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At least 19 recordsLinked to original sources
PubMed1985

X-ray microanalysis of uremic nephrocalcinosis: cellular distribution of calcium, aluminium and silicon in uremic nephrocalcinosis.

Nephrocalcinosis with a deposition of aluminum and silicon has been previously reported in uremic rats. To clarify the origin of these elements thin sections of renal cortex were examined by means of electron microscopy and energy dispersive x-ray microanalysis. Studies were performed on subtotally nephrectomized rats (SNX) and sham-operated control animals. Electron microscopy of proximal tubular epithelial cells in SNX rats unlike control rats revealed severe mitochondrial disorganization; irregularity of the tubular basement membrane which exhibited various inclusions; and lamellar bodies within the brush border membrane. On x-ray microanalysis disorganized mitochondria contained calcium and silicon, while secondary lysosomes displayed aluminum and silicon. The tubular basement membrane of SNX rats, as well as lamellar body-like inclusions within the brush border contained calcium, aluminum and silicon together. It is suggested that lysosomal and mitochondrial interaction in proximal tubular cells of uremic rats may contribute to the deposition of calcium together with aluminum and silicon in the renal parenchyma, resulting in nephrocalcinosis.

Aluminum↗
PubMed1995

Medullary nephrocalcinosis in nephropathic cystinosis.

Children with nephropathic cystinosis excrete large amounts of calcium and phosphate due to renal tubular Fanconi syndrome, and also receive substantial supplements of phosphate and alkalinizing agents. Since these constitute risk factors for nephrocalcinosis, we evaluated 41 children age 2 months to 15 years with nephropathic cystinosis and good renal function by performing retroperitoneal ultrasound examinations in a blinded fashion. We also retrospectively analyzed parameters of calcium and phosphate metabolism representing 216 person-years of data on these children. Fifteen children had no evidence of medullary nephrocalcinosis, while 18 had mild nephrocalcinosis, and 8 severe nephrocalcinosis; 5 had renal stones. Mean urine calcium and phosphate concentrations increased from 1.47 mM and 5.30 mM, respectively, in children without nephrocalcinosis to 1.60 mM and 5.69 mM in children with mild nephrocalcinosis to 1.66 mM and 6.19 mM in children with severe nephrocalcinosis. Mean urine pH ranged from 7.5 to 8.1. The mean (+/- SD) age of the 26 patients with nephrocalcinosis was 9.4 +/- 3.8 years compared with 5.1 +/- 3.8 years for those without nephrocalcinosis (P < 0.005). Serum calcium, phosphate, vitamin D, and parathyroid hormone did not correlate with frequency or degree of nephrocalcinosis. We conclude that nephrocalcinosis frequently accompanies nephropathic cystinosis, can be detected by ultrasound examination, and might be managed by reducing oral replacement of phosphate, calcium, vitamin D, and citrate. Consideration should be given to truncating phosphate replacement once bone growth ceases.

Adolescent↗
PubMed1995

Nephrocalcinosis in X-linked hypophosphatemia: effect of treatment versus disease.

While the literature has suggested that vitamin D and phosphate therapy benefits children, and possibly adults, with X-linked hypophosphatemia (XLH), there have been increasing reports of nephrocalcinosis by renal ultrasound examination in treated patients. Although it has been assumed that nephrocalcinosis is the result of treatment, there has been no systematic comparison of treated and untreated XLH patients with long-term follow-up. Therefore, we studied 10 adults and 4 children by renal ultrasound examination with no history of medical therapy and 10 adults and 8 children with a history of medical therapy. None of the untreated patients had nephrocalcinosis; 5 treated adults and 5 treated children had nephrocalcinosis. In 3 of 4 treated children, serial renal ultrasounds did not show progression of the nephrocalcinosis. One patient progressed from baseline to year 1 only. Comparisons of means between treated patients without and with nephrocalcinosis showed statistically significant differences for urine calcium/creatinine ratios and urine phosphorus/creatinine ratios, differences not seen between untreated patients and treated patients without nephrocalcinosis. Phosphate dose, but not vitamin D dose, was statistically significantly different between the two treated groups. Our studies point to a convincing role for the association between nephrocalcinosis, as diagnosed by renal ultrasound examination, and medical therapy.

Child↗
PubMed1984

Nephrocalcinosis and diets containing alkali- and non-alkali-treated soy protein.

