Acute phase proteins and vitamin D seasonal variation in end-stage renal disease patients

: End-stage renal disease (ESRD) patients are vulnerable to vitamin D deficiency due to impaired renal hydroxylation, low dietary intake and inadequate sun exposure. Vitamin D plays a role in innate and adaptive immunity and its seasonal variation has been linked to mortality. ESRD is associated with inadequate removal of pro-inflammatory cytokines regulating acute phase protein (APP) synthesis. Our aim was to look for associations between lifestyle factors, diet, and vitamin D seasonal variation and their relationship with selected APPs and calcium-phosphate metabolism. The study included 59 ESRD patients treated with maintenance hemodialysis. A 24-hour dietary recall was conducted in the post-summer (November 2018, PS) and post-winter (February/March 2019, PW) period, and blood was collected for the measurements of serum total vitamin D, α1-acid glycoprotein (AGP), C-reactive protein (CRP), albumin, prealbumin (PRE), parathormone, calcium and phosphate. A self-constructed questionnaire gathered information on vitamin D supplementation, sun exposure and physical activity. Higher caloric intake was observed PW compared PS. Less than 15% of participants met the dietary recommendations for energy, protein, fiber, vitamin D and magnesium intake. Vitamin D supplementation was associated with higher serum vitamin D regardless of season. AGP, PRE, albumin, and vitamin D presented seasonal changes (higher values PS). In patients with serum vitamin D below 25 ng/mL, vitamin D seasonal change correlated with CRP and prealbumin change. Phosphate and Ca × P correlated positively with AGP. A low vitamin D serum level could impact the inflammatory process; however, more studies are needed to confirm the relationship

Urinary Neutrophil Gelatinase-Associated Lipocalin Is Complementary to Albuminuria in Diagnosis of Early-Stage Diabetic Kidney Disease in Type 2 Diabetes

Background. Two clinical phenotypes of diabetic kidney disease (DKD) have been reported, that is, with or without increased albuminuria. The aim of study was to assess the usefulness of urinary neutrophil gelatinase-associated lipocalin (uNGAL) for the early diagnosis of DKD in the type 2 diabetes mellitus (T2DM). Methods. The study group consisted of 123 patients with T2DM (mean age 62 ± 14 years), with urine albumin/creatinine ratio (uACR) 39.64 µg/g, 13 (54%) did not have markedly increased albuminuria. Women with T2DM had higher uNCR than men (p<0.001), without difference in uACR (p=0.09). uNCR in T2DM patients correlated significantly with HbA1c. Sex, total cholesterol, and uACR were independent predictors of uNCR above 39.64 µg/g. Conclusions. Increased uNGAL and uNCR may indicate early tubular damage, associated with dyslipidemia and worse diabetes control, especially in females with T2DM

Pentraxin 3 as a new indicator of cardiovascular-related death in patients with advanced chronic kidney disease

Pentraxin 3 (PTX3) is involved in inflammatory response by recognizing pathogens and damaged tissues. The aim of this study was to assess the relationship between PTX3 levels and all‑cause and cardiovascular (CV) mortality in patients with chronic kidney disease (CKD) during 5‑year follow‑up. The study included 78 patients (51 on hemodialysis and 27 on predialysis). We measured the levels of PTX3, calcium, phosphate, intact parathyroid hormone, high-sensitivity Creactive protein (hs-CRP), interleukin 6 (IL‑6), fibroblast growth factor 23 (FGF‑23), osteopontin (OPN), osteocalcin (OC), osteoprotegerin (OPG), fetuin A, tumor necrosis factor receptor 2 (TNFR2), transforming growth factor $\beta1$ ($TGF‑\beta 1$), hepatocyte growth factor (HGF), stromal cell‑derived factor $1\alpha$ ($SDF‑1\alpha$), and thrombomodulin (TM). In a subgroup of 45 patients, fragments of the radial artery obtained during creation of hemodialysis access were stained for calcifications. In 51 patients, ultrasonography was performed to assess common carotid artery intima–media thickness (CCA‑IMT). The median serum concentrations of PTX3 were 1.43 ng/ml (interquartile range, 0.74–2.50). Higher concentrations of fibrinogen, hs‑CRP, IL‑6, TNFR2, $TGF‑\beta$ 1, HGF, OPN, OPG, FGF‑23, TM, and $SDF‑1\alpha$ and lower albumin and uric acid levels were observed in patients with PTX3 above the median. During follow‑up, 27 patients (35%) died, including 25 due to CV causes. In contrast to hs-CRP levels, baseline PTX3 levels predicted CV mortality independently of classic CV risk factors. PTX3 levels also significantly predicted mortality after adjustment for age, baseline dialysis status, serum OPG and CRP levels, radial artery calcifications, and CCA‑IMT. We postulate that PTX3 might be an early marker of CV mortality in patients with advanced CKD, yet before the increase in the levels of a specific marker for systemic inflammation such as hs‑CRP

The marker of tubular Injury, kidneyiInjury molecule-1 (KIM-1), in acute kidney injury complicating acute pancreatitis : a preliminary sttudy

Acute pancreatitis (AP) may be associated with severe inflammation and hypovolemia leading to organ complications including acute kidney injury (AKI). According to current guidelines, AKI diagnosis is based on dynamic increase in serum creatinine, however, creatinine increase may be influenced by nonrenal factor and appears late following kidney injury. Kidney injury molecule-1 (KIM-1) is a promising marker of renal tubular injury and it has not been studied in AP. Our aim was to assess if urinary KIM-1 may be used to diagnose AKI complicating the early stage of AP. We recruited 69 patients with mild to severe AP admitted to a secondary care hospital during the first 24 h from initial symptoms of AP. KIM-1 was measured in urine samples collected on the day of admission and two subsequent days of hospital stay. AKI was diagnosed based on creatinine increase according to Kidney Disease: Improving Global Outcomes 2012 guidelines. Urinary KIM-1 on study days 1 to 3 was not significantly higher in 10 patients who developed AKI as compared to those without AKI and did not correlate with serum creatinine or urea. On days 2 and 3, urinary KIM-1 correlated positively with urinary liver-type fatty acid-binding protein, another marker of tubular injury. On days 2 and 3, urinary KIM-1 was higher among patients with systemic inflammatory response syndrome, and several correlations between KIM-1 and inflammatory markers (procalcitonin, urokinase-type plasminogen activator receptor, C-reactive protein) were observed on days 1 to 3. With a limited number of patients, our study cannot exclude the diagnostic utility of KIM-1 in AP, however, our results do not support it. We hypothesize that the increase of KIM-1 in AKI complicating AP lasts a short time, and it may only be observed with more frequent monitoring of the marker. Moreover, urinary KIM-1 concentrations in AP are associated with inflammation severity