scholarly journals Alkali supplementation as a therapeutic in chronic kidney disease: what mediates protection?

2020 ◽  
Vol 319 (6) ◽  
pp. F1090-F1104
Author(s):  
Elinor C. Mannon ◽  
Paul M. O’Connor
Keyword(s):  
Chronic Kidney Disease ◽  
Clinical Trials ◽  
Kidney Disease ◽  
Functional Decline ◽  
Physiological Mechanism ◽  
Basic Research ◽  
Ph Homeostasis ◽  
Disease States ◽  
Kidney Disease Progression ◽  
Acid Base Status

Sodium bicarbonate (NaHCO3) has been recognized as a possible therapy to target chronic kidney disease (CKD) progression. Several small clinical trials have demonstrated that supplementation with NaHCO3 or other alkalizing agents slows renal functional decline in patients with CKD. While the benefits of NaHCO3 treatment have been thought to result from restoring pH homeostasis, a number of studies have now indicated that NaHCO3 or other alkalis may provide benefit regardless of the presence of metabolic acidosis. These data have raised questions as to how NaHCO3 protects the kidneys. To date, the physiological mechanism(s) that mediates the reported protective effect of NaHCO3 in CKD remain unclear. In this review, we first examine the evidence from clinical trials in support of a beneficial effect of NaHCO3 and other alkali in slowing kidney disease progression and their relationship to acid-base status. Then, we discuss the physiological pathways that have been proposed to underlie these renoprotective effects and highlight strengths and weaknesses in the data supporting each pathway. Finally, we discuss how answering key questions regarding the physiological mechanism(s) mediating the beneficial actions of NaHCO3 therapy in CKD is likely to be important in the design of future clinical trials. We conclude that basic research in animal models is likely to be critical in identifying the physiological mechanisms underlying the benefits of NaHCO3 treatment in CKD. Gaining an understanding of these pathways may lead to the improved implementation of NaHCO3 as a therapy in CKD and perhaps other disease states.

A Comparative Review of Erythropoiesis Stimulating Agents

2008 ◽  
Vol 21 (6) ◽  
pp. 424-430
Author(s):  
Nicole L. Metzger ◽  
Kerry E. Francis ◽  
Stacy A. Voils
Keyword(s):  
Chronic Kidney Disease ◽  
Clinical Trials ◽  
Kidney Disease ◽  
Tumor Progression ◽  
Safety And Efficacy ◽  
Regulatory Issues ◽  
Erythropoiesis Stimulating Agents ◽  
Disease States ◽  
Comparative Review ◽  
The Us

Erythropoiesis stimulating agents have been used for more than a decade in patients with chronic kidney disease, malignancy, and other disease states where anemia is common. Recently, several clinical trials have questioned the safety and efficacy of these agents. Thrombosis and increase in tumor progression as well as a potential increase in mortality have been noted in some trials and have generated growing concern regarding whether these agents should remain on the US market. Subsequently, reimbursement from some payers for erythropoiesis stimulating agent administration has become somewhat restrictive. We address the pharmacology, pharmacokinetics, pharmacodynamics, safety, efficacy, and pharmacoeconomics of erythropoiesis stimulating agents as well as emerging regulatory issues pertaining to the administration of erythropoiesis stimulating agents.

Effect of coronavirus disease in patients with kidney disease in India

2020 ◽  
Vol 11 (SPL1) ◽  
pp. 1255-1259
Author(s):  
Shashi Prabha Singh ◽  
Preeti Sharma ◽  
Durgesh singh ◽  
Pradeep kumar ◽  
Rakesh Sharma ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Clinical Trials ◽  
Kidney Disease ◽  
Meta Analysis ◽  
Tertiary Care ◽  
Type Ii Diabetes Mellitus ◽  
Asymptomatic Infection ◽  
Type Ii ◽  
Cardiorespiratory Failure ◽  
Inflammatory State

Coronavirus disease 19 is a global pandemic which infects over millions of people worldwide in a limited time and changes the lifestyle, clinical spectrum lies from asymptomatic infection to pneumonitis with cardiorespiratory failure and finally death. Higher mortality occurs in senior and who are suffering from co-morbidities like chronic kidney disease, (HTN) hypertension, (DM TYPE II) diabetes mellitus or (CVD) cardiovascular diseases. However, rather than normal individuals, patients with chronic kidney disease (CKD) are under higher risk for infections. The chronic systemic inflammatory state is a significant cause for morbidity and mortality in CKD patients. The objective of this review is to discuss the pathogenesis of COVID-19 in CKD, changes observed in the immune system of CKD patients, COVID-19 infections risk in CKD and therapeutic approach of COVID-19 in CKD patients. From the standpoint of frequent renal co-morbidities in covid19 patients, renal complications were explored in covid19 patients received at level 2 tertiary care Santosh Hospital, Ghaziabad, U.P. Delhi-NCR India during March to August 2020 as per the protocol of Nephrology Society of India. Relevant clinical trials were reviewed in support. Meta-analysis and clinical trials are covered in this review study. Duplicate studies are not taken into account. The outcome of the studies shows that CKD patients are more prone to COVID-19. CKD patients are more likely infected with COVID-19 virus. Whereas in intensive care, CKD occurs more frequent than DM type II and CVD. So,COVID-19 pathogenesis in CKD patients, risk of COVID-19, immunologic changes and therapy COVID-19 in CKD can add support in the effective management of COVID-19.

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

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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