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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↗
PubMed1996

Nephrocalcinosis is associated with renal tubular acidosis in children with X-linked hypophosphatemia.

BACKGROUND: X-linked hypophosphatemia is characterized clinically by rickets and growth retardation. Therapy of this disorder with phosphate and vitamin D often produces nephrocalcinosis. The long-term effects of nephrocalcinosis on renal function in patients with X-linked hypophosphatemia are unknown. The purpose of this study was to evaluate the prevalence of glomerular and tubular disorders in patients with X-linked hypophosphatemia who developed nephrocalcinosis. METHODS: The creatinine clearance and the prevalence of renal tubular acidosis were compared in 19 patients with X-linked hypophosphatemia and nephrocalcinosis with 15 patients with X-linked hypophosphatemia without nephrocalcinosis. RESULTS: Sixteen of the 19 patients (84%) with nephrocalcinosis had a hyperchloremic metabolic acidosis compared with one of the 13 patients without nephrocalcinosis (P < .01). The serum bicarbonate of patients with nephrocalcinosis was 20.0 +/- 0.7 as compared to 24.5 +/- 0.6 mmol/L in patients without nephrocalcinosis (P < .01). The urinary anion gap was positive in all patients with acidosis (+62.1 +/- 13.3 mmol/L). The creatinine clearance was 125 +/- 6 mL/min/1.73 m2 in patients with nephrocalcinosis and 124 +/- 7 mL/min/1.73 m2 in those without nephrocalcinosis. CONCLUSION: Therapy of X-linked hypophosphatemia is often associated with nephrocalcinosis. Nephrocalcinosis is associated with renal tubular acidosis in patients with X-linked hypophosphatemia.

Acidosis, Renal Tubular↗
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↗
PubMed1999

Incidence, ultrasonic patterns and resolution of nephrocalcinosis in very low birthweight infants.

This longitudinal study was undertaken in order to elucidate the incidence and natural course of nephrocalcinosis in preterm infants and to evaluate whether the ultrasonic classification for nephrocalcinosis used here is suitable for predicting subsequent resolution of the condition. A total of 129 very low birthweight infants were screened for nephrocalcinosis by renal ultrasonography at 2 wk, 6 wk and 3 mo. The pyramidal changes were classified as peripheral, scattered or extensive. Follow-up renal ultrasonography was performed on the infants with nephrocalcinosis at 6, 12, 18 and 24 mo, and thereafter annually up to 6 y of age, or until ultrasonic resolution. The overall incidence of nephrocalcinosis was 20% (26/129). Nephrocalcinotic changes were peripheral in 14 out of the 26 infants (54%), scattered in 7 (27%) and extensive in 5 (19%). Ultrasonic resolution had taken place in all the cases with peripheral nephrocalcinosis by 12 mo, but 3 of the 7 infants with the scattered pattern and 3 of the 4 with the extensive pattern (1 died) were still affected at 24 mo. In two cases with extensive nephrocalcinosis the condition still persisted at 5-6 y of age. We conclude that about 20% of very low birthweight infants develop nephrocalcinosis during the first 3 mo of life. In about half of the affected infants renal changes are restricted and transient, but more extensive forms may last several years. The classification of nephrocalcinosis used here is appropriate for predicting later ultrasonic resolution.

Anti-Inflammatory Agents↗
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↗
PubMed1999

Nephrocalcinosis in full-term infants receiving furosemide treatment for congestive heart failure: a study of the incidence and 2-year follow up.

UNLABELLED: In order to study the incidence and course of nephrocalcinosis in full-term infants with congestive heart failure receiving long-term furosemide treatment, 36 such infants (median age 2.9 months, range 1.2-8.0) and 36 full-term control infants not receiving any diuretics (median age 3.4 months, range 1.1-8.4) were studied by renal ultrasonography and random urine calcium variables. The infants with nephrocalcinosis were followed at 3-6 month intervals up to 2 years of age, or until ultrasonic resolution. Nephrocalcinosis was found in 5 out of the 36 (14%) treated infants, but in none of the controls (P = 0.03). The dose of furosemide was higher in the infants with nephrocalcinosis than in those without (1.9+/-0.6 vs. 1.3+/-0.4 mg/kg per day; P = 0.01). The urinary calcium concentration was higher in the infants receiving furosemide than in controls and a similar trend was observed in the urinary calcium/creatinine ratio, but these variables did not differ between the study infants with and without nephrocalcinosis. Ultrasonic resolution of nephrocalcinosis was observed in 3 of the 5 infants at 12 months, but in the other 2 the condition still persisted at 24 months. CONCLUSIONS: Long-term furosemide treatment in full-term infants with congestive heart failure entails a considerable risk of developing nephrocalcinosis. Renal ultrasonography is warranted in these patients within a few months after initiation of the treatment and in the case of nephrocalcinosis alteration of the diuretic regimen is to be considered.

