Long-Term Phosphorus Restriction Prevents Corticomedullary Nephrocalcinosis and Sustains Reproductive Performance but Delays Bone Mineralization in Rats

Ritskes-Hoitinga, J.; Mathot, J. N. J. J.; Lemmens, A. G.; Danse, L. H. J. C.; Meijer, G.W.; Tintelen, G. van; Beynen, A.C.

doi:10.1093/jn/123.4.754

Cited by 15 publications

(13 citation statements)

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“…To overcome the obstacle of rat being phosphate sensitive, we used male rats that are reported to be more resistant to dietary phosphate than females. (19) In fact, the Ca:P 1:2 rats did not have a significant rise in S-PTH compared with controls, although many of the parameters measured declined, indicating that high dietary phosphate intake has a weakening effect beyond PTH.…”

Section: High-phosphate Intake Reduces Bone Strength 89mentioning

confidence: 81%

“…Male rats were used because they are reported to be relatively insensitive to diet-induced nephrocalcinogenesis, which could produce interindividual variation in results. (19) BMD measurement with DXA Right femur bone area (cm 2 ), bone mineral content (BMC, g), and bone mineral density (BMD, g/cm 2 ) were determined in vivo with a dual-energy X-ray bone densitometry device (Lunar PIXImus; GE Medical Systems). Analyses of the areas were carried out with the image of the animal on the screen using a region of interest for the segments.…”

Section: Animals and Dietsmentioning

confidence: 99%

“…With rats, these include continuous longitudinal growth, periosteal modeling, lack of a Haversian system, and the sensitivity to dietary phosphate. (19,41) Our study describes the effect of high dietary phosphate on the growing skeleton; therefore, the first two obstacles are overcome, because they are also present in the growing human skeleton.…”

Section: High-phosphate Intake Reduces Bone Strength 89mentioning

confidence: 99%

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High Dietary Phosphate Intake Reduces Bone Strength in the Growing Rat Skeleton

Huttunen

Tillman

Viljakainen

et al. 2007

Journal of Bone and Mineral Research

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Nutrition influences peak bone mass development in early adulthood. The effect of high dietary phosphate intake on the growing skeleton of 1-month-old male rats (n = 30) was assessed in an 8-week intervention. High dietary phosphate intake increased bone remodeling and impaired bone material properties, diminishing bone mechanical strength.Introduction: High dietary phosphate intake is typical in the Western diet. Abundant phosphate intake enhances parathyroid secretion and bone metabolism. To study the influence of high dietary phosphate intake on growing bone homeostasis and structure, we submitted growing rats to experimental diets that varied in their phosphate content. Materials and Methods: One-month-old intact male rats (n ‫ס‬ 30) were fed a control diet (Ca:P 1:1) or an experimental diet of either Ca:P 1:2 or Ca:P 1:3 for 8 weeks. At the beginning and the end of the study period, the right femurs were measured using DXA. Double labeling with tetracycline injection was performed 12 and 2 days before death. After death, hind legs were cut loose. Left femurs were processed for histomorphometry. Right femurs were measured with pQCT. Mechanical testing was performed on the right femoral neck and tibial shaft. Six right tibias were analyzed with CT. Serum PTH, calcium, and phosphate contents were analyzed. Results: High-phosphate intake impaired growth of the animal, limited bone longitudinal growth, and restricted femur BMC and BMD build-up. Osteoclast number, osteoblast perimeter, and mineral apposition rate were increased, and trabecular area and width were decreased. Phosphate decreased femur midshaft total bone BMD, cortical bone BMD, and mean cortical thickness. High-phosphate diet reduced femoral neck and tibial shaft ultimate strength and tibia stiffness and toughness. In addition, serum PTH increased. Conclusions: High dietary phosphate intake reduced growth, skeletal material, and structural properties and decreased bone strength in growing male rats. Adequate calcium could not overcome this.

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Section: High-phosphate Intake Reduces Bone Strength 89mentioning

confidence: 81%

Section: Animals and Dietsmentioning

confidence: 99%

Section: High-phosphate Intake Reduces Bone Strength 89mentioning

confidence: 99%

See 1 more Smart Citation

High Dietary Phosphate Intake Reduces Bone Strength in the Growing Rat Skeleton

Huttunen

Tillman

Viljakainen

et al. 2007

Journal of Bone and Mineral Research

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“…However, adult female rats have the role to breed offspring. In a study of three successive generations of rats, Ritskes-Hoitinga et al 15) have reported that 0.2% P in the diet sustained reproduction, but delayed bone mineralization in the first-and second-generation offspring after 4-12 week compared to 0.4% P in the diet. It was suggested that keeping the serum P concentration at the normal level might be necessary to sustain bone mineralization in next-generation offspring, although a low-P diet was effective for bone mineralization in adult females.…”

mentioning

confidence: 99%

Effects of Dietary Phosphorus Intake on Bone Mineralization and Calcium Absorption in Adult Female Rats

