Terapevticheskii arkhiv · 2011
[An IL-6 level in the serum and urine in estimation of cryoglobulinemic vasculitis activity in patients with chronic hepatitis C associated with renal damage].
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Korotchaeva Iu V, Kozlovskaia L V, Gordovskaia N B, Speranskiĭ A I
Аннотация
AIM: To estimate serum and urine IL-6 levels and to study its role in diagnosis of nephritis activity in patients with cryoglobulinemic glomerulonephritis (CGN) associated with chronic hepatitis C (CHC).
MATERIAL AND METHODS: Enzyme immunoassay was used to assay IL-6 in blood serum of 124 patients having different stages of CHC. IL-6 was also estimated in the urine of 57 patients with CHC systemic manifestations including renal damage.
RESULTS: Abnormal serum IL-6 level was seen in 36% CHC patients. Patients with elevated level of IL-6 in the serum vs. patients with normal IL-6 level had cryoglobulinemia (CGE) (56% vs. 26%, p < 0.01) and related systemic manifestations including cryoglobulinemic glomerulonephritis (30% vs. 9%, p < 0.01). Most of (90%) patients with CHC-associated CGN had urinary IL-6 excretion correlating with severity of renal damage: the highest urinary level of IL-6 was seen in development of acute nephritic and nephritic syndromes (from 83.5 to 250 pg/ml). It did not correlate with IL-6 in the serum and proteinuria. This is evidence that IL-6 in the urine had a local origin (intrarenal), reflecting activity of immune inflammation in the kidney.
CONCLUSION: Control of IL-6 levels in the blood serum and urine of patients suffering from CHC with cryoglobulinemic syndrome and renal damage can be used for monitoring of the disease activity.
MATERIAL AND METHODS: Enzyme immunoassay was used to assay IL-6 in blood serum of 124 patients having different stages of CHC. IL-6 was also estimated in the urine of 57 patients with CHC systemic manifestations including renal damage.
RESULTS: Abnormal serum IL-6 level was seen in 36% CHC patients. Patients with elevated level of IL-6 in the serum vs. patients with normal IL-6 level had cryoglobulinemia (CGE) (56% vs. 26%, p < 0.01) and related systemic manifestations including cryoglobulinemic glomerulonephritis (30% vs. 9%, p < 0.01). Most of (90%) patients with CHC-associated CGN had urinary IL-6 excretion correlating with severity of renal damage: the highest urinary level of IL-6 was seen in development of acute nephritic and nephritic syndromes (from 83.5 to 250 pg/ml). It did not correlate with IL-6 in the serum and proteinuria. This is evidence that IL-6 in the urine had a local origin (intrarenal), reflecting activity of immune inflammation in the kidney.
CONCLUSION: Control of IL-6 levels in the blood serum and urine of patients suffering from CHC with cryoglobulinemic syndrome and renal damage can be used for monitoring of the disease activity.