Switching from Allopurinol to Febuxostat: A Comparison of The Rate of Renal Functional Decline in Patients With Moderate and Severe Chronic Kidney Disease

Background: Despite of considerable advances in its diagnosis and management, heart failure remains an unsettled problem and life threatening. Heart failure with a growing prevalence represents a burden to healthcare system, responsible for deterioration of patient’s daily activities. Galectin-3 is a new cardiac biomarker in prognosis for heart failure. Serum galectin-3 has some relation to heart failure NYHA classification, acute coronary syndrome and clinical outcome. Level of serum galectin-3 give information for prognosis and help risk stratifications in patient with heart failure, so intensive therapeutics can be approached to patients with high risk. Objective: To examine plasma galectin-3 level in hospitalized heart failure patients, investigate the relationship between galectin-3 level with associated diseases, clinical conditions and disease progression in hospital. Methodology: Cross sectional study. Result: 20 patients with severe heart failure as NYHA classification were diagnosed by The ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure (2012) and performed blood test for serum galectin-3 level. Increasing of serum galectin-3 level have seen in all patients, mean value is 36.5 (13.7 – 74.0), especially high level in patient with acute coronary syndrome and patients with severe chronic kidney disease. There are five patients dead. Conclusion: Serum galectin-3 level increase in patients with heart failure and has some relation to NYHA classification, acute coronary syndrome. However, level of serum galectin-3 can be affected by severe chronic kidney disease, more research is needed on this aspect Key words: Serum galectin-3, heart failure, ESC Guidelines, NYHA

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Faculty Opinions recommendation of Dulaglutide versus insulin glargine in patients with type 2 diabetes and moderate-to-severe chronic kidney disease (AWARD-7): a multicentre, open-label, randomised trial.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.733467482.793553182 ◽

2018 ◽

Author(s):

Vlado Perkovic ◽

Brendan Smyth

Keyword(s):

Type 2 Diabetes ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Insulin Glargine ◽

Randomised Trial ◽

Open Label ◽

Severe Chronic Kidney Disease

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A phosphate and calcium-enriched diet promotes progression of 5/6-nephrectomy-induced chronic kidney disease in C57BL/6 mice

Scientific Reports ◽

10.1038/s41598-021-94264-8 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

J. Radloff ◽

N. Latic ◽

U. Pfeiffenberger ◽

C. Schüler ◽

S. Tangermann ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Calcium Phosphate ◽

Kidney Disease ◽

Renal Fibrosis ◽

Time Course ◽

Bone Mineralization ◽

Fibroblast Growth Factor 23 ◽

Functional Decline ◽

Left Ventricular ◽

Normal Diet

AbstractC57BL/6 mice are known to be rather resistant to the induction of experimental chronic kidney disease (CKD) by 5/6-nephrectomy (5/6-Nx). Here, we sought to characterize the development of CKD and its cardiac and skeletal sequelae during the first three months after 5/6-Nx in C57BL/6 mice fed a calcium- and phosphate enriched diet (CPD) with a balanced calcium/phosphate ratio. 5/6-NX mice on CPD showed increased renal fibrosis and a more pronounced decrease in glomerular filtration rate when compared to 5/6-Nx mice on normal diet (ND). Interestingly, despite comparable levels of serum calcium, phosphate, and parathyroid hormone (PTH), circulating intact fibroblast growth factor-23 (FGF23) was 5 times higher in 5/6-Nx mice on CPD, relative to 5/6-Nx mice on ND. A time course experiment revealed that 5/6-Nx mice on CPD developed progressive renal functional decline, renal fibrosis, cortical bone loss, impaired bone mineralization as well as hypertension, but not left ventricular hypertrophy. Collectively, our data show that the resistance of C57BL/6 mice to 5/6-Nx can be partially overcome by feeding the CPD, and that the CPD induces a profound, PTH-independent increase in FGF23 in 5/6-Nx mice, making it an interesting tool to assess the pathophysiological significance of FGF23 in CKD.

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