Hematological Parameters and Clinical Features in Patients with Advanced Chronic Kidney Disease.

BACKGROUND: Hematological parameters like red cell distribution width (RDW) and mean platelet volume (MPV) were reported to be associated with inflammation, atherosclerosis, and chronic kidney disease (CKD) progression. In this study, we evaluated RDW and MPV along with clinical features in patients with advanced CKD. We also aimed to detect clues for causative relations concerning these parameters, renal function and comorbidities. METHODS: Stage 3-5 CKD patients (627 total) were included (mean age 63.1 years, 48.3% male). Patients with malignancies, cirrhosis, infections, severe anemia, and systemic inflammation were excluded. Patients were evaluated for clinical features and grouped for comparison using median RDW and MPV. Linear regression models were generated to predict potential influences on RDW and MPV. RESULTS: Mean estimated glomerular filtration rate (eGFR) was 27.3 mL/min/1.73m2. Mean Charlson Comorbidity Index (CCI) score was 5.83 ± 2.06. Patients with high RDW (n = 303) were older with higher CRP and CCI, they also had lower eGFR, hemoglobin, and albumin (P < 0.001 for all). Patients with low MPV (n = 311) had lower eGFR, and platelet counts (P = 0.015 and 0.017). eGFR was negatively correlated with RDW after adjusting for age, gender and comorbidities. In a further adjusted model RDW was associated with CRP, CCI, hemoglobin and albumin (P < 0.05 for all), not with eGFR. MPV was positively correlated with eGFR in our adjusted, and fully adjusted regression models (P = 0.003). CONCLUSION: In this study, we found that high RDW is associated with comorbidity burden, anemia, and inflammatory status in patients with advanced CKD. Meanwhile, low MPV seems to be associated with worse renal function.

Renal Tubular Acidosis in Patients with Systemic Lupus Erythematosus.

OBJECTIVE: Renal tubular acidosis (RTA) is a clinical manifestation that occurs with insufficiency in restoring bicarbonate or disruption in hydrogen ion elimination as a result of a disruption in tubulus functions, causing normal anion gap-opening metabolic acidosis. In the present study, we aimed to investigate the prevalence of RTA in the largest systemic lupus erythematosus (SLE) patient population to date. MATERIALS AND METHODS: SLE patients, who were followed up in 2 different healthcare centers, were included. Patients with metabolic acidosis (pH <7.35 and HCO3 <22 mEq/L) in venous blood gas analysis were determined. The serum and urine anion GAP of these patients were estimated, and the urine pH was assessed. RTA presence was evaluated as metabolic acidosis with a normal serum anion gap and a positive urine anion GAP. RESULTS: A total of 108 patients were included in the present study. The mean age of the patients was 41.5 ± 1.2 and 87% were female. The SLE diagnosis duration was 75 ± 5 months. The mean creatinine value ​​was 0.6 ± 0.1 mg/dL and the mean eGFR was 111 ± 2 mL/min. According to the blood gas analysis, 18 patients (16.7% of the total) had RTA. Sixteen of these patients had type 1 RTA and 2 had type 2 RTA; type 4 RTA was not determined in any of the patients. CONCLUSION: RTA should be considered in SLE patients even if they have normal eGFR values. This is the largest study to examine the prevalence of RTA in SLE patients in the literature.

Can vasohibin-1, an endothelium-derived angiogenesis inhibitor, be a marker of endothelial dysfunction in hemodialysis patients?

BACKGROUND: Endothelial dysfunction (ED) is associated with high cardiovascular disease burden in hemodialysis (HD) patients. Vasohibin-1, an endothelium-derived angiogenesis inhibitor, is essential for endothelial cell survival, therefore it may be a promising marker of ED. We aimed to investigate whether vasohibin-1 levels are associated with ED markers in HD patients. METHODS: Fifty HD patients and 30 healthy controls were included in the study. As markers of ED, endothelium-dependent flow-mediated dilatation (FMD), carotid intima-media thickness (CIMT), and pulse wave velocity (PWV) were examined. Serum vasohibin-1 levels were measured with ELISA. RESULTS: Serum vasohibin-1 levels were low (387.7 ± 115.7 vs 450.1 ± 140.1 P = .02), FMDs' were impaired (6.65 ± 2.50 vs 10.95 ± 2.86 P < .001), PWV (7.92 ± 1.964 vs 6.79 ± 0.96 P = .01) and CIMT (0.95 ± 0.20 vs 0.60 ± 0.11 P < .001) were increased in HD patients compared to healthy controls. In regression analysis, vasohibin-1 levels were not related with FMD, PWV, or CIMT. CONCLUSIONS: Hemodialysis patients have low serum vasohibin-1 levels but serum levels of vasohibin-1 did not show any significant relationship with FMD, PWV, and CIMT in HD patients. Since vasohibin-1 acts via paracrine pathways, serum levels may be insufficient to explain the relationship between vasohibin and ED. Local vasohibin-1 activity on tissue level may be more important instead of circulating levels.

