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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↗

PubMedDate not supplied

Hypercalciuria and nephrocalcinosis in cystic fibrosis patients.

The objective of this study was to determine the frequency of nephrocalcinosis and hypercalciuria in cystic fibrosis (CF) patients, and to search possible causes of this phenomenon. Forty-three CF children (24 boys, 19 girls; mean age 64.9 months, range 5 months-18 years) were included in this study. Plasma sodium, potassium, chloride, BUN, creatinine, calcium, phosphorus, magnesium, alkaline phosphatase; spot urine sodium, potassium, chloride, creatinine, calcium, magnesium; and serum 25-hydroxyvitamin-D levels were measured in all patients. Urine samples were examined for microscopic hematuria. Fractional sodium, potassium, chloride excretion and estimated glomerular filtration rate (GFR) were calculated. All patients underwent renal ultrasonography. Hypercalciuria, nephrocalcinosis and microscopic hematuria were detected in 15 patients (34.2%), 10 patients (23.2%) and two patients (5%), respectively. There was no significant but borderline correlation between 25-hydroxyvitamin-D levels and hypercalciuria (r: 0.308, p:0.05). There were no correlations between Shwachman clinical scoring system results and hypercalciuria (r: 0.221, p: 0.148) and age and hypercalciuria (r: -0.229, p: 0.135). Patients with chronic Pseudomonas colonization showed no hypercalciuria or nephrocalcinosis. There was no difference for plasma biochemical results, renal function tests, hypercalciuria and nephrocalcinosis between CF patients who had or had not experienced pseudo Bartter's syndrome (PBS) before. There was no relation between detected CF mutations of the patients and hypercalciuria and nephrocalcinosis. These results suggested that it is a primary abnormality of calcium metabolism in the kidney.

Adolescent↗

PubMed2004

[Nephrocalcinosis].

Nephrocalcinosis is used to describe renal parenchymal calcification. Causes of nephrocalcinosis include persistent hypercalcemia, hypercalciuria, acid-base disorders, hyperoxaluria and urinary stasis. Patients with nephrocalcinosis initially present no symptom. However, advanced nephrocalcinosis is irreversible and causes impaired renal function. Therefore, careful observation for the presence and progression of nephrocalcinosis is necessary for patients who have risk factors for this disorder.

Acid-Base Imbalance↗

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↗

PubMed1984

The pathogenesis and effect on renal function of nephrocalcinosis induced by different diets in female rats.

The ability of three diets to produce nephrocalcinosis in female rats has been compared after 30, 60 and 90 days of feeding. Severe nephrocalcinosis with associated tubular damage was induced with a standard laboratory maintenance low-protein diet and with a diet containing a single-cell protein (Pruteen) but not with a casein-containing diet. Both the Pruteen and casein diets were high-protein diets. The development of the lesion was equally rapid following feeding of either the laboratory maintenance diet or the Pruteen diet. Nephrocalcinosis was present, with body kidneys similarly affected, at each 30-day interval with either diet. A severe degree of nephrocalcinosis was associated with widespread renal damage although signs of tubular regeneration and repair were evident at 30 days. Nephrocalcinosis induced by the Pruteen diet was accompanied by enlargement of the kidney. Renal function was assessed at each time by the measurement of urine volume, specific gravity and protein content, inulin clearance, and the excretion of the urinary enzymes N-acetyl-beta-glucosaminidase and alkaline phosphatase. Despite extensive calcification and some tubular damage, renal function was unimpaired, reflecting the capacity of the functional reserve of the kidney.

Animals↗

PubMed1999

[Early hypomagnesemia, hypercalciuria and nephrocalcinosis: two cases in a family].

