Vitamin D receptor gene polymorphisms and prostate cancer.

Prostate cancer (PC) is the most common cancer among men worldwide and its pathogenesis is complex. The development of PC depends on family and environmental factors. Vitamin D can be associated with both of these factors. Its reduced serum concentration has been reported in a number of tumors. However, in the case of PC, the study results are conflicting. Polymorphism of VDR gene may also be involved in the development of this cancer. The aim of the study was to compare the frequency of selected polymorphisms in patients with PC and in men without this disease. Seventy-two Caucasian males aged 35-75 years with histologically proven PC (T1/T2) were enrolled in the study group. Seventy-two random age-matched Caucasian out-patient subjects formed the control group. VDR (FokI, BsmI and TaqI) gene polymorphism (rs2228570, rs1544410, rs731236) was determined by TaqMan® SNP Genotyping. The Hardy-Weinberg Equilibrium (HWE) - p> 0.05 was in all studied polymorphisms. Deviations from the HWE were not found. There were no differences between the study group and the control group. No difference was found when the groups were compared in terms of age or the Gleason score.

Risk Factors for Fractures Identified in the Algorithm Developed in 5-Year Follow-Up of Postmenopausal Women From RAC-OST-POL Study.

The aim of the study was to establish factors with an impact on fracture risk and to develop an algorithm to predict osteoporotic fracture. A total of 978 postmenopausal women from the epidemiological, population-based RAC-OST-POL study with a mean age of 65.7 ± 7.3 years were enrolled. At baseline, bone mineral density at hip and clinical risk factors for fracture were collected. Afterward, each person was asked annually on fracture incidence in the 5-year follow-up. Finally, data for complete 5-year observation were gathered for the group of 802 patients. During the follow-up, 92 osteoporotic fractures occurred in 78 women. The most common fracture site was the forearm (n = 45). The following baseline factors were found as significant for fracture incidence: femoral neck bone mineral density, prior fractures, steroid use, falls within previous 12 months, and height. Fracture risk was predicted by the following formula: Riskoffractureincidence=11+e-(-9.899+1.077∗STEROIDS+0.681∗PRIORFALLS+0.611∗PRIORFRACTURES-0.483∗FNTscore+0.042∗HEIGHT). In our current longitudinal study, an algorithm predicting fracture occurrence over a period of 5 years was developed. It may find application in daily medical practice.

Inducible T-cell costimulator (ICOS) and CD28 polymorphisms possibly play a role in the pathogenesis of chronic autoreactive urticaria.

BACKGROUND: Clinical experience emphasizes the coexistence of chronic spontaneous urticaria (CSU) and autoimmune disturbances. In chromosome 2q33-34, there is a cluster of homologous genes that are considered promising candidate genes for susceptibility to autoimmune diseases. AIM: To examine the possible role of polymorphisms in the genes for CD28 and inducible T-cell costimulator (ICOS) in the background of CSU. METHODS: In total, 149 patients with CSU with positive autologous serum skin test were enrolled in the study. The healthy control (HC) group consisted of 100 healthy volunteers. In all subjects, the CD28 rs2140148 and rs3116496 and the ICOS rs6726035 polymorphisms were analysed. Disease severity was assessed by means of Urticaria Activity Score. RESULTS: We found a statistically significantly lower prevalence of the ICOS rs6726035 TT genotype among patients with CSU compared with HCs. Furthermore, the haplotype rs2140148A, rs3116496T and rs6726035C presented a possible association with CSU. We did not find any association between the examined polymorphisms and either urticaria severity or age of disease onset. CONCLUSIONS: Our results underline the role of autoimmune components in the pathogenesis of chronic autoreactive urticaria, and indicate it as a potentially genetically related disorder.

High fracture probability predicts fractures in a 4-year follow-up in women from the RAC-OST-POL study.

