Acid–base status and progression of chronic kidney disease

2012 ◽  
Vol 21 (5) ◽  
pp. 552-556 ◽  
Author(s):  
Nimrit Goraya ◽  
Donald E. Wesson
2013 ◽  
Vol 33 (2) ◽  
pp. 229-235 ◽  
Author(s):  
Luciano H. Giovaninni ◽  
Marcia M. Kogika ◽  
Marcio D. Lustoza ◽  
Archivaldo Reche Junior ◽  
Vera A.B.F. Wirthl ◽  
...  

Chronic kidney disease (CKD) is frequently observed in cats and it is characterized as a multisystemic illness, caused by several underlying metabolic changes, and secondary renal hyperparathyroidism (SRHPT) is relatively common; usually it is associated with the progression of renal disease and poor prognosis. This study aimed at determining the frequency of SRHPT, and discussing possible mechanisms that could contribute to the development of SRHPT in cats at different stages of CKD through the evaluation of calcium and phosphorus metabolism, as well as acid-base status. Forty owned cats with CKD were included and divided into three groups, according to the stages of the disease, classified according to the International Renal Interest Society (IRIS) as Stage II (n=12), Stage III (n=22) and Stage IV (n=6). Control group was composed of 21 clinically healthy cats. Increased serum intact parathyroid hormone (iPTH) concentrations were observed in most CKD cats in all stages, and mainly in Stage IV, which hyperphosphatemia and ionized hypocalcemia were detected and associated to the cause for the development of SRHPT. In Stages II and III, however, ionized hypercalcemia was noticed suggesting that the development of SRHPT might be associated with other factors, and metabolic acidosis could be involved to the increase of serum ionized calcium. Therefore, causes for the development of SRHPT seem to be multifactorial and they must be further investigated, mainly in the early stages of CKD in cats, as hyperphosphatemia and ionized hypocalcemia could not be the only factors involved.


2021 ◽  
Vol 99 (1) ◽  
pp. 208-217 ◽  
Author(s):  
Fabiola G. Gianella ◽  
Victor E. Prado ◽  
John R. Poindexter ◽  
Beverley Adams-Huet ◽  
Xilong Li ◽  
...  

2009 ◽  
Vol 19 (2) ◽  
pp. 178-182 ◽  
Author(s):  
Viviane O. Leal ◽  
Alvimar G. Delgado ◽  
Maurilo Leite ◽  
William E. Mitch ◽  
Denise Mafra

2020 ◽  
Vol 319 (6) ◽  
pp. F1090-F1104
Author(s):  
Elinor C. Mannon ◽  
Paul M. O’Connor

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.


2010 ◽  
Vol 4 (3) ◽  
pp. 367-372
Author(s):  
James C. M. Chan

Abstract Background and objectives: This review focuses on three areas, basic acid-base physiology especially concerning hydrogen ion balance, development of acidosis in chronic kidney disease (CKD), and the consequences of acidosis. We highlight what is well established, what is less certain, and what is unknown. Method and results: The literature on acidosis in CKD were searched from 2004 to 2010 utilizing PubMed, Google Scholar, and Ovid to augment the classic work on acid base physiology over the past three decades. The original research in endogenous acid production and net acid excretion were reviewed. Touching upon the development of metabolic acidosis in CKD, we focused on the consequences of chronic metabolic acidosis on growth and other important variables. Finally, we recognize the significant issue of patients’ medical non-compliance and presented treatment strategy to counter this problem. Conclusion: The correction of acidosis in chronic kidney disease needs no advocacy. The case is made conclusively. Patient non-compliance because of the medication that needs to be taken several times a day is a problem, requiring due diligence.


2021 ◽  
Vol 39 (Supplement 1) ◽  
pp. e298
Author(s):  
Giuseppe Mule’ ◽  
Caterina Carollo ◽  
Alessandra Sorce ◽  
Marta Giambrone ◽  
Alida Ferrara ◽  
...  

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