BACKGROUND: Hypomagnesemia-hypercalciuria and nephrocalcinosis is a rare inherited syndrome which is characterized by persistent hypomagnesemia despite supplementation, hypercalciuria, nephrocalcinosis and progressive renal failure. OBSERVATIONS: Case 1. A girl was referred at the age of 18 months because of polyuria, polydipsia and vitamin-resistant rickets. There was hypomagnesemia, hypercalciuria and mild renal insufficiency; ultrasonography showed nephrocalcinosis. For two years, she received hydrochlorothiazide and the course of the disease was marked by a significant reduction of urine output and hypercalciuria, recurrent urinary tract infections and a progression toward chronic renal failure. Case 2. The brother of this child was investigated at the age of nine months because of polyuria and polydipsia. He also had hypomagnesemia, hypercalciuria and nephrocalcinosis. Renal function was initially normal. After two years on continuous treatment with hydrochlorothiazide, hypercalciuria decreased without deterioration of renal function. No signs of rickets were noted and nephrocalcinosis remained stable. CONCLUSION: To our knowledge, these two patients are the youngest reported in the literature. The long-term deterioration of renal function is hazardous but rickets may be avoided by early administration of hydrochlorothiazide.

Calcinosis↗

PubMedDate not supplied

Nephrocalcinosis in childhood.

Charts of 16 children with nephrocalcinosis between 1990 and 1997 were reviewed. The cause of nephrocalcinosis was believed to be iatrogenic in 7 patients (43.8%) and non-iatrogenic in 9 (56.2%). Vitamin D therapy was responsible for 5 patients of iatrogenic nephrocalcinosis, and furosemide therapy for the remaining iatrogenic patients. Non-iatrogenic cases consisted of 3 patients with renal tubular acidosis, 3 patients with idiopathic hypercalciuria, and the 3 other patients with rare underlying conditions. Abdominal X-ray detected nephrocalcinosis in only 2 (12.5%) of the total 16 patients. None showed resolution of nephrocalcinosis during these years of follow-up.

Adolescent↗

PubMed1995

Medullary nephrocalcinosis: sonographic findings in adult patients.

Medullary nephrocalcinosis occurs in various diseases as a non-specific renal manifestation. We present 5 patients (hypophosphataemic rickets, type 1 renal tubular acidosis, primary hyperparathyroidism, hypercalcaemia of unclear origin, chronic renal insufficiency requiring dialysis) in whom a medullary nephrocalcinosis was demonstrated by means of sonographically detectable changes in the renal medulla region. The sonographic appearance of medullary nephrocalcinosis is characterized by detection of echo-enhanced structures in the region of the renal pyramids. The presence of a medullary nephrocalcinosis can generally be confirmed with adequate reliability on the basis of sonographic findings and characteristic clinical pictures. In individual cases it is difficult to distinguish between medullary nephrocalcinosis and renal calyx calculi.

Acidosis, Renal Tubular↗

PubMed1996

Histological long-term outcome of furosemide-induced nephrocalcinosis in the young rat.

The long-term prognosis of furosemide-associated nephrocalcinosis in the infant is still unclear. Although discontinuation of the diuretic often results in radiological resolution of the calcifications, functional abnormalities may persist. The natural history of the renal histopathology of these patients is yet unknown. In the present study we investigated the histological long-term outcome of furosemide-induced nephrocalcinosis in the young rat. Thirty-six weanling male Sprague-Dawley rats were divided into three groups: A controls, B furosemide given for 8 weeks, and C furosemide given for 2 weeks followed by 6 weeks of observation. Metabolic studies at the end of the experiment demonstrated a significant diuretic and natriuretic effect in group B. Kidney histology showed nephrocalcinosis scores (mean +/- SD) of 0.0 +/- 0.0 in A, 2.6 +/- 1.5 in B, and 0.8 +/- 0.6 in C, with B significantly higher than A and C, and C greater than A. Kidney calcium content in B (3,421.9 +/- 2,558.7 micrograms/g dry tissue) was significantly greater than in A (310.4 +/- 21.3) and C (1470.1 +/- 932.2). Another group of 6 rats receiving 2 weeks treatment of furosemide showed a nephrocalcinosis score of 2.2 +/- 1.5, not different from group B, and an additional group of 6 rats treated with furosemide for 2 weeks and observed for another 12 weeks showed a score of 1.3 +/- 0.4, not different from group C. We conclude that most of the renal calcifications induced by furosemide occur during the early days of treatment and that up to 12 weeks after discontinuation of the diuretic, the resolution of the calcifications is only partial.

Animals↗

PubMed1991

Dietary fluoride, unlike bromide or iodide, counteracts phosphorus-induced nephrocalcinosis in female rats.

