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Biomedical subjects

K T Woo

Publications and source records attributed to K T Woo.

At least 109 records · Page 6Linked to original sources
PubMed1985

Antithrombin III in mesangial IgA nephritis.

Plasma Antithrombin III (A T III) was measured in 97 patients with IgA nephritis, 30 patients with non IgA idiopathic mesangial proliferative glomerulonephritis and 40 healthy subjects. The mean plasma A T III levels in the patients with IgA nephritis (105 +/- 10%) was significantly higher than those of normal controls (96 +/- 5%) (p less than 0.0005). The mean plasma A T III levels in the patients with non IgA nephritis (101 +/- 10%) was not different from those of the normal controls or the patients with IgA nephritis. A T III levels were significantly correlated with proteinuria (p less than 0.0001), segmental sclerosis (p less than 0.001), crescents (p less than 0.01), medial hypertrophy (p less than 0.001) and intensity of IgA staining on IMF (p less than 0.02). Patients with IgA nephritis with raised A T III levels had significantly more proteinuria (p less than 0.003), more segmental sclerosis (p less than 0.007) as well as a greater intensity of IgA staining on IMF (p less than 0.02) when compared to patients with normal A T III levels. The data suggest that raised plasma A T III levels may serve as a prognostic marker in IgA nephritis.

Antithrombin III↗
PubMed1985

Antithrombin III in renal transplant recipients.

Antithrombin III (AT III) is increased in situations where there is increased platelet turnover. Plasma AT III levels measured in 39 renal transplant recipients were significantly higher than in 20 healthy subjects (p less than 0.001) and 20 patient controls (p less than 0.025). AT III levels were significantly correlated with the patients' platelet counts (r = 0.4, p less than 0.02). Transplant patients with less than 1 year follow up had significantly higher AT III levels than patients with more than 1 year follow up (p less than 0.01). All 5 patients with transplant rejection in the study had elevated plasma AT III levels. The data suggest that elevation of plasma AT III may be related to graft rejection.

Adult↗
PubMed1985

Beta-2-microglobulin in the assessment of renal function of the transplanted kidney.

Plasma and urine beta-2-microglobulin (B2m) were measured in 37 renal transplant recipients and 34 healthy subjects. Serum B2m was found to be a more sensitive index of renal function than serum creatinine. Renal transplant recipients had significantly higher urine B2m when compared with normal controls. Normal subjects had a higher serum to urine B2m ratio (SUR) while those with renal impairment had a lower SUR. Serum B2m used alone or together with urine B2m and SUR appears a useful index for assessment of renal allograft function as well as detection of potential renal damage.

Adult↗
PubMed1985

Effects of hemodialysis and peritoneal dialysis on antithrombin III and platelets.

Plasma antithrombin III (AT III) levels in hemodialysis patients, low prior to dialysis, improved after dialysis (p less than 0.01). The platelet counts before and after dialysis, did not change significantly. In peritoneal dialysis patients the AT III levels, which were normal before dialysis, increased significantly after dialysis (p less than 0.01). The platelet counts before and after peritoneal dialysis also improved (p less than 0.005). No correlation was found between AT III levels and platelet counts. Although platelet damage has a contributory role in increasing AT III levels during hemodialysis, the data on peritoneal dialysis suggest that there may be other factors affecting platelets and AT III during dialysis.

Adult↗
PubMed1985

Ampicillin-induced interstitial nephritis with generalised exfoliative dermatitis.

Drug induced renal failure is a serious, potentially, fatal illness that is preventable. Hypersensitivity reactions involving the kidneys can occur with any of the penicillin groups. However, there are few reports in the literature of ampicillin as a cause of acute interstitial nephritis. In the following case report, a patient developed acute interstitial nephritis with renal failure and exfoliative dermatitis following ampicillin therapy. The diagnosis was based on the rapid onset of renal failure, presence of eosinophilia, skin rash, and characteristic renal biopsy finding, following the administration of ampicillin. Renal function returned to normal eventually, but she continued to have relapses of exfoliative dermatitis up to a year later.

