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.
A successful kidney transplantation does not lead to a significant reduction in the prevalence of pain when compared to chronic HD patients. Pain relief medications are underused in KTx patients.
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.
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