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Background/Aims: Desphospho-uncarboxylated matrix Gla protein (dp-ucMGP) is formed as a result of vitamin K insufficiency. The aim of this study was to investigate the association between plasma dp-ucMGP, kidney function and cardiovascular risk factors before and after 9-months substitution of vitamin K2 in non-dialysis patients with chronic kidney disease (CKD) stage 4 and 5. Methods: 38 CKD patients were supplemented for 270±12 days with 90 µg vitamin K2 and 10 µg cholecalciferol or 10 µg cholecalciferol alone. At baseline and at follow-up circulating calcium, phosphate, lipids, hemoglobin, albumin and total protein, dp-ucMGP, osteoprotegerin, fetuin A, osteocalcin and fibroblast grown factor 23 (FGF-23) were assessed. Proteinuria was assessed in the first morning void. Results: Baseline plasma dp-ucMGP was 1018.6±498.3 pmol/l and was significantly higher in patients at stage 5 CKD (1388.3 ±505.4 pmol/l) than at stage 4 (885.1±419.7 pmol/l), p=0.04. Vitamin K2 supplementation resulted in a decrease of dp-ucMGP level by 10.7%. Plasma dp-ucMGP was positively associated with proteinuria, serum creatinine, PTH and FGF-23; and inversely associated with glomerular filtration rate, serum hemoglobin and albumin. Conclusions: High dp-ucMGP level, reflecting a poor vitamin K status seems to be associated with kidney damage and may be also a marker of cardiovascular risk in CKD patients. Supplementation with vitamin K2 may improve the carboxylation status of MGP.

Background: The aim of this prospective cohort study was to evaluate the progression of coronary artery calcification (CAC), and atherosclerosis in hemodialysis (HD) patients and to relate them to novel biomarkers, i.e. serum osteoprotegerin (OPG) and fibroblast growth factor 23 (FGF-23). Material and Methods: Forty-seven HD patients were followed up for 30 months or until death. Intima media thickness (CCA-IMT), atherosclerotic plaques and CAC were assessed at baseline and after 30 months. Serum mineral parameters, lipids, OPG and plasma FGF-23 were also measured. Results: At baseline, 70% HD patients presented detectable CAC. The patients without calcification at baseline remained calcification free at 30 months and presented lower serum OPG and FGF-23 than those with CAC. A 64.4% progression of CAC was observed in all patients with CAC at baseline. In parallel, a 13% increase in CCA-IMT was found. Both ΔCAC and ΔCCA-IMT correlated positively with baseline and follow-up serum OPG. The patients who died had significantly higher baseline CAC and serum OPG. Conclusion: The plasma level of OPG could serve as a surrogate marker of progression of atherosclerosis and calcification in patients with end-stage renal disease. Therefore, the serum OPG may be a candidate biomarker of cardiovascular complications and poor outcome among dialysis patients.

Background: There is a paucity of epidemiological data on biopsy-proven glomerulonephritis (GN) in Poland. The aim of this study was to assess the epidemiology of renal diseases based on histological diagnosis in the region of Central Poland over the last two decades. Methods: Retrospective analysis of the results of 746 consecutive native kidney biopsies performed in the Caucasian adults from 1990 to 2010 in a single tertiary nephrology center serving an area of Central Poland. Results: Primary GN was found in 81.4% of all biopsies. The mesangioproliferative GN including IgA nephropathy was the most frequent type of primary GN (51.2%). Membranoproliferative GN was diagnosed between 1990 and 2000 more frequently than in the following decade (26.7 vs. 7.3%, p < 0.001). There was a significant increase in the incidence of FSGS (4.8 vs. 17.3%, p < 0.001) and MCD (5.1 vs. 11.2%, p < 0.001) over time. Secondary GN was documented in 18.6% of biopsies and lupus nephritis was the most frequent cause (34.5%). Conclusion: Our analysis showed the decrease in the incidence of membranoproliferative GN with the parallel increase of FSGS and MCD over the last twenty years. Mesangioproliferative GN including IgA nephropathy remains the most frequent type of GN observed in our region.

