Association of ADP-Induced Whole-Blood Platelet Aggregation with Serum Low-Density Lipoprotein Cholesterol in Patients with Coronary Artery Disease When Receiving Maintenance Ticagrelor-Based Dual Antiplatelet Therapy.

The degree of platelet inhibition in patients undergoing dual antiplatelet therapy (DAPT) affects cardiovascular outcomes after acute coronary syndromes (ACS) and/or percutaneous coronary intervention. Our aim was to search for correlates of residual ex vivo platelet reactivity and circulating soluble P-selectin (sP-selectin), an index of in vivo platelet activation, in patients being treated by DAPT with ticagrelor. Adenosine diphosphate (ADP)-induced platelet aggregability (by multiple electrode aggregometry) and plasma sP-selectin were estimated in 62 stable post-ACS subjects (46 men and 16 women; mean age: 64 ± 10 years; 30 with type 2 diabetes (T2DM)) undergoing maintenance DAPT with ticagrelor and aspirin. These patients did not exhibit heart failure or other relevant coexistent diseases except for properly controlled T2DM, mild renal insufficiency, and hypertension. We also assessed this in 64 subjects on clopidogrel-based DAPT matched for age, sex, and T2DM status. ADP-induced platelet aggregation was below the optimal levels (190-460 arbitrary units (AU) * min) in most patients receiving ticagrelor-based DAPT, especially in those with below-median (<1.9 mmol/L) serum concentrations of low-density lipoprotein cholesterol (LDL-c) (128 ± 61 vs. 167 ± 73 AU * min for below-median and above-median LDL-c, respectively, p = 0.025). In contrast, platelet reactivity did not differ by LDL-c on clopidogrel-based DAPT (246 ± 101 vs. 268 ± 108 AU * min for below-median and above-median LDL-c, respectively, p > 0.4). Plasma sP-selectin was found to be unrelated to serum LDL-c when receiving DAPT with ticagrelor (p > 0.4) or clopidogrel (p > 0.8). In conclusion, our preliminary observational study suggests the association of lower residual ex vivo platelet aggregability with better LDL-c control in patients undergoing ticagrelor-based maintenance DAPT, which does not appear to be reflected by plasma sP-selectin. Whether the serum LDL-c level should be considered among the factors affecting the degree of platelet inhibition for those treated with ticagrelor-based DAPT needs to be investigated in larger studies.

Diagnostic Ability of Peguero-Lo Presti Electrocardiographic Left Ventricular Hypertrophy Criterion in Severe Aortic Stenosis.

Traditional electrocardiographic (ECG) criteria for left ventricular hypertrophy (LVH), introduced in the pre-echocardiographic era of diagnosis, have a relatively low sensitivity (usually not exceeding 25-40%) in detecting LVH. A novel Peguero-Lo Presti ECG-LVH criterion was recently shown to exhibit a higher sensitivity than the traditional ECG-LVH criteria in hypertension. Our aim was to test the diagnostic ability of the novel Peguero-Lo Presti ECG-LVH criterion in severe aortic stenosis. We retrospectively analyzed 12-lead ECG tracings and echocardiographic records from the index hospitalization of 50 patients with isolated severe aortic stenosis (mean age: 77 ± 10 years; 30 women and 20 men). Exclusion criteria included QRS > 120 ms, bundle branch blocks or left anterior fascicular block, a history of myocardial infarction, more than mild aortic or mitral regurgitation, and significant LV dysfunction by echocardiography. We compared the agreement of the novel Peguero-Lo Presti criterion and traditional ECG-LVH criteria with echocardiographic LVH (LV mass index > 95 g/m2 in women and >115 g/m2 in men). Echocardiographic LVH was found in 32 out of 50 study patients. The sensitivity of the Peguero-Lo Presti criterion in detecting LVH was improved (55% vs. 9-34%) at lower specificity (72% vs. 78-100%) in comparison to 8 single traditional ECG-LVH criteria. Additionally, the positive predictive value (77% vs. 72%), positive likelihood ratio (2.0 vs. 1.5), and odds ratio (3.2 vs. 2.4) were higher for the Peguero-Lo Presti criterion versus the presence of any of these 8 traditional ECG-LVH criteria. Cohen's Kappa, a measure of concordance between ECG and echocardiography with regard to LVH, was 0.24 for the Peguero-Lo Presti criterion, -0.01-0.13 for single traditional criteria, and 0.20 for any traditional criterion. However, by the receiver operating characteristics (ROC) curve analysis, the overall ability to discriminate between patients with and without LVH was insignificantly lower for the Peguero-Lo Presti versus Cornell voltage as a continuous variable (area under the ROC curve: 0.65 (95% CI, 0.48-0.81) vs. 0.71 (0.55-0.86), p = 0.5). In conclusion, our preliminary results suggest a slightly better, albeit still low, agreement of the novel Peguero-Lo Presti ECG criterion compared to the traditional ECG-LVH criteria with echocardiographic LVH in severe aortic stenosis.