Relationship Between Osteoporosis and Serum Sclerostin Levels in Kidney Transplant Recipients.

OBJECTIVES: Sclerostin, a peptide secreted primarily by osteocytes, suppresses osteoblast maturation, thus reducing bone formation. Here, we evaluated the relationship between sclerostin levels and osteoporosis in kidney transplant recipients. MATERIALS AND METHODS: This cross-sectional study included 78 kidney transplantrecipients > 18 years old and at least 6 months posttransplant. In our center, unrelated living-donor kidney transplants are not performed. Patients with parathyroid adenoma or parathyroidectomy history were excluded. Lumbar and femoral neck bone mineral densities andT and Z scores were obtained by dual-energy X-ray absorptiometry; results were used to divide patients into osteoporotic and nonosteoporotic groups. Serum sclerostin was measured by enzyme-linked immunosorbent assay. RESULTS: : Of total patients, 43% had osteoporosis, mean age was 40.8 years, and 70% were male. Groups had similar ages, male-female distribution, time posttransplant, cumulative corticosteroid dose, estimated glomerular filtration rates, and 25-hydroxyvitamin D2 levels (P > .05). The osteoporotic group had lower sclerostin (405.9 ± 234.9 vs 521.7 ± 233.5 ng/dL; P = .035) and higherintact parathyroid hormone levels (110.9 ± 68.0 vs 84.8 ± 41.4 pg/mL; P = .04) than the nonosteoporotic group. Sclerostin levels were not correlated with cumulative corticosteroid dose, intact parathyroid hormone, bone mineral density, and T scores at any site but were weakly negatively correlated with age (P = .04, r = -0.25). In multiple regression analyses, only intact parathyroid hormone had negative effects on lumbar bone mineral density (P = .02) andT scores (P = .036). Serum sclerostin levels, age, and cumulative corticosteroid dose did not affect lumbar or hip bone mineral density and T scores (P > .05). CONCLUSIONS: Sclerostin levels were low in our osteoporotic patients;therefore, sclerostin may not be a contributing factor to osteoporosis development. Because sclerostin is an osteocyte-derived peptide, its serum levels only reflect total osteocyte number and bone mass.

Does neutrophyl to lymphocyte ratio really predict chronic kidney disease progression?

PURPOSE: Chronic kidney disease (CKD) is an inflammatory process. In addition to increased morbidity and mortality, inflammation also contributes to the progression of CKD. Neutrophil/lymphocyte ratio (NLR) is a marker of inflammation. Some recent data suggest that NLR may predict the progression of CKD. METHODS: In this study, 5-year data of 740 patients with stage 2-4 CKD were reviewed retrospectively. Demographic data, NLR, CRP, albumin, the amount of proteinuria were recorded. At the beginning and the end of follow-up the glomerular filtration rate (GFR) and the annual GFR decline rate were calculated. Patients were divided to high and low NLR group according to median value of their baseline NLR. Reaching stage 5 CKD or initiation of renal replacement therapy was determined as end-point for follow-up. RESULTS: The mean age was 62.8 ± 0.57 years, eGFR 40 ml/min/1.73 m2, median NLR was 2.76. NLR increased as the CKD-stage increased. Mean follow-up time was 51.2 ± 30 months and 21.4% of patients reached the end-point. NLR was significantly increased at follow-up (from 3.22 to 5.68, p < 0.001). Annual GFR loss and baseline CRP were higher but baseline albumin and GFR were lower of patients with high NLR. The percent of patients reaching the end-point was not different between the groups with high and low baseline NLR. Kaplan Meier analysis showed that patients with high NLR had significantly lower mean renal survival (86.5 months) than patients with low NLR (105 months) (p < 0.001). In the Cox-regression analysis NLR was not an independent predictor in reaching the end-point but presence of diabetes mellitus, younger age and low baseline eGFR were found effective. CONCLUSIONS: NLR is an indicator of inflammation in chronic kidney disease. It may not be an independent predictor of CKD progression except that the CKD is in a more advanced stage and reflects the associated inflammation. Classical risk factors such as DM and lower GFR are more powerful predictors of progression.