Estimation and Comparison of Serum Levels of Sodium, Potassium, Calcium and Phosphorus in Different Stages of Chronic Kidney Disease

Poudel, Bibek; Mittal, Ankush; Yadav, Binod Kumar; Sharma, Prakriti; Jha, Bharat; Raut, K B

doi:10.3126/nje.v1i5.6154

Cited by 4 publications

(4 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On biochemical level and in the same line with Nasir, 2013;Poudel et al, 2011), significant elevations of circulated urea, creatinine, BUN, and uric acid in AD treated animals are indicators of impaired kidney function. These data are in consistency with other studies (Ali et al, 2010;Saad, 2013;Saad et al, 2017c;2017d;Toson et al, 2014).…”

Section: Discussionmentioning

confidence: 70%

Hepato-toxic risk of gum arabic during adenine-induced renal toxicity prevention

2018

J App Pharm Sci

View full text Add to dashboard Cite

Objective: Lately, gum arabic (GA) is traditionally used in Middle East countries to ameliorate renal function of patients with chronic renal failure (CRF). This action is controversial and it is still experimentally under evaluation. We aimed to shed more light on the potential effects of GA administration to rats with adenine (AD)-induced CRF through investigating kidney and liver changes. Material and Methods: Rats were divided into four groups treated for consecutive 28 days. Control group was given normal food and water. GA group was given GA (15% w/v/day) in drinking water. AD group; received AD (50 mg/ kg/day, intraperitoneally). GA + AD group received both AD (50 mg/kg/day) and GA (15% w/v/day). On day 29, rats were sacrificed and serum creatinine, urea, uric acid, blood urea nitrogen (BUN), aspartate aminotransferase (AST), alanine aminotransferase (ALT), albumin, bilirubin, cholesterol levels, and renal/hepatic malondialdehyde (MDA), superoxide dismutase (SOD), and catalase were estimated. Kidney/liver histo-pathological studies were performed. Results: GA supplement efficiency in preventing AD-induced renal toxicity is clearly evident from histo-pathological examination and reduced urea, BUN, and creatinine levels. Also, it is proven that GA supplementation produces harmful effects on the liver as it increases ALT and AST levels. Conclusion:Liver function tests should be monitored in chronic kidney disease (CKD) patients who utilize GA supplement.

show abstract

Section: Discussionmentioning

confidence: 70%

Hepato-toxic risk of gum arabic during adenine-induced renal toxicity prevention

2018

J App Pharm Sci

View full text Add to dashboard Cite

show abstract

“…CsA has been shown to reduce bile flow in animal studies, which could explain why high doses cause hyperbilirubinemia [ 41 ]. Furthermore, it is rapidly metabolized in the liver and interacts with the cytochrome P450 system (CYP 3A4), making it vulnerable to severe drug–drug interactions [ 42 ]. In comparison, mice that were given UGT1A1 antisense morpholino oligonucleotide alone or in combination with CsA every third day had significantly higher serum UCB levels than CsA- and CsA + CH-treated mice, owing to increased total bilirubin and decreased conjugated bilirubin.…”

Section: Discussionmentioning

confidence: 99%

The Potential Protective Effect and Underlying Mechanisms of Physiological Unconjugated Hyperbilirubinemia Mediated by UGT1A1 Antisense Oligonucleotide Therapy in a Mouse Model of Cyclosporine A-Induced Chronic Kidney Disease