Novel antidiabetic drugs in diabetic kidney disease accompanying type 2 diabetes - a minireview.

Intensive hypoglycemic treatment is the strongest preventive strategy against the development of microvascular complications of type 2 diabetes (T2DM), including diabetic nephropathy. However, some antidiabetic drugs, i.e. sodium-glucose cotransporter-2 inhibitors (SGLT-2i) and glucagon-like peptide-1 receptor agonists (GLP1-RA) have an additional renoprotective effect beyond glucose control by itself. Similar, both SGLT-2i and GLP1-RA have been demonstrated to decrease the risk of adverse cardiovascular (CV) events in CV outcome trials. Nevertheless, there are relevant differences in CV and renal effects of SGLT-2i and GLP1-RA. First, SGLT2i reduced the incidence and progression of albuminuria and prevented loss of kidney function, while predominant renal benefits of GLP1-RA were driven by albuminuria outcomes. Second, the risk of heart failure (HF) hospitalizations decreased on SGLT2i but not on GLP1-RA, which gives priority to SGLT2i in T2DM and HF, especially with depressed EF. Third, either GLP1-RA (reducing predominantly atherosclerosis-dependent events) or SGLT-2i, should be used in T2DM and established atherosclerotic CV disease (ASCVD) or other indicators of high CV risk. In this review, we have briefly compared clinical practice guidelines of the American Diabetes Association (2020 and 2021 versions), Polish Diabetes Association (2020) and the European Society of Cardiology/European Association for the Study of Diabetes (2019), with a focus on the choice between SGLT-2i and GLP1-RA in patients with diabetic kidney disease.

Distinct associations between plasma osteoprotegerin, homoarginine and asymmetric dimethylarginine in chronic kidney disease male patients with coronary artery disease.

High plasma osteoprotegerin (OPG) and asymmetric dimethylarginine (ADMA) and low homoarginine (hArg) predict adverse renal and cardiovascular (CV) outcomes. In patients with chronic kidney disease and stable coronary artery disease, plasma OPG correlated with hArg (r = - 0.37, P = 0.03) and the hArg/ADMA molar ratio (r = - 0.46, P = 0.009), which was maintained upon adjustment for renal function. Elevated OPG levels and decreased hArg/ADMA ratios independently predicted 4-year composite CV and renal endpoints (CV death or progression to dialysis). Thus, high OPG and low hArg/ADMA ratio, albeit interrelated, appear to independently contribute to adverse clinical outcome.

Association of Inadequately Low Left Ventricular Mass with Enhanced Myocardial Contractility in Severe Degenerative Aortic Stenosis.

