The aim of this study was to investigate the effects of antidepressant treatment on serum cytokines and nutritional status in hemodialysis patients. Twenty-eight hemodialysis patients with a depressed mood were given 20 mg of fluoxetine for 8 weeks. The degree of depressive symptoms, the serum levels of interleukin-1beta, interleukin- 2, interleukin-6, tumor necrosis factor-alpha, c-reactive protein, and markers of nutritional status were assessed at baseline and after treatment. The outcome was assessed in terms of response to treatment (>50% reduction in the score of the Hamilton depression rating scale). Antidepressant treatment decreased the serum level of interleukin- 1 in both response and nonresponse groups, and increased the serum level of interleukin-6 only in the response group. At baseline, the level of interleukin-6 in the response group was lower than in the nonresponse group. Antidepressant treatment also increased fat distribution significantly in the response group which might have slightly improved the nutritional status. This study suggests that antidepressant treatment improve depressive symptoms and may affect immunological functions and nutritional status in chronic hemodialysis patients with depression.
Adult ; Antidepressive Agents, Second-Generation/*pharmacology ; C-Reactive Protein/biosynthesis ; Cytokines/*blood ; Depression/*drug therapy ; Electric Impedance ; Female ; Fluoxetine/*pharmacology ; Human ; Interleukin-1/blood ; Interleukin-2/blood ; Interleukin-6/blood ; Male ; Middle Aged ; Nutrition ; Renal Dialysis/*methods ; Support, Non-U.S. Gov't ; Treatment Outcome ; Tumor Necrosis Factor/biosynthesis

OBJECTIVES: Apoptosis is a physiologic or programmed cell death in contrast with necrotic cell death. Recently it has been known that apoptosis are concerned in the effects of chemotherapeutic agents or radiation therapy on tumor cells. Cyclosporine a(CsA), a potent immunosuppressant, has been effectively used in organ transplantaion, but it also has a significant toxicity in the kidneys. However the exact mechanism of CsA nephrotoxicity has not been ellucidated yet. This study was performed to investigate whether apoptosis particiates in CsA nephrotoxicity or not. METHODS: Twenty seven Sprague-Dawley rats were divided into 5 groups. 1) Vehicle group(n=7) as a control: Cremopbor 50mg/kg/day/subcutaneously (sc) for 7 days, 2) CsA4 group(n=5): CsA 50mg/kg/day/sc for 4 days, 3) CsA7 group(n=5): CsA 50mg/kg/day/sc for 7 days, 4) R4 group(n=5): 4 days after CsA 50mg/kg/day/se for 7 days, and 5) R8 group(n=5): 8 days after CsA 50mg/kg/day/sc for 6 days, Biochemical parameters including blood pressure were measured in each group and the cell count of apoptosis in rat kidney was evaluated by in situ end labelling(ISEL) method. RESULTS: 1) The increase of serum creatinine, blood pressure and decrease of creatinine clearance appeared in CsA4 and CsA7 groups. 2) The ce11 counts of apoptosis on tubular cells in CsA4 and CsA7 groups were significantly increased more than in control group(79.0 +/- 16.9, 98.4 +/- 11.4 vs 35.4 +/- 8.8, p<0.05), and the cell counts of apoptosis on tubular cells in R4 and R8 groups were not significantly different from that in control group(53.8 +/- 12.5, 65.2 +/- 7.1 vs 35.4 +/- 8.8, p>0.05), 3) The cell count of apoptosis on the interstitium in each group was not significantly different from that in control group(p>0.05). 4) The cell count of apaptosis on tubular cells was increased more than that on the interstitium in all groups. 5) The cell count of apoptosis on cortex only in CsA7 group was significantly increased more than that io control group(57.8 +/- 11.5 vs 21.8 +/- 2.6, p<0.05), 6) The cell count of apoptosis on medulla only in CsA4 group was significantly increased more than that in control group(636. +/- 17.9 vs 22.6 +/- 9.7, p<0.05). 7) Total cell counts of apoptosis only in CsA4 and CsA7 groups were significantly increased more than in contral group(96.0 +/- 21.1, 99.8 +/- 11.8 vs 46.6 +/- 11.4, p<0.05). CONCLUSION: CsA caused apoptosis mainly on tubular cells rather than the interstitial cells and apoptotic cells in CsA nephrotoxicity were not increased during the recovery phase. With the results apoptosis may play an important role in CsA nephrotoxicity.
Animals ; Apoptosis* ; Blood Pressure ; Cell Count ; Cell Death ; Creatinine ; Cyclosporine* ; Kidney ; Rats* ; Rats, Sprague-Dawley

