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Background: Ankylosing spondylitis (AS) is an inflammatory autoimmune disorder that manifested with sacroiliitis at its early stage and developed extensive inflammation with syndesmophytes of the lumbar, thoracic and cervical spines at its later stage. In the present study, we characterized the trunk isometric strength in patients with AS with different disease severity, defined by the radiological images. Methods: In a cross-sectional study conducted in a university-affiliated hospital, thirty-eight male AS patients (23 in the early AS group whose radiological findings showed no syndesmophyte, Modified Stoke Ankylosing Spinal Score (m-SASSS

IgG Fcγ receptors (FcγRs) mediate a variety of immune functions that are critical in immune responses. In humans, 5 classic low-affinity FcγRs (FcγRIIA, FcγRIIB, FcγRIIC, FcγRIIIA, and FcγRIIIB) are coded by 5 genes (FCGR2A, FCGR2B, FCGR2C, FCGR3A, and FCGR3B, respectively) in the FCGR cluster on chromosome 1. Activating FcγRs (FcγRIIA, FcγRIIC, FcγRIIIA, and FcγRIIIB) mediate immune cell activation promoting inflammation, while the classic inhibitory FcγRIIB dampens immune responses and restricts inflammation (1,2). Activating FcγRs mediate functions including immune complex clearance, phagocytosis, antigen presentation, antibody-dependent cellular cytotoxicity, and cytokine production (3). In contrast, the inhibitory FcγRIIB abrogates immune cell activation. FcγRIIB also plays a role in the maintenance of peripheral B cell tolerance and the prevention of autoimmunity (2). The variations in FcγR expression significantly affect IgG immune complex–mediated signal thresholds (3,4). Notably, proinflammatory and antiinflammatory cytokines could modulate the expression levels of activating and inhibitory FcγRs (5) that affect the threshold immune cell response to IgG immune complexes (6). FcγR-knockout mouse models indicate that both activating and inhibitory FcγRs influence the development of autoimmune diseases (7–9). The contributions of FcγR genes to autoimmune diseases have attracted substantial attention, and functional FcγR polymorphisms have been reported to play important roles in the pathogenesis of autoimmune diseases (4,10,11). Gene copy number variation (CNV) is a rich source of genetic heterogeneity (12,13). The FCGR cluster on chromosome 1q23 shows a complex pattern of CNVs. Among 5 FcγR genes in the cluster, 3 genes (FCGR3A, FCGR2C, and FCGR3B) have CNVs, while FCGR2A and FCGR2B do not have CNVs (14,15). CNVs play important roles in human disease pathogenesis (16). FCGR3B copy number deficiency is associated with autoimmune disease, including systemic lupus erythematosus (SLE) (17–19), Sjogren's syndrome (20), and systemic sclerosis (21). Although FCGR3B CNVs were reported to associate with rheumatoid arthritis (RA) (22–24), no association between RA and FCGR3B CNVs was observed in other studies (25,26). Moreover, no association between FCGR3A CNVs and RA was observed (24,27). In the current study, we investigated whether FCGR3A and FCGR3B CNVs are associated with susceptibility to SLE and RA in Taiwanese individuals. The results provide new insights into the role of FcγRIII family members in the pathogenesis of SLE and RA in an Asian population.

Background/PurposeCryoglobulinemic vasculitis is a systemic vasculitis resulting from circulating immune complex deposition in the small vessels and is characterized by variable clinical features, including purpura, Raynaud’s syndrome, ulcerations, arthralgia, glomerulonephritis, and peripheral neuropathy. Cryoglobulinemia can also result from hepatitis C virus (HCV) infection. The clinical spectrum and associated or underlying diseases of cryoglobulinemia in different age groups is not well understood. This study investigated the demographic, clinical, serologic features, and associated or underlying diseases in children and adult patients with cryoglobulinemia.MethodsThe retrospective study included 114 patients (18 children, 96 adults) who presented with cryoglobulinemia between 2000 and 2010 at the Chang Gung Memorial Hospital. Their medical records were reviewed and serological and virologic assessments were analyzed.ResultsIn this group of patients, children had a significantly higher prevalence of prolonged fever (16.7% vs. 3.13%; p=0.018), arthralgia (66.67% vs. 16.67%; p