Supplemental dietary F has been shown to counteract P-induced nephrocalcinosis in female rats. In order to obtain information as to the specificity of this F effect, the effect of other halogens, namely Br and I, on P-induced nephrocalcinosis was studied in weanling female rats. Supplemental dietary Br (5.24 mmol/kg of diet) and I (1.43 mmol/kg of diet) did not influence P-induced nephrocalcinosis, whereas F at equimolar dietary concentrations had marked antinephrocalcinogenic activity. The halogens were added to the diets in the form of KBr, KI, and NaF; the diets were balanced for the kations with Cl salts. The addition of KI to the diet to a concentration of 5.24 mmol/kg caused pronounced growth retardation, decreased feed intake, hepatomegaly, and signs of lethargy. It is concluded that the protective effect of dietary F against P-induced nephrocalcinosis does not extend to other halogens.

Animals↗

PubMed1991

Dietary fluoride prevents phosphorus-induced nephrocalcinosis in female rats.

The effect of dietary fluoride (F) on nephrocalcinosis was studied in young, female rats. Nephrocalcinosis was induced by a diet rich in phosphorus (P). F in the diet effectively counteracted P-induced nephrocalcinosis in a dose-dependent fashion. The feeding of increasing amounts of F caused decreasing calcium (Ca) and F concentrations in kidney. This suggests that the amount of Ca in kidney determines F accumulation in this organ, rather than F intake. Increasing amounts of F in the diet caused increasing rates of urinary and fecal excretion and whole-body retention of F. Dietary F did not influence urinary and fecal excretion and plasma concentrations of Ca, magnesium (Mg), and P. The metabolic basis for the protective effect of F against the development of nephrocalcinosis remains to be established.

Animals↗

PubMed1996

Nephrocalcinosis in a patient with primary hyperoxaluria type 2.

Although nephrocalcinosis is a classical finding in primary hyperoxaluria type 1 (PH 1) associated with a poor renal survival it is exceptional in patients with PH type 2 (PH 2), characterized by a more favorable outcome. We describe an 8-month-old girl who suffered from recurrent urinary tract infections. Imaging studies revealed a profound corticomedullary nephrocalcinosis with no evidence of calculi. Urinary oxalate and D-glycerate excretion were massively elevated, while urinary glycolate or glyoxylate could not be detected, confirming the diagnosis of PH 2. Although the nephrocalcinosis progressed radiologically, renal function remained stable for over 2 years. Only further follow-up will show whether the associated nephrocalcinosis worsens the prognosis of our patient and of PH 2 in general.

Child↗

PubMedDate not supplied

Nephrocalcinosis complicating medical treatment of posthemorrhagic hydrocephalus.

Furosemide and acetazolamide are often used concurrently to treat posthemorrhagic hydrocephalus in premature infants with intraventricular hemorrhage. Eleven premature infants with posthemorrhagic hydrocephalus were monitored for the development of hypercalciuria during treatment using urine calcium/creatinine (Ca/Cr) ratios (normal: less than or equal to 0.21). Seven of 11 infants (64%) developed hypercalciuria; 5 of those 7 infants had nephrocalcinosis on renal ultrasonography. Infants who developed nephrocalcinosis had urine Ca/Cr ratios of 0.5-4.0. In all 5 infants with nephrocalcinosis, renal calculi decreased and urine Ca/Cr improved after drug therapy was discontinued. The combined use of acetazolamide and furosemide as therapy for posthemorrhagic hydrocephalus places premature infants at high risk for nephrocalcinosis. It is suggested that urine Ca/Cr be monitored closely in infants receiving these drugs and that other treatment modalities be considered when the urine Ca/Cr ratio exceeds 0.21.

Acetazolamide↗

PubMed2004

Renal failure due to acute nephrocalcinosis following oral sodium phosphate bowel cleansing.

