Relationship of Serum Kallistatin Level With Arterial Stiffness and Metabolic Parameters in Obesity-Related Chronic Kidney Disease.

Abstract

We investigated the relationship between serum kallistatin and kidney disease and proteinuria in nondiabetic obesity-related chronic kidney disease and observed the effects on arterial stiffness. We included 40 patients with nondiabetic obesity-related chronic kidney disease followed in our nephrology clinic and a control group of 40 participants without chronic kidney disease matched by age, sex, and mean body mass index (measured as weight in kilograms divided by height in meters squared). Pulse-wave velocity and augmentation index were measured oscillometrically by pulse-wave analysis (Mobil-O-Graph) by the same operator. Serum kallistatin levels were measured by sandwich enzyme-linked immunosorbent assay. Mean age of patients was 51 ± 7.5 years (range, 29-62 years), and 40% were female. Mean body mass index was 35 ± 3.1. Four patients (10%) had morbid obesity; 21 (52.5%) had hypertension. Glomerular filtration rate (42 ± 18 vs 83 ± 15 mL/min/1.73 m², respectively; P < .001) were significantly lower. However proteinuria (671 ± 1031 vs 80 ± 30 mg/d, respectively; P < .001) were significantly higher in patients than in controls. Also, serum kallistatin and arterial stiffness were significantly higher in patients (P < .05).''The Pulse Wave Velocity was higher in patients with hypertension (P = .01); GFR was lower (P < .01); serum uric acid level was higher (P < .001); and neutrophil-to-lymphocyte ratio (P < .05), C-reactive protein level (P < .05), and serum kallistatin level were higher (P < .05). Serum kallistatin levels increase in patients with obesity-related kidney disease. Especially hypertension and hyperuricemia are associated with an increase in serum kallistatin.