UNLABELLED: In 770 postmenopausal women, the fracture incidence during a 4-year follow-up was analyzed in relation to the fracture probability (FRAX risk assessment tool) and risk (Garvan risk calculator) predicted at baseline. Incident fractures occurred in 62 subjects with a higher prevalence in high-risk subgroups. Prior fracture, rheumatoid arthritis, femoral neck T-score and falls increased independent of fracture incidence. INTRODUCTION: The aim of the study was to analyze the incidence of fractures during a 4-year follow-up in relation to the baseline fracture probability and risk. METHODS: Enrolled in the study were 770 postmenopausal women with a mean age of 65.7 ± 7.3 years. Bone mineral density (BMD) at the proximal femur, clinical data, and fracture probability using the FRAX tool and risk using the Garvan calculator were determined. Each subject was asked yearly by phone call about the incidence of fracture during the follow-up period. RESULTS: Of the 770 women, 62 had a fracture during follow-up, and 46 had a major fracture. At baseline, BMD was significantly lower, and fracture probability and fracture risk were significantly higher in women who had a fracture. Among women with a major fracture, the percentage with a high baseline fracture probability (>10 %) was significantly higher than among those without a fracture (p < 0.01). Fracture incidence during follow-up was significantly higher among women with a high baseline fracture probability (12.7 % vs. 5.2 %) and a high fracture risk (9.2 vs. 5.3 %) so that the "fracture-free survival" curves were significantly different (p < 0.05). The number of clinical risk factors noted at baseline was significantly associated with fracture incidence (chi-squared = 20.82, p < 0.01). Prior fracture, rheumatoid arthritis, and femoral neck T-score were identified as significant risk factors for major fractures (for any fractures, the influence of falls was also significant). CONCLUSIONS: During follow-up, fracture incidence was predicted by baseline fracture probability (FRAX risk assessment tool) and risk (Garvan risk calculator). A number of clinical risk factors and a prior fracture, rheumatoid arthritis, femoral neck T-score, and falls were independently associated with an increased incidence of fractures. [Corrected]

The rs1800471 Polymorphism of TGFB1 Gene, Serum TGF-Beta1 Level and Chronic Kidney Disease Progression.

The aim of the study was to investigate whether rs1800471 polymorphism in TGFB1 gene is associated with the development and progression of non-diabetic chronic kidney disease. Moreover, we examined the serum TGF-beta1 concentration and its association with that polymorphism and progression of the disease. We applied two different methodological approaches. Firstly, a family based study was carried out, comprised of 109 patients with non-diabetic chronic kidney disease and their 218 healthy parents, using the transmission/disequilibrium test. The rs1800471 polymorphism and serum TGF-beta1 level were determined in all subjects. Serum TGF-beta1 concentration was also measured in 40 healthy controls. Secondly, we performed a case-control orientated study to determine whether rs1800471 polymorphism and other factors influence the progression of renal impairment. We found no relationships between rs1800471 polymorphism allele transfer and the incidence or progression of non-diabetic chronic kidney disease. We found, however, that the serum TGF-beta1 was significantly higher in patients than in controls. In conclusion, rs1800471 polymorphism in TGFB1 gene does not have an impact on the development and progression of non-diabetic chronic kidney disease caused by primary glomerulopathy and chronic interstitial nephritis. The increased serum TGF-beta1 concentration in such patients suggests its role in the pathomechanism of the disease. Circulating TGF-beta1 level is determined in a multifactorial way, not by rs1800471 polymorphism in TGFB1 gene.

Nephroprotective effect of pentoxifylline in renal ischemia-reperfusion in rat depends on the timing of its administration.

BACKGROUND: Renal ischemia-reperfusion injury (IRI) induces inflammatory reaction damaging kidney. Pentoxifylline (PTX) given before IRI attenuates inflammation and prevents ischemic acute kidney injury (iAKI). Given that in clinical settings IRI is not always predictable, we aimed to assess whether PTX administration during or shortly after IRI affects the course of iAKI in the rat. METHODS: In 58 male 10-week-old Sprague-Dawley rats, 14 days after right nephrectomy, a 45-minute clamping of solitary renal pedicle was conducted. PTX 100 mg/kg body weight or 0.9% NaCl 1 mL were given subcutaneously either 60 minutes before renal ischemia, 1 minute into ischemia, or 60 minutes after clamp release. Creatinine clearance (ClCr; mL/min/kg body weight), fractional excretions of sodium (FENa [%]) and potassium (FEK [%]), and urine protein/ClCr ratio (Uprot/ClCr [mg/1 mL ClCr]) at 48 hours after IRI were compared between PTX-treated animals and respective controls (Mann-Whitney U test). RESULTS: Kidney function was improved in rats given PTX before IRI compared with controls: ClCr 2.10 ± 0.44 versus 1.03 ± 0.18; FENa 0.16 ± 0.12 versus 0.84 ± 0.55; FEK 40.3 ± 13.0 versus 75.5 ± 17.9, respectively (all P < .001). There was no difference in proteinuria: Uprot/ClCr 0.004 ± 0.002 versus 0.004 ± 0.002. Conversely, the analyzed parameters did not differ between animals administered PTX during IRI and controls: ClCr 0.42 ± 0.34 versus 0.73 ± 0.43; FENa 2.98 ± 2.71 versus 3.16 ± 3.05; FEK 280.1 ± 155.7 versus 206.2 ± 154.1; and Uprot/ClCr 0.031 ± 0.029 versus 0.029 ± 0.031, respectively, nor between rats given PTX after IRI and controls: ClCr 0.29 ± 0.38 versus 0.40 ± 0.47; FENa 4.25 ± 3.55 versus 3.80 ± 3.94; FEK 284.9 ± 117.5 versus 243.0 ± 150.6; and Uprot/ClCr 0.044 ± 0.018 versus 0.055 ± 0.061, respectively. CONCLUSIONS: PTX given only before, and not at the time of renal ischemia or after reperfusion, alleviates subsequent iAKI in the rat. This implicates usefulness of PTX in the clinical settings of expected renal ischemia, like kidney transplantation, and suggests potential benefits of PTX in peritransplant period foremost with donor pretreatment.

