In a previous report, we showed that nutritional status and especially serum albumin had great predictive value for death in chronic hemodialysis patients, whereas blood pressure did not. In the present study, we analyzed the causes of death in consideration of the relationship between serum albumin and blood pressure. A total of 1,243 Okinawan patients (719 males, 524 females) undergoing hemodialysis in January 1991 were followed up through the end of 1995. Three hundred forty-two of the patients died, 45 received transplants, and 12 were transferred by the end of the follow-up period. The total duration of observation was 5,110.3 patient-years. Blood pressure as well as clinical and laboratory variables were determined immediately prior to the first dialysis session in January 1991. The crude death rate was 40.0% when the diastolic blood pressure (DBP) <70 mm Hg, 35.0% at 70 to 79 mm Hg, 25.0% at 80 to 89 mm Hg, 25.0% at 90 to 99 mm Hg, and 13.0% at >100 mm Hg. The death rate showed an inverse correlation with DBP. DBP showed a significant positive correlation with serum albumin (r = 0.137, P < 0.001) and age (r = -0.325, P < 0.0001). The adjusted odds ratio (95% confidence interval) of death was 0.84 (0.71 to 0.99) with 10 mm Hg increments in DBP when the reference DBP was less than 69 mm Hg. Low DBP may be a manifestation of malnutrition and/or cardiovascular disease in chronic hemodialysis patients. Target DBP levels may be higher levels in chronic hemodialysis patients than the general population.
Here we report a community-based epidemiologic study of patients who received renal biopsy in Okinawa, Japan between 1967 and 1994. The total number of cases was 2832 (1395 men and 1437 women), and the mean (SD) age at biopsy was 30.0 (10.0) years (range 1.0 to 88.0 years). The most common clinical indications for renal biopsy were proteinuria/hematuria (46.7%), nephrotic syndrome (21.2%), acute glomerulonephritis (10.1%), and systemic lupus erythematosus (7.5%). Patients who received renal biopsy between 1985 and 1994 (N= 1480) were much less likely to have acute glomerulonephritis than patients treated between 1967 and 1984 (N= 1352); the rates of proteinuria/hematuria, renal failure, and diabetes mellitus were slightly higher in the later period. Okinawa patients who began dialysis between 1971 and 2000 (N= 5246) were also studied. Among them, a total of 468 patients (260 men and 208 women) began dialysis after renal biopsy. The cumulative incidence of end-stage renal disease (ESRD) among these patients was 17% in 17 years. Half of these patients developed ESRD in the 5.8 years after renal biopsy. Among the dialysis patients, the biopsy rate was 12.6% in chronic glomerulonephritis, 1.7% in diabetes mellitus, 2.6% in nephrosclerosis, and 52.1% in systemic lupus erythematosus. The diagnoses of primary renal diseases were primarily made clinically. The survival rate after starting dialysis therapy was slightly better in those with than in those without renal biopsy but this finding was not statistically significant (adjusted hazards ratio 0.855, 95% CI 0.711-1.028, P= 0.095). The clinical significance of renal biopsy, other than its provision of histologic evidence, remains to be shown.
Striking renal involvement occurs in NZB and particularly in NZB-NZW F1 hybrid mice. In this paper we describe the morphologic changes observed by light and electron microscopy in the kidneys of both strains during a study of the natural history of the disease. A semiquantitative analysis of the histologic findings was made and was compared with previously published observations in human systemic lupus erythematosus. In the NZB strain, normal kidneys were found in 30 mice of all ages up to 96 weeks; glomerulitis, in which intraglomerular thrombi were often observed, in 19; and glomerulonephritis in four. In the NZB-NZW F1 hybrid, nine kidneys were considered normal (10–28 weeks of age); five had glomerulitis (32–42 weeks); and 17 had glomerulonephritis (34–84 weeks). Morphologically, there are definite similarities between human lupus glomerulitis and the disease seen in the NZB mouse; and, between human lupus glomerulonephritis and that seen in the NZB-NZW F1 hybrid.