To estimate the mortality rate and identify factors predicting survival in patients with polymyositis (PM) and dermatomyositis (DM). The medical records of 192 PM/DM patients who were treated at Chang Gung Memorial Hospital from 1999 through 2008 were retrospectively reviewed. The Taiwan National Death Registry (1999–2008) was used to obtain their survival status. Thirty-one (16.1%) of the 192 patients with PM/DM had an associated malignancy; 41 (21.4%) had interstitial lung disease (ILD). During the follow-up period, 55 (28.6%) patients died and the overall cumulative survival rate was 79.3% at 1 year, 75.7% at 2 years, 69.9% at 5 years, and 66.2% at 10 years. In univariate analysis, older age at PM/DM onset, anemia, thrombocytopenia, leukopenia, diabetes mellitus, ILD, cancer, and non-use of azathioprine were associated with higher mortality (p = 0.0172, 0.0484

Objective.To investigate the association of the functional FCRL3 single-nucleotide polymorphism (SNP) −169T/C with disease phenotypes and susceptibility to systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) in Taiwanese.Methods.FCRL3 SNP −169T/C was genotyped in 573 patients with SLE, 670 patients with RA, and 758 controls. Genotype distributions and allele frequencies were compared among the 3 groups as aggregates or as stratified by clinical characteristics, autoantibody profile, and sex within patient groups.Results.Overall, FCRL3 SNP −169T/C was not associated with susceptibility to either SLE or RA. However, −169CC genotype was significantly reduced in leukopenia-positive SLE patients as compared to the leukopenia-negative SLE patients (CC vs CT+TT, p = 6 × 10−4, OR 0.444, 95% CI 0.279–0.708) and controls (p = 6.1 × 10−3, OR 0.583, 95% CI 0.396–0.857). On the other hand, −169TT genotypes were significantly more numerous in RA patients with non-destructive disease as compared with patients with destructive disease (CC+CT vs TT: p = 0.007, OR 1.672, 95% CI 1.149–2.432). The −169T allele frequency was also significantly increased in non-destructive RA compared with patients with destructive disease (C vs T: p = 0.010, OR 1.423, 95% CI 1.089–1.859). FCRL3 SNP −169TT homozygous donors were significantly more numerous among female cyclic citrullinated peptide (CCP)-negative RA patients versus female CCP-positive RA patients (CC+CT vs TT: p = 0.019, OR 1.64, 95% CI 1.085–2.479).Conclusion.The functional FCRL3 SNP −169T/C appears to play important roles in the development of certain phenotypes such as SLE leukopenia and RA disease severity in Taiwanese patients with SLE and RA.

Objectives. To estimate the incidence, characteristics and predictors of infections in patients with PM and DM. Methods. The medical records of 192 PM/DM patients followed up in a tertiary teaching medical centre from 1999 to 2008 were retrospectively reviewed. Results. Seventy-six episodes of major infection, defined as infections requiring >1 week of treatment with anti-microbial agents, occurred in 53 (27.6%) patients, and 15 (7.8%) patients had two or more episodes. The incidence rate of major infections was 11.1 episodes per 100 patient-years in PM/DM patients. Aspiration pneumonia [n (%)=16 (21.1)] was the leading cause of major infections, followed by opportunistic infection [n (%)=14 (18.4)]. A variety of pathogens were isolated, mainly including Staphylococcus aureus, Klebsiella, Escherichia coli, Salmonella and Mycobacterium. Overall patient survival rates were 85.0% at 1 year, 78.0% at 5 years and 78.0% at 10 years. However, after one episode of major infection, survival rates decreased to 84.7% at 30 days and 68.3% at 1 year. Multivariate analysis indicated that independent predictors of major infection were age >45 years at PM/DM onset [odds ratio (OR) 5.26; 95% CI 2.01, 13.77; P=0.001], presence of arthritis/arthalgia (OR 2.59; 95% CI 1.12, 6.02; P= 0.027), co-present interstitial lung disease (OR 7.24; 95% CI 2.67, 19.65; P < 0.001 current use of AZA (OR 6.07; 95% CI 2.39, 15.42; P < 0.001) or IVIG (OR 6.33; 95% CI 1.50, 26.77; P= 0.012). Conclusions. This study underlines the high frequency of major infections in PM/DM, which is significantly detrimental to patient survival rates. Close follow-up of PM/DM patients with risk factors for developing major infections is mandatory.

