The relationship between serum trimethylamine n-oxide (TMAO), asprosine and neutrophil gelatinase-associated lipocalin (NGAL) levels and hypertensive nephropathy in patients with hypertension

ABSTRACT THE RELATIONSHIP BETWEEN SERUM TRIMETHYLAMINE N-OXIDE (TMAO), ASPROSINE AND NEUTROPHIL GELATINASE-ASSOCIATED LIPOCALIN (NGAL) LEVELS AND HYPERTENSIVE NEPHROPATHY IN PATIENTS WITH HYPERTENSION Hypertension is defined as a systolic blood pressure of 140 mmHg or more and/or a diastolic blood pressure of 90 mmHg or more. It is the leading modifiable risk factor for morbidity and mortality worldwide. Hypertension is the most common cardiovascular disorder in the world, affecting 1.28 billion adults aged 30-79 years worldwide according to the World Health Organisation. Hypertension is the second most common underlying cause of end-stage renal disease (ESRD), with 30% of all patients on renal replacement therapy developing end-stage renal failure due to hypertensive nephropathy. The study group consisted of individuals aged 30-75 years. Patients were divided into 2 groups as hypertensive patients with and without hypertensive nephropathy. The study group consisted of 64 patients, 31 with HT and hypertensive nephropathy and 33 without hypertensive nephropathy. The control group consisted of 22 healthy individuals of similar age and sex who were non-hypertensive and had no comorbidities and lipid metabolism disorders. Patient group: Patients who were admitted to the outpatient clinic and outpatient clinic of the Department of General Internal Medicine, Firat University, Faculty of Medicine, were recruited based on the data obtained from retrospective file review. TMAO is a metabolite and biologically active molecule derived from trimethylamine (TMA). Dietary sources of TMA are foods rich in choline, L-carnitine and phosphatidylcholine such as red meat, saltwater fish, eggs, dairy products and some fruits, vegetables and cereals. Asprosin is a protein hormone whose release is stimulated by starvation and induces hepatic glucose production. It is mainly secreted from white adipose tissue. NGAL is a lipocalin family protein released mainly from activated neutrophils. Since it is released from the distal tubule in case of damage, NGAL can be shown as a marker of renal tubular damage. In our study, we aimed to determine the relationship between these molecules and hypertension and hypertensive nephropathy by comparing TMAO, asprosin and NGAL levels between patient groups. In our study, a statistically significant difference was found between the median values of asprosin (p=0.002), TMAO (p=0.001) and NGAL (p=0.020). A statistically significant difference was found between the median plasma TMAO values of the participants (p=0.001). The TMAO median value of the control group was significantly higher than both hypertensive patients with nephropathy (p2-p3=0.006) and hypertensive patients without nephropathy (p1-p3<0.001). There was a statistically significant difference between the plasma asprosine median values of the participants (p=0.002). The asprosin median value of hypertensive patients without nephropathy was significantly higher than both the control group (p1-p3=0.001) and hypertensive patients with nephropathy (p1-p2=0.010). There was a statistically significant difference between the plasma NGAL median values of the participants (p=0.020). The NGAL median value of the control group was statistically significantly higher than hypertensive patients without nephropathy (p1-p3=0.006). There was no statistically significant difference between the NGAL median values of the control group and hypertensive patients with nephropathy (p2-p3=0.194). Similarly, no statistically significant difference was found between the NGAL median values of hypertensive patients with and without nephropathy. There was a significant negative correlation between TMAO and NGAL values in hypertensive patients with nephropathy (r:-0.368; p=0.042). In conclusion, contrary to some studies in the literature, TMAO was found to be higher in the control group in our study and we can say that it may be protective against hypertension. NGAL is a molecule evaluated as an early marker of acute kidney injury and contrary to what is known in our study, it was found to be lower in patients with and without nephropathy compared to the control group. Since the limited number of patients and the single-centre study affected the diversity of results, more extensive studies are needed for the relationship between NGAL and hypertensive nephropathy. Asprosin, which is effective on glucose homestasis, was found to be high in hypertensive patients without nephropathy. Since asprosin may also be involved in the pathophysiology of hypertension, more comprehensive studies are needed. Finally, hypertension is a common cause of morbidity and mortality worldwide, hypertensive nephropathy is the second most common cause of end-stage renal failure, and we can say that more comprehensive studies on these diseases are needed. Keywords: Hypertension, Hypertensive nephropathy, TMAO, Asprosin, NGAL