Since autoimmune heinolytic anemia wasAll 3-and 9-month mice were clinically first demonstrated in NZB/Bl mice, these healthy when blood was drawn. Many of the animals have been investigated in detail by 18-month-old mice of the NZB and NZBmany workers( 1,2,3), and the role of heredity NZW strains were ill. In our colony of NZB has been demonstrated clearly(4,5,6,7). I n mice the Coombs test was positive in none of patients with Systemic Lupus Erythematosus (SLE) serum gamma globulin levels are significantly elevated (8) , and agammaglobulinemia may occur in association with connective tissue diseases including SLE( 9~0 ) . Some authors (1 1) reported elevation of serum gamma globulin levels in relatives of patients with SLE; others did not( 1243).In view of these observations in human SLE, we studied the serum protein levels of NZBJBl mice and related pure and hybrid strains in order to determine whether or not hypergammaglobulinemia occurred in these mice and its possible relationship to heredity and to disease activity, Mateyial and methods. The inbred strains used in this study were NZB, NZW, NZC and the F1 hybrids NZB-NZW and NZB-NZC. Animals were grouped a t 3, 9, and about 18-20 months of age. Where possible, equal numbers of each sex were studied, but breeding difficulties with the colony inevitably resulted in unequal numbers in the various groups. * These studies were supported by research grants AM05374 and AM10281 from Sat. Inst. of Arthritis and Metab. Dis., USPHS. t This work was done during the tenure of a Career Development Award USPHS (l-K3-HE-22,492-01). Present address: Michael Reese Hospitalthe 3-month animals, in 55% of the 9-month animals, and 100% of the 18-month animals (14). In the NZB-NZW colony the test for antinuclear antibodies was positive in about 1270 a t 3 months, 75% at 9 months, and 100% at 18 months; the test for LE cells was positive in none at 3 months; 35% a t 9 months; and looL% a t 18 months(l5).Controls used were 3-and 9-month-old mice of the C3H, NHA, Cb, and Strong A strains. All were clinically healthy, were housed in the same laboratory and received the same diet and care. Blood samples were drawn in capillary tubes from the retro-orbital venous plexus under light ether anesthesia. Sera were frozen if not used immediately, and were thoroughly mixed in siliconized wells prior to analysis. Total protein was determined in duplicate by a minor modification of the method of Lowry and his colleagues ( 16). Freshly dissolved crystalline bovine albumin$ was used as the standard, and was checked by micro-Kjeldahl, using a conversion factor of 6.54(17). Electrophoresis was done in duplicate on cellulose acetate strips (18).Resuhs. The results are summarized in Tables I and 11. There were no significant differences among the 4 control strains and the results therefore have been pooled in Ta-
The possible pathogenetic role of the thymus in autoimmune disease has been the subject of much recent investigation. Tumors and other thymic abnormalities occur in patients with dysgammaglobulinemia ; thymic epithelial hyperplasia and/or germinal center formation are described in systemic lupus erythematosus (SLE) and myasthenia gravis ( 1 ) .Atypical epithelial hyperplasia and structures resembling germinal centers were described by Holmes ,and Burnet in the thymus of NZB mice with autoimmune hemolytic anemia and nephritis( 2). These authors considered the changes to be representative of the development of "forbidden clones" which initiate autoimmune reactions. As neonatal thymectomy is known to impair the full development of i m u n d o g i c competence in many animal species, it was logical to attempt to determine the effect of neonatal thymectmny in murine strains with autoimmune disease. On the one hand, Helyer and Howie reported the earlier appearance of auto antibodies and more florid renal disease in neonatally thymectomized animals (3,4) ; whereas Holmes and Burnet noted that the appearance of Coombs antibodies was delayed 2 to 3 months in NZB mice thymectomized 2 to *These studies were supported by research grants AM05374 land AM10281 from Nat. Inst. od Arthritis & Metab. Dis., USPHS. 6 days after birth( 5,6). We report herein on the effect of neonatal thymectomy in two F1 hybrid strains, NZB-NZW and NZB-NZC.t Nephritis is the major manifestation of the disease in the former, hemolytic anemia in the latter ( 7 ) .Mat eria2 and met hods. Thymectomies were done within 24 hours of birth by the technique of Helyer & Howie(3). Two groups served as controls: nonthymectomized and sham thymtomized animals. In the latter the thymus was dissected but left in place. Mice from newborn litters were assigned at random to the 3 groups.Studies were made on mice which survived to weaning: 24 neonatally thymectomized (Tx) NZB-NZW F1 mice and 25 controls( 1 1 sham operated; 14 unoperated) ; 2 1 Tx NZB-NZC F1 mice and 17 sham operated and unoperated controls. As there were no differences in the 2 control groups of each strain they are considered together. All mice were inspected and weig,hed weekly; blood was drawn biweekly for hematocrit, Cmrnbs tests, antinuclear antibodies and LE cells (8). Animals were sacrificed when ill. A complete autopy was done in 66 mice; completeness of thymectomy was confirmed by gross inspection and histologic examination in all but 2 NZB-NZC mice.tA breeding colony of mice of the NZB, NZW & NZC strains was kindly provided by Dr. B. J. Ho'wie, Dundin, New Z d a n d .
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