Evaluation of four animal models of intrarenal calcium deposition and assessment of the influence of dietary supplementation with essential fatty acids on calcification

Burgess, N; Reynolds, Tim; Williams, N. E.; Pathy, A.; Smith, Shawn J.

doi:10.1007/bf00393305

Cited by 24 publications

(9 citation statements)

References 18 publications

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“…103,104 Dietary supplementation with essential fatty acids reduced calcium glucanate-induced renal calcification. 105 Reduction in calcific deposits improved renal function. 104,105 The dietary calcium to phosphorus ratio appears to play a significant role in calcification, and female weanling rats are more susceptible to calcification than are mature females or weanling or mature males.…”

Section: Animal Model Studiesmentioning

confidence: 98%

“…105 Reduction in calcific deposits improved renal function. 104,105 The dietary calcium to phosphorus ratio appears to play a significant role in calcification, and female weanling rats are more susceptible to calcification than are mature females or weanling or mature males. 106 Diet-induced calcification is primarily seen in renal tubules of the corticomedullary junction.…”

Section: Animal Model Studiesmentioning

confidence: 98%

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Crystal-induced inflammation of the kidneys: results from human studies, animal models, and tissue-culture studies

2004

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Calcium oxalate (CaOx), calcium phosphate (CaP), and uric acid or urate are the most common crystals seen in the kidneys. Most of the crystals evoke an inflammatory response leading to fibrosis, loss of nephrons, and eventually to chronic renal failure. Of the three, CaOx monohydrate is the most reactive, whereas some forms of CaP do not evoke any discernible response. Reactive oxygen species are produced during the interactions between the crystals and renal cells and are responsible for the various cellular responses. CaOx crystals generally form in the renal tubules. Exposure of renal epithelial cells to CaOx crystals results in the increased synthesis of osteopontin, bikunin, heparan sulfate, monocyte chemoattractant protein 1 (MCP-1), and prostaglandin (PG) E2, which are known to participate in inflammatory processes and in extracellular matrix production. CaOx crystal deposition in rat kidneys also activates the renin-angiotensin system. Both Ox and CaOx crystals selectively activate p38 mitogen-activated protein kinase (MAPK) in exposed tubular cells. CaP crystals can form in the tubular lumen, tubular cells, or tubular basement membrane. Renal epithelial cells exposed to brushite crystals produce MCP-1. Basic CaP and calcium pyrophosphate dihydrate induce mitogenesis in fibroblasts, stimulate production of PGE2, and up-regulate the synthesis of metalloproteinases (MMP) while down-regulating the production of inhibitors of MMPs through activation of p42/44 MAPK. Deposition of urate crystals in the kidneys becomes associated with renal tubular atrophy, interstitial fibrosis, and development of inflammatory infiltrate. Renal epithelial cells exposed to uric acid crystals synthesize MCP-1 as well as PGE2. Monocytes or neutrophils exposed to urate crystals produce tumor necrosis factor alpha, interleukin-1 (IL-1), IL-6, and IL-8. Expression of IL-8 is mediated through extracellular signal-regulated kinase 1 (ERK-1)/ERK-2 and nuclear transcription factors activated protein 1 and nuclear factor kappabeta. Urate crystals also stimulate the macrophages to produce MMPs.

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Section: Animal Model Studiesmentioning

confidence: 98%

Section: Animal Model Studiesmentioning

confidence: 98%

Crystal-induced inflammation of the kidneys: results from human studies, animal models, and tissue-culture studies

2004

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“…50 Essential fatty acids Greenland Eskimos and coastal Japanese are reported to have a very low incidence of renal stone disease. 51 One theory to explain this ''immunity'' is that n-3 and n-6 polyunsaturated fatty acids affect the activity of cell membrane transporter proteins. 52 The administration of fish oil (n-3) and evening primrose oil (n-6) has been shown to have significant effects in rat models of nephrolithiasis.…”

Section: Vitamin Cmentioning

confidence: 99%

Best Practice No 181: Table 1

Reynolds

2005

J Clin Pathol

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Renal stones have afflicted humans for millennia but there is still no solution to this problem. This review discusses the laboratory and metabolic aspects of the clinical management of patients with renal stones, both primary and secondary in origin. First, non-pharmacological interventions such as increased fluid intake, decreased protein consumption, dietary changes in sodium, calcium, oxalate, potassium, purine, vitamins, and essential fatty acids are considered. Then specific pharmacological treatment to modify urine calcium, oxalate, urate, citrate, and acidity are considered. Finally, more unusual types of stone are examined.

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“…Fish oil and gamma-linolenic acid (glA), alone or combined, significantly reduced renal calcification, with a possible synergistic effect between the two 27 . epA could also limit induced abdominal aorta medial (but not iliac) calcification by lowering the expression of osteogenic markers and suppressing matrix metalloproteinase-9 activity 28 , although monoester epA plus lA increased renal and aortic calcification, while high dose epA given with antioxidant lipoic acid prevented calcification 29 .…”

Section: Animal Studies Ectopic Calcificationmentioning

confidence: 99%

Cardiovascular and Renal Calcification and Bone: A comparison of the effect of Dietary Fatty Acids

Nicoll¹,

Howard²,

Henein³

2015

ICFJ

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Cardiovascular (CV) and renal calcification is regularly found with osteoporosis and both are conditions of chronic inflammation and oxidative stress. Intake of dietary fatty acids is known to impact on the incidence of CV disease and bone loss but few studies have specifically looked at their impact on CV or renal calcification. this review found that although a very high total fat intake is likely to prove detrimental to both tissues and bone, particularly with low calcium intake, human studies often show mixed results, possibly because fatty acid intake shows a u-shaped dose/response curve, contrary to the expected linear relationship. Nevertheless, intake of fish and fish oil are generally found to protect against ectopic calcification and bone loss, with a low omega 6 to omega 3 ratio (preferably <5:1) proving critical. Fish intake of 3-4 servings a week was believed to be optimal. In arteries, the relationship between fish oil intake and other markers of sub-clinical atherosclerosis, such as intima-medial thickness, may be stronger than their relationship with arterial calcification. Any association with arterial calcification often lost significance after adjustment for CV risk factors, suggesting that fish oil may act principally by lowering risk factors and calling into question whether CV calcification is a condition of dyslipidaemia.

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Evaluation of four animal models of intrarenal calcium deposition and assessment of the influence of dietary supplementation with essential fatty acids on calcification

Cited by 24 publications

References 18 publications

Crystal-induced inflammation of the kidneys: results from human studies, animal models, and tissue-culture studies

Crystal-induced inflammation of the kidneys: results from human studies, animal models, and tissue-culture studies

Best Practice No 181: Table 1

Cardiovascular and Renal Calcification and Bone: A comparison of the effect of Dietary Fatty Acids

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