PubMed Health⌕ Search

Biomedical subjects

B K Bang

Publications and source records attributed to B K Bang.

At least 37 records · Page 2Linked to original sources
PubMed2000

Determinants of plasma total homocysteine levels in Korean chronic renal transplant recipients.

OBJECTIVE: Study the determinants of plasma total homocysteine (tHcy) levels, such as fasting levels of serum creatinine (SCr), albumin, plasma tHcy, folate, B(12), and pyridoxal-5'-phosphate (PLP) in chronic Korean renal transplant recipients (RTR). DESIGN: Cross-sectional study. SETTING: Nephrology & Transplant Service in Catholic University Kangnam St. Mary's Hospital, Seoul, Korea. PARTICIPANTS: Ninety-one chronic Korean RTR with stable renal function who were > or =6 months post-transplant. MEASURES: Used medical record review and anthropometric measurements, and overnight (10 to 14 hours) fasting blood samples were measured for plasma tHcy, PLP, folate, B(12), SCr, and albumin. RESULTS: The prevalence of hyperhomocysteinemia (tHcy > 12 micromol/L) was 56%, and 47% had low plasma folate levels (<3 ng/mL). Linear modeling with analysis of covariance adjusted for age, sex, albumin, SCr, and plasma B-vitamin status revealed that only SCr (standard regression coefficient R = +0.663, P<.001), plasma folate (R = -0.276, P =.001), and B(12) (R = -0.149, marginal, P =.08) were independent determinants of fasting tHcy levels in this patient population. CONCLUSION: Renal function is the major independent determinant of the fasting tHcy levels among chronic, stable Korean RTR, and that B-vitamin status plays a secondary role among such patients.

Adult↗
PubMed2000

Intestinal protein loss in patients with haemorrhagic fever with renal syndrome.

BACKGROUND: In haemorrhagic fever with renal syndrome (HFRS) vascular dysfunction has been observed in various organs, but the involvement of the intestine has not yet been reported. This study was performed to evaluate the association of intestinal protein loss in this disease with other clinical parameters reflecting vascular permeability or disease severity. METHODS: Twenty patients with HFRS were included in this study. Intestinal protein loss was measured by (99m)Tc-human serum albumin ((99m)Tc-HSA) scintigraphy in the acute stage, and quantitative analysis of protein loss was measured by the faecal clearance of alpha 1-antitrypsin (C(AT)) in the acute and the recovery stages. C(AT) was then compared with clinical parameters reflecting disease activity and vascular permeability. RESULTS: (99m)Tc-HSA scintigraphy was positive in 13 (65%) patients, and C(AT) in the acute stage was significantly increased as compared with C(AT) in the recovery stage (40.5+/-24.1 vs 9.2+/-4.2 ml/day, P<0.001). C(AT) was associated with serum albumin levels, frequency of hypotensive episodes, severity of acute renal failure, and degree of thrombocytopenia. CONCLUSIONS: Our data suggest that the increased vascular permeability of HFRS is associated with the increased intestinal loss of plasma proteins, which might represent one of the parameters of disease severity in HFRS.

Adult↗
PubMed2000

A case of Goodpasture's syndrome with massive pulmonary hemorrhage.

We present a typical case of Goodpasture's syndrome with massive pulmonary hemorrhage and acute deterioration of renal function. A 20-year-old male was admitted due to severe azotemia (blood urea nitrogen 214.7 mg/dL, serum creatinine 30.2 mg/dL) and was treated with emergency hemodialysis. On the 4th hospital day, a sudden onset of pulmonary hemorrhage developed. The circulating level of anti-glomerular basement membrane antibody was then elevated highly, and the kidney biopsy showed crescentic glomerulonephritis and linear deposition of IgG along the glomerular capillary. The patient was treated with intravenous high dose-steroid, oral cyclophosphamide and plasma exchanges. The pulmonary hemorrhage improved with the therapy, however, his renal function did not improve. He is currently on a regular schedule of hemodialysis.

Adult↗
PubMed2000

Comparison of acquired cystic kidney disease between hemodialysis and continuous ambulatory peritoneal dialysis.

