IgA glomerulonephritis (IgAGN) is a kidney disease with variable prognosis. Several known risk factors exist for a more progressive course. Some population studies indicate that moderate alcohol consumption might protect kidney function, but the relationship between alcohol intake and IgAGN has not previously been examined.
We examined 158 (95 men) IgAGN patients (37 abstainers, 80 light drinkers, 25 moderate drinkers and 16 heavy drinkers) in a cross-sectional study. The definition of alcohol consumption was based on interviews on the amounts of alcohol intake combined with measurements of serum carbohydrate-deficient transferrin, a specific biomarker of alcohol abuse. Longitudinal data on renal function were available from 117 patients (76 men) in whom an analysis with respect to progression was also performed.
Moderate drinkers showed the best kidney function. When adjusted by hypertension and 24-hour protein excretion, moderate alcohol consumption in a cross-sectional multivariate analysis, and both light and moderate alcohol consumption in a longitudinal multivariate analysis were significant factors of better kidney function. When the study population was divided by gender, the best kidney function was among light drinkers in women and among moderate drinkers in men.
Moderate alcohol consumption might have a favorable impact on the progression of IgAGN. Light alcohol consumption in women and moderate consumption in men are associated with improved indices of the glomerular filtration estimates in patients with IgAGN.
Costs for treating patients with end-stage renal disease (ESRD) have grown noticeably. However, most of the cost estimates to date have taken the perspective of the payers. Hence, direct costs of treating ESRD are not accurately known.
Files of all adult patients with ESRD who entered dialysis therapy between January 1, 1991, and December 31, 1996, were studied retrospectively, and all use of health care resources and services was recorded. Follow-up continued until December 31, 1996.
Two hundred fourteen patients fulfilled the study criteria, 138 patients started with in-center hemodialysis (HD) therapy, and 76 patients started with continuous ambulatory peritoneal dialysis (CAPD) therapy. Patients were followed up until death (72 patients) or treatment modality changed for more than 1 month. Fifty-five patients received a cadaveric transplant, and after transplantation (TX), they were examined as a separate group of TX patients. Direct health care costs for the first 6 months in the HD, CAPD, and TX groups were 32,566 US dollars, 25,504 dollars, and 38,265 dollars, and for the next 6 months, 26,272 dollars, 24,218 dollars, and 7,420 dollars, respectively. During subsequent years, annual costs were 54,140 US dollars and 54,490 dollars in the HD group, 45,262 dollars and 49,299 dollars in the CAPD group, and 11,446 dollars and 9,989 dollars in the TX group. Regression analyses showed 4 variables significantly associated with greater daily costs in dialysis patients: age, ischemic heart disease, nonprimary renal disease, and HD treatment.
Compared with HD, CAPD may be associated with lower costs, yet the absolute difference is not striking. After the TX procedure is performed once, annual costs decline remarkably, and cadaveric TX is less costly than both dialysis modalities.
The reported biopsy-proven glomerulonephritis incidence varies according to population characteristics, the unknown true glomerulonephritis incidence and biopsy rate. Reported glomerulonephritis incidence should be evaluated against the biopsy rate.
We report here the glomerulonephritis incidence in our University Hospital (UH) consecutive biopsy material. It is compared to those from surrounding central hospitals (CH), previous single-centre studies and European biopsy registries (EBR). Biopsy rate, when reported, has been considered.
The annual biopsy rate/10(5), median (min-max), at the UHs was 25.4 (15.6-35.1). At the CHs it was 8.7 (5.1-12.6). In previous single-centre studies it has been 18.7-21.5. In the EBRs it has been between 1.0 and 6.9 when reported. The annual incidences (median, min-max) per 10(5) (1980-2000) at the UH were as follows: proliferative glomerulonephritis (9.5, 6.8-18.1), non-proliferative glomerulonephritis (6.7, 3.4-12.6), the four major glomerulonephritis groups MesGN (7.7, 4.4-15.9), ECGN/FPGN-complex (1.4, 0.5-3.2), MCGP/FSGS-complex (0.9, 0.2-2.7) and MGN (1.4, 0.5-2.4) these which findings were compatible with the single-centre studies and higher than those of the CHs and in the EBRs. Biopsy rate had a major impact on the annual glomerulonephritis incidences explaining 60% of the variation. The relative frequency of MesGN was the highest by all observers, followed by the ECGN/FPGN-complex, MGN and MCGP/FSGS-complex whose frequencies did not differ much. For every patient commencing renal replacement therapy (Finnish Renal Replacement Registry Data) due to glomerulonephritis there were about 11 subjects with biopsy-proven glomerulonephritis, a relationship compatible with previous reports.