Nephrocalcinosis is a chronic tubulointerstitial nephropathy characterized by tubular calcium phosphate deposition and slowly progressive renal insufficiency. We report a novel association of acute nephrocalcinosis and acute renal failure (ARF) with colonoscopy preceded by a bowel-cleansing regimen consisting of oral sodium phosphate solution (OSPS). A cohort of 5 patients (mean age, 69.2 years) had normal renal function (mean serum creatininem 0.9 mg/dL) before colonoscopy and presented with ARF (mean serum creatinine, 4.9 mg/dL) from 3 days to 2 months postcolonoscopy. Past medical history included hypertension in all 5 patients. Medications included an angiotensin-converting enzyme (ACE) inhibitor (ACE-I) or angiotensin receptor blocker (ARB) in 4 patients and diuretics in 2 patients. In all patients, colonoscopy was preceded by bowel cleansing with OSPS; OSPS was contraindicated in a single patient with hyperparathyroidism and was used at excessive doses in another. Renal biopsy specimens obtained from all 5 patients revealed diffuse tubular injury and abundant tubular deposition of calcium phosphate. Although the tubular injury involved all tubular segments, lectin and immunohistochemical staining disclosed calcium phosphate deposition confined to distal tubules and collecting ducts. At a mean of 5.8 weeks of postbiopsy follow-up, renal function was unchanged in 4 patients and mildly improved in 1 patient. We conclude that acute nephrocalcinosis is a seemingly rare complication of bowel cleansing with OSPS. The pathophysiology of acute nephrocalcinosis after treatment with OSPS likely involves transient hyperphosphatemia; volume depletion exacerbated by intercurrent ACE-I, ARB, and diuretic use; and elevated distal tubular phosphate and calcium concentrations. Greater awareness of this entity is needed to identify potential risk factors.

Administration, Oral↗

PubMed1992

Metabolic and histologic investigation of the nature of nephrocalcinosis in children with hypophosphatemic rickets and in the Hyp mouse.

To investigate the biochemical nature of nephrocalcinosis in children with hypophosphatemic rickets treated with orally administered phosphate and vitamin D, we studied five such patients, aged 3.7 to 12.3 years, during treatment and again 3 days after it had been discontinued. Treatment was associated with significant increases in mean serum phosphate concentration and urine phosphate/creatinine ratio, from 0.71 to 1.03 mmol/L and from 3.61 to 9.42 mmol/mmol, respectively. Significant correlation was found between urine phosphate/creatinine and oxalate/creatinine ratios (r = 0.670; p less than 0.01); however, the mean urine oxalate/creatinine ratio of 65.0 mumol/mmol while patients were taking phosphate orally was not significantly different from the ratio of 59.0 mumol/mmol when treatment was discontinued. Kidney biopsy specimens from three of the patients showed that the renal calcifications were located mainly intratubularly and were composed exclusively of calcium phosphate. In a further investigation of the nature of phosphate-induced nephrocalcinosis, six 6-week-old male Hyp mice, the murine analog of the human disease, received oral phosphate therapy with drinking water for 48 days; six others served as control animals. Mice in the experimental group excreted more phosphate (p less than 0.001) and less calcium (p less than 0.01) than control mice did, and medullary nephrocalcinosis, with a high kidney calcium content, developed (p less than 0.001). Histologic sections showed that the renal calcifications were located intratubularly and were composed of calcium phosphate. We conclude that, both in children with hypophosphatemic rickets and in the Hyp mouse, the development of nephrocalcinosis is associated with high oral phosphate intake and subsequent deposition of calcium phosphate precipitates in the kidney.

Animals↗

PubMed2001

Bisphosphonates and nephrocalcinosis in a rabbit leg lengthening model: a histological and therapeutic comparison.

We performed a comparison of the effects of two bisphosphonates, pamidronate and zoledronic acid, on regenerate bone mineral content in distraction osteogenesis in an immature rabbit model. Single dose zoledronic acid was found to be 18 times more potent at producing an increase in bone mineral content than pamidronate per mg/kg of drug infused at surgery. Histological examination of all rabbit kidneys was performed at trial completion. Nephrocalcinosis was identified in 14 of 20 kidneys of rabbits infused with pamidronate, but was not detected in the 20 kidneys of those rabbits infused with zoledronic acid. A further 20 kidneys from rabbits given a second dose of zoledronic acid were also found to be free of signs of nephrocalcinosis. Three of 40 control kidneys exhibited signs of nephrocalcinosis. The increased potency of zoledronic acid allowed us to give one-tenth the dose of pamidronate, with increased therapeutic efficacy and no evidence of nephrocalcinosis.

Animals↗