BACKGROUND: Left ventricular hypertrophy (LVH), traditionally considered an adaptive mechanism that is aimed at the maintenance of LV systolic function, is absent in 10%⁻35% of patients with severe aortic stenosis (AS). Our aim was to estimate the clinical and hemodynamic characteristics in patients with severe AS and absent LVH, or inadequately low LV mass (i-lowLVM) relative to an individual hemodynamic load. METHODS: We retrospectively analyzed in-hospital records of 100 patients with pure severe degenerative AS, preserved LV systolic function and without relevant coexistent diseases, except for well-controlled hypertension or diabetes. RESULTS: Clinical characteristics were similar in patients with and without LVH, as well as those with and without i-lowLVM, except for slightly lower GFR at i-lowLVM. When compared to their counterparts, subjects without LVH or with i-lowLVM had smaller LV cavities, decreased LV wall thicknesses and higher EF. There were no significant differences in stenosis severity and indices of afterload (valvulo-arterial impedance and circumferential end-systolic LV wall stress), according to the presence or absence of either LVH or i-lowLVM. However, LV fractional shortening at the midwall level was elevated only in patients with i-lowLVM, but not in those without LVH, compared to the remainder (15.8 ± 3.3 vs. 12.9 ± 3.2%, p < 0.001 for those with and without i-lowLVM, respectively; 13.7 ± 3.7 vs. 13.8 ± 3.6% for LVH presence and absence, p = 0.9). CONCLUSIONS: Inadequately low LVM relative to the individual hemodynamic load could potentially reflect a different mode of the LV response to severe AS, associated with enhanced load-independent LV systolic performance, i.e., better LV contractility. If confirmed in a large series of patients, our small preliminary study may add to the possible mechanisms of a previously reported counterintuitive tendency of a lower, not higher, risk of adverse outcome in patients with low LV mass despite severe AS. Prospective studies are warranted, in order to determine a potential utility of LVM inadequacy in the risk stratification of patients with AS.

How does preclinical laboratory training impact physical examination skills during the first clinical year? A retrospective analysis of routinely collected objective structured clinical examination scores among the first two matriculating classes of a reformed curriculum in one Polish medical school.

OBJECTIVE: As a result of a curriculum reform launched in 2012 at our institution, preclinical training was shortened to 2 years instead of the traditional 3 years, creating additional incentives to optimise teaching methods. In accordance with the new curriculum, a semester-long preclinical module of clinical skills (CS) laboratory training takes place in the second year of study, while an introductory clinical course (ie, brief introductory clerkships) is scheduled for the Fall semester of the third year. Objective structured clinical examinations (OSCEs) are carried out at the conclusion of both the preclinical module and the introductory clinical course. Our aim was to compare the scores at physical examination stations between the first and second matriculating classes of a newly reformed curriculum on preclinical second-year OSCEs and early clinical third-year OSCEs. DESIGN: Analysis of routinely collected data. SETTING: One Polish medical school. PARTICIPANTS: Complete OSCE records for 462 second-year students and 445 third-year students. OUTCOME MEASURES: OSCE scores by matriculation year. RESULTS: In comparison to the first class of the newly reformed curriculum, significantly higher (ie, better) OSCE scores were observed for those students who matriculated in 2013, a year after implementing the reformed curriculum. This finding was consistent for both second-year and third-year cohorts. Additionally, the magnitude of the improvement in median third-year OSCE scores was proportional to the corresponding advancement in preceding second-year preclinical OSCE scores for each of two different sets of physical examination tasks. In contrast, no significant difference was noted between the academic years in the ability to interpret laboratory data or ECG - tasks which had not been included in the second-year preclinical training. CONCLUSION: Our results suggest the importance of preclinical training in a CS laboratory to improve students' competence in physical examination at the completion of introductory clinical clerkships during the first clinical year.

No Association of Proton Pump Inhibitor Use with Fasting or Postload Glycaemia in Patients with Cardiovascular Disease: A Cross-Sectional Retrospective Study.

