Acute effects of moderate dietary protein restriction in patients with idiopathic hypercalciuria and calcium nephrolithiasis

Giannini, Sandro; Nobile, M.; Sartori, Leonardo; Carbonare, Luca Dalle; Ciuffreda, Matteo; Corrò, Paolo; D’Angelo, Angela; Calò, Lorenzo A.; Crepaldi, Gaetano

doi:10.1093/ajcn/69.2.267

Cited by 97 publications

(52 citation statements)

References 28 publications

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“…The main responsible mechanism for these effects is the acid load produced by proteins, especially by those rich in sulfur-containing amino acids (11). Accordingly, it was demonstrated that sulfate excretion and some markers of protein intake, such as urinary or serum urea, well correlate with bone turnover markers and density (25,27,28,61). We also found that a moderate protein restriction was accompanied by a proportional reduction in calcium excretion and bone turnover markers in patients with nephrolithiasis and PH (61).…”

Section: Pathophysiologymentioning

confidence: 52%

“…Accordingly, it was demonstrated that sulfate excretion and some markers of protein intake, such as urinary or serum urea, well correlate with bone turnover markers and density (25,27,28,61). We also found that a moderate protein restriction was accompanied by a proportional reduction in calcium excretion and bone turnover markers in patients with nephrolithiasis and PH (61). Since dietary protein excess was repeatedly reported in hypercalciuric stone formers (11,61) and hypersensitivity to protein effects on bone was also suggested, normalization of protein intake is highly recommended in hypercalciuric patients.…”

Section: Pathophysiologymentioning

confidence: 99%

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Bone Disease in Primary Hypercalciuria

Giannini

Nobile

Sella

et al. 2005

Critical Reviews in Clinical Laboratory Sciences

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SummaryPrimary Hypercalciuria (PH) is very often accompanied with some degrees of bone demineralization. The most frequent clinical condition in which this association has been observed is calcium nephrolithiasis. In patients affected by this disorder bone density is very frequently low and increased susceptibility to fragility fractures is reported. The very poor definition of this bone disease from a histomorphometric point of view is a crucial aspect. At present, the most common finding seems to be a low bone turnover condition. Many factors are involved in the complex relationships between bone loss and PH. Since bone loss was mainly reported in patients with fasting hypercalciuria, a primary alteration in bone metabolism was proposed as a cause of both hypercalciuria and bone demineralization. This hypothesis was strengthened by the observation that some bone resorbing-cytokines, such as IL-1, IL-6, and TNF-α α are high in hypercalciuric patients. The effect of an excessive response to the acid load induced by dietary protein intake seems an additional factor explaining a primitive alteration of bone. The intestine plays a major role in the clinical course of bone disease in PH. Patients with absorptive hypercalciuria less frequently show bone disease and a reduction in dietary calcium greatly increases the probability of bone loss in PH subjects. It has recently been reported that greater bone loss is associated with a larger increase in intestinal calcium absorption in PH patients. Considering the absence of PTH alterations, it was proposed that this is not a compensatory phenomenon, but probably the marker of disturbed cell calcium transport, involving both intestinal and bone tissues. While renal hypercalciuria is rather uncommon, the kidney still seems to play a role in the pathogenesis of bone loss of PH patients, possibly via the effect of mild to moderate urinary phosphate loss with secondary hypophosphatemia. In conclusion, bone loss is very common in PH patients. Even if most of the factors involved in this process have been identified, many aspects of this intriguing clinical condition remain to be elucidated.

