No abstract available.
Glomerulonephritis, Membranoproliferative* ; Hepatitis B* ; Hepatitis*

No abstract available.
Diabetic Nephropathies*

IgA nephropathy is characterized by the predominant deposition of IgA in a granular fashion diffusely in the mesangial zones of glomeruli. IgA nephropathy was first described over four decades ago and is now the most common form of primary glomerular disease. Much progress has been made in the elucidation of potential pathogenetic mechanisms such as undergalactosylated IgA1 as well as in the fields of clinical features, prognosis, and treatment. This knowledge is being applied in the development of new diagnostic methods and hopefully in the future the creation of novel and rational therapeutic approaches.
Glomerulonephritis, IGA ; Immunoglobulin A ; Kidney Failure, Chronic ; Prognosis

Much progress has been made in the elucidation of potential pathogenetic mechanisms of glomerulonephritis such as anti-PLA2R autoantibody in membranous nephropathy and under-galactosylated IgA1 in IgA nephropathy as well as in the fields of treatment. This knowledge is, hopefully in the future, being applied in the development of the creation of rational therapeutic approaches. Current treatment strategies for glomerular diseases recommended by many clinical studies include high-dose glucocorticoids, calcineurin inhibitors, cyclophosphamide, mycophenolate mofetil, and rituximab. Although these therapies have been effective in treating immune-mediated glomerular diseases, they all have potentially serious side effects.
Antibodies, Monoclonal, Murine-Derived ; Calcineurin ; Cyclophosphamide ; Glomerulonephritis ; Glomerulonephritis, IGA ; Glomerulonephritis, Membranous ; Glucocorticoids ; Immunoglobulin A ; Mycophenolic Acid ; Rituximab

No abstract available.
Collagen* ; Heparin* ; Mesangial Cells*

No abstract available.
Collagen* ; Glucose* ; Insulin* ; Mesangial Cells* ; Somatostatin*

BACKGROUND: Thyroid status in uremia is still inconclusive due to the complexicity of the system. No single pathogenetic event may explain the thyroid function abnormalities in end stage renal disease (ESRD). Defects at all levels of the hypothalamic-pituitary-thyroid axis have been identified. Regarding the thyroid dysfunction in ESRD it is well recognized that the TSH response to TRH is blunted and serum concentrations of thyroid hormones are decreased in patients with ESRD. Whether or not on maintenance hemodialysis. Restoration of renal function with renal transplantation resulted in normalization of all parameters of thyroid function with exception of blunted TSH response to TRH. We evaluated the long-term changes of the thyroid function in 10 patients to know whether the thyroid function and the hypothalamo-pituitary axis were improved with the recovery of the renal function under maintenance low-dosage steroid administration after renal transplantation. METHODS: These tests were performed during the morning in the fasting state in 10 ESRD patients before, 1 month and 6 years after renal transplantation (RT). Thyroid function tests. Serum T3, T4 were measured by RIA kit and serum TSH was measured by IRMA kit. TRH stimulation test. Serum blood samples were obtained 0, 30, 60, 90, 120 min after TRH (400microgram) administration. Statistical analysis. All grouped data were expressed as mean+/-SD. Student t-test was used to assess the statistical difference between any two means. RESULTS: 1) The mean basal level of serum T3 was reduced in ESRD patients (53.6+/-33.2ng/dL) and increased to the low normal level 1 month after RT (87.8+/-25.4ng/dL), improved to the normal level 6 years after RT (116.3+/-28.8ng/dL). 2) The mean basal level of T4 was within normal range before RT (5.9+/-1.1microgram/dL), after 1 month (6.2+/-1.2microgram/dL) and after 6 years (6.5+/-1.4microgram/dL) of RT. 3) The mean basal level of TSH was within normal range before RT (2.0+/-1.2microU/mL), after 1 month (1.1+/-0.7microU/mL), and after 6 years (0.7+/-0.5microU/mL) of RT. Rut the mean TSH level of 6 years of RT was significantly decreased within the normal range. 4) In ESRD the TSH response to TRH was blunted, had a diminished peak and delayed fall before RT. After 1 month of RT, the TSH response to TRH was persistently blunted, however showed more rapid fall of TSH. After 6 years of RT, the TSH response to TRH normalized, but the absolute level of TSH and the peak level of TSH to TRH were less than before and after 1 month of RT. CONCLUSIONS: The abnormalities of thyroid hormones in uremic patients were improved partially after 1 month of RT and almost completely after 6 years of RT. But the level of T3H and the peak level of TSH to TRH were low within normal range, these results may be a direct consequence of low-dosage and long-term glucorcorticoid administration.
Axis, Cervical Vertebra ; Fasting ; Follow-Up Studies* ; Humans ; Kidney Failure, Chronic ; Kidney Transplantation* ; Reference Values ; Renal Dialysis ; Thyroid Function Tests ; Thyroid Gland* ; Thyroid Hormones ; Uremia

No abstract available.
Peritoneal Dialysis, Continuous Ambulatory* ; Peritonitis, Tuberculous*

No abstract available.
Humans ; Nephrotic Syndrome* ; Renal Veins* ; Thrombosis*

No abstract available.
Humans ; Kidney Failure, Chronic* ; Kidney Transplantation* ; Thyroid Gland*