全部 标题 作者
关键词 摘要


Moderately Decreased Dietary Salt Intake Suppresses the Progression of Renal Insufficiency in Rats with 5/6 Nephrectomy

DOI: 10.1155/2014/701487

Full-Text   Cite this paper   Add to My Lib

Abstract:

Aim. Up to now, an appropriate salt intake in renal insufficiency has not been clearly determined. We hypothesize that even a moderate decrease in salt intake may affect functional and morphologic response of the rat remnant kidney after 5/6 nephrectomy. Methods. Subtotal nephrectomy was performed in 77 inbred 12 week-old-female AVN Wistar rats. The two groups of rats were fed either a standard or a low salt diet. Median of salt intake was 14.6 and 10.4?mg/100?g/24?h in the two groups. Results. Ten weeks after ablation, the remnant kidney parenchyma wet weight was 0.66 ± 0.16?g/100?g of body weight and 0.56 ± 0.11?g/100?g of body weight () in rats with a standard and low salt diet, respectively. In these two groups, systolic blood pressure was 151 ± 29 versus 126 ± 21?mmHg (), serum creatinine levels were 164 ± 84 versus 106 ± 29?μmol/L (), proteinuria was 84 ± 37 versus 83 ± 40?mg/100?g/24?h (N.S.), and the glomerular injury score was 2.06 ± 0.49 versus 1.43 ± 0.62 (), respectively. Conclusion. Moderately decreased salt intake slowed down the development of ablation nephropathy in AVN inbred strain of rats. 1. Introduction Ablation of 5/6 (83%) of renal parenchyma in rats is an experimental model of chronic renal failure. Remnant “intact” nephrons respond by increasing single nephron filtration rate and with an impaired regulation of inflammatory mediators production. Later, the systemic hypertension and proteinuria develop. The final fatal consequence is the remnant glomeruli sclerosis, tubular atrophy and interstitial sclerosis (i.e., ablation nephropathy), and renal failure. This process can be reduced by a low protein diet and/or angiotensin converting enzyme inhibitors administration [1] or by the early kidney transplantation [2]. It is well known that low salt intake decreases systemic blood pressure in experimental animals and men [3–7] as well as the incidence of cardiovascular accidents [8]. Low salt intake suppresses asymmetric dimethylarginine (ADMA) formation and therefore nitric oxide (NO) production and downregulates the activity of platelet-derived growth factor (PDGF), interleukin-1 (IL-1), and other proinflammatory cytokines. Consequently, the endothelial function may be modified [8–11] and therefore atherosclerosis and cardiovascular and renal damages reduced [7]. Low salt intake also decreases proximal tubular epithelia hypertrophy [12–14]. In hemodialyzed patients with severe hypertension, low salt intake (5?g/24?h) caused a decrease in blood pressure due to the decrease in total peripheral resistance [7]. The normotension persisted

