Various cytokines and growth factors may be involved in IgA nephropathy. To clarify whether interleukin-6 was a prognostic factor for this disease, we investigated interleukin-6 positivity of renal biopsy specimens and its relationship with the prognosis. The subjects were 90 patients with IgA nephropathy (42 males and 48 females with a median age of 32.7 ± 13.8 years). Renal biopsy specimens were stained for interleukin-6 using an enzyme-antibody method. Fifty-two of 90 patients showed glomerular positivity for interleukin-6. Among the patients positive for interleukin-6, 24-hour urinary protein excretion and serum creatinine levels were significantly higher at the time of biopsy than in the patients without interleukin-6 positivity, while creatinine clearance was significantly lower. In the interleukin-6-positive patients without steroid therapy, serum creatinine increased significantly after 1 year (Δs-Cr; 1.04 ± 0.45 mg/dl) and creatinine clearance decreased significantly (ΔCcr; –11.7 ± 3.2 ml/min) compared to the interleukin-6-negative patients without steroid therapy. Steroid therapy improved 24-hour urinary protein excretion, serum creatinine, and creatinine clearance in the interleukin-6-positive patients, while these parameters worsened without steroid therapy. On the other hand, the IL-6-negative patients showed no differences of clinical parameters irrespective of the presence or absence of steroid therapy. In conclusion, glomerular interleukin-6 positivity may be a prognostic factor and an indicator of the need for steroid therapy in IgA nephropathy.
We report a myeloperoxidase antineutrophil cytoplasmic antibody-positive rheumatoid arthritis patient who developed necrotizing crescentic glomerulonephritis. Steroid therapy was given combined with an immunosuppressant agent, and double-filtration plasmapheresis was started with the aim of removing antibodies from the blood. This therapeutic regimen was found to be useful.
We report on a 22-year-old female with focal glomerular sclerosis and hyperlipidemia who did not respond to long-term steroid or immunosuppressant therapy. When low-density lipoprotein (LDL) apheresis was performed, her total daily protein excretion decreased, serum albumin increased, total cholesterol decreased from 1,052 mg/dl to 148 mg/dl after 3 months, and the serum lipoprotein(a) level also decreased from 117.8 mg/dl to 9.1 mg/dl. After this therapy, her clinical course was well maintained. By controlling hyperlipidemia, including oxidized low-density lipoprotein and lipoprotein(a), low-density lipoprotein apheresis may produce clinical improvement in focal glomerular sclerosis.
Although the mechanism of unresponsiveness to recombinant human erythropoietin therapy in dialysis patients has been studied extensively in recent years, many aspects remain unclear. We previously found that administration of erythropoietin induces interleukin-1beta, a cytokine that inhibits erythropoiesis. The present study investigated the involvement of tumour necrosis factor-alpha, another cytokine which inhibits erythropoiesis. Peripheral blood mononuclear cells were obtained from 18 patients on continuous ambulatory peritoneal dialysis, who were being treated with erythropoietin for renal anaemia, and were cultured with various concentrations of erythropoietin (0, 1, 5, 10, and 50 U/ml). Then the tumour necrosis factor-alpha level in the culture supernatant was assayed. The 18 patients were divided into four groups on the basis of the haematocrit after treatment: group A (n = 3), <23.0%; group B (n = 5), 23.0-24.9%; group C (n = 7), 25.0-26.9%; and group D (n = 3), > or =27.0%. In group A, the tumour necrosis factor-alpha level in the culture supernatant was increased by incubation with erythropoietin, while it was not increased in other groups. The tumour necrosis factor-alpha level was significantly higher in group A than in the other groups at erythropoietin concentrations of 5 U/ml. These results suggested that induction of tumour necrosis factor-alpha is one of the reasons for unresponsiveness to recombinant human erythropoietin.
We report on a patient with myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA) associated glomerulonephritis who had an elevated MPO-ANCA level and necrotizing crescentic glomerulonephritis on renal biopsy. She was treated by double filtration plasmapheresis and immunoadsorption plasmapheresis combined with steroid therapy and immunosuppressive agents. After plasmapheresis, the MPO-ANCA level decreased, and the cellular crescents were reduced. We conclude that plasmapheresis combined with steroid and immunosuppressive therapy may be useful to decrease the activity of MPO-ANCA associated crescentic glomerulonephritis.
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