IntroductionNeutrophil gelatinase-associated lipocalin (NGAL) has been recently proved useful in the quantitation of chronic kidney disease (CKD). The aim of the study was to assess prevalence of CKD according to the Modification of Diet in Renal Disease (MDRD), Cockcroft-Gault, and the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formulae in 412 patients with normal serum creatinine and markers of kidney function/injury such as NGAL, cystatin C, and kidney injury molecule-1 (KIM-1) in these patients in relation to age (below and over 65 years).Material and methodsWe included in the study 1005 patients with coronary artery disease and normal serum creatinine. However, markers of kidney function/injury were assessed in 412 patients. The NGAL, cystatin C and KIM-1, were assessed using commercially available kits.ResultsPatients over 65 years had significantly lower estimated glomerular filtration rate (eGFR) than their younger counterparts despite identical creatinine. They also had significantly lower haematocrit, despite similar Hb, lower platelet count, higher serum fibrinogen, higher systolic (SBP) and lower diastolic blood pressure, higher serum NGAL and cystatin C, but similar urinary NGAL and KIM-1. Serum NGAL correlated with age, haematocrit, leukocyte, platelet and erythrocyte count, eGFR, creatinine, fasting glucose, HbA1c, fibrinogen, SBP, and diabetes duration. In multiple regression analysis kidney function (eGFR, creatinine clearance or creatinine), cystatin C and SBP were predictors of serum NGAL.ConclusionsIn our study we found a very high prevalence of CKD up to 61% in elderly patients with coronary artery disease and normal serum creatinine. Neutrophil gelatinase-associated lipocalin could be a sensitive marker of kidney function, particularly in elderly patients with another risk factor for kidney damage, i.e. hypertension.

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INTROduCTION Iron metabolism has been studied for many years. New substances involved in iron metabolism continue to be described. Functional iron deficiency (FID) is characterized by the presence of adequate iron stores (as defined by standard criteria) but insufficient iron mobilization required for erythropoiesis during administration of erythropoiesis-stimulating agents. ObjECTIvEs The aim of the study was to evaluate new parameters of iron metabolism and the prevalence of FID as well as to assess potential correlations in patients on hemodialysis (HD). PATIENTs ANd mEThOds The study included 98 patients on maintenance HD. Standard laboratory methods were used to measure the iron status, complete blood count, creatinine, calcium, phosphorus, albumin, intact parathyroid hormone, and lipids. Commercially available kits were used to measure high-sensitivity C-reactive protein (hsCRP), interleukin 6 (IL-6), tumor necrosis factor-α, N-terminal pro-B-type natriuretic peptide (NT-proBNP), growth differentiation factor (GDF15), bone morphogenetic protein (BMP6), hemojuvelin, and hepcidin. REsuLTs FID was present in 23% of the patients on HD and was associated with significantly higher serum ferritin, IL-6, hsCRP, hepcidin, and NT-proBNP levels. There were no significant differences in BMP6 and GDF15 levels between patients with and without FID. Patients on HD had increased prevalence of hypertension, diabetes, and left ventricular hypertrophy and required slightly, but insignificantly, higher erythropoietin doses. Predictors of FID included serum iron levels and residual renal function. CONCLusIONs FID is present in a substantial proportion of patients on HD, who thus should be screened for reversible causes of inflammation. New parameters in iron metabolism do not seem to be related to FID in patients on HD.

We tested the hypothesis whether midkine could represent an early biomarker of contrast-induced acute kidney injury (CIAKI) in 89 patients with normal serum creatinine undergoing PCI. Midkine, serum and urinary NGAL, and cystatin C were evaluated before and 2, 4, 8, 24, and 48 hours after PCI using commercially available kits. Serum creatinine was assessed before and 24 and 48 hours after PCI. We found a significant rise in serum midkine as early as after 2 hours (P < 0.001) when compared to the baseline values. It was also significantly higher 4 hours after PCI and then returned to the baseline values after 24 hours and started to decrease after 48 hours. When contrast nephropathy was defined as an increase in serum creatinine by >25% of the baseline level 48 hours after PCI, the prevalence of CIN was 10%. Patients with CIN received significantly more contrast agent (P < 0.05), but durations of PCI were similar. Midkine was significantly higher 2, 4, and 8 hours after PCI in patients with CIN. Since the “window of opportunity” is narrow in CIAKI and time is limited to introduce proper treatment after initiating insult, particularly when patients are discharged within 24 hours after the procedure, midkine needs to be investigated as a potential early marker for renal ischemia and/or nephrotoxicity.

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