Background: Proton pump inhibitor (PPI) use was reportedly associated with an excess of adverse cardiovascular (CV) events, thus making their systemic effects relevant to public health. PPIs reduce gastric acid secretion, causing increased gastrin release. Gastrin stimulates ß-cell neogenesis and enhances insulin release, exerting an incretin-like effect. Our aim was to assess, if PPI usage is associated with altered glycaemia in patients with CV disease. Methods: We retrospectively analyzed medical records of 102 subjects (80 with ischemic heart disease) who underwent a routine oral glucose tolerance test while hospitalized in a cardiology department. Fasting and 2-h postload glucose levels were compared according to PPI use for ≥1 month prior to admission. Results: Compared to 51 subjects without PPIs, those on a PPI were older, more frequently male, had a lower body-mass index and a tendency to a worse renal function. PPI users and non-users exhibited similar glucose levels at baseline (5.6 ± 0.9 vs. 5.5 ± 1.1 mmol/l, P = 0.5) and 2-hrs post glucose intake (9.8 ± 3.0 vs. 9.9 ± 3.4 mmol/l, P = 0.9). This was consistent across subgroups stratified by gender or diabetes status. The results were substantially unchanged after adjustment for different characteristics of subjects with and without PPIs. Conclusions: PPI use does not appear associated with altered glycaemia in subjects with CV disease. Unchanged glucose tolerance despite PPI usage may result from simultaneous activation of pathways that counteract the putative PPI-induced incretin-like effect.

Clinical Correlates and Prognostic Value of Plasma Galectin-3 Levels in Degenerative Aortic Stenosis: A Single-Center Prospective Study of Patients Referred for Invasive Treatment.

Galectin-3 (Gal-3), a ß-galactoside-binding lectin, has been implicated in myocardial fibrosis, development of left ventricular (LV) dysfunction and transition from compensated LV hypertrophy to overt heart failure (HF), being a novel prognostic marker in HF. Risk stratification is crucial for the choice of the optimal therapy in degenerative aortic stenosis (AS), affecting elderly subjects with coexistent diseases. Our aim was to assess correlates and prognostic value of circulating Gal-3 in real-world patients with degenerative AS referred for invasive treatment. Gal-3 levels were measured at admission in 80 consecutive patients with symptomatic degenerative AS (mean age: 79 ± 8 years; aortic valve area (AVA) index: 0.4 ± 0.1 cm²/m²). The therapeutic strategy was chosen following a dedicated multidisciplinary team-oriented approach, including surgical valve replacement (n = 11), transcatheter valve implantation (n = 19), balloon aortic valvuloplasty (BAV) (n = 25) and optimal medical therapy (n = 25). Besides routine echocardiographic indices, valvulo-arterial impedance (Zva), an index of global LV afterload, was computed. There were 22 deaths over a median follow-up of 523 days. Baseline Gal-3 correlated negatively with estimated glomerular filtration rate (eGFR) (r = -0.61, p < 0.001) and was unrelated to age, symptomatic status, AVA index, LV ejection fraction, LV mass index or Zva. For the study group as a whole, Gal-3 tended to predict mortality (Gal-3 >17.8 vs. Gal-3 <17.8 ng/mL; hazard ratio (HR): 2.03 (95% confidence interval, 0.88-4.69), p = 0.09), which was abolished upon adjustment for eGFR (HR: 1.70 (0.61-4.73), p = 0.3). However, in post-BAV patients multivariate-adjusted pre-procedural Gal-3 was associated with worse survival (HR: 7.41 (1.52-36.1), p = 0.01) regardless of eGFR. In conclusion, the inverse eGFR-Gal-3 relationship underlies a weak association between Gal-3 and adverse outcome in patients with degenerative AS referred for invasive therapy irrespective of type of treatment employed. In contrast, pre-procedural Gal-3 appears an independent mortality predictor in high-risk AS patients undergoing BAV.

Serum uromodulin concentrations correlate with glomerular filtration rate in patients with chronic kidney disease.