Possible contribution of chemokine receptor CCR2 and CCR5 polymorphisms in the pathogenesis of chronic spontaneous autoreactive urticaria

BACKGROUND: Autoimmune mechanisms play a role in the pathophysiology of chronic urticaria. As the genetic background of autoimmunity is well proven, the role of genetics in chronic urticaria is hypothesised. METHODS: 153 unrelated chronic spontaneous urticaria patients with a positive result of autologous serum skin test were included into the study, as were 115 healthy volunteers as control group. In all subjects we analysed CCR2 G190A and CCR5 d32 polymorphisms. RESULTS: We noticed higher prevalence of CCR2 A allele as well as lower frequency of CCR5 d32 in chronic urticaria group in comparison to control group, with borderline statistical significance. Additionally, we assumed haplotype Gd statistically significant negative chronic urticaria association with tendency to higher frequency of Aw haplotype in this group. CONCLUSIONS: The results of our study imply the role of autoimmune components in chronic urticaria pathogenesis and present chronic urticaria as possibly genetically related disorder

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CTLA-4 polymorphism in the pathogenesis of chronic spontaneous autoreactive urticaria

BACKGROUND: Autoimmune mechanisms are considered to play a significant role in chronic urticaria pathophysiology. Additionally, clinical experience emphasises the coexistence of chronic urticaria manifestation with thyroid autoimmunity. As the role of CTLA-4 polymorphism in autoimmune thyroid diseases is well proven we speculated on the possible role of this polymorphism in the background of chronic urticaria. MATERIALS AND METHODS: We included 128 chronic spontaneous autoreactive urticaria patients (87 females and 41 males) and 101 healthy volunteers (71 females and 30 males). In all examined subjects CTLA-4 A49G polymorphism was analysed. Disease severity with Urticaria Activity Score as well as age of disease onset was also studied. RESULTS: No statistically significant differences in the allele or genotype distribution between urticaria patients and controls were observed. Furthermore, we found no association between CTLA4 polymorphism and urticaria severity as well as the age of disease onset. CONCLUSIONS: Our data suggest that there is no contribution of CTLA-4 A49G polymorphism to chronic spontaneous autoreactive urticaria susceptibility. We recommend further research on other polymorphisms in chronic urticaria patients to explore in detail the potent role of the genetic background in the pathogenesis of this disorder

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CTLA-4 polymorphism in the pathogenesis of chronic spontaneous autoreactive urticaria.

BACKGROUND: Autoimmune mechanisms are considered to play a significant role in chronic urticaria pathophysiology. Additionally, clinical experience emphasises the coexistence of chronic urticaria manifestation with thyroid autoimmunity. As the role of CTLA-4 polymorphism in autoimmune thyroid diseases is well proven we speculated on the possible role of this polymorphism in the background of chronic urticaria. MATERIALS AND METHODS: We included 128 chronic spontaneous autoreactive urticaria patients (87 females and 41 males) and 101 healthy volunteers (71 females and 30 males). In all examined subjects CTLA-4 A49G polymorphism was analysed. Disease severity with Urticaria Activity Score as well as age of disease onset was also studied. RESULTS: No statistically significant differences in the allele or genotype distribution between urticaria patients and controls were observed. Furthermore, we found no association between CTLA4 polymorphism and urticaria severity as well as the age of disease onset. CONCLUSIONS: Our data suggest that there is no contribution of CTLA-4 A49G polymorphism to chronic spontaneous autoreactive urticaria susceptibility. We recommend further research on other polymorphisms in chronic urticaria patients to explore in detail the potent role of the genetic background in the pathogenesis of this disorder.

