renin during acute ischemic renal injury. METHODS: The Sprague-Dawley rats were divided into 4 groups, group I(n=3) as the control, group II (n=3) as the sham operation group, group III(n=15) as the ischemic renal injury group without nifedipine pretreatment, and group IV(n=15) as the ischemic renal injury model by right nephrectomy and left renal artery clamping for 40 minutes with systemic nifedipine pretreatment(10mg/kg), 1n ischemic renal injury model(group III and IV), rats were further divided into three subgroups according to reperfusion time of 1,24,72 hours. The non-ischemic right kidney removed at the time of initial procedure served as paired control. Total renal RNA was extracted by Chomczynskis method and electrophoresis was done in a 1% agarose gel containing 2,2M formaldehyde. Northern was performed at 42degrees C with isotope labeled renin probe for 18 hours, Autoradiographs were obtained and quantitated by a densitometer measured at 530nm. RESULTS: 1) The expression of renin gene was markedly decreased after renal ischemia and slowly recovered to one half of the control level after 72 hours of reperfusion. 2) Renin gene expression pattern of ischemic renal injury with prior nifedipine treatment was similar to the ischemic group without nifedipine pretreatment. CONCLUSION: These findings suggest that the renin gene expression was markedly decreased after renal ischemia and slowly recovered. Systemic nifedipine pretreatment does not have a significant effect on gene expression pattern of renin in ischemic renal injury.
Adenosine Triphosphate ; Angiotensins ; Animals ; Calcium Channel Blockers ; Calcium Channels* ; Calcium* ; Cell Membrane ; Constriction ; Electrophoresis ; Formaldehyde ; Gene Expression* ; Humans ; Ischemia ; Kidney ; Membranes ; Nephrectomy ; Nifedipine ; Rats ; Rats, Sprague-Dawley ; Regeneration ; Renal Artery ; Renal Circulation ; Renin* ; Renin-Angiotensin System ; Reperfusion ; RNA ; Sepharose

No abstract available.
Acute Kidney Injury* ; Lymphoma*

Diabetic kidney disease, as one of the important diabetic complication, developed in 20% to 40% of patients with diabetes and is now the most common cause of end-stage renal disease. Although it has been recommended that annual screening of renal function including microalbuminuria in diabetic patients, many patients are currently under-diagnosed state. Early recognition of diabetic renal complication has a pivotal role in the management of diabetic patients for improvement of patient's prognosis. The detection of microalbuminuria is particularly important as a marker of early diabetic kidney disease, and is related with an elevated cardiovascular complications. Like other chronic renal disease, diabetic kidney disease has characteristic to show a progressive decline in renal function, but significantly increased cardiovascular mortality even in the early stage of diabetic kidney disease. Therefore, more aggressive trials for detection of the presence of diabetic kidney disease and comorbid cardiovascular disease and management for cardiovascular risk factor reduction and adequate therapeutic intervention for slowing the progression of renal disease is essential to proper management for patients with diabetic kidney disease.
Cardiovascular Diseases ; Diabetes Complications ; Diabetic Nephropathies ; Diabetic Retinopathy ; Humans ; Kidney Failure, Chronic ; Mass Screening ; Prognosis ; Renal Insufficiency, Chronic ; Risk Factors

Diabetic kidney disease, as one of the important diabetic complication, developed in 20% to 40% of patients with diabetes and is now the most common cause of end-stage renal disease. Although it has been recommended that annual screening of renal function including microalbuminuria in diabetic patients, many patients are currently under-diagnosed state. Early recognition of diabetic renal complication has a pivotal role in the management of diabetic patients for improvement of patient's prognosis. The detection of microalbuminuria is particularly important as a marker of early diabetic kidney disease, and is related with an elevated cardiovascular complications. Like other chronic renal disease, diabetic kidney disease has characteristic to show a progressive decline in renal function, but significantly increased cardiovascular mortality even in the early stage of diabetic kidney disease. Therefore, more aggressive trials for detection of the presence of diabetic kidney disease and comorbid cardiovascular disease and management for cardiovascular risk factor reduction and adequate therapeutic intervention for slowing the progression of renal disease is essential to proper management for patients with diabetic kidney disease.
Cardiovascular Diseases ; Diabetes Complications ; Diabetic Nephropathies ; Diabetic Retinopathy ; Humans ; Kidney Failure, Chronic ; Mass Screening ; Prognosis ; Renal Insufficiency, Chronic ; Risk Factors

No abstract available.
Acute Kidney Injury* ; Nifedipine* ; Plasma* ; Renin*

No abstract available.
Receptors, Mineralocorticoid*

No Abstract Available.
Knee* ; Synovitis, Pigmented Villonodular*

As a result of the energy overload in obesity, insulin resistance, type 2 diabetes, dyslipidemia, hypertension, and atherosclerosis develop, which together comprise the metabolic syndrome. Although the kidney becomes a victim of hyperglycemia in diabetes mellitus, recent work has shown that the abnormalities of lipid and glucose metabolism in the kidney are similarly important to those in adipose tissue. Interestingly, obesity triggers the release of adipokines such as leptin, resistin, and visfatin, and these can then be associated with the progression of diabetic nephropathy and other vascular complications. These adipokines, which are also synthesized in the kidney, appear to have an important role in renal injury associated with insulin resistance. Our studies found that visfatin is not only a surrogate marker of systemic inflammation in type 2 diabetic patients but is also up-regulated in diabetic kidney through the uptake of glucose into renal cells, which leads to the activation of the intracellular insulin signaling pathway and pro-inflammatory mechanisms. However, we also observed a beneficial effect of visfatin administration to type 2 diabetic mice. Visfatin injection improved diabetic nephropathy in vivo, in contrast to our previous in vitro study of cultured renal mesangial cells. These results suggest the possibility of multiple cross-talk between adipose tissue and kidney in the metabolic syndrome, particularly in diabetic nephropathy. Further study should be undertaken to understand the role of adipose tissue and kidney as major organs in the metabolic syndrome.
Adipokines ; Adipose Tissue ; Animals ; Atherosclerosis ; Biomarkers ; Diabetes Mellitus ; Diabetic Nephropathies ; Dyslipidemias ; Glucose ; Humans ; Hyperglycemia ; Hypertension ; Inflammation ; Insulin ; Insulin Resistance ; Kidney ; Leptin ; Mesangial Cells ; Mice ; Nicotinamide Phosphoribosyltransferase ; Obesity ; Resistin