INTRODUCTION Urinary uromodulin excretion has been associated with kidney diseases. However, serum uromodulin concentrations have not been extensively studied in patients with chronic kidney disease (CKD), and the results of published studies are inconsistent. OBJECTIVES The aims of the study were to evaluate serum uromodulin concentrations in patients with CKD and to assess the utility of serum uromodulin measurements for diagnosing CKD stages. PATIENTS AND METHODS This observational study included 170 patients with CKD stages 1 to 5, not treated by renal replacement therapy, and 30 healthy individuals. The serum levels of creatinine, cystatin C, and uromodulin were measured, and estimated glomerular filtration rate (eGFR) was calculated according to the 2012 CKD Epidemiology Collaboration cystatin­creatinine equation. RESULTS Among patients with CKD, serum uromodulin concentrations were significantly lower than in controls, and were strongly negatively correlated with renal retention markers (ie, serum creatinine and cystatin C) and strongly positively correlated with eGFR. An inverse, hyperbolic relationship between serum creatinine and uromodulin levels was analogous to the well­known association between serum creatinine concentrations and eGFR. A receiver­operating characteristic curve analysis showed a high diagnostic accuracy of the measurement of serum uromodulin concentrations in the assessment of CKD stages. CONCLUSIONS Serum uromodulin concentrations are closely correlated with eGFR, which is the recommended measure of renal function. As uromodulin is produced exclusively by renal tubular cells, the assessment of uromodulin levels in patients with CKD may be an alternative method for evaluating the number of functioning nephrons.

Effects of Atorvastatin Dose and Concomitant Use of Angiotensin-Converting Enzyme Inhibitors on Renal Function Changes over Time in Patients with Stable Coronary Artery Disease: A Prospective Observational Study.

Angiotensin-converting enzyme inhibitors (ACEI) and statins are widely used in patients with coronary artery disease (CAD). Our aim was to compare changes in glomerular filtration rate (GFR) over time in subjects with stable CAD according to atorvastatin dose and concomitant use of ACEI. We studied 78 men with stable CAD referred for an elective coronary angiography who attained the then-current guideline-recommended target level of low-density lipoproteins (LDL) cholesterol below 2.5 mmol/L in a routine fasting lipid panel on admission and were receiving atorvastatin at a daily dose of 10-40 mg for ≥3 months preceding the index hospitalization. Due to an observational study design, atorvastatin dosage was not intentionally modified for other reasons. GFR was estimated during index hospitalization and at about one year after discharge from our center. Irrespective of ACEI use, a prevention of kidney function loss was observed only in those treated with the highest atorvastatin dose. In 38 subjects on ACEI, both of the higher atorvastatin doses were associated with increasing beneficial effects on GFR changes (mean ± SEM: -4.2 ± 2.4, 1.1 ± 1.6, 5.2 ± 2.4 mL/min per 1.73 m² for the 10-mg, 20-mg and 40-mg atorvastatin group, respectively, p = 0.02 by ANOVA; Spearman's rho = 0.50, p = 0.001 for trend). In sharp contrast, in 40 patients without ACEI, no significant trend effect was observed across increasing atorvastatin dosage (respective GFR changes: -1.3 ± 1.0, -4.7 ± 2.1, 4.8 ± 3.6 mL/min per 1.73 m², p = 0.02 by ANOVA; rho = 0.08, p = 0.6 for trend). The results were substantially unchanged after adjustment for baseline GFR or time-dependent variations of LDL cholesterol. Thus, concomitant ACEI use appears to facilitate the ability of increasing atorvastatin doses to beneficially modulate time-dependent changes in GFR in men with stable CAD.

Parental history of premature coronary artery disease does not affect plasma levels of asymmetric dimethylarginine in young healthy adults.

