Effect of Hyperlipidemia on Glomerular Sclerosis in Unilateral Nephrectomized Rats

Miyata, Junichi; Takebayashi, Shigeo

doi:10.1111/j.1440-1827.1987.tb02265.x

Cited by 6 publications

(2 citation statements)

References 14 publications

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“…In rats fed on different oils, or butter, decline in glomerular fi ltration rate (GFR) was found to be greatest in those receiving butter, perhaps because of a higher percentage of saturated fat. It has been convincingly demonstrated that rats with chronic hyperlipidemia and hypercholesterolemia develop glomerulosclerosis in kidneys (51,55,53). Hyperlipidemia was also supposed to be associated with chronic tubulointerstitial damage (15,56).…”

Section: Discussionmentioning

confidence: 99%

High cholesterol diet leads to oxidant load and peroxidation in the rabbit kidney tissue

Öztürk¹,

Özer²,

Billur³

et al. 2016

BLL

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Section: Discussionmentioning

confidence: 99%

High cholesterol diet leads to oxidant load and peroxidation in the rabbit kidney tissue

Öztürk¹,

Özer²,

Billur³

et al. 2016

BLL

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“…It has been convincingly demonstrated that rats with chronic hyperlipidemia and hypercholesterolemia develop glomerulosclerosis in kidneys without immune complex disease (14,34,45,53). The present study confirms these data.…”

Section: Discussionmentioning

confidence: 99%

Oxidant stress in hyperlipidemia-induced renal damage

Scheuer

Gwinner

Hohbach

et al. 2000

American Journal of Physiology-Renal Physiology

137

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Hyperlipoproteinemia can aggravate glomerulosclerosis and chronic tubulointerstitial (ti) damage in kidneys without primary immunologic disease. We evaluated whether the effect of hyperlipidemia on progression of renal damage differed between kidneys without preexisting glomerular disease and kidneys with mesangioproliferative glomerulonephritis and whether the renal actions of hyperlipidemia were dependent on oxidant-antioxidant balance. Hyperlipidemia was induced by high-fat and high-cholesterol diet in uninephrectomized rats. In rats without glomerulonephritis, hyperlipidemia led to a rise in glomerular and ti generation of reactive oxygen species (ROS). Oxygen radicals were mainly generated by enhanced xanthine oxidoreductase (XO), which rose with protein concentration and activity during hyperlipidemia; concurrently, glomerulosclerosis and chronic ti injury were noticed during hyperlipidemia [ti damage (% of total tubulointerstitium (TI) after 150 days): normolipidemia 0.1 +/- 0% vs. hyperlipidemia 3.4 +/- 0. 9%; P < 0.05]. In mesangioproliferative Thy-1 nephritis, ti injury was significantly accelerated by hyperlipidemia (ti damage after 150 days: normolipidemic Thy-1 nephritis 2.5 +/- 0.6% vs. hyperlipidemic Thy-1 nephritis 12.5 +/- 3.1%; P < 0.05). Antioxidant enzyme activities decreased and XO activity rose markedly in the TI (XO activity in TI after 150 days: normolipidemic Thy-1 nephritis 2.2 +/- 0.5 vs. hyperlipidemic Thy-1 nephritis 4.5 +/- 0.7 cpm/microg protein; P < 0.05). In hyperlipidemic Thy-1 nephritis rats, which had a higher urinary protein excretion than normolipidemic rats, hypochlorite-modified proteins, an indirect measure for enhanced myeloperoxidase activity, were detected in renal tissue and in urine, respectively. During hyperlipidemia, chronic damage increased in renal TI. Enhanced generation of ROS, rise in oxidant enzyme activity, and generation of hypochlorite-modified proteins in renal tissue and urine were noticed. These data suggest that oxidant stress contributed to the deleterious effects of hyperlipidemia on the renal TI.

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Arterial hypertension and hyperlipidemia as determinants of glomerulosclerosis

1993

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Arterial hypertension is a dominant pathogenetic factor for glomerulosclerosis. Nevertheless metabolic factors such as hyper- or dyslipoproteinemia may significantly modify and accelerate the process of glomerular scarring. Hyperlipidemia and lipoprotein abnormalities are often encountered in patients with nephrotic syndrome and chronic renal disease. Although the significance of lipid deposition in renal tissue and the role of lipoproteins in the pathogenesis of renal disease in man has not yet been clearly defined, experimental and clinical data indicate a damaging effect of disturbed lipid metabolism on the kidney. In humans glomerular lipid deposition is observed in several genetic diseases, including lecithin-cholesterol acyltransferase activity deficiency. Studies on animals with reduced renal mass, diabetes mellitus or arterial hypertension have shown that hypercholesterolemia increases the incidence of glomerulosclerosis. Especially the interaction of arterial hypertension and dyslipoproteinemia leads to a rapid and pronounced development of glomerulosclerosis. As most of these studies have been performed in the rat, which has a different lipoprotein profile than man, these results should be carefully interpreted with regard to their relevance for humans. In vitro cell culture studies on human glomerular cells have provided insight into the possible cellular mechanisms of lipid-induced glomerular damage. Apoprotein E containing lipoproteins that are pathologically elevated in many renal diseases are avidly taken up by human glomerular cells. Mesangial cells seem to play a central role in the initiation of glomerulosclerosis by proliferation and production of excess extracellular matrix. Lipoproteins are able to stimulate DNA synthesis in these cells and increase the synthesis of mitogens and matrix proteins. The pathogenetic role of modified, oxidized lipoproteins has not yet been elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effect of Hyperlipidemia on Glomerular Sclerosis in Unilateral Nephrectomized Rats

Cited by 6 publications

References 14 publications

High cholesterol diet leads to oxidant load and peroxidation in the rabbit kidney tissue

High cholesterol diet leads to oxidant load and peroxidation in the rabbit kidney tissue

Oxidant stress in hyperlipidemia-induced renal damage

Arterial hypertension and hyperlipidemia as determinants of glomerulosclerosis

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