Objective To assess the changes in static and dynamic balance and movement strategies in patients with severe osteoporotic vertebral compression fracture while wearing and not wearing the Knight-Taylor (K-T) spinal brace. Subjects 47 patients with severe osteoporotic vertebral compression fracture, which was confirmed on radiographs and with bone density measurements obtained by dual energy X-ray absorption. Intervention Patients were randomly subjected to computerized dynamic posturography, which contained sensory organization tests, motor control balance test at 75% limit of stability (LOS) in 8 movement directions, and left/right rhythmic weight shift test (L/R RWS), while wearing and not wearing the K-T spinal brace, respectively. Results Patients wearing the spinal brace had significantly increased average stability, significantly increased average maximal stability under the swayed vision with fixed support surface condition and under the eye open with swayed support surface condition, significantly increased ankle strategy and decreased average velocity of COG target sway under the eye open with swayed support surface condition, significantly reduced the frequency of falls under the eye closed with swayed support surface condition and swayed vision with swayed support surface condition, and significantly decreased in the percentage of directional control with no difference of reaction time in the LOS test, and an increase in the on-axis velocity in the L/R RWS test. Conclusions The K-T spinal brace efficiently enables the subjects to maintain static and dynamic motor balance. Its use decreases the fall frequency but limits the directional control in severe osteoporotic patients with vertebral compression fracture.

The aim of the study was to estimate the prevalence, characteristics, and prognostic factors of interstitial lung disease (ILD) in patients with polymyositis (PM) and dermatomyositis (DM). The medical records of 151 PM/DM patients treated at Chang Gung Memorial Hospital between January, 2000 and June, 2007 were retrospectively reviewed. Thirty of 151 (19.9%) PM/DM patients had developed ILD. Older age at PM/DM onset, anti-Jo-1 antibody, and arthritis/arthralgia were associated with the presence of ILD (p = 0.004, p = 0.008, and p = 0.026, respectively). Anti-Jo-1 was initially excluded from the multivariate analysis because only 80 patients underwent the test. An older age at onset above 45 years (odds ratio 3.28, 95% confidence interval (CI) 1.15-9.34, p = 0.026) and arthritis/arthralgia at onset (odds ratio (OR) 2.57, 95% CI 1.09-6.08, p = 0.032) were the two independent risk factors for developing ILD. If anti-Jo-1 was included in the multivariate analysis (n = 80), then an older age at onset above 45 years (OR 7.30, 95% CI 1.70-31.40, p = 0.008) and anti-Jo-1 positive (OR 7.89, 95% CI 1.18-52.87, p = 0.033) were associated with ILD, while arthritis/arthralgia was no longer significant (OR 2.64, 95% CI 0.70-10.01, p = 0.153). Of the 30 ILD patients, 16 (53.3%) died. The survival time was significantly shorter in ILD patients than in patients without ILD (p < 0.001). Poor survival in ILD patients was associated with male gender (p = 0.039), a Hamman-Rich-like presentation (p = 0.039), and a clinical diagnosis of acute interstitial pneumonia (p = 0.007).

The aim of the current study was to determine whether the FcgammaRIIb 187-Ile/Thr polymorphism is a predisposition factor for subtypes of RA defined by disease severity and production of autoantibodies against cyclic citrullinated peptides (anti-CCPs) in Taiwanese RA patients. Genotype distributions and allele frequencies of FcgammaRIIb 187-Ile/Thr were compared between 562 normal healthy controls and 640 RA patients as stratified by clinical parameters and autoantibodies. Significant enrichment of 187-Ile allele was observed in RA patients positive for anti-CCP antibodies as compared with the anti-CCP negative RA patients (P=0.001, OR 1.652 (95% CI 1.210-2.257)) or as compared with the normal controls (P=0.005, OR 1.348 (95% CI 1.092-1.664)). In addition, 187-Ile allele was found to be enriched in RA patients positive for rheumatoid factor (RF) compared to the RF negative RA patients (P=0.024, OR 1.562 (95% CI 1.059-2.303)). Furthermore, the homozygotes were enriched in destructive male RA patients (P=0.035; OR 2.038 (95% CI 1.046-3.973)) and the 187-Ile allele was associated with early-onset of RA in Taiwanese patients (P=0.045, OR 1.548 (95% CI 1.007-2.379)). Thus, FcgammaRIIb SNP 187-Ile/Thr may influence the RA phenotypes in Taiwanese RA.