INTRODUCTION: Family history of premature coronary artery disease (CAD) is a risk factor of atherogenesis and adverse coronary events. OBJECTIVES: The aim of the study was to establish whether asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide formation, might be elevated in the asymptomatic offspring of patients with early­onset CAD and whether it might contribute to subclinical atherosclerosis. PATIENTS AND METHODS: We studied 20 healthy subjects (10 men and 10 women) aged from 19 to 30 years with a parental history of documented CAD before 60 years of age, and 20 controls with no evidence of parental CAD. ADMA and its isomer, symmetric dimethylarginine (SDMA), were determined by enzyme­linked immunosorbent assays. Mean intima­media thickness (IMT) of the common carotid arteries was assessed by B­mode ultrasound. RESULTS: Characteristics of the 2 groups were similar, except for insignificant tendencies towards higher low­density lipoprotein (LDL) cholesterol (P = 0.07) and estimated glomerular filtration rate (eGFR) (P = 0.06) in the group with a positive family history. Compared with controls, subjects with a parental history of premature CAD had increased IMT (0.54 ±0.05 vs. 0.48 ±0.05 mm; P <0.001) and similar levels of ADMA (0.66 ±0.17 vs. 0.74 ±0.15 µmol/l; P = 0.14) and SDMA (0.49 ±0.07 vs. 0.50 ±0.07 µmol/l; P = 0.61). The results did not change substantially on adjustment for LDL cholesterol and eGFR. In a multivariate analysis, parental CAD (P = 0.005) and LDL cholesterol (P = 0.06), but not ADMA, were independent positive IMT predictors. CONCLUSIONS: Our preliminary data suggest that elevated ADMA is not a part of the proatherogenic risk profile in the young adult offspring of patients with premature CAD.

[Rapidly progressive ANCA-negative glomerulonephritis in the course of pauci immune microscopic vasculitis with hemolytic anemia probable in the course of Wilson's disease]. / Gwaltownie postepujace klebuszkowe zapalenie nerek w przebiegu ANCA-negatywnego "niemego- immunologicznie" mikroskopowego zapalenia naczyn z towarzyszaca anemia hemolityczna prawdopodobnie w przebiegu choroby Wilsona.

Pauci-immune glomerulonephritis, i.e., with no evidence of immune deposits in the blood vessel, is the most prevalent form of rapidly progressive glomerulonephritis (RPGN). In the pathogenesis of pauci-immune renal disease inflammation of blood vessels in the presence of circulating anti-neutrophil cytoplasm antibodies (ANCA) takes place. However the lack of ANCA (about 5-30% of patients) does not exclude pauci-immune vasculitis. The patients without circulating ANCA might have fewer extrarenal symptoms than those who are ANCA-positive. We describe a case of a 40-year old women with ANCA-negative renal limited pauci-immune small-vessel vasculitis with rapidly decreasing kidney function. She was ineffectively treated with plasmapheresis combined with a puls of cyclophosphamide (i.v.) and 3 pulses of methyloprednisolone (i.v.). The patient progressed to end-stage renal disease and should be treated with renal replacement therapy. In differential diagnosis we excluded other causes of pauci-immune vasculitis (Churg-Strauss syndrome, Wegener's granulomatosis), vasculitis with immune complexes deposition (systemic lupus erythematosus, Schoenlein-Henoch purpura, post-infection RPGN), Goodpasture disease, haemolytic-uremic syndrome (HUS), disseminated intravascular coagulation (DIC) and Wilson's disease.

Synergistic effects of asymmetrical dimethyl-L-arginine accumulation and endothelial progenitor cell deficiency on renal function decline during a 2-year follow-up in stable angina.