The incidence of any glomerulonephritis of 17.6 per 10(5) population was comparable to those from the single-centre studies, but higher than in European biopsy registries, a fact largely explained by biopsy rates.
To evaluate mortality and causes of death in patients with rheumatoid arthritis (RA) treated with low-dose oral glucocorticoids.
Mortality was analyzed in population-based data of 604 patients with RA. In the original study in 1988, state of general health, severity of RA, and treatment including the use of oral glucocorticoids were recorded. In 1999 vital status and causes of death were evaluated. Mortality in patients with RA who had not received glucocorticoids (Group A, n = 209) was compared to that in patients treated with glucocorticoids for less than 10 years (Group B, n = 276) or for more than 10 years (Group C, n = 119).
From onset of RA to 1999, 395 (65%) patients had been treated with oral glucocorticoids. In 1999 a total of 160 (26%) patients had died, 23% of patients in Group A, 21% in Group B, and 45% in Group C. In multivariate Cox regression analysis, male sex (hazard ratio 2.50; 95% CI 1.74-3.59), impaired functional capacity by Health Assessment Questionnaire (HR 2.11; 95% CI 1.65-2.96), heart failure (HR 1.96; 95% CI 1.36-2.84), and diabetes (HR 1.87; 95% CI 1.17-3.01) predicted increased mortality. In the same analysis glucocorticoid treatment for 1 year increased the mortality risk by 14% (HR 1.14; 95% CI 0.98-1.27, p = 0.057) and treatment over 10 years by 69% (HR 1.69; 95% CI 1.12-2.56, p = 0.011) compared to RA patients without treatment. The major cause of death was cardiovascular disease in all groups, but infections and intestinal perforations due to amyloidosis were more frequent in patients with long-lasting glucocorticoid therapy. Lymphomas were more frequent in all patients treated with glucocorticoids (Groups B and C) than in those not receiving glucocorticoids.
Patients with RA treated with low-dose oral glucocorticoids for more than 10 years had increased mortality compared to those who did not receive glucocorticoids or whose duration of treatment was less than 10 years. The increased mortality was related mainly to infections and complications caused by systemic amyloidosis.
The Centre for Cardiovascular Genetics, British Heart Foundation Laboratories, Royal Free and University College Medical School, University College London, Rayne Building, 5 University Street, UK. email@example.com
A 53G>A polymorphism identified in the 5' untranslated region (5'UTR) of the platelet endothelial cell adhesion molecule-1 (PECAM-1) gene alters a putative shear stress responsive element (SSRE). PECAM-1 was shown to be responsive to shear stress and transient transfection of human umbilical vein endothelial cell (HUVECs) with two luciferase reporter constructs driven by the PECAM-1 promoter and 5'UTR showed a response of the 53G allele, not the 53A allele, to shear stress. Association between the 53G>A, and the previously published L125V polymorphism, and coronary atherosclerosis was examined in two angiographic studies. The frequencies of the rare alleles of the 53G>A and L125V polymorphisms were 0.01 and 0.49, respectively, in the Lopid Coronary Angiography Trial (LOCAT) study and 0.02 and 0.49, respectively, in the Regression Growth Evaluation Statin Study (REGRESS) study. Compared with 53G homozygotes, carriers of the 53A allele showed less focal progression of disease in the LOCAT study and a similar trend in the diffuse progression of disease in the REGRESS study, whereas no association between L125V and coronary atherosclerosis was observed in either study. These data demonstrate that the PECAM-1 gene is responsive to shear stress in vitro and that decreased PECAM-1 gene expression in 53A carriers may influence reduced progression of vessel stenosis in patients with coronary artery disease.