Diets containing alkali-treated soy protein have been shown to cause nephrocalcinosis in rats. In order to determine if alkali-treated soy protein is the dietary component that induces nephrocalcinosis, the effects of a purified diet containing 20% alpha-protein (an alkali-treated soy protein) were compared with the effects of the same diet containing 20% promine-D (a non-alkali-treated soy protein) on renal morphology and renal calcium and phosphorus metabolism. After a 9-week feeding trial, light and transmission electron microscopy revealed that the animals fed either the alpha-protein or promine-D diet developed nephrocalcinosis. In fact, the type of nephrocalcinosis was the same in both groups of animals. Moreover, quantitative determinations of total renal calcium and phosphorus showed that the severity of nephrocalcinosis was also the same in the two groups. No signs of nephrocalcinosis were detected in rats fed a standard commercial laboratory diet. Since nephrocalcinosis was present in the animals fed the promine-D diet, and that it was identical to that found in the animals fed the alpha-protein diet, it appears that alkali-treated soy protein is not the factor responsible for nephrocalcinosis in rats fed a diet containing the protein.

Alkalies↗
PubMed1989

Familial distal renal tubular acidosis with neurosensory deafness: early nephrocalcinosis.

Nephrocalcinosis was observed in 3 children of one family with distal renal tubular acidosis (dRTA). At presentation, all 3 patients had failure to thrive, rickets, hyperchloremic metabolic acidosis, hypokalemia, hypophosphatemia and hypercalciuria. At a later age, sensorineural hearing impairment was detected. Nephrocalcinosis was diagnosed in the index case at the age of 5 years, when a plain abdominal roentgenogram was first made; in the younger brother and sister, nephrocalcinosis was detected earlier at the age of 4 months and 5 weeks, respectively. All 3 patients required large doses of alkali (7.5-9.5 mEq/kg body weight/day) during infancy and early childhood to correct the acidosis and to prevent progression of the nephrocalcinosis. Contrary to the current notion that in children with dRTA, nephrocalcinosis is observed only after the age of 3 years, it appears that in some instances nephrocalcinosis may develop in early infancy. The occurrence of nephrocalcinosis at a very young age may be a manifestation of a severe genetically transmitted variant of dRTA and emphasizes the need for early diagnosis and optimal treatment of these patients from the first days of life.

Acidosis, Renal Tubular↗
PubMed1991

Phosphorus-induced nephrocalcinosis in female rats: a study on regression and clinical abnormalities.

The question addressed was whether preestablished phosphorus (P)-induced nephrocalcinosis would regress after dietary P restriction. Female rats were fed purified diets containing either 0.2% (w/w) P (low P) or 0.6% P (high P). After 29 days, the high-P diet had caused massive nephrocalcinosis as demonstrated chemically (by the analysis of calcium in kidney) and histologically (by inspection of kidney sections stained for calcium phosphate deposits). Switching rats from the high P to the low P diet did not result in a decrease in the degree of nephrocalcinosis within 91 days. Thus, P-induced nephrocalcinosis may not regress upon subsequent P restriction. Rats that had been fed either the 0.2 or 0.6% P diet for 56 days were examined clinically with respect to 14 selected variables. None of the variables discriminated between rats with or without nephrocalcinosis. This might imply that P-induced nephrocalcinosis in female rats does not cause significant discomfort.

Animals↗
PubMed1975

The development of nephrocalcinosis in the rat following injections of neutral sodium phosphate.

The development of nephrocalcinosis in the rat following intraperitoneal injections of various concentrations of neutral sodium phosphate (pH 7-4) was studied using histology, histochemistry, electron microscopy and quantitative techniques. Daily injections of 0-5 M phosphate consistently produced nephrocalcinosis after 6 days or more. Calcium deposits were at first confined to the basement membranes of proximal tubules; but a longer course of injections, up to 10 days, resulted in additional basement membrane calcification in the outer cortes, and outer medulla, together with intra-luminal casts, often calcified, in the outer medulla and papilla. Calcification was not found in other organs such as liver, lung, heart or aorta. Results from quantitative estimations of total kidney calcium and phosphorus suggested that it was the calcium content which was important to the initiation of nephrocalcinosis. Ultrastructural changes, suggestive of degeneration or alteration in function, were found in mitochondria of proximal tubules in experimental animals before the onset of histologically evident nephrocalcinosis. Later changes, especially to the basal part of proximal tubular cells and their basal laminae, were thought to be consequent upon the mitochondrial changes. It is suggested that the initial renal damage was caused both directly, by a toxic effect of the phosphate load on the kidney and, indirectly, by stimulation of the parathyroid glands as a result of the hypocalcaemia and hyperphosphataemia which followed an injection of phosphate. Daily doses of 1 M phosphate for 3 days produced a type of nephrocalcinosis which was more typical of that reported by previous investigators, who used high doses of phosphate. Twice daily injections of 0-25 M phosphate for 6 days did not induce nephrocalcinosis, whereas 0-375 M phosphate given twice daily for 6 days produced only minimal calcium deposits compared with animals given 0-5 M phosphate once daily for the same period. This may have important clinical implications, since phosphate has been used to control hypercalcaemia of various etiologies.

