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1.
Korean Journal of Medicine ; : 528-536, 2005.
Article in Korean | WPRIM | ID: wpr-209710

ABSTRACT

BACKGROUND: Chronic systemic inflammation in ESRD patients due to uremia and hemodialysis procedure itself comes into notice as a main factor for premature mortality secondary to rapid progressing atherosclerosis. Various pro-inflammatory cytokine, known to mediate these reaction of malnutrition, inflammation and atherosclerosis, are regulated by anti-inflammatory cytokine, such as IL-10. Quantitative production of IL-10 shows interindividual variability determined genetically by polymorphisms of promotor gene. The aim of this study was to measure the degree of IL-10 synthesis in ESRD patients treated with hemodialysis and evaluate the association with genotypes and cardiovascular risk factors. METHODS: The IL-10 genotypes for polymorphic bases at position at -1082 was determined in 66 chronic hemodialysis patients and 98 healthy subjects using highly specific PCR and the lipopolysaccharide (LPS)-stimulated IL-10 (sIL-10) release from whole blood were measured by ELISA. RESULTS: The distribution of the IL-10 genotypes in hemodialysis patients were similar to the general population, but the proportion of A allele in hemodialysis group was significantly higher (72.3% vs 59.8%, p=0.05). sIL-10 concentration were lower in hemodialysis patients compared with normal control (21.1 pg/mg vs 36.1 pg/mg, p=0.001) and both groups showed same relationship of sIL-10 with genotypes, that AA type was low producer. In multiple regression analysis, sIL-10 of normal group correlated negatively with age, creatinine, uric acid and existence LVH, and positively with albumin, hemoglobin. On the other hand, lower albumin, lower ejection fraction on echocardiography and existence of left ventricular hypertrophy were associated with higher sIL-10 in hemodialysis group. CONCLUSION: Polymorphisms by IL-10 genotypes were associated with production of IL-10 by endotoxin stimulation, and sIL-10 was lower in hemodialysis patients than in normal control. According to relation of sIL-10 with cardiovascular risk factors such as existence LVH, ejection fraction and malnutrition, it could be suggested that sIL-10 is useful marker in evaluating the risk of cardiovascular events.


Subject(s)
Humans , Alleles , Atherosclerosis , Cardiovascular Diseases , Creatinine , Echocardiography , Enzyme-Linked Immunosorbent Assay , Genotype , Hand , Hypertrophy, Left Ventricular , Inflammation , Interleukin-10 , Kidney Failure, Chronic , Malnutrition , Mortality, Premature , Polymerase Chain Reaction , Renal Dialysis , Risk Factors , Uremia , Uric Acid
2.
Korean Journal of Nephrology ; : 970-974, 2004.
Article in Korean | WPRIM | ID: wpr-224246

ABSTRACT

Scleroderma renal crisis is defined as rapidly progressive renal failure and/or new onset of malignant hypertension during the course of systemic sclerosis. Most patients show clinical features of malignant hypertension, but there have been several reports of normotensive renal crisis. We have experienced a 63 year old female patients with acute renal failure due to scleroderma renal crisis who did not show the clinical features of malignant hypertension. She had taken steroid for the treatment of degenerative osteoarthritis and gradually developed shortness of breath and edema. Her blood pressure on admission was 150/90 mmHg and easily controlled by diuretics. Renal biopsy showed onion-skin appearance in the interlobular arteries with varying degree of tubulointerstitial changes. Her renal function rapidly deteriorated despite ACE inhibitor therapy and cytotoxic therapy had to be initiated because of progressive interstitial pneumonitis and myocarditis. We describe a patient with scleroderma renal crisis who did not show the clinical features of malignant hypertension following steroid treatment.


Subject(s)
Female , Humans , Middle Aged , Acute Kidney Injury , Arteries , Biopsy , Blood Pressure , Diuretics , Dyspnea , Edema , Hypertension, Malignant , Lung Diseases, Interstitial , Myocarditis , Osteoarthritis , Renal Insufficiency , Scleroderma, Systemic
3.
Korean Journal of Nephrology ; : 975-981, 2004.
Article in Korean | WPRIM | ID: wpr-224245

ABSTRACT

Light chain deposition disease is caused by systemic paraprotein deposition resulting from monoclonal plasma cell dyscrasia. It is usually characterized rapidly progressive renal failure and multiple organ dysfunctions. Besides deposition of light chain, it can lead to multiple organ dysfunctions due to hyperviscosity syndrome. We experienced a case of 54-year-old man who presented as an acute renal failure, and elevation of liver enzyme. Radiologically, there was no abnormal finding except enlargement of both kidney in abdominal sonogram. Globulinuria was noticed on 24 hrs-urine study. The histologic findings of kidney showed lambda chain deposits in basement membrane of tubules and glomeruli, interstitium, and vessel walls. On 10th day of hospitalization, he developed sudden hypoxia that was not corrected by oxygen supplementation, and focal neurologic signs accompanied with a change of consciousness. We report a case of light chain deposition disease manifested as an acute renal failure and liver enzyme elevation with suspicious multiple organ embolic events later.


Subject(s)
Humans , Middle Aged , Acute Kidney Injury , Hypoxia , Basement Membrane , Consciousness , Hospitalization , Kidney , Liver , Neurologic Manifestations , Oxygen , Paraproteinemias , Renal Insufficiency
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