Calcium↗
PubMed1999

Prematurity-associated nephrocalcinosis and kidney function in early childhood.

To assess the impact of prematurity-associated nephrocalcinosis on kidney function later in life, 20 premature children with neonatal nephrocalcinosis and 20 controls, matched for birth weight and postnatal age but without nephrocalcinosis, were examined (birth weight 905+/-209 vs. 957+/-226 g; study age 4.7+/-1.1 vs. 4.6+/-0.9 years). Distal tubular acidification capacity was measured with the oral acetazolamide test, in which the response was abnormal in 1 out of the 20 children with a history of nephrocalcinosis, but in none of the controls. Urinary calcium and beta(2)-microglobulin excretion were higher in the children with nephrocalcinosis, but no differences were found in fractional excretion of sodium and potassium or tubular reabsorption of phosphate. Estimated creatinine clearance was not different between the groups. Of the 6 children with nephrocalcinosis lasting beyond 2 years of age, 5 had had chronic lung disease neonatally and exhibited a tendency for compensated respiratory acidosis at the time of the examination. Neonatal nephrocalcinosis seems to lead to some signs of renal tubular dysfunction in early childhood of preterm infants. Glomerular function, however, appears not to be specifically disturbed by nephrocalcinosis.

Calcium↗
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↗
PubMed1996

The natural history of nephrocalcinosis in premature infants treated with loop diuretics.

PURPOSE: We investigated the natural history of nephrocalcinosis in premature infants treated with furosemide and attempted to identify factors to predict infants most at risk. MATERIALS AND METHODS: We evaluated 13 preterm infants in this longitudinal pilot study. During hospitalization and while receiving a loop diuretic nephrocalcinosis developed in each patient. Patients were divided into groups based on resolution (6) and nonresolution (7) according to spontaneous resolution of nephrocalcinosis at any point during followup. The 2 groups were compared to each other and to a control group. RESULTS: Mean followup after discontinuation of furosemide in the resolution versus nonresolution groups was 10.3 and 7.7 months, respectively. Between the 2 groups there was no significant difference in average gestational age, birth weight, number of days hospitalized or on furosemide, or total furosemide dose. Mean calcium-to-creatinine ratio while receiving furosemide at the time nephrocalcinosis developed was 0.38 in the resolution group but 2.23 in the nonresolution group (p < 0.005). Initial calcium-to-creatinine ratio in age matched infants who did not have nephrocalcinosis was 0.4. Frank renal stones developed in 2 of the 7 patients without resolution and 0 of the 6 with resolution. When nephrocalcinosis resolved, it was at a mean of 5.2 months following discontinuation of the diuretic. CONCLUSIONS: Early data indicate that nephrocalcinosis resolves in approximately 50% of premature infants 5 to 6 months after discontinuation of furosemide. The only factor that appears to be predictive of the infants who will have resolution is the calcium-to-creatinine ratio when nephrocalcinosis is diagnosed. In patients without resolution this ratio is much higher than in age adjusted normal controls, while in those with resolution it appears normal for age.

Diuretics↗
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↗
PubMed1997

Salt supplementation, growth, and nephrocalcinosis in the furosemide-treated weanling rat.

OBJECTIVE: Furosemide treatment in the human neonate is associated with sodium depletion, growth retardation, hypercalciuria and nephrocalcinosis. Dietary sodium intake is known to directly influence urinary calcium excretion. The objectives of this study were to create a rat model of furosemide-induced nephrocalcinosis and to test the effects of dietary sodium supplementation on growth, electrolyte balance, calciuria, and renal calcifications. METHODS: Initially, 18 weanling Sprague-Dawley rats were randomly divided into three groups. Groups A (control) and B were fed a basal diet. Group C was fed a sodium-enriched diet. Groups B and C received furosemide (40 mg/kg) intraperitoneally daily for 28 days. At the end of the study, serum, urine, and kidney samples were obtained for biochemical and histologic analyses. The three groups were then compared for differences in growth, electrolyte homeostasis, calcium excretion and nephrocalcinosis. Subsequently an additional 15 rats were studied to confirm our findings regarding urinary calcium excretion and kidney calcifications. RESULTS: Treatment with furosemide without sodium supplementation (group B) resulted in decreased weight gain compared with group A (137.5 +/- 12.9 vs 154.0 +/- 10.6 g; p < 0.05), hypokalemia (3.7 +/- 0.1 vs. 4.4 +/- 0.4 mEq/l; p < 0.05), and nephrocalcinosis (187.1 +/- 155 vs. 18.8 +/- 6.9 micrograms Ca/g dry kidney; p < 0.05). Sodium supplementation (group C) normalized weight gain and corrected electrolyte abnormalities without increasing calciuria or nephrocalcinosis. CONCLUSIONS: We conclude that in this animal model, chronic furosemide treatment results in growth failure and development of nephrocalcinosis. Sodium supplementation protects against the deleterious effects of furosemide on weight gain and electrolyte homeostasis with no adverse effect on nephrocalcinosis.