BACKGROUND: Renal insufficiency predisposes to coronary artery disease (CAD), but also CAD and traditional risk factors accelerate renal function loss. Endothelial progenitor cell (EPC) deficiency and elevated asymmetrical dimethyl-L-arginine (ADMA), an endogenous nitric oxide (NO) formation inhibitor, predict adverse CAD outcome. Our aim was to assess changes in estimated glomerular filtration rate over time (DeltaeGFR) in relation to baseline EPC blood counts and ADMA levels in stable angina. METHODS: Eighty non-diabetic men with stable angina were followed up for 2 years after elective coronary angioplasty. Exclusion criteria included heart failure, left ventricular systolic dysfunction, eGFR <30 ml/min/1.73 m(2) and coexistent diseases. Those with cardiovascular events or ejection fraction <55% during the follow-up were also excluded. A baseline blood count of CD34+/kinase-insert domain receptor (KDR)+ cells, a leukocyte subpopulation enriched for EPC, was quantified by flow cytometry (percentage of lymphocytes). RESULTS: A synergistic interaction (P = 0.015) between decreased CD34+/KDR+ cell counts and increased plasma ADMA, but not symmetrical dimethyl-L-arginine, was the sole significant multivariate DeltaeGFR predictor irrespective of baseline eGFR. DeltaeGFR was depressed in the simultaneous presence of high ADMA (>0.45 micromol/l, median) and low CD34+/KDR+ cell counts (<0.035%, median) compared to either of the other subgroups (P = 0.001-0.01). DeltaeGFR did not correlate with traditional risk factors, angiographic CAD extent, levels of C-reactive protein and soluble vascular cell adhesion molecule-1. CONCLUSIONS: Elevated ADMA and EPC deficiency may synergistically contribute to accelerated renal function decline in stable angina. This could result from the impairment of the EPC-dependent endothelial renewal in the kidney, an NO-dependent process.

[Chronic kidney disease in the source documentation of the outpatient clinic Department of Nephrology. Part II. Comparison of the three different methods of glomerular filtration rate estimation]. / Przewlekla choroba nerek w materiale Poradni Nefrologicznej. Czesc II. Porównanie trzech róznych metod oceny filtracji klebuszkowej.

The aim of the study was to compare three methods of GFR estimation as simplified MDRD formula, Cockcroft-Gault formula and 24 hour urine collection used in evaluation of kidney function. The study was conducted at the outpatient clinic and enclosed 1183 patients aged between 17 and 98 years (mean 64.7) with creatinine level >120 micromol/l and/or creatinine clearance <90 ml/min/1.73 m2, described in detail in part I. After calculation we obtained different mean GFR values adequately to the method: 38.4 +/- 15.13 ml/min/1.73 m2 (simplified MDRD formula), 44.51 +/- 20.59 ml/min/1.73 m2 (Cockcroft-Gault formula) and 45.63 +/- 25.55 ml/min/1.73 m2 (24-h urine collection). Results of the GFR assessment were different according to the applied method of calculation. The smallest data dispersion was observed in GFR values calculated based on abbreviated MDRD formula and the highest when obtained based on to the 24-hour urine collection. The GFR values obtained based on 24 hour urine collection showed positive correlations with BMI (p<0.01), hemoglobine (p<0.01), hematocrite (p<0.01), diastolic blood pressure (p=0.01), albumin (p=0.041), iron (p=0.03), AIAT activity (p=0.01), and negative with age (p<0.01), phosphate (p<0.01), alkaline phosphatase activity (p=0.039), parathormone (p=0.03), potassium (p<0.01) and magnesium (p<0.01). In the group of patients with GFR values below 30 ml/min in comparison with patients with GFR values above 30 ml/min, in all three methods of GFR estimation it was shown significantly higher values of phosphate, potassium, age, and lower hemoglobin, hematocrite. It was shown also in the group with GFR below 30 ml/min values estimated based on Cockcroft-Gault formula and 24 hour urine collection significantly lower BMI.

[Chronic kidney disease in the source documentation of the outpatient clinic Department of Nephrology. Part I. Causes of renal failure and characteristics of the studied population]. / Przewlekla choroba nerek w materiale Poradni Nefrologicznej. Czesc I. Przyczyny uszkodzenia nerek oraz charakterystyka badanej populacji.