of hypertension in pregnancy 757 to 10% of pregnancies in the United States and Europe. Women with chronic HT (1%-5% of the general population) have a higher risk of PE than women without pre existing HT (17%-25% vs 3%-5%, respectively). Furthermore, 7% to 20% of women with chronic HT have poor BP control in pregnancy (excluding those with PE). Significantly elevated BP in pregnancy is a di rect threat to maternal and fetal health and life. According to the World Health Organization (WHO), HT and its complications are among the leading causes of mortality in pregnancy in developed countries (approx. 16%). 9-11 HT promotes low birth weight (LBW), increas es the risk of PE superimposed on chronic HT and preterm birth, may cause placental abrup tion, leads to complications which require pro longed intensive care of a neonate with special ist neonatal treatment, and may cause intrauter ine fetal death. 12,13 PE is the most dangerous maternal complica tion of HT. PE is associated with a particularly high risk of complications harmful to the mother

The study revealed close relationships between CAC, intima media thickness and the thickness of atherosclerotic plaques in dialysis patients. It may indicate that both vascular calcification and atherosclerotic lesions frequently coexist in patients with ESRD and that the intima media thickness could serve as a surrogate marker of vascular calcification.

Introduction: Tacrolimus (TAC) metabolism rate has the potential to impact graft function after kidney transplantation (KTx). We aimed to analyze the relationship between the early post-KTx TAC C/D ratio (blood trough concentration normalized by total daily dose) and kidney graft function in a 2-year follow-up. Methods: We retrospectively analyzed data from 101 post-KTx patients at 3, 6, 12, and 24 months after KTx to identify the C/D ratio cutoff value optimal for dividing patients into fast and slow TAC metabolizers. We investigated the relationship between their TAC metabolism rate and graft function. Results: Patients were divided based on the TAC C/D ratio at 6 months after KTx of 1.47 ng/mL * 1 mg. Fast metabolizers (C/D ratio <1.47 ng/mL * 1 mg) presented with significantly worse graft function throughout the whole study period (p < 0.05 at each timepoint) and were significantly less likely to develop good graft function (estimated glomerular filtration rate ≥45 mL/min/1.73 m2) than slow metabolizers. Our model based on donor and recipient age, recipient sex and slow/fast metabolism status allowed for identification of patients with compromised graft function in 2-year follow-up with 66.7% sensitivity and 94.6% specificity. Conclusion: Estimating TAC C/D ratio at 6 months post-KTx might help identify patients at risk of developing deteriorated graft function in a 2-year follow-up.

BackgroundA new serum marker of inflammation copeptin (CPP) a stable C-terminal pro-vasopressin was assessed along with conventional markers such as C-reactive protein (CRP), procalcitonin (PCT) and IL-6 to discriminate between lower and upper bacterial urinary tract infections (UTI).MethodsStudy population comprised 45 patients including 13 with lower UTI (L-UTI) and 32 with upper UTI (U-UTI) and 24 healthy controls. Serum markers, blood cultures and urine cultures were assessed before commencing antibiotic treatment and repeated 24, 48 h and 7 days thereafter. Receiver operating curves (ROC) were plotted to assess a diagnostic utility of different inflammatory markers.ResultsBefore antibiotic therapy all inflammatory markers including serum CPP (2821.1 ± 1072.4 pg/ml vs. 223.8 ± 109.3 pg/ml; p < 0.05) were higher in UTI than in controls. CPP was not different between L- and U-UTI (2253 ± 1323 pg/ml vs 3051 ± 1178 pg/ml; p = 0.70) despite significant differences in hsCRP (2.09 ± 1.7 mg/dl vs 127.3 ± 62.4 mg/dl; p < 0.001), PCT (0.05 ± 0 vs 5.02 ± 0.03 ng/ml p < 0.001) and IL-6 (22.5 ± 1.6 vs 84.8 ± 67 pg/ml p < 0.001). For U-UTI the areas under the ROC curves were 1.0 for both hsCRP and CPP, 0.94 for PCT and 0.7 for IL-6 and for L-UTI 0.571, 1, 0.505 and 0.73, respectively. After 7 days of treatment all markers decreased in parallel to clinical response.ConclusionAlthough elevated serum copeptin may become a marker of UTI it seems to be inferior compared to traditional serum inflammation markers for differentiation of bacterial infections involving upper and lower urinary tract.