et al. 2022

View full text Add to dashboard Cite

Cyclosporine A (CSA) is an immunosuppressive drug that has improved transplant survival rates. However, its use is often limited because it is thought to be linked to the development of chronic kidney disease after kidney transplants. This study aimed to investigate the protective effects and underlying mechanisms of physiological unconjugated (UC) hyperbilirubinemia mediated by UGT1A1 antisense oligonucleotide in a mouse model of CsA-induced chronic kidney disease, and match these with that of chitosan (CH) as a natural chelator against kidney injury. In the current study, CsA-treated mice were given an intravenous injection of UGT1A1 antisense morpholino oligonucleotide (16 µg/kg) every third day for 14 days. In serum samples, bilirubin, creatinine, and urea were determined. Markers of oxidative stress, antioxidant activities, and mRNA expression of target genes PPAR-α, cFn, eNOS, NF-B, AT1-R, ETA-R, Kim-1, and NGAL were measured in the kidney tissues. Moreover, histopathological examinations were carried out on the kidney tissue. Physiological UC hyperbilirubinemia could be a promising protective strategy against CsA-induced kidney disease in transplant recipients. UGT1A1 antisense oligonucleotide-induced physiological UC hyperbilirubinemia serum significantly protected against CsA-induced kidney dysfunction. UCB acts as a signaling molecule that protects against kidney disease through different mechanisms, including antioxidant, anti-inflammatory, and hormonal action, by activating nuclear hormone receptors (PPAR-α). Moreover, it significantly downregulated mRNA expression of NF-kB, ETA-R, iNOS, AT1-R, cFn, Kim-1, and NGAL in the kidney tissue and alleviated CsA-induced kidney histological changes in CsA-treated mice.

show abstract

“…Impaired kidney function is reflected by the kidneys’ tubules ability to maintain plasma urea and creatinine clearance 32 . Kidney dysfunction was manifested by a significant elevation of serum urea and creatinine concentrations in adenine-treated animals at day 0 versus baseline (−10).…”

Section: Discussionmentioning

confidence: 99%

Endogenously elevated bilirubin modulates kidney function and protects from circulating oxidative stress in a rat model of adenine-induced kidney failure

Boon

Lam

Gopalan

et al. 2015

Sci Rep

View full text Add to dashboard Cite

Mildly elevated bilirubin is associated with a reduction in the presence and progression of chronic kidney disease and related mortality, which may be attributed to bilirubin’s antioxidant properties. This study investigated whether endogenously elevated bilirubin would protect against adenine-induced kidney damage in male hyperbilirubinaemic Gunn rats and littermate controls. Animals were orally administered adenine or methylcellulose solvent (vehicle) daily for 10 days and were then monitored for 28 days. Serum and urine were assessed throughout the protocol for parameters of kidney function and antioxidant/oxidative stress status and kidneys were harvested for histological examination upon completion of the study. Adenine-treated animals experienced weight-loss, polyuria and polydipsia; however, these effects were significantly attenuated in adenine-treated Gunn rats. No difference in the presence of dihydroadenine crystals, lymphocytic infiltration and fibrosis were noted in Gunn rat kidneys versus controls. However, plasma protein carbonyl and F2-isoprostane concentrations were significantly decreased in Gunn rats versus controls, with no change in urinary 8-oxo-7,8-dihydro-2′-deoxyguanosine or kidney tissue F2-isoprostane concentrations. These data indicated that endogenously elevated bilirubin specifically protects from systemic oxidative stress in the vascular compartment. These data may help to clarify the protective relationship between bilirubin, kidney function and cardiovascular mortality in clinical investigations.

show abstract

Estimation and Comparison of Serum Levels of Sodium, Potassium, Calcium and Phosphorus in Different Stages of Chronic Kidney Disease

Abstract: Background

Cited by 4 publications

References 31 publications

Hepato-toxic risk of gum arabic during adenine-induced renal toxicity prevention

Hepato-toxic risk of gum arabic during adenine-induced renal toxicity prevention

The Potential Protective Effect and Underlying Mechanisms of Physiological Unconjugated Hyperbilirubinemia Mediated by UGT1A1 Antisense Oligonucleotide Therapy in a Mouse Model of Cyclosporine A-Induced Chronic Kidney Disease

Endogenously elevated bilirubin modulates kidney function and protects from circulating oxidative stress in a rat model of adenine-induced kidney failure

Contact Info

Product

Resources

About