Alkaline Phosphatase↗
PubMed1980

Nephrocalcinosis in radiographs, computed tomography, sonography and histology.

In 12 patients with nephrocalcinosis, radiographs were compared with computed tomography, sonography and histology. Computed tomography detects nephrocalcinosis at a very early stage of the disease, gives a better picture of the density and extent of nephrocalcinosis and may detect other findings (e. g. cysts). Radiographs may show many more details than computed tomography; they seem to be more suitable for observing the course of the disease and have a lower radiation dose. Sonography has not been helpful in the diagnosis of nephrocalcinosis. Histology correlates only moderately with the degree of nephrocalcinosis demonstrated in radiographs and computed tomography.

Adolescent↗
PubMed1984

Influence of diet on the development of nephrocalcinosis in the rat.

A histological examination of the effect of a purified diet containing 20% alpha protein (an alkali-treated soyprotein) on the development of nephrocalcinosis induced by intraperitoneal injections of 0.5 neutral (pH 7.4) sodium phosphate was carried out in female weanling rats. Animals that were fed a standard commercial laboratory diet and given daily injections of phosphate for six or ten days developed a form of nephrocalcinosis that consisted mainly of intraluminal (intratubular) calcification at the junction of the outer and inner stripes of the outer medulla and in the inner stripe of the outer medulla. By contrast, rats that were fed the alpha protein diet and given injections of phosphate for six or ten days developed a form of nephrocalcinosis that was characterized primarily by a type of tubular basement membrane calcification at the junction of the inner stripe of the outer medulla and the inner medulla. The differences in nephrocalcinosis between the two dietary groups and the fact that an alpha protein diet by itself can cause renal calcification, leads to the suggestion that some component(s) or factor(s) in the alpha protein diet strongly influence(s) the development of nephrocalcinosis induced by injected neutral sodium phosphate.

Animals↗
PubMed1989

[Nephrocalcinosis in childhood. Sonographic findings and differential diagnosis].

Ultrasonography is the method of choice for the detection of medullary or cortical nephrocalcinosis in infancy and childhood. Compared with abdominal radiographs and computed tomography even smallest calcifications are detected more accurately. Using furosemide, ACTH, steroids or high doses of vitamin D, early forms of medullary nephrocalcinosis associated with a faint hyperechogenic rim at the margins of the renal pyramids can be diagnosed by ultrasound. Idiopathic hypercalciuria, Bartter's syndrome and renal tubular acidosis cause medullary nephrocalcinosis, whereas cortical nephrocalcinosis is the result of renal vein thrombosis; primary hyperoxaluria is associated with cortico-medullary calcifications. Due to the localisation of the nephrocalcinosis and the age distribution of the diseases, sonography merely enables us to narrow down differential diagnosis.

Aging↗
PubMed1988

Microscopic nephrocalcinosis in cystic fibrosis.

Airway, sweat-duct, and other epithelial cells in patients with cystic fibrosis display abnormal ion transport. To test whether the kidney, the organ most exquisitely adapted for ion transport, has a similar defect, we measured the levels of calcium excretion and searched for microscopic nephrocalcinosis in patients with cystic fibrosis. Thirty-eight specimens of kidney tissue were stained for calcium deposits, and 24-hour levels of urinary calcium excretion were measured in 14 patients and 15 control subjects. Microscopic nephrocalcinosis was observed in 35 of the 38 specimens (92 percent), and hypercalciuria (greater than 182 mg per gram of creatinine) in 5 of the 14 patients (36 percent). Notably, nephrocalcinosis was detected near the time of birth (in six patients under one year old, including two neonates and one stillborn infant), which supports the hypothesis that such renal calcium deposits reflect the genomic defect and are not due to longstanding pulmonary dysfunction, chronic infection, therapeutic agents, or disease progression. None of the patients with hypercalciuria or nephrocalcinosis had clinical evidence of renal dysfunction. The finding of microscopic nephrocalcinosis near the time of birth in patients with cystic fibrosis suggests a primary abnormality of calcium metabolism in the kidney. Studies of the pathophysiologic features of the kidney in cystic fibrosis may elucidate the molecular alterations observed in this disorder.

Adolescent↗
PubMed1990

X linked hypophosphataemia: treatment, height gain, and nephrocalcinosis.