OBJECTIVES: ACKD has been described mainly in patients treated with hemodialysis(HD), and there are only a few reports about the prevalence of ACKD in continuous ambulatory peritoneal dialysis (CAPD) patients. Therefore, we compared the prevalence of ACKD in patients receiving HD and CAPD, and evaluated the possible factors which may affect the development of ACKD. METHODS: Forty nine HD and 49 CAPD patients who had received dialysis therapy for at least 12 months were enrolled in this cross-sectional study. Patients who had a past history of polycystic kidney disease and had acquired cystic kidney disease on predialysis sonographic exam were excluded. Detection of ACKD was made by ultrasonography and ACKD was defined as 3 or more cysts in each kidney. RESULTS: The prevalence of ACKD was about 31% (30/98) and there was no significant difference between HD and CAPD patients(27% vs. 34%, p > 0.05). The prevalence of ACKD was not associated with age, sex, primary renal disease, the levels of hemoglobin, BUN, and serum creatinine. However, the duration of dialysis was significantly related to the development of ACKD (presence of ACKD, 74.4 +/- 42.4 months vs. absence of ACKD, 37.8 +/- 24.1 months, p < 0.05). CONCLUSION: The prevalence of ACKD is not different according to the mode of dialysis, and the major determinant of acquired cyst formation is duration of dialysis.

Adolescent↗
PubMed1999

Intravenous calcitriol regresses myocardial hypertrophy in hemodialysis patients with secondary hyperparathyroidism.

To evaluate the response of circulating intact parathyroid hormone (iPTH) on myocardial hypertrophy in hemodialysis (HD) patients with secondary hyperparathyroidism (SHPT), echocardiographic and neurohormonal assessments were performed over a 15-week period in 15 HD patients with SHPT before and after calcitriol treatment and 10 HD control patients with SHPT not receiving calcitriol therapy. We prospectively studied a group of 15 patients with significantly elevated iPTH levels (iPTH >450 pg/mL) receiving calcitriol (2 microg after dialysis twice weekly). Clinical assessment, medication status, and biochemical and hematological measurements were performed once a month. Throughout the study, calcium carbonate levels were modified to maintain serum phosphate levels at less than 6 mg/dL, but body weight, antihypertensive medication, and ultrafiltration dose remained constant. In patients treated with calcitriol, an adequate reduction of iPTH levels was found (1,112 +/- 694 v 741 +/- 644 pg/mL; P < 0.05) without changes in values of serum ionized calcium (iCa++), phosphate, or hematocrit. Blood pressure (BP), cardiac output (CO), and total peripheral resistance (TPR) did not significantly change. After 15 weeks of treatment with calcitriol, M-mode echocardiograms showed pronounced reductions in interventricular wall thickness (13.9 +/- 3.6 v 12.8 +/- 3.10 mm; P = 0.01), left ventricular posterior wall thickness (12.5 +/- 2.4 v 11.3 +/- 1.8 mm; P < 0.05), and left ventricle mass index (LVMi; 178 +/- 73 v 155 +/- 61 g/m2; P < 0.01). However, in control patients, these changes were not found after the treatment period. In addition, sequential measurements of neurohormonal mediator levels in patients receiving calcitriol showed that plasma renin (18.5 +/- 12.7 v 12.3 +/- 11.0 pg/mL; P = 0.007), angiotensin II (AT II; 79.7 +/- 48.6 v 47.2 +/- 45.7 pg/mL; P = 0.001), and atrial natriuretic peptide (ANP; 16.6 +/- 9.7 v 12.2 +/- 4.4 pg/mL; P = 0.03) levels significantly decreased, whereas antidiuretic hormone (ADH), epinephrine, and norepinephrine levels did not change significantly. The percent change in LVMi associated with calcitriol therapy had a strong correlation with the percent change in iPTH (r = 0.52; P < 0.05) and AT II (r = 0.47; P < 0.05) levels. We conclude that the partial correction of SHPT with intravenous calcitriol causes a regression in myocardial hypertrophy without biochemical or hemodynamic changes, such as heart rate, BP, and TPR. The changes in plasma levels of iPTH and, secondarily, plasma levels of neurohormones (especially AT II) after calcitriol therapy may have a key role in attenuating ventricular hypertrophy in SHPT.