Acute Kidney Injury↗
PubMed1985

Suppressor cell function in renal failure and transplant patients.

Suppressor cell function was assessed in 13 patients with chronic renal failure not on dialysis, 10 patients on regular hemodialysis and 11 renal transplant patients by means of the Concanavalin A inducible Suppressor Cell Assay. The mean Suppression Index (S.I.) in the undialysed patients (0.76 +/- 0.39) and those of the dialysed patients (0.72 +/- 0.18) were not significantly different from the 25 healthy controls (0.68 +/- 0.22). However the S.I. in the renal transplant patients (1.11 +/- 0.41) was significantly different from the normal controls as well as the undialysed and dialysed patients. Although there was no correlation between S.I. and age, post transplant follow up period, serum creatinine concentration, prednisolone or azathioprine dosage it is likely that the cause of the impaired suppressor cell function was due to the immunosuppressive agents used.

Adult↗
PubMed1985

Galloway memorial lecture. Platelet injury and antithrombin III in clinical nephrology.

Plasma Antithrombin III (AT III) has been shown to be elevated in certain conditions like diabetes mellitus and coronary artery disease as well as in situations where there is increased platelet turnover. This study attempts to define the role of platelet injury in Clinical Nephrology and assesses the clinical value of ATT III. In IgA Nephritis, plasma AT III levels (105 +/- 10%) in 97 patients were higher than those of normal controls (96 +/- 5%) (p less than 0.0005). AT III levels were significantly correlated with proteinuria (p less than 0.0001), segmental sclerosis (p less than 0.01), crescents (p less than 0.01), medial hypertrophy (p less than 0.001) and intensity of IgA staining on IMF (p less than 0.02). Patients with IgA nephritis with raised AT III had more proteinuria (p less than 0.003), more segmental sclerosis (p less than 0.007) as well as a greater intensity of IgA on IMG (p less than 0.02) when compared to patients with normal AT III levels. The data suggest that plasma AT III may serve as a marker of disease activity in IgA nephritis. Plasma AT III levels in hemodialysis patients, low prior to dialysis, improved after dialysis (p less than 0.01). Pre and post hemodialysis platelet counts however did not change significantly. In peritoneal dialysis patients, AT III levels which were normal before dialysis, increased significantly after peritoneal dialysis (p less than 0.01). The platelet counts before and after peritoneal dialysis also improved (p less than 0.005). No correlation was found between AT III levels and platelet counts. Although platelet damage has a contributory role in increasing AT III levels during hemodialysis, the data on peritoneal dialysis suggest that there may be other factors affecting platelets and AT III during dialysis.

Adult↗
PubMed1984

Beta-2-microglobulin in mesangial IgA nephropathy.

This study measured plasma beta 2-microglobulin (beta 2-m) in patients with mesangial IgA nephritis. Plasma beta 2-m was measured in 51 patients with IgA mesangial nephritis and in 50 normal controls using a Phadebas beta 2-m RIA kit available from Pharmacia Diagnostics (Uppsala, Sweden). The mean plasma beta 2-m in IgA nephritic patients (1.92 +/- 0.67 mg/l) was significantly different from that of healthy controls (1.33 +/- 0.41 mg/l; p less than 0.001). The mean plasma beta 2-m in non-IgA nephritic patients (1.83 +/- 0.73 mg/l) was also significantly different (p less than 0.001). Patients with IgA nephritis with glomerular sclerosis (n = 33) had significantly higher levels of beta 2-m (2.02 +/- 0.70 mg/l) than IgA nephritic patients without glomerular sclerosis (n = 18, 1.72 +/- 0.65 mg/l; p less than 0.025). In the group with IgA nephritis and glomerulosclerosis, raised beta 2-m levels were correlated with the severity of proteinuria (r = 0.41) (p less than 0.02) as well as the intensity of IgA staining on immunofluorescence (r = 0.34; p less than 0.05). Elevated beta 2-m levels in IgA nephritis may serve as a useful prognostic marker.