Animals↗
PubMed1997

Nephrocalcinosis.

The routine use of ultrasonography has resulted in an explosion in the number of conditions reported to be associated with nephrocalcinosis. It has also been increasingly recognized that urolithiasis and nephrocalcinosis can coexist in the same patient. The two conditions most commonly associated with nephrocalcinosis in childhood are the use of furosemide in infancy and the treatment of patients with hypophosphatemic rickets with phosphate and vitamin D preparations. Although originally thought to be related to hypercalciuria, more recent studies in humans and research animals indicate a multifactorial etiology for furosemide-related nephrocalcinosis. In patients with hypophosphatemic rickets, it seems that the dose of phosphate and in particular the development of secondary hyperparathyroidism play a central role in the development of nephrocalcinosis. Among the entities recently reported to be associated with nephrocalcinosis are some that characteristically include Fanconi's syndrome. These findings dispute the previous teaching of lack of renal calcifications in this syndrome, which involves proximal renal tubular acidosis. The diagnosis of nephrocalcinosis requires a metabolic work-up to identify the offending factor. When identified, appropriate intervention should be instituted.

Furosemide↗
PubMed1999

Observer reliability in grading nephrocalcinosis on ultrasound examinations in children.

BACKGROUND: Nephrocalcinosis is often associated with a variety of hypercalcemic conditions. Diagnostic ultrasound is often used for assessing nephrocalcinosis in children, but its reliability has not been proven. OBJECTIVE: To determine the reliability of expert interpretation of sonographic films with a grading scale of severity for nephrocalcinosis. MATERIALS AND METHODS: Fifty-eight ultrasonographic films of 30 children with Williams syndrome and other conditions know to be associated with nephrocalcinosis were assessed. We used a blinded randomized design to assess intra- and interobserver reliability. RESULTS: Grades I, II, and III nephrocalcinosis were noted in 13 %, 19 %, and 27 % of the examinations, respectively. The weighted kappa coefficient was 0.80 (standard error 0.12; 95 % confidence interval 0.68-0.92) for intraobserver agreement and 0.76 (standard error 0.13; 95 % confidence interval 0.63 to 0.89) for interobserver agreement. Reliability in assessing change from one examination to the next, with independently graded films, was fair with an unweighted kappa coefficient of 0.68 (95 % confidence interval 0.38-0.96) and 0.51 (95 % confidence interval 0.21-0.80) for intra- and interobserver reliability, respectively. CONCLUSION: The severity of nephrocalcinosis can be reliably interpreted with an ultrasonography grading scale.

Child↗
PubMed1993

Hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets.

The treatment of X-linked hypophosphatemia (XLH) consists of phosphate and vitamin D3 derivatives. Transient hypercalciuria and hypercalcemia are well-known signs of vitamin D intoxication. Despite urinary calcium excretion control, the danger of nephrocalcinosis in treated patients has been emphasized. It has recently been suggested that hyperoxaluria might be a causative factor of nephrocalcinosis other than calcium in phosphate-treated XLH patients. We measured urinary oxalate and phosphate excretion in 12 patients with the syndrome of hereditary hypophosphatemic rickets with hypercalciuria (HHRH) receiving only oral phosphates and in 5 XLH patients receiving both oral phosphates and vitamin D. No correlation was found between the dosage of phosphate supplements or urinary phosphate excretion and urinary oxalate excretion, in either group of patients. Nephrocalcinosis, presenting as hyperechogenicity of the medullary pyramids, was found in 2 of the 5 XLH patients and only in 2 HHRH patients who had been treated with excessive doses of vitamin D2 and calcium, prior to the true diagnosis being established. We conclude: (1) hyperoxaluria is not a cause of nephrocalcinosis in phosphate-treated patients with hereditary hypophosphatemic rickets; (2) prolonged phosphate treatment alone does not induce nephrocalcinosis in HHRH patients, and (3) we believe that in XLH patients, nephrocalcinosis is essentially due to vitamin D overdosage at some stage, or noncompliance in phosphate intake, leading to repeated undetected hypercalciuric periods.

Adolescent↗
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↗