Experimentally induced puromycine aminonucleoside nephrosis (PAN) in rats: evaluation of angiogenic protein platelet-derived endothelial cell growth factor (PD-ECGF) expression in glomeruli

<p>Abstract</p> <p>Background</p> <p>In experimentally induced puromycine aminonucleoside nephrosis (PAN) animal models, nephrotic syndrome with minimal change disease and focal and segmental sclerosis-like nephritis similar to that in human is demonstrated; however, the real mechanism of PAN is not yet elucidated. Platelet derived endothelial cell growth factor (PD-ECGF), an endothelial mitogen protein, is believed to take part in microvessel formation and in stimulation of angiogenesis and its expression has not been totally demonstrated in PAN rats yet. In this study, we aimed to examine PD-ECGF expression in acute and chronic PAN induced in rats and find out the association between its expression and the stages of angiogenesis in kidney.</p> <p>Methods</p> <p>For the experiment, twenty-four Male Wistar Albino rats were used and divided into four groups; control group (n = 6), pre-proteinuria group (n = 6), acute group (n = 6) and chronic group (n = 6). We compared statistically all data by One-way ANOVA Test followed by Dunn Multiple Comparison Test.</p> <p>Results</p> <p>Proteinurea levels in control and pre-proteinuria groups were not statistically different; however, it was remarkably higher in the acute nephrosis group and significantly greater in the chronic nephrosis group than control group (<it>p </it>< 0.0025). In pre-proteinuria group, the serum albumin and creatinine clearances also did not significantly differ from the control group. On the other hand, in the acute and chronic nephrosis groups, serum albumin and creatinine clearances progressively decreased (<it>p </it>< 0.05). In our immunohistochemical studies, we showed elevated PD-ECGF expression in glomeruli of acute and chronic PAN rats. Microscopic and ultrastructural appearances of the glomeruli of acute and chronic PAN showed various sequential steps of angiogenesis, macrophages and immature capillaries with primitive lumens and apoptotic endothelial cells in the increased mesangial matrix.</p> <p>Conclusions</p> <p>It is reported that acute and chronic PAN progressively increase PD-ECGF expression and following induction of angiogenesis in the affected glomeruli.</p

PROCALCITONIN AND MALONDIALDEHYDE AS MARKERS OF INFLAMMATION IN HEMODIALYSIS PATIENTS

Aim: Procalcitonin (PCT) is known as an infection marker. Malondialdehyde (MDA) is considered as a marker of oxidative stress. Both have been found to be elevated in peritoneal dialysis patients. In this study, we measured procalcitonin, malondialdehyde, and traditional inflammation markers, including albumin, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), fibrinogen, lymphocyte counts, and white blood cell counts (WBC) in hemodialysis (HD) patients, patients with moderate chronic kidney disease (CKD), and healthy subjects. Material and Method: We measured PCT, MDA, albumin, CRP, ESR, fibrinogen, lymphocyte counts, and WBC in 35 maintenance HD patients, 30 patients with moderate chronic kidney disease and a control group with normal kidney functions. The correlation of PCT and MDA with traditional inflammation markers (albumin, CRP, ESR, fibrinogen, lymphocyte counts, and WBC) was also evaluated. Results: PCT levels were significantly higher and were correlated with CRP levels in the HD group (r=0.89). MDA was significantly higher in HD patients and non-dialysis CKD patients as compared to healthy controls. Discussion: Higher PCT levels in HD patients might be caused by minimal endotoxin contamination. Elevated CRP levels, known as a marker of inflammation, were correlated with elevated PCT levels. PCT may also be a marker of inflammation

Renal Osteodystrophy

Chronic renal insufficiency is a functional definition which is characterized by irreversible and progressive decreasing in renal functions. This impairment is in collaboration with glomeruler filtration rate and serum creatinine levels. Besides this, different grades of bone metabolism disorders develop in chronic renal insufficiency. Pathologic changes in bone tissue due to loss of renal paranchyme is interrelated with calcium, phosphorus vitamine-D and parathyroid hormone. Clinically we can see high turnover bone disease, low turnover bone disease, osteomalacia, osteosclerosis and osteoporosis in renal osteodystropy. In this article we aimed to review pathology of bone metabolism disorders due to chronic renal insufficiency, clinic aspects and treatment approaches briefly