Possible contribution of chemokine receptor CCR2 and CCR5 polymorphisms in the pathogenesis of chronic spontaneous autoreactive urticaria.

BACKGROUND: Autoimmune mechanisms play a role in the pathophysiology of chronic urticaria. As the genetic background of autoimmunity is well proven, the role of genetics in chronic urticaria is hypothesised. METHODS: 153 unrelated chronic spontaneous urticaria patients with a positive result of autologous serum skin test were included into the study, as were 115 healthy volunteers as control group. In all subjects we analysed CCR2 G190A and CCR5 d32 polymorphisms. RESULTS: We noticed higher prevalence of CCR2 A allele as well as lower frequency of CCR5 d32 in chronic urticaria group in comparison to control group, with borderline statistical significance. Additionally, we assumed haplotype Gd statistically significant negative chronic urticaria association with tendency to higher frequency of Aw haplotype in this group. CONCLUSIONS: The results of our study imply the role of autoimmune components in chronic urticaria pathogenesis and present chronic urticaria as possibly genetically related disorder.

Acarbose improves glycemic control and reduces body weight: Subanalysis data of South Asia region.

Alpha-glucosidase inhibitors (AGIs) are widely used especially in Asian countries as a treatment option for type 2 diabetes patients with high postprandial glycaemia. However, data from South Asia region is very limited. In order to examine the effect of AGI in real-life setting, 10 PMS/NIS from all over the world from the launch of acarbose to date were pooled in one database and exploratory analysis was performed for glycemic parameters and weight. In total 62,905 patients were pooled from 21 countries and regions. Mean follow up (± SD) was 12.2 ± 4.8 weeks (range 0.1-108.9). From South Asia region (India and Pakistan), 8,738 Asian patients were enrolled. Mean PPG decreased from 240.0 and 261.1 mg/dl at baseline by 70.26 ± 65.10 and 82.96 ± 56.59 mg/dl at the last visit in total and South Asian populations, respectively (n = 53,883; n = 7,991, P < 0.0001 for both). Mean FPG decreased from 171.6 and 176.5 mg/dl at baseline by 38.48 ± 47.83 and 49.59 ± 41.41 mg/dl at the last visit in total and South Asian populations, respectively (n = 56,672; n = 7,837, P < 0.0001 for both). Mean HbA1c decreased from 8.4 and 8.4% at baseline by 1.11 ± 1.31% and 0.91 ± 0.93% at the last visit in total and South Asian populations, respectively (n = 38,843; n = 2,343, P < 0.0001 for both). Mean relative reduction of body weight (BW) was 1.40 ± 3.28% and 1.10 ± 3.39% at the last visit for mean baseline BW 73.6 and 74.2 kg in total and South Asian populations, respectively (n = 54,760; n = 7,718, P < 0.0001 for both). Consistent with RCT meta-analyses, post-hoc analysis of real-life data showed acarbose treatment improved glycaemic control and reduced the BW. Acarbose treatment in real life setting showed significant reductions in all glycemic parameters and BW in Asian patients from South Asia region.

Alpha-glucosidase inhibitor, acarbose, improves glycamic control and reduces body weight in type 2 diabetes: Findings on indian patients from the pooled data analysis.

Alpha-glucosidase inhibitors are widely used especially in Asian countries as a treatment option for type 2 diabetes patients with high postprandial glycemia (PPG). The higher carbohydrate in the Indian diets lead to greater prandial glycemic excursion, increased glucosidase, and incretin activity in the gut and may need special therapeutic strategies to tackle these glucose peaks. This is the subgroup analysis of Indian subjects who participated in the GlucoVIP study that investigated the effectiveness and tolerability of acarbose as add-on or monotherapy in a range of patients with type 2 diabetes mellitus. A total of 1996 Indian patients were included in the effectiveness analysis. After 12.5 weeks (mean), the mean change in 2-hour PPG from baseline was -74.4 mg/dl, mean HbA1c decreased by -1.0%, and mean fasting blood glucose decreased by -37.9 mg/dl. The efficacy of acarbose was rated "very good" or "good" in 91.1% of patients, and tolerability as "very good" or "good" in 88.0% of patients. The results of this observational study suggest that acarbose was effective and well tolerated in the Indian patients with T2DM.

