Kidney dysfunction in the arthritic rat

DiJoseph, John F.; Walter, T. L.; Hartman, David S.; Carlson, Richard P.

doi:10.1016/0192-0561(93)90011-m

Cited by 8 publications

(5 citation statements)

References 10 publications

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“…Both plasma creatinine (Perrone et al, 1992) and BUN (Schnellmann, 2001) reflect the glomerular filtration rate. Our observation in Pre-AA rat model is consistent with that reported for the full adjuvant arthritis (DiJoseph et al, 1993). This lends support to the suggestion (Ling and Jamali, 2005) that these types of experiments can be carried out before the development of the full adjuvant arthritis and its associated pain and stress.…”

Section: Discussionsupporting

confidence: 94%

Effect of inflammation on kidney function and pharmacokinetics of COX‐2 selective nonsteroidal anti‐inflammatory drugs rofecoxib and meloxicam

Harirforoosh

Jamali

2008

J of Applied Toxicology

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Chronic arthritis adversely affects glomerular function and nonsteroidal anti-inflammatory drugs (NSAIDs) reduce electrolyte urinary excretion. In addition, both acute and chronic inflammations may alter clearance of drugs. We studied (a) the effects of inflammation on the renal function and pharmacokinetics of rofecoxib and meloxicam; (b) whether inflammation could exacerbate reduced electrolytes excretion changes observed with NSAIDs; and (c) the influence of inflammation on distribution of these drugs into the kidney. Single oral doses of rofecoxib (10 mg kg(-1)), meloxicam (3 mg kg(-1)) or placebo were administered to normal or pre-adjuvant arthritic rats. Blood and urine samples were collected for the measurement of plasma nitrite, BUN and creatinine. The urinary excretion of sodium and potassium was also determined. Nitrite, BUN and plasma creatinine were increased starting on day 9 in the groups with inflammation. Sodium and potassium excretion rates were not affected by inflammation. Meloxicam did not alter the electrolyte excretion in any of the groups. Rofecoxib significantly decreased sodium and potassium excretion in normal rats and potassium excretion in inflamed rats. Inflammation significantly increased plasma concentrations of rofecoxib, but not meloxicam. The ratios of the kidney:plasma concentrations were not significantly altered by inflammation following either drug. Inflammation altered kidney function, demonstrated by increases in BUN and plasma creatinine. However, it did not influence the urinary electrolytes excretion. Since we have observed similar patterns of the effect of NSAIDs on kidney under healthy and inflammatory conditions, one may conclude that inflammation does not exacerbate the adverse effect.

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Section: Discussionsupporting

confidence: 94%

Effect of inflammation on kidney function and pharmacokinetics of COX‐2 selective nonsteroidal anti‐inflammatory drugs rofecoxib and meloxicam

Harirforoosh

Jamali

2008

J of Applied Toxicology

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“…As expected, injection of M. butyricum induced joint swelling [51] and leukocytosis with neutrophilia [50][51][52]. Whereas the effective dosage for treatment of joint pain by the Unani system may exceed amounts normally consumed in a typical diet, the effect of boron on arthritis in the present study cannot be considered pharmacologic, because the total amount of boron in the boron supplemented diet (2 mg B/kg) was only one-sixth of that typically present in commercial rodent chow (∼13.0 mg B/kg) [8].…”

Section: Findings and Discussionsupporting

confidence: 50%

“…Adjuvant arthritis is a well-recognized model of rheumatoid arthritis in humans because of the considerable overlap of clinical and pathologic features of each [50,51]. As expected, injection of M. butyricum induced joint swelling [51] and leukocytosis with neutrophilia [50][51][52].…”

Section: Findings and Discussionmentioning

confidence: 97%

Dietary boron as a physiological regulator of the normal inflammatory response: A review and current research progress