PERSISTENCE OF ANTIBODIES AFTER SARS-COV-2 VACCINES IN HAEMODIALYSIS PATIENTS: A 6 MONTHS FOLLOW-UP

BACKGROUND AND AIMS: As COVID-19 related mortality is higher in haemodialysis patients than in the general population, proper vaccination strategies against the SARS-CoV-2 virus have utmost importance. It has been previously shown that mRNA vaccines (e.g. BNT162b2) can generate >95% of seropositivity in haemodialysis patients [1]. On the other hand, the seropositivity rate reached by the inactivated vaccine (CoronaVac®) was around 80%. In this study, we aimed to analyse the persistence of SARS-CoV-2 antibodies in haemodialysis patients for 6 months and compare it with the healthy controls. METHOD: Haemodialysis patients who were vaccinated either by BNT162b2 or CoronaVac® and who continued their regular controls for 6 months were involved in the study. Those who had previous or active SARS-CoV-2 infection, who had malignancies and those who had received immunosuppressive drugs in the previous 12 month were excluded from the study. SARS-CoV-2 IgG levels were measured by a commercial test after the first doses of the vaccines and at the end of the sixth month. Healthy healthcare workers who were vaccinated with similar vaccine schemes were taken as the control group. RESULTS: We recruited 85 haemodialysis patients who had received their first doses of either vaccine. Of them, 4 patients died; 3 patients were hospitalized because of COVID-19 infection during the follow-up; 9 patients missed at least one of their regular controls; and 2 patients were diagnosed with malignancy. A total of 26 patients experienced asymptomatic or mild COVID-19 infection during the follow-up period. SARS-CoV-2 IgG levels were measured at the end of the sixth month for the remaining 41 patients. Sero-positivity significantly decreased at the end of the sixth month for both vaccines, but the BNT162b2 group (n = 22) still had better seropositivity than CoronaVac® (n = 19) group (81% versus 50%; P = .03). In contrast, the seropositivity of healthy controls, even with the inactivated vaccine, was 96%. When one booster dose was applied, 90% of seropositivity could be maintained in the BNT162b2 group at the sixth month. CONCLUSION: BNT162b2 vaccine generates more persistent antibodies than inactivated vaccines in haemodialysis patients. However, when compared with the healthy controls at the end of the sixth month, antibody titers decrease more profoundly in haemodialysis patients. The booster dose can maintain the antibody levels and should be applied at least every 6 months

Assessment of DNA Oxidation and Antioxidant Activity in Hypertensive Patients with Chronic Kidney Disease

The aim of this study was to evaluate the oxidative DNA damage, antioxidant activity, and effects of antihypertensive drugs on oxidative stress in hypertensive patients with different stages of chronic kidney disease (CKD). Fifty-three non-dialyzed hypertensive CKD patients were included by the study. Serum and urinary 8-hydroxydeoxy guanosine (8-OHdG) levels (as a marker of oxidative DNA damage), serum superoxide dismutase (SOD), and glutathione peroxidase (G-Px) activities (as antioxidant enzymes) were measured. SOD activity was higher and G-Px activity was lower in the patient group as compared to control group. Serum and urinary 8-OHdG levels were found to be higher in the patients with proteinuria greater than 3 g/day than those in the patients with proteinuria less than 3 g/day. It has been determined that G-Px activity and urinary 8-OHdG level were lower in the patients treated with angiotensin-converting enzyme (ACE) inhibitor compared to patients treated with calcium channel blocker. The present data show oxidative DNA damage at a higher level in the patients with proteinuria greater than 3 g/day. In comparison to a calcium channel blocker, an ACE inhibitor seems much more protective against oxidative DNA damage in hypertensive patients with different stages of CKD