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Section: Pathophysiologymentioning

confidence: 52%

Section: Pathophysiologymentioning

confidence: 99%

Bone Disease in Primary Hypercalciuria

Giannini

Nobile

Sella

et al. 2005

Critical Reviews in Clinical Laboratory Sciences

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“…However, only a handful of studies have reported dietary patterns (8,9,11,35). The present pattern of low protein intake by post-BS patients, evidenced by the food recalls and the lower urea, uric acid, and creatinine excretion, may have interfered with our rates of hyperoxaluria (36,37). The observed decrease in creatinine excretion was not only secondary to lower protein intake but was also most likely due to weight loss and decreased muscle mass (38).…”

Section: Discussionmentioning

confidence: 78%

Response to Dietary Oxalate after Bariatric Surgery

Froeder

Arasaki

Malheiros³

et al. 2012

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Bariatric surgery (BS) may be associated with increased oxalate excretion and a higher risk of nephrolithiasis. This study aimed to investigate urinary abnormalities and responses to an acute oxalate load as an indirect assessment of the intestinal absorption of oxalate in this population.Design, setting, participants, & measurements Twenty-four-hour urine specimens were collected from 61 patients a median of 48 months after BS (post-BS) as well as from 30 morbidly obese (MO) participants; dietary information was obtained through 24-hour food recalls. An oral oxalate load test (OLT), consisting of 2-hour urine samples after overnight fasting and 2, 4, and 6 hours after consuming 375 mg of oxalate (spinach juice), was performed on 21 MO and 22 post-BS patients 12 months after BS. Ten post-BS patients also underwent OLT before surgery (pre-BS).Results There was a higher percentage of low urinary volume (,1.5 L/d) in post-BS versus MO (P,0.001). Hypocitraturia and hyperoxaluria (P=0.13 and P=0.36, respectively) were more frequent in BS versus MO patients. The OLT showed intragroup (P,0.001 for all periods versus baseline) and intergroup differences (P,0.001 for post-BS versus MO; P=0.03for post-BS versus pre-BS). The total mean increment in oxaluria after 6 hours of load, expressed as area under the curve, was higher in both post-BS versus MO and in post-BS versus pre-BS participants (P,0.001 for both).Conclusions The mean oxaluric response to an oxalate load is markedly elevated in post-bariatric surgery patients, suggesting that increased intestinal absorption of dietary oxalate is a predisposing mechanism for enteric hyperoxaluria.

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“…This can mean that a low-protein diet will induce the changes in the binding of calcium in the intestine and bone (Giannini et al 1999;Kerstetter et al 2003).…”

Section: Calcium Levelmentioning

confidence: 99%

Blood cockle (Anadara granosa) supplementation to increase serum calcium level and femur growth of low-protein diet rat

Solang

2017

Nusantara Biosci

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Abstract. Solang M. 2017. Blood cockle (Anadara granosa) supplementation to increase serum calcium level and femur growth of lowprotein diet rat. Nusantara Bioscience 9: 62-67. Blood cockle (Anadara granosa) contains protein, zinc and calcium. The aim of this study was to evaluate the effects of blood cockle flour supplement on serum calcium level, rat femur length and weight of rat femur on low-protein diet. The design of research used The Separate Sample Pre-Post Test Design. Forty eight Wistar male rats were randomly grouped into 2 groups, 12 rats as normal control group and 36 rats as malnourished group. After eight weeks, 4 rats from each group were sacrificed. Furthermore, 8 rats as normal control and 32 rats as malnourished group were randomly grouped. Malnourished rats were treated with blood cockle flour of 12.5%/kg diet, 25%/kg diet, and 50%/kg diet ad libitum for 8 weeks. Data analysis was performed with One Way ANOVA, LSD, Kruskal-Wallis and Mann-Whitney tests. The results of study showed that the supplementation of blood cockle flour of 12.5%/kg diet was significantly increase the serum calcium level (p=0.003), rat femur length (p=0.000) and rat femur weight (p=0.002) on low-protein diet. This study demonstrated that blood cockle flour can be used as alternative food to improve the growth of rat femurs in a malnutrition condition.

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Acute effects of moderate dietary protein restriction in patients with idiopathic hypercalciuria and calcium nephrolithiasis

Cited by 97 publications

References 28 publications

Bone Disease in Primary Hypercalciuria

Bone Disease in Primary Hypercalciuria

Response to Dietary Oxalate after Bariatric Surgery

Blood cockle (Anadara granosa) supplementation to increase serum calcium level and femur growth of low-protein diet rat

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