Toll-like receptors (TLRs), as innate immunity sensors, play critical roles in immune responses. Six SNPs of TLR3, TLR7, and TLR8 were genotyped to determine their associations with systemic lupus erythematosus (SLE) and clinical manifestations of SLE. TLR7 SNP rs3853839 was independently associated with SLE susceptibility in females (G vs. C: p = 0.0051). TLR7 rs3853839-G (G vs. C: p = 0.0100) and TLR8 rs3764880-G (recessive model: p = 0.0173; additive model: p = 0.0161) were associated with pericardial effusion in females relative to healthy females. Anti-SSA positive cases were more likely to have the dominant TLR7 rs179010-T allele than normal controls (p = 0.0435). TLR3 rs3775296-T was associated with photosensitivity (p = 0.0020) and anemia (p = 0.0082). The "G-G" haplotype of TLR7 rs3853839 and TLR8 rs3764880 increased risk of SLE in females (age adjusted p = 0.0032). These findings suggest that TLR variations that modify gene expression affect risk for SLE susceptibility, clinical phenotype development, and production of autoantibodies.

Ankylosing spondylitis (AS) is a common rheumatic disease in the Chinese population, which is the largest population in the world associated with the global burden of health care. Herein we review and report the epidemiology and specific clinical characteristics of Chinese AS. More than 90 % of Chinese AS patients are HLA-B27 positive with the predominant HLA-B*2704 subtype; the incidence of HLA-B27 positivity ranges from 4 to 8 % in the general Chinese population. The first-degree relatives of AS probands often develop atypical AS with relatively mild disease and particularly undifferentiated spondyloarthropathy in females. Chinese AS patients have higher frequencies of juvenile-onset AS and peripheral arthritis. Of extra-articular manifestations, AS patients have earlier onset and more recurrent attacks of HLA-B27-related acute anterior uveitis. Cardiac arrhythmias or other cardiovascular disorders and metabolic syndrome are not infrequently found. Importantly, apical lung diseases in Chinese AS patients are also frequently associated with tuberculosis infection.

Introduction Ankylosing spondylitis (AS) is a familial, heritable disease specified by syndesmophyte formation leading to an ankylosed spine. Endoplasmic reticulum aminopeptidase 1 (ERAP1) genetic variations have been widely proved to be associated with AS in several ethnic populations. The aim of this study was to investigate whether ERAP1 single nucleotide polymorphisms (SNPs) are associated with AS susceptibility and disease severity in Taiwanese. Methods Four ERAP1 SNPs (rs27037, rs27980, rs27044 and rs30187) were genotyped in 797 Taiwanese AS patients and 1,150 healthy controls. Distributions of genotype and alleles were compared between AS patients and healthy controls, and among AS patients stratified by clinical parameters. Results The SNP rs27037T allele appeared to be a risk factor for AS susceptibility (P = 5.5 × 10-5, OR 1.30, 95% CI: 1.15 to 1.48; GT+TT vs. GG P = 9.3 × 10-5, OR 1.49, 95% CI: 1.22 to 1.82). In addition, the coding SNP (cSNP) rs27044G allele (P = 1.5 × 10-4, OR 1.28, 95% CI: 1.13 to 1.46; CG+GG vs. CC, P = 1.7 × 10-3, OR 1.44, 95% CI: 1.15 to 1.81) and the cSNP rs30187T allele (P = 1.7 × 10-3, OR 1.23, 95% CI: 1.08 to 1.40; CT+TT vs. CC P = 6.1 × 10-3, OR 1.38, 95% CI: 1.10 to 1.74) were predisposing factors for AS. Notably, the rs27044G allele carriers (CG+GG vs. CC, P = 0.015, OR 1.59, 95% CI: 1.33 to 2.30) and rs30187T allele carriers (CT+TT vs. CC, P = 0.011, OR 1.63, 95% CI: 1.12 to 2.38) were susceptible to syndesmophyte formation in AS patients. Furthermore, two cSNPs (rs27044 and rs30187) strongly associated with HLA-B27 positivity in AS patients. Finally, the ERAP1 SNP haplotype TCG (rs27037T/rs27980C/rs27044G) is a major risk factor for AS (adjusted P

Objectives To investigate the associations of paroxysmal supraventricular tachycardia (PSVT) and Wolff–Parkinson–White (WPW) syndrome with ankylosing spondylitis (AS). Methods We conducted a retrospective cohort study by reviewing the medical records of 1503 consecutive AS patients diagnosed at a tertiary medical center. The clinical and electrocardiographic (ECG) characteristics of 641 AS patients having 12-lead ECG available were further analyzed in a precise manner. Results Among the 641 AS patients with 12-lead ECG available for detecting cardiac abnormalities, 14 were identified as having PSVT, including 3 with WPW syndrome and 1 having a WPW (ventricular preexcitation) ECG pattern. A higher proportion of AS patients presented with PSVT (21.8/1000) compared with a general population-based study (2.25/1000). Also, AS patients demonstrated a higher prevalence of WPW syndrome or WPW pattern (6.24/1000) than found in general population-based studies (0.9 to 1.5/1000). Ankylosing spondylitis patients with PSVT or WPW syndrome had significantly higher rates of peripheral arthritis (78.6%; P = 0.002), acute anterior uveitis (64.3%; P = 0.003), bamboo spine (64.3%; P = 0.001), and other cardiovascular disorders (85.7%; P Conclusions Ankylosing spondylitis patients had a high probability of developing PSVT and WPW syndrome. Detailed ECG and electrophysiological examinations are required for early detection of PSVT and WPW syndrome for prompt resolution of potentially life-threatening complications in all AS patients, especially those presenting with the symptoms of palpitation, dizziness, dyspnea, or syncope.