References

[1]  Z. Krivosíkova, K. Sebekova, V. Spustova, I. Lajdova, and R. Dzurik, “Enalapril in subantihypertensive dosage attenuates kidney proliferation and functional recovery in normotensive ablation nephropathy of the rat,” Physiological Research, vol. 48, no. 6, pp. 429–435, 1999.
[2]  P. Rossmann, I. Ríha, K. Matousovic, M. Bohdanecka, and A. Buckovsky, “Experimental ablation nephropathy: fine structure, morphometry, cell membrane epitopes, glomerular polyanion and effect of subsequent transplantation,” Pathology—Research and Practice, vol. 186, no. 4, pp. 491–506, 1990.
[3]  T. H. Hostetter, T. W. Meyer, H. G. Rennke, and B. M. Brenner, “Chronic effects of dietary protein in the rat with intact and reduced renal mass,” Kidney International, vol. 30, no. 4, pp. 509–517, 1986.
[4]  J. M. Geleijnse, F. J. Kok, and D. E. Grobbee, “Blood pressure response to changes in sodium and potassium intake: a metaregression analysis of randomised trials,” Journal of Human Hypertension, vol. 17, no. 7, pp. 471–480, 2003.
[5]  P. Ylitalo, R. Hepp, and P. Oster, “Effects of varying sodium intake on blood pressure and renin angiotensin system in subtotally nephrectomized rats,” Journal of Laboratory and Clinical Medicine, vol. 88, no. 5, pp. 807–816, 1976.
[6]  G. A. MacGregor, N. D. Markandu, G. A. Sagnella, D. R. J. Singer, and F. P. Cappuccio, “Double-blind study of three sodium intakes and long-term effects of sodium restriction in essential hypertension,” The Lancet, vol. 2, no. 8674, pp. 1244–1247, 1989.
[7]  S. Shaldon and J. Vienken, “The long forgotten salt factor and the benefits of using a 5-g-salt-restricted diet in all ESRD patients,” Nephrology Dialysis Transplantation, vol. 23, no. 7, pp. 2118–2120, 2008.
[8]  B. D. Dickinson and S. Havas, “Reducing the population burden of cardiovascular disease by reducing sodium intake: a report of the council on science and public health,” Archives of Internal Medicine, vol. 167, no. 14, pp. 1460–1468, 2007.
[9]  C. Jones-Burton, S. I. Mishra, J. C. Fink et al., “An in-depth review of the evidence linking dietary salt intake and progression of chronic kidney disease,” The American Journal of Nephrology, vol. 26, no. 3, pp. 268–275, 2006.
[10]  C. Zoccali and F. Mallamaci, “The salt epidemic: old and new concerns,” Nutrition, Metabolism and Cardiovascular Diseases, vol. 10, no. 3, pp. 168–171, 2000.
[11]  P. W. Sanders, “Salt intake, endothelial cell signaling, and progression of kidney disease,” Hypertension, vol. 43, no. 2, pp. 142–146, 2004.
[12]  L. D. Dworkin, J. A. Benstein, E. Tolbert, and H. D. Feiner, “Salt restriction inhibits renal growth and stabilizes injury in rats with established renal disease,” Journal of the American Society of Nephrology, vol. 7, no. 3, pp. 437–442, 1996.
[13]  S. Kuriyama, H. Tomonari, Y. Ohtsuka, H. Yamagishi, I. Ohkido, and T. Hosoya, “Salt intake and the progression of chronic renal diseases,” Nippon Jinzo Gakkai Shi, vol. 45, no. 8, pp. 751–758, 2003.
[14]  K. Okada and K. Matsumoto, “Effect of dietary salt restriction on tubular hypertrophy in rats with early-stage chronic renal failure,” Scandinavian Journal of Urology and Nephrology, vol. 38, no. 4, pp. 326–331, 2004.
[15]  E. Ritz, N. Koleganova, and G. Piecha, “Role of sodium intake in the progression of chronic kidney disease,” Journal of Renal Nutrition, vol. 19, no. 1, pp. 61–62, 2009.
[16]  E. Ritz and O. Mehls, “Salt restriction in kidney disease—a missed therapeutic opportunity?” Pediatric Nephrology, vol. 24, no. 1, pp. 9–17, 2009.
[17]  J. Titze and E. Ritz, “Salt and its effect on blood pressure and target organ damage: new pieces in an old puzzle,” Journal of Nephrology, vol. 22, no. 2, pp. 177–189, 2009.
[18]  D. S. Lax, J. A. Benstein, E. Tolbert, and L. D. Dworkin, “Effects of salt restriction on renal growth and glomerular injury in rats with remnant kidneys,” Kidney International, vol. 41, no. 6, pp. 1527–1534, 1992.
[19]  C. Kitiyakara, T. Chabrashvili, Y. Chen, et al., “Salt intake, oxidative stress, and renal expression of NADPH oxidase and superoxide dismutase,” Journal of the American Society of Nephrology, vol. 14, no. 11, pp. 2775–2782, 2003.
[20]  C. Chatziantoniou and J.-C. Dussaule, “Is kidney injury a reversible process?” Current Opinion in Nephrology and Hypertension, vol. 17, no. 1, pp. 76–81, 2008.
[21]  C. H. Espinel, “The influence of salt intake on the metabolic acidosis of chronic renal failure,” Journal of Clinical Investigation, vol. 56, no. 2, pp. 286–291, 1975.
[22]  P. A. Stewart, “Modern quantitative acid-base chemistry,” Canadian Journal of Physiology and Pharmacology, vol. 61, no. 12, pp. 1444–1461, 1983.
[23]  E. Matyas, K. Jeitler, K. Horvath et al., “Benefit assessment of salt reduction in patients with hypertension: systematic overview,” Journal of Hypertension, vol. 29, no. 5, pp. 821–828, 2011.
[24]  E. Ritz, “Salt and hypertension,” Nephrology, vol. 15, supplement 2, pp. 49–52, 2010.
[25]  M. H. Alderman, “Dietary sodium and cardiovascular health in hypertensive patients: the case against universal sodium restriction,” Journal of the American Society of Nephrology, vol. 15, supplement 1, pp. S47–S50, 2004.
[26]  T. F. Antonios and G. A. MacGregor, “Salt—more adverse effects,” The Lancet, vol. 348, no. 9022, pp. 250–251, 1996.
[27]  J. A. Krikken, G. U. Laverman, and G. Navis, “Benefits of dietary sodium restriction in the management of chronic kidney disease,” Current Opinion in Nephrology and Hypertension, vol. 18, no. 6, pp. 531–538, 2009.
[28]  M. R. Weir, D. R. Dengel, M. T. Behrens, and A. P. Goldberg, “Salt-induced increases in systolic blood pressure affect renal hemodynamics and proteinuria,” Hypertension, vol. 25, no. 6, pp. 1339–1344, 1995.
[29]  E. Ritz, R. Dikow, C. Morath, and V. Schwenger, “Salt—a potential “uremic toxin”?” Blood Purification, vol. 24, no. 1, pp. 63–66, 2006.
[30]  G. K?kény, Z. Németh, M. Godó, and P. Hamar, “The Rowett rat strain is resistant to renal fibrosis,” Nephrology Dialysis Transplantation, vol. 25, no. 5, pp. 1458–1462, 2010.

Full-Text

comments powered by Disqus