During the last years the incidence of chronic kidney disease (CKD) is permanently increasing and has become a global social and economical problem in the world as well as in Poland. The aim of the study was the retrospective analysis of medical records of patients with renal failure under supervision at the outpatient clinic, Department of Nephrology, University Hospital in Cracow. The study population enclosed 1183 patients (640 men and 543 women) aged between 17 and 98 years (mean 64.7) with creatinine concentration >120 micromol/l and/or creatinine clearance <90 ml/min/1.73 m2. Hemoglobin, iron, creatinine, urea, sodium, potasium, calcium, phosphate, magnesium, PTH, uric acid, albumin, total protein, bilirubin, glucose, total cholesterol, LDL and HDL cholesterol, triglicerydes concentration and values of hematocrite, MCV, HbA1, as well as alkaline phosphatase, AspAT, AIAT activity were estimated based on standard laboratory methods. Creatinine clearances were evaluated based on 3 different methods: simplified MDRD formula, Cockcroft-Gault formula and 24-h urine collection. Mean creatinine concentration in the studied population was 172.8 micromol/l (1.95 mg/dl). Hypertension was diagnosed in 65% of patients. In spite of treatment, more than half of the patients (51.9%) have increased systolic blood pressure and above 1/3 (35%) increased diastolic blood pressure. Mean hemoglobin concentration was 13.02 g/dl; more than 12% of patients had decreased hemoglobin below 11 g/dl. Mean values of parameters discovering calcium-phosphate metabolism were: calcium--2.33 mmol/l, phosphate--1.23 mmol/l and parathormon--169.3 pg/ml. Increased value of total serum cholesterol level was noted more than half of the patients (56.5%). Significant positive correlations were found between GFR calculated based on Cockcroft-Gault formula and BMI, hemoglobin, hematocrite, serum iron, diastolic blood pressure, total and LDL serum cholesterol, triglicerydes level, as well as AIAT activity and % values of HbA1c and negative with age, serum potassium, phosphorus, PTH and uric acid.

Association between endothelial progenitor cell depletion in blood and mild-to-moderate renal insufficiency in stable angina.

BACKGROUND: Low blood counts of CD34/kinase-insert domain receptor double-positive cells (CD34(+)/KDR(+) cells)-a leukocytes subpopulation enriched for bone marrow-derived endothelial progenitor cells (EPC)- predict adverse outcomes in coronary artery disease (CAD). The dependence of EPC numbers on the glomerular filtration rate (GFR), another prognostic factor, has not been reported in CAD yet. Our aim was to assess CD34(+)/KDR(+) cell counts versus GFR in stable angina. METHODS: We studied 102 stable angina men with severe angiographic CAD and normal left-ventricular systolic function. CD34(+)/KDR(+) cells were enumerated by flow cytometry. RESULTS: With lowering GFR, CD34(+)/KDR(+) cell numbers (% of lymphocytes, median and interquartile range) decreased: 0.04 (0.03-0.06), 0.03 (0.02-0.05) and 0.02 (0.01-0.03)% for GFR >or=90, 60-89 and 30-59 ml/min/1.73 m(2), respectively (P < 0.001 for trend). CD34(+)/KDR(+) cell counts correlated with GFR (r = 0.25, P = 0.01), CAD extension score (r = -0.20, P = 0.04), soluble form of vascular cell adhesion molecule-1 (sVCAM-1) (r = -0.22, P = 0.03) and homocysteine (r = -0.20, P = 0.04) levels. A GFR <90 ml/min/1.73 m(2) was associated with insignificantly higher plasma erythropoietin concentrations (r = -0.22, P = 0.09 for trend) that correlated with haemoglobin levels (r = -0.33, P = 0.01, n = 59). The GFR-CD34(+)/KDR(+) cells relation was attenuated, yet maintained (beta = 0.19 +/- 0.09, P = 0.04) on adjustment for the remaining multivariate determinants of CD34(+)/KDR(+) cell numbers: sVCAM-1 (beta = -0.20 +/- 0.09, P = 0.03) and haemoglobin (beta = 0.18 +/- 0.09, P = 0.05). CONCLUSIONS: Mild-to-moderate renal dysfunction accompanying stable angina is associated with CD34(+)/KDR(+) cell depletion, which partially depends on concomitant endothelial dysfunction and a tendency to anaemia (despite insignificantly higher erythropoietin) irrespective of an angiographic CAD extent. This may exacerbate an imbalance between endothelial injury and EPC-mediated repair, thus contributing to high cardiovascular risk in CAD coexisting with renal insufficiency.