OBJECTIVE: Graft survival rate has been improved due to newly developed immunosuppressive agents, care of recipient and operative method. However, since many risk factors are still threatening the graft survival, many studies have been underway to identify such factors, one of which has been on delayed graft function(DGF). Extending the definition of DGF to oliguria within 2 months postoperative period(POP), we began this study in order to evaluate what effects oliguria within 2 months POP have on graft survival and what are the risk factors involved. METHODS: 103 patients who have had renal transplantation performed were divided into two groups (oliguric group and non-oliguric group), based on the presence or absence of oliguria within 2 months POP. Risk factors such as the recipient factors(age, gender), donor factors(age, gender), operative factors(warm ischemia time, intraoperative urine volume), HLA typing, postoperative hypotension, postoperative hypovolemia were compared between the two groups and the impact of oliguria on graft outcome was also analysed. RESULTS: 1) 14 were Oliguric patients and 89 were nonoliguric patients. 2) One-year graft survival rate was 40% in the oliguric group and 98% in the non-oliguric group(P<0.05). 3) As the result of analyzing the risk factors, non living related donor(living non-related donor and cadaver donor) were 7(50%) in the oliguric group and 16(18%) in the non-oliguric group(P<0.05). The mean intraoperative urine volume was 442m1 in the oliguric group and 774m1 in the non-oliguric group(P<0.05). The occurrence of postoperative hypotension were 5(36%) in the oliguric group and 1(1%) in the non-oliguric group(P<0.05). Other risk factors such as the recipient fractors, donor factors, warm ischemia time, HLA typing and postoperative hypovolemia were not significantly different between the two groups. CONCLUSION: Graft survival rate in the oliguric group was lower than in the non-oliguric group. The risk factors for oliguria were non living related donor, intraoperative urine volume lower than 500m1 and postoperative hypotension. In conclusion, renal transplantation from non living related donor needs to be proceeded with caution; the maintenance of intraoperative urine volume and the prevention of postoperative hypotension are essential for better graft outcome.
Cadaver ; Graft Survival ; Histocompatibility Testing ; Humans ; Hypotension ; Hypovolemia ; Immunosuppressive Agents ; Ischemia ; Kidney Transplantation* ; Oliguria* ; Postoperative Period* ; Risk Factors ; Tissue Donors ; Transplants* ; Warm Ischemia

RPGN is a catastrophic form of acute glomerulonephritis characterized by an abrupt onset and rapid deterioration of renal function resulting in oliguria within weeks or months. RPGN is seen in a variety of systemic disorders, including systemic lupus erythematosus, poly arteritis nodosa, Wegener's granulomatosis and subacute bacterial endocarditis. In addition, RPGN is seen in association with a variety of primary renal diseases such as poststreptococcal glomerulonephritis, membranoproliferative glomerulonephritis, and IgA nephropathy, Goodpasture's syndrome. Toxic epidermal necrolysis(TEN) is a drug induced life threatening disease characterized by extensive epidermal detachment, necrosis, and mucosal erosion. TEN may involve liver, lung, intestine, and kidney. But renal involvement has seldom been reported. We report on a 63-year-old patient who developed a RPGN with a TEN. Renal biopsy showed pauci-immune crescentric glomerulonephritis and skin biopsy showed edematous change with extravasated erythrocytes in upper dermis and several individually necrotic keratinocytes. ANCA and FANA test was negative. Our patient recovered renal function with steroid pulse therapy. The pathophysiology of TEN is unresolved but abnormal cytokine release(e.g., tumor necrosis factor) has been implicated in pathogenesis of TEN. Because various cytokines have direct toxic effect on kidney structure, the tubular and glomerular damage may be related to the cytokines involved in TEN. To our knowledge, this is the first case documenting the presence of RPGN in patients with TEN. And there maybe some relations between PRGN and TEN which require further study.
Anti-Glomerular Basement Membrane Disease ; Antibodies, Antineutrophil Cytoplasmic ; Arteritis ; Biopsy ; Cytokines ; Dermis ; Endocarditis, Subacute Bacterial ; Erythrocytes ; Glomerulonephritis ; Glomerulonephritis, IGA ; Glomerulonephritis, Membranoproliferative ; Humans ; Intestines ; Keratinocytes ; Kidney ; Liver ; Lung ; Lupus Erythematosus, Systemic ; Middle Aged ; Necrosis ; Oliguria ; Skin ; Stevens-Johnson Syndrome* ; Wegener Granulomatosis