The clinical data of 18 patients with X linked hypophosphataemia were analysed retrospectively. The height data were expressed as SD scores. There was no difference in the final height of patients treated with vitamin D (or 1,25-dihydroxyvitamin D) and phosphate for at least two years (n = 12) and that of 16 hypophosphataemic family members who had never been treated. The mean final SD score (-2.07) of treated patients, however, was significantly higher than the value before treatment (-2.79), which indicated an average absolute height gain of 4-4.5 cm compared with the expected height values. Six of the treated patients developed ultrasonographically detectable nephrocalcinosis with normal renal function. The daily phosphate intake and excretion of patients with nephrocalcinosis was significantly higher than that of patients with normal renal morphology. There was no difference in the doses of vitamin D between the two groups. The average urinary calcium:creatinine ratio of the two groups was similar to and below the hypercalciuric 0.6 mmol:mmol limit. The group with nephrocalcinosis, however, had a higher incidence of hypercalciuric episodes than the group without nephrocalcinosis (12 in 130 observations compared with six in 334 observations, respectively). The benefits and risks of treatment of patients with X linked hypophosphataemia must be further evaluated. The high dose of phosphate seems to be an important factor in the development of nephrocalcinosis in this group of patients.

Adolescent↗
PubMed1984

Age and the development of nephrocalcinosis induced by injections of neutral phosphate in rats.

A morphological characterization of nephrocalcinosis induced by injected neutral phosphate was made in both female weanling and young adult rats in order to determine the effects of age on the development of this type of phosphate-induced renal calcification. Nephrocalcinosis was induced by giving the rats single daily intraperitoneal injections of 0.5 M neutral phosphate (15.5 mg Pi/100 g bw/24 h) for 10 days. Following the experimental period, the kidneys of the animals were fixed and processed for general histology and for the histochemical localization of calcium-phosphate salts. The weanling rats developed nephrocalcinosis that was characterized mainly by large intraluminal calciferous deposits in terminal segments of proximal tubules at the junction of the outer and inner stripes of the outer medulla, and in collecting ducts and descending thin limbs and ascending thick limbs of Henle in the inner stripe of the outer medulla. In contrast, the young adult rats developed nephrocalcinosis that was characterized primarily by small granular calciferous deposits in the basement membranes of proximal tubules in the mid-cortex. The results of the present study indicate that some factor(s) associated with age and development of female rats influence(s) the development of nephrocalcinosis induced by injected neutral phosphate.

Aging↗
PubMed1983

The effects of parathyroidectomy on the development of nephrocalcinosis in rats fed phosphate-supplemented and unsupplemented diets containing alpha protein.

The effects of parathyroidectomy (PTX) on the development of nephrocalcinosis in rats fed a diet containing alpha protein were investigated for the purpose of determining whether the nephrocalcinosis was phosphate-induced. PTX completely prevented the occurrence of nephrocalcinosis in rats fed a phosphate-supplemented commercial laboratory diet for 4 weeks. However, PTX did not completely prevent the occurrence of nephrocalcinosis in rats fed a phosphate-supplemented alpha protein diet. Several calciferous deposits were found in the inner medulla. The same was also found in rats that underwent sham operations and PTX rats fed the basal alpha protein diet. Total renal calcium and phosphorous levels in these three groups were also similar and were about twice as great as those in corresponding groups fed phosphate-supplemented and unsupplemented commercial laboratory diets. Therefore, we conclude that the nephrocalcinosis in rats fed a basal alpha protein diet is not induced by PTH or excess phosphate, but is induced by some other factor associated with the diet.

Animals↗
PubMed1987

Prevention of parathyroid hormone-dependent nephrocalcinosis by chronic administration of the organic phosphorothioate WR-2721.

Pharmacological inhibition of parathyroid hormone (PTH) secretion has been the object of several experimental and clinical trials in the past. It is only recently that a drug, WR-2721 [S-,2-(3-aminopropylamino)-,ethylphosphorothioic acid], has been shown to effectively inhibit PTH secretion in euparathyroid subjects and in parathyroid cancer patients within a few hours after its administration. In the present study we tested its long term efficacy as a PTH inhibitor in a model of nephrocalcinosis resulting from secondary hyperparathyroidism. Intact and thyroparathyroidectomized (TPTX) rats were pair-fed on a low Ca (0.2%)-high phosphorus (1.6%) diet (nephrocalcinotic diet) or on a normal Ca (1.1%)-normal phosphorus (0.8%) diet for 7 days. Simultaneously, either 0.2 mmol/kg of WR-2721 or its solvent was injected subcutaneously twice daily. The intact animals on the nephrocalcinotic diet had an increased urinary cyclic AMP excretion and important renal Ca accumulation. This nephrocalcinosis was markedly reduced by WR-2721 treatment. The kidney Ca content of the WR-2721-treated rats was 58 +/- 6% lower than that of the nontreated animals. The low Ca-high phosphorus diet did not cause nephrocalcinosis in the TPTX rats. WR-2721 failed to reduce the nephrocalcinosis induced by 1,25 dihydroxyvitamin D3 intoxication in TPTX rats fed the normal Ca-normal phosphorus diet. In conclusion, the present study suggests that chronic treatment with WR-2721, a potent inhibitor of PTH secretion, may be effective for preventing the deleterious consequences of hyperparathyroidism, such as nephrocalcinosis.

Amifostine↗