Lack of association of programmed cell death 1 gene (PDCD1) polymorphisms with susceptibility to chronic urticaria in patients with positive autologous serum skin test.

BACKGROUND: Autoimmune mechanisms play an important role in the pathophysiology of chronic urticaria (CU), and the autologous serum skin test (ASST) helps to identify patients with autoreactive CU. One of the factors involved in autoreactive mechanisms is the cell surface receptor programmed death-1 which is encoded by the programmed cell death 1 gene (PDCD1). OBJECTIVE: To investigate whether PDCD1 polymorphisms influence susceptibility to CU. METHODS: We enrolled 93 ASST-positive patients with CU and a control group consisting of 105 healthy volunteers. In all individuals, PD1.3 (7146 A/G; rs 11568821) and PD1.5 (7785 C/T; rs 2227981) polymorphisms were analyzed. RESULTS: No statistically significant differences were found between CU patients and controls for allele or genotype distribution. We also did not observe any association between PDCD1 genotypes and severity of urticaria or age of disease onset. CONCLUSIONS: PD1.3 and PD1.5 polymorphisms were not proven to be implicated in susceptibility to ASST-positive CU in the Polish population. A more comprehensive analysis of the 2q33-2q37 genomic region might reveal whether variants of 1 or more of the genes in this region are involved in susceptibility to CU.

PTPN22 polymorphism presumably plays a role in the genetic background of chronic spontaneous autoreactive urticaria.

BACKGROUND: The association of chronic urticaria (CU) with autoimmune disorders is relatively well proved. Protein tyrosine phosphatase-22 (PTPN22) is considered to be one of the strongest genetic factors for human autoimmunity. We decided to evaluate whether additional, non 1858C>T, PTPN22 variants are independent contributors to the risk of CU occurrence in the Polish population. METHODS: A total of 91 CU patients with a positive result of autologous serum skin test and 100 healthy volunteers were enrolled in the study. The Urticaria Activity Score was used in disease intensity assessment. In all subjects rs3811021, rs1310182 and rs2488457 polymorphisms were genotyped. RESULTS: We found a higher prevalence of -1123 C allele among CU patients. No differences in the allele and genotype distribution were found in the other analyzed polymorphisms. Haplotype construction of the three SNPs revealed statistically significant CU association of rs2488457C, rs1310182T and rs3811021T. CONCLUSIONS: Contrary to previous findings, the contribution of PTPN22 to disease susceptibility is suggested. We can speculate that CU is a genetically complex disease and that its occurrence needs multiple genetic and environmental risk factors.

Systemic vascular hemodynamics and transplanted kidney survival.

INTRODUCTION: High blood pressure and arterial stiffness contribute independently to cardiovascular mortality in uremic patients. High blood pressure is an established risk factor for chronic allograft nephropathy, recently named interstitial fibrosis/tubular atrophy (IF/TA). We sought to assess whether heart afterload determinants: arterial stiffness and vascular resistance or impedance accelerate kidney graft failure upon long-term observation. METHODS: Using a noninvasive method of blood pressure waveform analysis, (HDI/PulseWave/CR-2000), we studied 160 consecutive kidney transplant recipients, who were at least 3 months after transplantation, for systolic (SBP), diastolic, and mean blood pressure; pulse rate; systemic vascular resistance and impedance as well as large and small artery compliance. The associations of the hemodynamic parameters with relative increases in serum creatinine for every year of graft survival (ΔCreat) were assessed using multiple linear regression analysis. Relationships between systemic hemodynamics and kidney graft loss due to IF/TA were evaluated by Cox regression analysis, including serum creatinine, time after transplantation, delayed graft function, human leukocyte antigen mismatch, panel-reactive antibodies, cold ischemia time, donor age glomerular filtration rate as well as prescribed cardiovascular and immunosuppressive drugs. RESULTS: Over 6.6±0.4 years of follow-up, excluding four noncompliant patients, 11 patients died and 32 lost their kidney grafts, including 25 due to IF/TA. ΔCreat (10.3%±22.0%/y) was independently and positively associated with the initial SBP (ß=0.26; P=.001) and serum creatinine values (ß=0.16; P=.04). The risk of graft loss due to IF/TA was greater among patients with an increased serum creatinine (relative risk [RR]=59.5 per nlog-unit increase; P<.001) or higher SBP (RR=51.1 per nlog-unit increase; P=.04). Besides SBP, no other hemodynamic parameter was associated with graft failure. CONCLUSIONS: The rate of kidney graft function deterioration and risk of transplant loss due to IF/TA are not independently influenced by systemic arterial compliance, resistance, or impedance. SBP appears to be the key circulatory parameter independently affecting the progression of IF/TA, and should be a therapeutic target.