Adult↗
PubMed1999

The possible role of c-fos protein in hypothalamus in sleep disturbance in chronic uremic rats.

Sleep disturbance is very common in patients with chronic renal failure, but its mechanism is not clear. The activity of c-fos protein (FOS) in ventrolateral preoptic neurons (VLPO) is associated with the sleep pattern. The purpose of this study was to evaluate the relationship between sleep disturbance and the expression of FOS in VLPO of chronic uremic rats. Chronic uremia was induced by the 5/6 nephrectomized model. The movements of the rats were measured with infrared monitoring during the daytime (8.00-20.00) and nighttime (20.00-8.00). Rats were killed at 10.00 or 16.00 h for the daytime (uremic rats 7, control 8) and at 22.00 h for the nighttime (uremic rats 7, control 9). The expression of FOS in VLPO was examined with the immunohistochemical method. The number of recorded daytime movements in uremic rats was significantly higher than in control rats (458 +/- 185 vs. 222 +/- 41, p < 0.001), but the number of recorded nighttime movements in uremic rats was lower than in control rats (949 +/- 430 vs. 1,618 +/- 261, p < 0.001). In the daytime, the number of FOS immunoreactive cells in uremic rats was lower than in control rats (18.4 +/- 5.3 vs. 42.8 +/- 6.3, p < 0. 001), but there was no difference between two groups in the nighttime (10.8 +/- 8.4 vs. 12.5 +/- 5.1, p = 0.62). There was a strong negative correlation between the number of recorded movements and the number of FOS immunoreactive cells in VLPO (r = -0.700, p < 0.001). This finding suggests that sleep disturbances in chronic uremic rats might be related to the decreased expression of FOS in VLPO.

Animals↗
PubMed1998

Immunotactoid glomerulopathy associated with idiopathic hypereosinophilic syndrome.

A case of immunotactoid glomerulopathy in an 18-year-old man with an idiopathic hypereosinophilic syndrome is presented. The patient showed cervical lymphadenopathy, asymptomatic proteinuria of nephrotic range, and hematuria without any defined immunologic disease. Marked and prolonged hypereosinophilia was found in peripheral blood (eosinophil count; 6,248/mm3) and bone marrow (eosinophil series; 32%). Diffuse and/or nodular eosinophilic infiltration was identified in multiple organs such as kidney, stomach, liver, lymph node, and skin. Renal biopsy revealed endocapillary proliferative features of typical immunotactoid glomerulopathy with IgG and C3 deposition and microtubular structures of variable size, 20-80 nm in diameter, mainly in the subendothelium. This study suggests that immunotactoid glomerulopathy may be a secondary immunologic manifestation of the tissue damage by eosinophils in the idiopathic hypereosinophilic syndrome.

Adolescent↗
PubMed1998

Clinical course of cytomegalovirus (CMV) viremia with and without ganciclovir treatment in CMV-seropositive kidney transplant recipients. Longitudinal follow-up of CMV pp65 antigenemia assay.

This study was designed to evaluate the longitudinal history of cytomegalovirus (CMV) infection and to test the capacity of ganciclovir as effective therapy in CMV-seropositive renal transplant recipients. The CMV viremia was detected with CMV pp65 antigenemia assay in 153 renal transplants. The recipients were classified as having low-grade and high-grade CMV infections according to the severity of CMV infection. The recipients with low-grade CMV infections were observed without ganciclovir treatment, and the recipients with high-grade CMV infection were randomly assigned to ganciclovir-treated and untreated groups. The clinical course between low-grade and high-grade CMV infections was evaluated. All recipients with low-grade CMV infection (n = 62) showed spontaneous remission regardless of immunosuppresants. In high-grade CMV infection (n = 31), the ciclosporin A treated group (n = 11) showed no evidence of CMV disease, and the methylprednisolone-treated group (n = 8) showed CMV disease in 1 (25%) of 4 ganciclovir-untreated recipients. In the OKT3 group (n = 12), symptomatic CMV infection was observed in 6 (100%) ganciclovir-untreated recipients contrary to no CMV disease in the ganciclovir-treated group (p < 0.05). In conclusion, the CMV antigenemia assay is effective in monitoring CMV viremia, and ganciclovir treatment should be done during early CMV viremia in OKT3-treated recipients.

