The Effect of High Animal Protein Intake on the Risk of Calcium Stone-Formation in the Urinary Tract

Robertson, William; Heyburn, P. J.; Hanes, F. A.; Swaminathan, R.

doi:10.1042/cs0570285

Cited by 207 publications

(85 citation statements)

References 11 publications

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“…High dietary animal protein intake decreases urinary pH (by increasing acid load) and increases urinary Ca 2ϩ excretion (38,39). An increase in urinary Ca 2ϩ predisposes individuals to formation of kidney stones (40). Administration of alkali in normal human subjects decreases urinary Ca 2ϩ excretion (41).…”

Section: Discussionmentioning

confidence: 99%

Mechanism and Molecular Determinant for Regulation of Rabbit Transient Receptor Potential Type 5 (TRPV5) Channel by Extracellular pH

Yeh

Sun

Lee

et al. 2003

Journal of Biological Chemistry

106

103

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The transient receptor potential type 5 (TRPV5) channel is present in kidney and intestine and important for transepithelial (re)absorption of calcium in these tissues. We report that in whole-cell patch clamp recording extracellular acidification inhibited rabbit TRPV5 with apparent pK a ϳ6.55. The two extracellular loops between the fifth and sixth transmembrane segments of TRPV5 presumably form part of the outer opening of the pore and likely are important in binding and regulation by external protons. We found that mutation of glutamate 522 to glutamine (E522Q) decreased the sensitivity of the channel to extracellular acidification. Mutations of other titratable amino acids within the two extracellular loops to non-titratable amino acids had no effect on pH sensitivity. Substitutions of aspartate or other titratable amino acids for glutamate 522 conferred an increase in pH sensitivity. The pH sensitivity mediated by glutamate 522 was independent of extracellular or intracellular Mg 2؉ . Single channel analysis revealed that extracellular acidification reduced single channel conductance as well as open probability of the wild type channel. In contrast to wild type channel, extracellular acidification did not reduce open probability for E522Q mutant. Methanethiosulfonate reagents inhibited the activity of glutamine 522 to cysteine mutant channel with a reaction rate constant approaching that with free thiols in solution, suggesting that glutamate 522 is located on the surface of the channel. These data suggest that glutamate 522 of the rabbit TRPV5 is a "pH sensor," and extracellular protons inhibit TRPV5 likely by altering conformation of the channel protein.

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Section: Discussionmentioning

confidence: 99%

Mechanism and Molecular Determinant for Regulation of Rabbit Transient Receptor Potential Type 5 (TRPV5) Channel by Extracellular pH

Yeh

Sun

Lee

et al. 2003

Journal of Biological Chemistry

106

103

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“…Excessive protein intake increases excretion of potentially lithogenic substances such as calcium and uric acid [99,100]. Reddy et al [101] noted that consumption of a high protein diet for six weeks was associated aciduria and urinary calcium and claimed that this constituted increased risk of stone formation in ten healthy subjects although none of the ten subjects developed renal stones.…”

Section: Dietary Protein and Kidney Stonesmentioning

confidence: 99%

Dietary Protein Intake and Renal Function

Martin¹,

Armstrong²,

Rodriguez³

2013

Clinical Nutrition

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Recent trends in weight loss diets have led to a substantial increase in protein intake by individuals. As a result, the safety of habitually consuming dietary protein in excess of recommended intakes has been questioned. In particular, there is concern that high protein intake may promote renal damage by chronically increasing glomerular pressure and hyperfiltration. There is, however, a serious question as to whether there is significant evidence to support this relationship in healthy individuals. In fact, some studies suggest that hyperfiltration, the purported mechanism for renal damage, is a normal adaptative mechanism that occurs in response to several physiological conditions. This paper reviews the available evidence that increased dietary protein intake is a health concern in terms of the potential to initiate or promote renal disease. While protein restriction may be appropriate for treatment of existing kidney disease, we find no significant evidence for a detrimental effect of high protein intakes on kidney function in healthy persons after centuries of a high protein Western diet.

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“…Previous studies examining the relationship between dietary protein and urinary oxalate excretion did not control dietary oxalate, a major limitation of these investigations [6][7][8][9][11][12][13][14]. Such dietary control is essential when urinary oxalate excretion is an endpoint in any investigation due to the important contribution that dietary oxalate makes to urinary oxalate excretion [27].…”

Section: Discussionmentioning

confidence: 99%

“…However, the impact of dietary protein on urinary oxalate excretion has not been clearly delineated. Some studies reported that urinary oxalate excretion increased with increased protein intake and decreased with protein restriction [6][7][8][9][10], whereas others noted no change [11][12][13][14]. A limitation of these studies is a lack of dietary oxalate control.…”

Section: Introductionmentioning

confidence: 99%

Increased Protein Intake on Controlled Oxalate Diets Does Not Increase Urinary Oxalate Excretion

Knight¹,

Easter²,

Neiberg³

et al. 2009

Journal of Urology

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High animal protein intake is a risk factor for calcium oxalate stone disease. The effect of dietary protein on the urinary excretion of calcium, acid and citrate is well established. However, its effect on oxalate excretion is unclear, due in part to an inadequate control of dietary oxalate intake in previous studies. This relationship warrants clarification due to the proposed important role of the metabolism of amino acids in endogenous oxalate synthesis. In this study, 11 normal subjects consumed controlled oxalate diets containing 0.6, 1.2 and 1.8 g protein/kg body weight/day. The analysis of 24 h urine collections confirmed that as protein intake increased, urinary calcium and glycolate increased and urinary pH and citrate decreased. The increased glycolate excretion was due in part to an increased hydroxyproline, but not glycolate consumption. Total daily urinary oxalate excretion did not change. When indexed to creatinine there was a small but significant decrease in oxalate excretion. This is most likely due to hyperfiltration. These results indicate that as dietary protein intake increases, the catabolism of diet-derived amino acids is not associated with an increased endogenous oxalate synthesis in normal subjects.

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The Effect of High Animal Protein Intake on the Risk of Calcium Stone-Formation in the Urinary Tract

Cited by 207 publications

References 11 publications

Mechanism and Molecular Determinant for Regulation of Rabbit Transient Receptor Potential Type 5 (TRPV5) Channel by Extracellular pH

Mechanism and Molecular Determinant for Regulation of Rabbit Transient Receptor Potential Type 5 (TRPV5) Channel by Extracellular pH

Dietary Protein Intake and Renal Function

Increased Protein Intake on Controlled Oxalate Diets Does Not Increase Urinary Oxalate Excretion

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