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The deletion polymorphism of the angiotensin-converting enzyme (ACE) gene has been considered as a risk factor for IgA nephropathy and for its progression to end-stage renal failure. However, results from various studies are conflicting. We had genotyped the ACE gene in 100 patients with IgA nephropathy, 32 of whom were in end-stage renal failure and in 90 normal adult subjects. All DD cases were subjected to confirmation with a second PCR, performed with the insert-specific forward primer. Similar genotype frequencies were obtained for the 90 normal control subjects (II: 47%, ID: 44%, DD: 9%); for the 68 patients not in end-stage renal failure (ESRF) (II: 47%, ID: 46%, DD: 7%) and for the 32 patients with ESRF (II: 53%, ID: 38%, DD: 9%). The genotype frequencies in all 3 series are in Hardy-Weinberg equilibrium. These results suggest that ACE gene polymorphism is not a risk factor for IgA nephropathy and is not a predictor for its progression. Definitive proof of association between ACE gene polymorphism and progression in IgA nephropathy will require a prospective study, controlled for important risk factors, with adequate patient numbers and facility for confirming DD genotypes., (Copyright 2002 S. Karger AG, Basel)

We compared cell-mediated immune responses in two groups of patients on hemodialysis. One group of patients were chronic carriers of hepatitis B virus (HBV), and the patients of the other group were HBV antigen negative. Our results show that despite the presence of normal numbers of T cells and an increased CD4/CD8 ratio in both groups of patients compared to healthy controls (p less than 0.0001), only the group of patients who were chronic HBV carriers showed depressed lymphoproliferative responses to phytohemagglutinin (p less than 0.001) and concanavalin A (p less than 0.0001). In contrast, a control group of healthy adult HBV carriers showed normal T cell subsets and lymphoproliferative responses to mitogens, indicating that HBV infection per se did not result in depressed lymphoproliferative responses. These results further substantiate the notion that depressed cell-mediated immunity in chronic renal failure is an important factor in predisposing patients to HBV infection with subsequent development of the chronic carrier state.

The factors influencing the development of electroencephalographic (EEG) abnormalities and hypertensive encephalopathy were studied in 31 children with acute glomerulonephritis and hypertension. Based on the degree of background slowing on the EEG, they were divided into 2 groups: group 1 had a percent EEG power for frequencies 1-4 Hz of less than or equal to 6.45 (upper 95th percentile confidence limit in 31 age- and sex-matched controls), while group 2 had values greater than 6.45. Six of 16 children in group 2 developed grand mal convulsions and had prolonged changes in the level of consciousness. There were no significant differences between the mean levels of peak blood pressures (systolic, diastolic and mean), degree of fluid overload, and fractional sodium excretion in the 2 groups. However, group 2 had significantly higher mean blood urea and creatinine levels (p less than 0.02 and p less than 0.03 respectively). These findings suggest that hypertension alone does not predict the subsequent development of EEG abnormalities and hypertensive encephalopathy. The concomitant presence of azotaemia may render the child more susceptible to cerebral autoregulatory dysfunction, resulting in hypertensive encephalopathy.

Among 98 patients with IgA nephritis who had protein selectivity studies performed, 54% had nonselective proteinuria and the remaining 46% had selective proteinuria. Patients with nonselective proteinuria had a higher incidence of glomerulosclerosis. At the end of a 4-year follow-up period, patients with nonselective proteinuria had lower creatinine clearance, higher incidence of hypertension and chronic renal failure when compared to patients with selective proteinuria. Six out of eleven patients (55%) in the study who had the nephrotic syndrome had selective proteinuria. Among these 6 patients, 1 had spontaneous remission and 5 responded to steroid or cyclophosphamide therapy. The remaining 5 patients with nonselective proteinuria did not respond to therapy. In the patients who had selectivity studies repeated, the data showed that the selectivity index (SI) can fluctuate depending on the clinical course of the patients. SI can therefore be used to monitor the progress of patients on long-term follow-up. Protein selectivity appears to be a useful prognostic index in IgA nephritis. For patients with the nephrotic syndrome it may serve as a guide to therapy.

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.