Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary chronic glomerulonephritis may emerge clinically as acute nephritis, the nephrotic syndrome as well as asymptomatic hematuria and proteinuria. Therapeutic consequences still depend on the morphological diagnosis. In cases of minor proteinuria [< 3,5 g/24 h] immunosuppressive therapy is not superior to symptomatic therapy. In patients with nephrotic syndrome immunosuppressive therapy depends on the morphological diagnosis. Glucocorticoids are the therapy of choice in minimal changes glomerulopathy and should be tried in focal segmental sclerosing glomerulonephritis. Steroids may be tried in pure mesangial as well as in IgA and IgM nephropathy. Especially Ponticelli claims significant therapeutic success in patients with membranous glomerulonephritis treated with Prednisolone and Chlorambucil. Failures and relapses may be treated with Cyclophosphamide, Chlorambucil or Cyclosporin A. Anticoagulants may be advantageous in the therapy of membranoproliferative glomerulonephritis.
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PMID:[Therapy of primary chronic glomerulonephritis]. 778 93

The usefulness of icodextrin-containing peritoneal dialysis (PD) solution for the management of body fluid and blood pressure has been reported. However, icodextrin PD solution is a foreign solution in the body, and the possible induction of intraperitoneal inflammation has been reported. In this study, we investigated at 6-month intervals the influence of icodextrin solution on peritoneal permeability and inflammatory reactions in patients in whom glucose solution had been changed to icodextrin solution for the overnight dwell. We enrolled 9 anuric PD patients (5 men, 4 women) of mean age 58 +/- 5.9 years (range: 45.6-64.8 years) into the study. The patients' mean duration of PD was 61.9 +/- 42 months (range: 6.7-142.5 months). The cause of end-stage renal disease was chronic glomerulonephritis in all patients. For evaluation ofperitoneal permeability, we performed peritoneal equilibration tests (PETs) immediately after an overnight dwell and determined the dialysate-to-plasma ratios of creatinine (D/P Cr), beta2-microglobulin (D/P beta2m), albumin (D/P Alb), immunoglobulin G (D/P IgG), and alpha2-macroglobulin (D/P alpha2m). We also measured interleukin-6 (IL-6) and fibrinogen degradation products (FDPs) in overnight effluent as indices of inflammation and of the fibrinolysis-coagulation system. The evaluation was performed every 6 months for 24 months. The FDPs in effluent increased significantly at 6 months after the change to icodextrin solution, and IL-6 tended to increase. The D/P beta2m, D/P Alb, D/P IgG, and D/P alpha2m all significantly increased in the course of follow-up. In the PETs, the D/P Cr increased slightly, but the change was nonsignificant. At 30 months after the change to icodextrin solution, 1 patient was diagnosed as having a risk of encapsulating peritoneal sclerosis (pre-EPS). In this patient, rapid increases in IL-6, D/P Cr and macromolecular and small molecular D/P by PET were noted after the change to icodextrin solution. Steroids were administered after the diagnosis of pre-EPS, with the result that the IL-6 level rapidly decreased and the D/P Cr and D/P of small molecules and macromolecules slightly decreased. Icodextrin dialysis solution increased peritoneal permeability. Although the cause was unclear, icodextrin may have changed peritoneal reactivity. Long-term use of icodextrin PD solution requires further investigation.
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PMID:Impact on peritoneal membrane of use of icodextrin-based dialysis solution in peritoneal dialysis patients. 1698 33

Steroids are still the mainstay of therapy in primary chronic glomerulonephritis (PCGN), regardless of underlying disturbance or pathology. Moreover, relationship between known abnormalities and disease manifestation is stochastic, therefore treatment continues to be empirical. It is not known whether responsiveness is related to immune phenotype. We performed flowcytometric lymphocyte (Ly) phenotyping (CD19, CD3, CD3CD4, CD3CD8, CD56/16) on 16 patients (pts) (12M, 4F), mean age 37.6+/-13 years with primary chronic glomerulonephritis (PCGN): minimal change disease (MCD)--6 pts, focal and segmental glomerulosclerosis (FSGS)--4 pts, mesangial proliferative glomerulonephritis--5 pts, mesangiocapillary glomerulonephritis--1 pt, before and at 7 days of oral Prednisone 1 mg/kg/day (in 2 divided doses). Before steroids: 4/16 pts(25%) had elevated BP; 9/16(56.2) showed nephrotic proteinuria. Serum creatinine was >1.2 mg% in 6/16(37.5%). At 7 days WBC count increased (13,079.37+/-4966.4/microl vs. 8021.25+/-2077.4/microl; p=0.0007), Ly percentage (%) decreased (20.30+/-9% vs. 29.9+/-10.4%; p=0.0095), while absolute (abs.) Ly count remained unchanged. Both CD19 Ly% and CD19 Ly abs. count increased (16.13+/-6.5% vs. 9.52+/-3.7%; p=0.0015, and 410.012+/-29.7/microl vs. 223.56+/-123.8/microl; p=0.0077, respectively). NK (natural killer)% decreased (9.15+/-5.2% vs. 14.19+/-7.1%; p=0.0296). CD3, CD3CD4, CD3CD8 Ly subsets and CD4/CD8 ratio showed no change. Variation in proteinuria (2.88+/-2.1 g/24 h vs. 3.45+/-1.7 g/24 h; p=0.4) did not reach statistical significance (Wilcoxon-Mann-Whitney). In 11 pts we performed an additional analysis at 1 month. Compared to levels before steroids, there was an increase in WBC, CD19 Ly% and CD19 Ly abs. count and a decrease in NK% and NK abs. count. Other Ly subsets and CD4/CD8 ratio remained unchanged. Variation in clinical parameters (proteinuria, serum Creatinine, BP) did not reach statistical significance. Changes in Ly profile precede changes in clinical parameters and thus are divergent. While our patients proved to be early non-responders, further studies to elucidate whether profile changes provide for response specification are warranted.
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PMID:The effect of steroids on lymphocyte profile in primary chronic glomerulonephritis. Empirical or tailored therapy? 1763 Feb 6