Koshihara

Katsumata

Uehara

et al. 2005

Bioscience, Biotechnology, and Biochemistry

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“…3 High-phosphate diets also can induce nephrocalcinosis in rats. 22 Hyperphosphaturia is a hallmark of XLH. 1 In our study, HCTZ therapy decreased urinary calcium excretion without affecting phosphate excretion measured by TmP/GFR (Table 1).…”

Section: Discussionmentioning

confidence: 99%

Thiazide Diuretics Arrest the Progression of Nephrocalcinosis in Children With X-Linked Hypophosphatemia

Seikaly

Baum

2001

Pediatrics

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ABSTRACT. Objective. X-linked hypophosphatemia (XLH) is characterized clinically by rickets, hypophosphatemia, and hyperphosphaturia. Conventional treatment of XLH with oral phosphate and vitamin D is associated with increased urinary calcium excretion and nephrocalcinosis. Thiazide diuretics decrease urinary calcium excretion. The objective of this study was to determine the effect of thiazide diuretics on the clinical and radiologic course of nephrocalcinosis in children with XLH.Methods. The effect of hydrochlorothiazide (HCTZ) on clinical and radiologic progression of nephrocalcinosis was evaluated in 11 children with XLH. All patients had been treated previously with vitamin D and oral phosphate and had radiologic evidence of nephrocalcinosis. The average age of the patients at the start of HCTZ was 6.6 ؎ 1.0 years. The effect of oral HCTZ at 0.8 ؎ 0.1 mg/kg body weight per day given for 3.3 ؎ 0.6 years on the progression of nephrocalcinosis and urinary calcium excretion was evaluated.Results. There was no change in serum phosphorous, calcium, potassium, and chloride after HCTZ therapy. HCTZ therapy increased serum bicarbonate and decreased urinary calcium excretion. The grade of nephrocalcinosis increased from 0.4 ؎ 0.2 to 1.5 ؎ 0.3 in the 2.3 ؎ 0.3 years before initiation of HCTZ therapy, whereas the degree of nephrocalcinosis was stable after 3.3 ؎ 0.6 years of HCTZ therapy (1.5 ؎ 0.3 vs 3.0 ؎ 0.3).Conclusion. HCTZ decreased urinary calcium excretion but did not result in the resolution of nephrocalcinosis. However, when compared with the control period, HCTZ prevented the progression of nephrocalcinosis in children with XLH. Pediatrics 2001;108(1). URL: http:// www.pediatrics.org/cgi/content/full/108/1/e6; X-linked hypophosphatemia, rickets, nephrocalcinosis, thiazide diuretics.ABBREVIATIONS. XLH, X-linked hypophosphatemia; HCTZ, hydrochlorothiazide; TmP/GFR, tubular maximum reabsorption of phosphate per deciliter of glomerular filtration; SEM, standard error of the mean. X -linked hypophosphatemia (XLH) is the most common inherited cause of rickets. It is characterized by hypophosphatemia caused by impaired proximal tubular reabsorption of phosphorous and an inappropriately normal serum level of 1,25(OH) 2 vitamin D. The resulting hypophosphatemia leads to defective bone mineralization. 1 Current therapy includes administration of 1,25(OH) 2 vitamin D (calcitriol) and phosphate to replete urinary phosphate losses without stimulating parathyroid hormone release. 2 Such therapy often leads to hypercalcuria and nephrocalcinosis. 3,4 Nephrocalcinosis can lead to renal tubular acidosis and possibly renal insufficiency. 4 -6 Hypercalcuria also has been shown to be associated with nephrocalcinosis in distal renal tubular acidosis, hyperparathyroidism, prolonged immobilization, Bartter's syndrome, hypophosphatasia, certain tumors, high-dose vitamin D therapy, and idiopathic and drug-induced hypercalcuria. 7-13 Hydrochlorothiazide (HCTZ) decreases urinary calcium excretion. The effect of HCTZ on nephrocalcino...

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Long-Term Phosphorus Restriction Prevents Corticomedullary Nephrocalcinosis and Sustains Reproductive Performance but Delays Bone Mineralization in Rats

Cited by 15 publications

References 10 publications

High Dietary Phosphate Intake Reduces Bone Strength in the Growing Rat Skeleton

High Dietary Phosphate Intake Reduces Bone Strength in the Growing Rat Skeleton

Effects of Dietary Phosphorus Intake on Bone Mineralization and Calcium Absorption in Adult Female Rats

Thiazide Diuretics Arrest the Progression of Nephrocalcinosis in Children With X-Linked Hypophosphatemia

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