The pathogenesis of adult-onset Still's disease (AOSD), which is currently thought to be an autoimmune disorder, may share similarities with autoimmune hyperthyroidism. This report describes a middle-aged woman in whom hyperthyroidism and Still's disease developed concurrently. During the course of her illness, the hyperthyroidism was observed to be aggravated whenever her AOSD was in the active stage. After her AOSD activity was controlled, her hyperthyroidism improved clinically. The extent of activation of her hyperthyroidism was observed in parallel to the extent of activation of her AOSD. Furthermore, the patient developed neutropenia after receiving either propylthiouracil (PTU) or methimazole, both of which are standard accepted medications for treatment of hyperthyroidism. Immune mechanisms contributed to PTU induced neutropenia have been proposed, and hyperthyroid patients treated with standard antithyroid agents should be monitored for blood cell counts especially for AOSD patients. Corticosteroid may effect Graves' disease activity, and steroids may play a role in the treatment of hyperthyroidism if a patient had drug allergies to antithyroid agents.

Objective.We investigated the etiological association and clinical characteristics of apical pulmonary fibrosis in ankylosing spondylitis (AS).Methods.We reviewed medical records of 2136 consecutive patients diagnosed with AS at a tertiary medical center. Clinical and radiographic characteristics were analyzed for evidence of apical lung fibrosis on chest radiographs.Results.Of 2136 patients with AS, 63 (2.9%) developed apical lung fibrosis, of which chronic infections were the cause in 41 and AS inflammation predisposed the fibrosis in 22 patients. Tuberculosis (TB) infection was considered to be the cause of apical lung fibrosis in 40 patients (63.5%) including 19 with bacteriologically-proven TB and 21 with chest radiographs suggestive of TB. Two were identified as having non-TB mycobacterial infection and one asAspergillusinfection. Lung cavity lesion appeared to be a crucial differentiator (p = 0.009, odds ratio 7.4, 95% CI 1.5–36.0) between TB infection and AS inflammation-induced apical fibrosis.Conclusion.Our study suggests that TB, instead ofAspergillus, is the most common pulmonary infection in patients with AS presenting with apical lung fibrosis. AS-associated apical lung fibrosis may mimic pulmonary TB infection. Thus, bacteriological survey and serial radiological followup of lung fibrocavitary lesions are critical for accurate diagnosis and treatment.

The aim of this study was to investigate the clinical characteristics of patients with coexisting ankylosing spondylitis (AS) and gout. Between July 1987, and October 2004, sixty-five patients with coexisting AS and gout were enrolled. The clinical manifestations of both AS and gout in these patients were studied. Of the 65 patients included in the study, 61 were men and four were women (men-to-women ratio, 15.3:1). Sixty-three subjects were Han Chinese, and two were Atayal Aborigines. Mean ages at onset of AS and gout were 29.3 +/- 15.6 years (range 7-63) and 42.2 +/- 13.2 years (range 20-74), respectively. Fifty-six patients developed gout after (15.5 +/- 11.2 years; range, 1-51 years) onset of AS; nine patients developed gout before (average, 3.4 +/- 2.2 years; range. 1-7 years) onset of AS. Forty-four (67.7%) patients had chronic peripheral arthritis and all 65 (100%) patients had acute peripheral arthritis. Thirty-three (50.8%) cases had heel pain (enthesopathy), including 22 (33.9%) with chronic heel pain, seven (10.8%) with acute heel pain, and four (6.2%) with concurrent acute and chronic heel pain. Sixty-one (93.9%) subjects were HLA-B27 antigen positive. Medical conditions potentially associated with hyperuricemia or gout were urolithiasis (n = 17), hypertension (n = 21), diabetes mellitus (n = 8), hyperlipidemia (n = 34), congestive heart failure (n = 6), coronary heart disease (n = 5), and stroke (n = 3). The following drugs were prescribed: diuretics (n = 7), low-dose aspirin (n = 4), antituberculous drugs (n = 1), and sulphasalazine (n = 34). Six (6.2%) patients had iatrogenic Cushing syndrome with adrenal insufficiency. Patients with coexisting AS and gout are not rare. Distinguishing between peripheral arthritis or enthesopathies of AS and gout is essential, especially when the course of AS arthritis becomes acute or the course of gout becomes chronic.

