ArticleBMC nephrology2012
Effects of a high-sodium diet on renal tubule Ca2+ transporter and claudin expression in Wistar-Kyoto rats.
Article in BMC nephrology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Unravelling the Complex Relationship between Diet and Nephrolithiasis: The Role of Nutrigenomics and Nutrigenetics.Nutrients · 2022Pooled it
- Defining the potential role of the mineralocorticoid receptor in musculoskeletal health and bone crosstalk with other tissues.The Journal of endocrinology · 2026Review
- Strategies for preventing bone loss in populations with insufficient calcium and vitamin D intake.Nutrition research and practice · 2025Review
- The importance of kidney calcium handling in the homeostasis of extracellular fluid calcium.Pflugers Archiv : European journal of physiology · 2022Review
- The impact of excessive salt intake on human health.Nature reviews. Nephrology · 2022Review
- Experimental rat model for acute tubular injury induced by high water hardness and high water fluoride: efficacy of primary preventive intervention by distilled water administration.BMC nephrology · 2020Article
- Effects of Doenjang, a Traditional Korean Soybean Paste, with High-Salt Diet on Blood Pressure in Sprague-Dawley Rats.Nutrients · 2019Article
- The Demographic Diversity of Food Intake and Prevalence of Kidney Stone Diseases in the Indian Continent.Foods (Basel, Switzerland) · 2019Review
- Loss-of-function mutations of SCN10A encoding NaScientific reports · 2018Article
- Activation of angiotensin II type 1 receptors increases DHypertension research : official journal of the Japanese Society of Hypertension · 2017Article
- Review
- The role of calbindin-D28k on renal calcium and magnesium handling during treatment with loop and thiazide diuretics.American journal of physiology. Renal physiology · 2016Article
- Effects of renal Na+/Ca2+ exchanger 1 inhibitor (SEA0400) treatment on electrolytes, renal function and hemodynamics in rats.Clinical and experimental nephrology · 2015Article
- Article
- Monosodium glutamate (MSG) consumption is associated with urolithiasis and urinary tract obstruction in rats.PloS one · 2013Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUrinary Ca2+ excretion increases with dietary NaCl. NaCl-induced calciuria may be associated with hypertension, urinary stone formation and osteoporosis, but its mechanism and long-term effects are not fully understood. This study examined alterations in the expressions of renal Ca2+ transporters, channels and claudins upon salt loading to better understand the mechanism of salt-induced urinary Ca2+ loss.
methodsEight-week old Wistar-Kyoto rats were fed either 0.3% or 8% NaCl diet for 8 weeks. Renal cortical expressions of Na+/Ca2+ exchanger 1 (NCX1), Ca2+ pump (PCMA1b), Ca2+ channel (TRPV5), calbindin-D28k, and claudins (CLDN-2, -7, -8, -16 and -19) were analyzed by quantitative PCR, western blot and/or immunohistochemistry.
resultsFractional excretion of Ca2+ increased 6.0 fold with high-salt diet. Renal cortical claudin-2 protein decreased by approximately 20% with decreased immunological staining on tissue sections. Claudin-16 and -19 expressions were not altered. Renal cortical TRPV5, calbindin-D28k and NCX1 expressions increased 1.6, 1.5 and 1.2 fold, respectively.
conclusionsChronic high-salt diet decreased claudin-2 protein and increased renal TRPV5, calbindin-D28k, and NCX1. Salt loading is known to reduce the proximal tubular reabsorption of both Na+ and Ca2+. The reduction in claudin-2 protein expression may be partly responsible for the reduced Ca2+ reabsorption in this segment. The concerted upregulation of more distal Ca2+-transporting molecules may be a physiological response to curtail the loss of Ca2+, although the magnitude of compensation does not seem adequate to bring the urinary Ca2+ excretion down to that of the normal-diet group.
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