1,720,970 research outputs found
Kinetics of the circulating levels of bone alkaline phosphatase in a case of hungry bone disease following total parathyroidectomy
No full textUric acid: a starring role in the intricate scenario of metabolic syndrome with cardio-renal damage?
No full textElevated uric acid levels are a common finding in patients with metabolic syndrome and in those with cardiovascular and renal disease, but the meaning of this elevation is still unclear. In patients with chronic kidney diseases, it could merely reflect the reduction in glomerular filtration rate: but uric acid levels are known to be elevated in people, also in younger ones, prior to the development of hypertension or renal disease, independently of several risk factors. Multiple potential mechanisms suggest a causative role for uric acid in vascular disease. Uric acid has been shown to be involved in metabolic pathways that lead to oxidative stress, endothelial disfunction, and to a vascular and systemic inflammatory response. Moreover, the elevation in uric acid levels observed after fructose ingestion, with a consequent reduction in nitric oxide, may lead to a reduced glucose uptake in the skeletal muscle, hyperinsulinemia, and insulin resistance. Besides these bench research data, also clinical studies showed the beneficial effects of lowering uric acid therapies on several markers of cardiovascular and renal disease. To date, however, there is no evidence indicating that such therapies, that are not free of risk, may reduce cardiovascular events; so that to manage our prescriptions, we need larger, prospective, interventional data
URINARY PROCOAGULANT AND FIBRINOLYTIC-ACTIVITY IN HUMAN GLOMERULONEPHRITIS - RELATIONSHIP WITH RENAL-FUNCTION
No full textA simple method for correcting overestimated glomerular filtration rate in obese subjects evaluated by the Cockcroft and Gault formula.
No full textUtilizzo di ferro liposomiale in pazienti con IRC in terapia conservativa intolleranti al solfato ferroso
No full textCoronary artery calcification and outcomes in diabetic patients with and without chronic kidney disease.
No full textAbstract
Background/Aims: Presence and progression of coronary
artery calcification (CAC) indicate severe atherosclerosis and
predict cardiovascular events (CVE) in dialysis (chronic kidney
disease, CKD, stage 2–5) and nondialysis patients (CKD
patients). This study aimed at evaluating the prevalence and
progression of CAC and CVE in CKD patients with diabetes in
whom atherosclerosis of coronary arteries is the leading
cause of CVE. Methods: This was a retrospective study conducted
in both out- and in-patients. CAC were assessed by
the total calcium (TC) score. CT scans were performed at the
entry and at the end of the study. Results: Patients (n = 341)
were divided into nondiabetic (n = 281) and diabetic patients
(n = 60). CAC prevalence and TC score were higher in
diabetics and associated with age, diabetes mellitus and
pulse pressure. Diabetics with CKD presented a higher percentage
of CAC progression and CVE. Conclusion: Prevalence,
extent, progression of CAC and CVE are higher in diabetics
with concomitant CKD. These findings may promote
a more aggressive protocol of screening and care in type 2
diabetics with concomitant CKD
Interference of angiotensin-converting enzyme inhibitors on erythropoiesis in kidney transplant recipients: role of growth factors and cytokines
No full textA simple method for correcting overestimated glomerular filtration rate in obese subject evaluated by the Cockcroft and Gault formula: a comparison with 51Cr EDTA clearance
No full textAIM: The Cockcroft and Gault formula is a quick and reliable method for
calculating creatinine clearance without a 24-hour urine collection (CG-cl). In
obese subjects an excess of fat mass provokes a reduction in daily creatinine
urine excretion per body kilo weight and is responsible for overestimated renal
function when calculated by CG-cl. The aim of this study was to devise a simple
correction method which could also make use of CG-cl in obese subjects. PATIENTS
AND METHODS: In 52 subjects with a body mass index (BMI) > 25, renal function was
assessed by simultaneously determining creatinine clearance using 24-hour urine
collection (Cr-cl) and the CG-cl. The percentage difference between the 2
clearances (delta %) was correlated with BMI for each patient using simple linear
regression analysis. The estimated regression model (delta% = 1.217 BMI-- 24.81)
provided the following CG-cl correction formula for obese subjects: Corrected
CG-cl = CG-cl (1.25 - 0.012 BMI). Its validity was evaluated in another group of
20 subjects with BMI > 25 by comparing the results obtained with Corrected CG-cl
to those obtained by CG-cl and MDRD formula (MDRD-cl) using the clearance of
51Cr-EDTA (5 Cr-EDTA-cl) as the GFR measurement gold standard. RESULTS AND
CONCLUSION: Linear regression analysis of CG-cl, MDRD-cl and Corrected CG-cl
compared to 5tCr-EDTA-cl (considered as the independent variable) resulted in the
following determination coefficients (R2): 0.687; 0.818; 0.947, respectively. In
conclusion, this formula can be considered a quick and reliable method for CG-cl
correction in obese subjects
Vitamin D in patients with chronic kidney disease: a position statement of the Working Group "Trace Elements and Mineral Metabolism" of the Italian Society of Nephrology.
No full textIn the late 1970s, calcitriol was introduced into clinical practice for the management of secondary renal hyperparathyroidism in chronic kidney disease (CKD). Since then, the use of calcifediol or other native forms of vitamin D was largely ignored until the publication of the 2009 Kidney Disease Improving Global Outcomes (KDIGO) recommendations. The guidelines suggested that measurement of circulating levels of 25(OH)D (calcifediol) and its supplementation were to be performed on the same basis as for the general population. This indication was based on the fact that the precursors of active vitamin D had provided to CKD patients considerable benefits in survival, mainly due to their pleiotropic effects on the cardiovascular system. However, despite the long-term use of various classes of vitamin D in CKD, a clear definition is still lacking concerning the most appropriate time for initiation of therapy, the best compound to prescribe (active metabolites or analogs), the proper dosage, and the most suitable duration of therapy. The aim of this position statement is to provide and critically appraise the current plentiful evidence on vitamin D in different clinical settings related to CKD, particularly focusing on outcomes, monitoring and treatment-associated risks. However, it should be taken in account that position statements are meant to provide guidance; therefore, they are not to be considered prescriptive for all patients and, importantly, they cannot replace the judgment of clinicians
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