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  • br Methods br Results Table

    2018-11-03


    Methods
    Results Table 1 presents the characteristics of the study population. The mean ages (±standard deviation) for the 3502 psoriatic patients and 10,506 matched THZ1 Hydrochloride comparisons were 45.9 ± 16.1 years and 45.7 ± 16.2 years, respectively. No statistically significant difference in age was found between psoriatic patients and the comparison group. All patients with psoriasis showed higher frequencies of comorbidities of hypertension, diabetes mellitus, hyperlipidemia, and circulatory disease (p < 0.05). Approximately 2.7% of the patients received prescriptions for cyclosporin (vs. 0.1% in controls, p < 0.0001), and the median drug usage quantity was 252.0 capsules [interquartile ranges (IQR), 56.0–735] in psoriatic patients and the median drug usage quantity was 15.0 capsules (IQR, 14.0–21.0) in controls (p = 0.0316). A total of 202 incident renal disease cases were identified. In univariate analyses, we found a significant association between psoriasis cases and renal disease incidence (RR = 1.27; 95% CI, 1.08–1.49; p = 0.0031; Table 2). In multivariate analyses, we found no significant association between psoriasis cases and renal disease incidence, regardless of their comorbidity status. Next, we examined the association between concomitant drug use and risk of chronic renal failure. Although risk of chronic renal failure was not significantly higher in psoriatic patients with concomitant drug use with cyclosporin, methotrexate, or NSAIDs, the risk became higher as NSAIDs exposure day increased (Table 3). Stratified by cyclosporin use, controls with cyclosporin use were at increased risk of renal disease independently (adjusted RR = 6.34; 95% CI, 3.57–11.26; p < 0.0001; Table 4). By contrast, psoriatic patients with cyclosporin use did not have increased risk of renal disease, regardless of their comorbidity status. During the follow-up period, 104 of 3502 psoriasis cases, excluding patients with other renal disease, and 200 of 10,506 matched controls experienced chronic renal failure events (Table 5). The median follow-up duration was 5.0 years (IQR, 2.5–7.4 years) in psoriasis cases and 9.3 years in the comparison group (IQR, 5.9–12.8 years; p < 0.0001; Table 1). The incidence of chronic renal failure events was significantly greater in psoriatic patients than in population comparisons (4.34/1000 person-years vs. 1.31/1000 person-years; IRR = 3.27; 95% CI, 2.58–4.15; p < 0.0001). Our results showed that psoriasis increased the risk of chronic renal failure (adjusted HR = 3.00; 95% CI, 2.30–3.93; p < 0.0001). The results were similar in men and women. After excluding patients with comorbidity, the incidence rate of psoriasis cases (2.48/1000 person-years) in chronic renal failure was still significantly higher than in controls (0.30/1000 person-years; IRR = 3.66; 95% CI, 1.96–6.82; p < 0.0001), suggesting that patients with psoriasis were at increased risk of incident chronic renal failure independently compared with the matched population comparisons. The incidence of ESRD events were also significantly greater in psoriasis cases than in controls (0.64/1000 person-years vs. 0.25/1000 person-years; IRR = 2.53; 95% CI, 1.39–4.60; p = 0.0024; Table 6). Finally, the Kaplan–Meier curves of disease-free probability for the matched psoriasis and nonpsoriatic groups are illustrated in Figure 2. The psoriasis group had a higher incidence of chronic renal failure than matched nonpsoriatic controls (log-rank test p < 0.0001).
    Discussion This retrospective cohort study revealed that psoriasis is an independent risk factor of chronic renal failure and ESRD, after adjusting for potential confounders, including comorbidities such as hypertension and diabetes mellitus. It is intriguing, however, that psoriasis may not increase the risk of overall renal disease. These results imply that systemic inflammation involved in psoriasis may exacerbate preexisting renal disease but not initiate renal disease. These results are in accordance with the finding that IL-17-producing Th17 cells induce renal inflammation by mediating preexisting cells, including tubular epithelial cells, mesangial cells, neutrophils, and macrophages. It has been known that certain inflammatory mediators correlate with disease activity of psoriasis. For example, chemerin, a chemokine that routes macrophages and dendritic cells toward inflammatory sites, correlates with Psoriasis Area and Severity Index as well as C-reactive protein level in patients with psoriasis. It is worthwhile to investigate whether these mediators have roles in chronic inflammation of renal disease.