Hunt

Idso

1999

J. Trace Elem. Exp. Med.

145

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“…The constant levels of plasma and urinary creatinine, as well as urinary a 1 -m, indicated that the kidney functions were intact throughout the period covered by our study. It has been shown that adjuvant-induced experimental arthritis in rats leads to kidney dysfunction and abnormal histopathology of the organs in rats [42]. In contrast, our results indicate that CII-induced arthritis yields an inflammation without secondary effects on the kidneys, which is of importance when studying protein metabolism during arthritis.…”

Section: Discussionmentioning

confidence: 46%

α₁‐Microglobulin and Bikunin in Rats with Collagen II‐Induced Arthritis: Plasma Levels and Liver mRNA Content

et al. 1997

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Falkenberg C, Blom A, Fries E, Ekström G, Särnstrand B, Salier J-P, Å kerström B. a 1 -Microglobulin and Bikunin in Rats with Collagen II-Induced Arthritis: Plasma Levels and Liver mRNA Content. Scand J Immunol 1997;46:122-128 The plasma proteins a 1 -microglobulin (a 1 -m) and bikunin are synthesized in the liver as a common precursor which is cleaved just before secretion. Half of plasma a 1 -m is covalently linked to fibronectin and a 1 -inhibitor-3, and more than 95% of bikunin is part of pre-a-inhibitor, inter-a-inhibitor and related large molecules. Both a 1 -m and bikunin have been shown to be involved in inflammation, but the regulation of their synthesis is not clear. The authors have measured the plasma and urinary concentrations of a 1 -m and bikunin as well as their hepatic mRNA levels in rats during the development of collagen-induced arthritis. Also, the plasma concentrations of acknowledged acute-phase proteins were measured. The results suggested a biphasic inflammatory reaction: an early response after 1 week, represented by an elevated fibronectin level; and a late response after 3 weeks, represented by elevated a 1 -acid glycoprotein and decreased albumin and a 1 -inhibitor-3 levels. The a 1 -m-bikunin mRNA content in liver was slightly reduced after 1 week and elevated after 3 weeks, but the total concentrations of free and bound a 1 -m and bikunin in plasma were unchanged. The free bikunin fraction as well as the fibronectin/a 1 -m complex in plasma, however, were elevated after 1 week. Urinary bikunin levels were also elevated after 1 week, whereas urinary a 1 -m levels remained unchanged. The results thus suggest that free bikunin in plasma is increased and excreted in the urine at an early stage during the development of collagen-induced arthritis. Later, when the synthesis rate of a 1 -m-bikunin is elevated, both proteins are most likely directed to other locations in the body.

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Kidney dysfunction in the arthritic rat

Cited by 8 publications

References 10 publications

Effect of inflammation on kidney function and pharmacokinetics of COX‐2 selective nonsteroidal anti‐inflammatory drugs rofecoxib and meloxicam

Effect of inflammation on kidney function and pharmacokinetics of COX‐2 selective nonsteroidal anti‐inflammatory drugs rofecoxib and meloxicam

Dietary boron as a physiological regulator of the normal inflammatory response: A review and current research progress

α₁‐Microglobulin and Bikunin in Rats with Collagen II‐Induced Arthritis: Plasma Levels and Liver mRNA Content

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Kidney dysfunction in the arthritic rat

Cited by 8 publications

References 10 publications

Effect of inflammation on kidney function and pharmacokinetics of COX‐2 selective nonsteroidal anti‐inflammatory drugs rofecoxib and meloxicam

Effect of inflammation on kidney function and pharmacokinetics of COX‐2 selective nonsteroidal anti‐inflammatory drugs rofecoxib and meloxicam

Dietary boron as a physiological regulator of the normal inflammatory response: A review and current research progress

α1‐Microglobulin and Bikunin in Rats with Collagen II‐Induced Arthritis: Plasma Levels and Liver mRNA Content

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Product

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α₁‐Microglobulin and Bikunin in Rats with Collagen II‐Induced Arthritis: Plasma Levels and Liver mRNA Content