Adolescent↗
PubMed1982

Beta-thromboglobulin in mesangial IgA nephritis.

Plasma beta-thromboglobulin (beta-TG) concentration were determined in 28 patients with mesangial IgA nephritis (17 with focal glomerular sclerosis and 11 without any glomerular sclerosis) and compared with those from 52 normal subjects and 24 patients controls with no evidence of renal disease. The mean beta-TG concentration in the patients with IgA nephritis [159 +/- 63 ng/ml (SD)] significantly different from the patients controls [32 +/- 25 ng/ml (SD)] (p less than 0.001) as well as the group of normal subjects [23 +/- 17 ng/ml (SD)] (p less than 0.001). In another group of 12 patients with diffuse mesangial proliferative glomerulonephritis with no IgA deposits (non IgA nephritis) the mean beta-TG concentration [126 +/- 86 ng/ml (SD)] though different from that of the normal as well as patient controls (p less than 0.001) was not significantly different from the IgA nephritis patients. The elevated beta-TG levels in the nephritic patients showed no correlation with serum creatinine, creatinine clearance or proteinuria but was significantly correlated with the degree of glomerular sclerosis (r = 0.44) (p less than 0.05). In vivo activation of the platelets is suggested by these findings of elevated beta-TG in patients with diffuse proliferative mesangial glomerulonephritis (IgA and non IgA).

Adolescent↗
PubMed1982

Loss of concanavalin A induced suppressor T-lymphocyte function in patients with mesangial IgA nephritis.

Using the method of concanavalin A (Con a) inducible suppressor activity the peripheral mononuclear cells (PMC) of 17 patients with Mesangial IgA nephritis, 13 patients with idiopathic mesangial proliferative glomerulonephritis but with no IgA deposits on immunofluorescence (Non-IgA nephritis) and 18 healthy subjects were studied. DNA synthesis was measured by incorporation of 3H Thymidine. The mean suppression index (S.I.) of 0.94 +/- 0.08 (SEM) in the IgA nephritic patients was significantly different from that of the non-IgA nephritic patients (0.67 +/- 0.05) (P less than 0.01) as well as the group of normal healthy controls (0.64 +/- 0.05) (P less than 0.0025). The data show that patients with IgA nephritis have abnormal suppressor cell function and suggest an autoimmune basis in the pathogenesis of IgA nephritis.

Adult↗
PubMed1982

Histopathological profile of adult nephrotic syndrome in Singapore.

The renal biopsies of 100 patients presenting with the Nephrotic Syndrome were analysed. Eighty-seven percent were due to primary glomerulonephritis and the other 13% due to secondary glomerulonephritis of which Systemic Lupus Erythematosus was the commonest. Diffuse mesangial proliferative glomerulonephritis (DPGN) formed the largest group (60%). Minimal lesion occurred in 15% of patients and only 5% had Membranous Glomerulonephritis. 63% of patients with DPGN had negative staining on immunofluorescence. Even though Mesangial IgA Nephritis is prevalent in Singapore, it accounted for only 4% of glomerulonephritis causing the Nephrotic Syndrome.

Adolescent↗
PubMed1982

Nephrotic syndrome associated with malignant tumours.

The nephrotic syndrome complicating malignancy is an unusual occurrence. We report here four cases of nephrotic syndrome associated with malignant tumours. Three cases were associated with bronchogenic carcinoma and one with adenocarcinoma of colon. One of the four cases developed nephrotic syndrome before the discovery of bronchogenic carcinoma. All patients had renal biopsies with light microscopy, immunofluorescence and electron microscopy. The findings suggest an immune-complex disease complicating malignancy. The true incidence of nephrotic syndrome associated with malignant tumours is unknown. However it is clinically prudent to screen for malignancy in older patients presenting with nephrotic syndrome.

Aged↗