Evaluation of renal functions and investigation of subclinical renal damage in patients with psoriasis vulgaris

Psoriasis is a hyperproliferative papulosquamous disease affecting approximately 2% of the population. It is known that psoriasis is a T cell-mediated inflammatory disease that occurs due to dysregulation in the innate and adaptive immune system. In recent years, it has been reported that psoriasis is not only a skin disease but also it is a systemic inflammatory disease. Studies have shown that patients with psoriasis are predisposed to many comorbid diseases such as metabolic syndrome and its components, especially cardiovascular diseases, and the inflammatory process is effective on the basis of these comorbidities. In the literature, there are conflicting results about the renal involvement of psoriasis vulgaris. Existing studies are generally aimed at demonstrating chronic renal damage. The number of studies examining subclinical renal damage is limited. In this study, we aimed to examine the presence of clinical and subclinical renal damage in patients with psoriasis vulgaris, with renal function parameters and spesific early renal damage biomarkers. In our study, 44 patients with psoriasis vulgaris and 44 healthy controls were included. There was no statistically significant difference between the patient and control groups in terms of age and gender distribution. Serum urea, creatinine, glomerular filtration rate (GFR), complete urinalysis, urine microscopy, albuminuria and proteinuria levels in spot urine, urinary kidney injury molecule-1 (KIM-1), urinary neutrophil gelatinase-associated lipocalin (NGAL) and urinary podocalyxin (PCX) levels were compared between the two groups to evaluate renal functions. Serum urea, creatinine and GFR levels were within normal limits in the patient and control groups. There was no significant differance between the two groups in terms of serum urea (p=0.246), serum creatinine (p=0.067) levels, GFR (p=0.069), complete urinalysis, urine microscopy and albuminuria levels (p=0.149). When proteinuria levels were compared, a statistically significant difference was found between the two groups, but higher in the patient group (p=0.021). There was no statistically significant difference between the two groups in terms of urinary KIM-1 (p=0.786), NGAL (p=0.170), podocalyxin (p=0.356) levels. Statistically significant difference between both groups in terms of urinary KIM-1/creatinine (p=0.246), urinary NGAL/creatinine (p=0.301) and urinary PCX/creatinine levels (p=0.611) was not detected. No correlation was found between serum urea, creatinine, GFR, albuminuria, proteinuria, urinary KIM-1, NGAL, PCX levels, urinary KIM-1/creatinine, urinary NGAL/creatinine, urinary PCX/creatinine ratio and disease duration and disease severity in the patient group. In conclusion, the results of our study suggest that psoriasis vulgaris does not cause clinical renal damage. In our study, proteinuria levels which is a subclinical renal damage marker were found to be higher in the patient group with psoriasis. Therefore, we think that monitoring proteinuria with a detailed anamnesis and physical examination at regular intervals in patients with psoriasis and repeated measurements of urinary KIM-1/creatinine, NGAL/creatinine levels and albuminuria levels that correlate with proteinuria levels may allow early detection of renal damage that may occur. In order to evaluate the presence of renal involvement in patients with psoriasis, large-scale studies with larger patient groups and long-term observation are needed. Keywords: Psoriasis vulgaris, Renal damage, KIM-1, NGAL, PCX