An age-related decrease in factor V Leiden frequency among Polish subjects.

Factor V Leiden (G1691A FV mutation) is a widely acknowledged risk factor of deep vein thrombosis, including pulmonary embolism as the most serious complication. However, its high prevalence of ~5%in the Caucasian population might be related to an unknown evolutionary advantage. It might exert a beneficial effect on the carrier, e.g. protecting women from excessive bleeding during labour or allowing increased survival in severe sepsis or with other inflammatory diseases. The aim of our study was to verify or contradict the hypothesis of a favourable association between the A allele (A1691) and longevity in the Polish population. For this purpose, the G1691A mutation was analyzed by PCR-RFLP in 1016 Poles: 400 neonates (187 female and 312 male), 184 healthy adults (129 female and 55 male), and 432 long-lived individuals (age ≥95 years: 343 women and 89 men). Frequencies of G1691A carriers and the A1691 allele in long-lived individuals (0.2% and 0.1%, respectively) were significantly lower than in neonates (4.2% and 2.2%, respectively) and adults (3.3% and 1.6%). The frequency of the G1691A factor V Leiden mutation decreased with age, which indicates a shorter survival time among A1691 allele carriers in the Polish population.

Association between anthropometric obesity measures and coronary artery disease: a cross-sectional survey of 16,657 subjects from 444 Polish cities.

BACKGROUND: Excessive body weight is known to cluster with cardiovascular (CV) risk factors, but it is not clear which anthropometric obesity measure provides best independent predictive value of coronary artery disease (CAD). METHODS AND RESULTS: We explored associations between CAD and four different obesity measures (body mass index (BMI), waist circumference, waist/height and waist/height(2)) in a cohort of 16 657 subjects (40.4% men; 20.8% CAD patients), recruited by 700 primary care physicians in 444 Polish cities. 42.8% of subjects were classified as overweight, 31.7% as obese and 39.8% had abdominal obesity. In univariate analyses all obesity measures correlated with CAD (p>0.001), but waist/height(2) was the strongest discriminator between CAD patients and controls. Age-adjusted and sex-adjusted analyses confirmed a graded increase in CAD risk across distributions of all four obesity measures-1 standard deviation (SD) increase in BMI, waist, waist/height and waist/height(2) increased the odds of CAD by 1.23, 1.24, 1.26 and 1.27, respectively (all p<0.001). In models fully adjusted for CV risk factors, waist/height(2) remained the strongest obesity correlate of CAD, being the only independent associate of CAD in men. In a fully adjusted BMI-waist circumference stratified model, sarcopenic obesity (waist > median, BMI < median) and simple obesity (waist and BMI > median) were the strongest independent associates of CAD in men (p = 0.008) and women (p>0.001), respectively. CONCLUSION: This cross-sectional study showed that waist/height(2) may potentially offer a slightly higher predictive value of CAD than BMI or waist circumference and revealed an apparent sexual dimorphism in correlations between obesity measures and CAD.

Quality of life among diabetic and non-diabetic patients on maintenance haemodialysis.

AIMS: To compare the quality of life of end stage renal disease (ESRD) diabetic and non-diabetic patients undergoing chronic haemodialysis. METHODS: A case-control study of 54 diabetic and 60 non-diabetic patients undergoing maintenance haemodialysis. All subjects completed the Kidney Disease Quality of Life Short Form (KDQOL-SF) version 1.3 questionnaire as well as the SF-36 Health Survey (SF-36). RESULTS: When compared to the control non-diabetic group, physical health was significantly impaired in diabetic dialysis patients (P<0.005) and staff encouragement was significantly worse (P<0.05). In both groups, all other compounds of the SF-46 and variables related to kidney disease were similar. CONCLUSIONS: To improve diabetic haemodialysis patients' quality of life, physical activity should be incorporated to the routine dialysis care and health care professionals should support them more intensively.