Objective. To estimate in a Chinese population the prevalence of undifferentiated spondyloarthropathy (USpA) among first-degree relatives (FDRs) of ankylosing spondylitis (AS) probands, and to compare the clinical features of familial USpA with those of sporadic USpA. Methods. The FDRs of two separate cohorts of consecutive AS probands were evaluated for the prevalence of USpA, using the Modified New York criteria and the European Spondylitis Study Group criteria for AS and SpA, respectively. Sporadic USpA and FDRs of non-SpA rheumatic patient probands served as separate controls. Results. Among the 301 FDRs of 102 AS probands, 7.0% were USpA. This was 1000 times higher than the 147 FDRs of 40 non-SpA probands (P^0.00230). Within the AS families, USpA was less male-dominated than AS (33.3 vs 72.5%) (P^0.006). The only feature distinguishing familial from sporadic USpA was that the percentages of HLA B27 were 100 and 50%, respectively (P

To determine whether the distribution of Fcgamma receptor IIa, IIIa, and IIIb polymorphisms confers a risk factor for disease susceptibility, and correlates with the clinical characteristics and serological parameters of patients with SLE in Taiwan.Genotyping of Fcgamma receptors IIa H/R131, IIIa F/V158, and IIIb NA1/NA2 was performed in 302 patients with SLE and 311 healthy blood donor controls. The distribution of Fcgamma receptor IIa, IIIa, and IIIb genotypes in patients and controls was analysed. Frequencies of three Fcgamma receptor polymorphisms were also compared between lupus patients with and without different clinical manifestations and autoantibodies.No significant skewing in the distribution of Fcgamma RIIa H/R131, Fcgamma RIIIa F/V158, and Fcgamma RIIIb NA1/NA2 was found between patients and controls in Taiwan. The following clinical associations were found: Fcgamma RIIIb NA1/NA1 protected against neuropsychiatric lupus (p = 0.028) but conferred susceptibility to discoid rash (p0.005); increased Fcgamma RIIIa V/V158 was associated with infections (p = 0.039); increased Fcgamma RIIa H/H131 was associated with earlier onset of lupus (p = 0.01).Fcgamma receptor IIa, IIIa, and IIIb polymorphisms may be responsible for the development of distinct manifestations of lupus patients in Taiwan, but there is no significantly skewed distribution in the susceptibility to lupus as a whole.

Nephropathy is known to occur in persons exposed to high levels of lead, but the question of whether long-term exposure to low levels of environmental lead is associated with impaired renal function remains controversial.To examine whether chelation therapy slows the progression of renal insufficiency in patients with mildly elevated body lead burden.Randomized, controlled trial.Academic medical center in Taiwan.32 patients with chronic renal insufficiency (serum creatinine level132.6 micromol/L [1.5 mg/dL] and353.8 micromol/L [4.0 mg/dL]), mildly elevated body lead burden (0.72 micromol [150 microg] of lead per 72-hour urine collection and2.90 micromol [600 microg] of lead per 72-hour urine collection [EDTA mobilization tests]), and no history of heavy lead exposure.The treatment group received 2 months of chelation therapy; the control group received no therapy.The reciprocal of serum creatinine (1/Cr) was used as an index of progressive renal insufficiency.Rates of progression of renal insufficiency were similar in the treatment group and the control group during a 12-month baseline observation period (1/Cr, 0.000054 L/micromol per month compared with 0.000046 L/micromol per month; P0.2). After the 2-month treatment period, improvement in renal function was greater in the treatment group than in the control group. In the 12 months after the treatment period, renal insufficiency progressed more slowly in the treatment group than in the control group (1/Cr, 0.000033 +/- 0.00038 L/micromol per month compared with 0.000045 +/- 0.000038 L/micromol per month; P = 0.0030).Chelation therapy seems to slow the progression of renal insufficiency in patients with mildly elevated body lead burden. This implies that long-term exposure to low levels of environmental lead may be associated with impaired renal function in patients with chronic renal disease.