Adult↗
PubMed1998

Urinary soluble HLA class I antigen in patients with minimal change disease: a predictor of steroid response.

In primary minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS), increased lymphocyte reactivity to renal antigens has been defined. Soluble HLA class I antigen (sHLA-I) is actively secreted by T and B lymphocytes when they are stimulated by mitogens, antigens and lymphokines. To determine if serum and urine sHLA-I levels could predict steroid response in patients with MCD and differentiate those from FSGS, we have investigated 45 healthy controls, biopsy-proven 17 patients with MCD (edema and 24-hour urine protein > 3.5 g/day), 8 patients with FSGS (24-hour urine protein > 1 g/day) and 10 patients with membranous nephropathy (MGN) (24-hour urine protein > 1 g/day). Before and after prednisone therapy (1 mg/kg/day or 2 mg/kg/EOD for 8 weeks), the levels of serum and urinary sHLA-I were measured by ELISA (sHLA-STAT; Sangstat Co., Calif., USA). After 8 weeks of treatment, 10 patients with MCD were responders (MCD-CR) while the other 7 patients with MCD were nonresponders (MCD-NR). Three of 7 patients with MCD-NR were re-biopsied and finally diagnosed as FSGS. They were included in the data of patients with FSGS. In healthy controls, serum sHLA-I was detected (415 +/- 256 ng/ml), but urinary sHLA-I was not. At entry, there were no differences in age, sex, serum Cr and 24-hour urine protein among the patients with MCD-CR, MCD-NR and FSGS, but serum albumin was significantly elevated in patients with FSGS and MGN (p < 0.05). Serum sHLA-I levels were notably elevated in MCD-CR (1,040 +/- 1,066 ng/ ml), in MCD-NR (668 +/- 315 ng/ml) and in FSGS (713 +/- 790 ng/ml), but not in patients with MGN (444 +/- 86 ng/ml) when compared with controls (p < 0.05). On the other hand, urinary sHLA-I levels in MCD-NR (541 +/- 239 ng/mg Cr) and in FSGS (457 +/- 239 ng/mg Cr) were significantly higher than those in MGN (125 +/- 28 ng/mg Cr) and in MCD-CR(100 +/- 42 ng/mg Cr, p < 0.05) and these substantial differences were maintained for 8 weeks. In all patients, serum and urinary sHLA-I levels were not reduced during 8 weeks of steroid therapy. We conclude that elevated serum and urinary sHLA-I levels reflect increased cellular immune response and disease activity in patients with MCD and FSGS. In patients with MCD, urinary sHLA-I may be an easily measurable indicator of predicting steroid response, while MCD-NR with high urinary sHLA-I levels might be re-evaluated for the possibility of FSGS.

Adolescent↗
PubMed1998

Inhibition of calbindin D28K expression by cyclosporin A in rat kidney: the possible pathogenesis of cyclosporin A-induced hypercalciuria.

A recent study by Steiner et al. (Biochem Pharmacol 51: 253-258, 1996) demonstrated a decreased calbindin D28K expression in the kidneys of cyclosporin A (CsA)-treated rats. To evaluate the association of renal calcium handling with calbindin D28K expression in CsA-treated rats, two separate experiments (vehicle [VH] versus CsA groups, 1,25-dihydroxyvitamin D3 [VitD] versus VitD + CsA groups) were done simultaneously. CsA (25 mg/kg per d, subcutaneously) and VitD (0.5 microg/kg per d, subcutaneously) were given for 7 d. The CsA group showed decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VH group. The VitD + CsA treatment decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VitD alone. CsA treatment did not affect the serum parathyroid hormone and VitD levels. This study demonstrates an association of calbindin D28K expression with the urinary calcium excretion in CsA-treated rats, and suggests that decreased calbindin D28K expression may play a role in renal calcium wasting.

Animals↗