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PubMed1995

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis.

Very few patients with familial hypomagnesemia, hypercalciuria and nephrocalcinosis have been described. Information about clinical course, familial studies or evolution after renal transplantation is very scant. We have studied eight patients with this syndrome who belong to five different families. The mean age at diagnosis was 15 +/- 7 years (5 to 25 years). The primary clinical data were polyuria-polydipsia (8 cases), ocular abnormalities (5), recurrent urinary tract infections (5) and recurrent renal colics with stone passage (2). Bilateral nephrocalcinosis was observed in all cases. Every patient showed hypomagnesemia (1.1 +/- 0.2 mg/dl) with inappropriately high urinary magnesium (Mg) excretions (70 +/- 17 mg/day), Mg clearances (4.4 +/- 1.2 ml/m) and Mg fractional excretions (16.2 +/- 7.1%). Hypercalciuria was present in every case except in those with advanced renal insufficiency. Serum parathormone levels were abnormally high. Serum calcium (Ca), phosphorus and potassium, and urinary excretions of uric acid and oxalate were normal. Neither chronic oral Mg administration nor thiazide diuretics normalized serum Mg levels or urinary Ca excretions, respectively. Follow-up was 6 +/- 4.5 years. Renal function worsened in every case with six patients starting on chronic dialysis after 4.3 +/- 3.8 years. The progression rate of renal insufficiency correlated with the severity of nephrocalcinosis. Five patients have received a kidney graft, and their serum Mg and urinary Ca have always been within normal values after transplantation. Twenty-six members of four of the affected families were studied: none of them showed hypomagnesemia, renal insufficiency or nephrocalcinosis. However, eleven cases (42%) had hypercalciuria and four of them presented with recurrent renal stones. Two family members had medullary sponge kidneys. In conclusion, progression to renal insufficiency is common in this syndrome; oral Mg and thiazide diuretics are ineffective to correct abnormalities. After kidney graft, tubular handling of Mg and Ca was normal. A striking incidence (42%) of hypercalciuria was found in the familial study.

Adolescent↗

PubMedDate not supplied

Nephrocalcinosis in premature infants: variability in ultrasound detection.

OBJECTIVE: To measure variability among radiologists in the ultrasound diagnosis of nephrocalcinosis in premature infants. METHODOLOGY: In this prospective multicenter study, renal ultrasounds were performed on 54 very low birth weight infants using a 5.0- and 7.5-MHz transducer, and these ultrasounds were read independently by three radiologists. kappa coefficients were calculated to assess variability in identification of nephrocalcinosis among the radiologists. RESULTS: The kappa coefficient (+/- confidence intervals) using a 5.0-MHz transducer was 0.143 (0.108, 0.178); using the 7.5-MHz transducer, the kappa coefficient was 0.268 (0.243, 0.293). All three radiologists agreed in their identification of nephrocalcinosis on 3 of 54 ultrasounds using a 5.0-MHz transducer; a total of 6 of 54 ultrasounds obtained using a 7.5-MHz transducer were read as positive by all three radiologists. CONCLUSION: There is significant variability among radiologists in the ultrasound identification of nephrocalcinosis in premature infants; a 7.5-MHz ultrasound transducer is associated with less variability in recognizing this lesion.

Evaluation Studies as Topic↗

PubMed2004

Nephrocalcinosis: molecular insights into calcium precipitation within the kidney.

Nephrocalcinosis may be defined as a generalized increase in the calcium content of the kidneys. This renal calcification may occur at a molecular, microscopic or macroscopic level leading to progressive amounts of renal damage. The major causes include those associated with an increase in urinary levels of calcium, oxalate and phosphate. Under these conditions, urine concentration and supersaturation leads to calcium crystal precipitation, which may be an intratubular event or initiate within the renal interstitium. The focus of discussion concerning renal calcification is often limited to factors that lead to renal stones (calculi and nephrolithiasis); however, nephrocalcinosis is a more sinister event, and often implies a serious metabolic defect. This review will discuss the hypotheses concerning initiating lesions of nephrocalcinosis using available laboratory and clinical studies and will examine whether new understanding of the molecular basis of tubulopathies, that lead to nephrocalcinosis, has given further insights.

Bartter Syndrome↗

PubMed1988

Influence of dietary calcium:phosphorus ratio on mineral excretion and nephrocalcinosis in female rats.

The effects of dietary calcium (Ca) concentration and calcium: phosphorus (Ca:P) ratio on mineral balance and nephrocalcinosis were studied in female rats. In the first experiment there were two dietary Ca concentrations (0.25 and 0.50%, wt/wt) at two different Ca:P ratios (0.6 and 1.3). In the second experiment the diets were formulated to contain 0.40% P and either 0.13, 0.25, 0.50 or 0.75% Ca. The diets contained 0.03% magnesium (Mg). The fecal outputs of Ca, P and Mg were lower (P less than 0.01) after feeding low Ca diets than after feeding high Ca diets. Urinary excretion of P decreased with increasing dietary Ca and increased with increasing P intake. In rats fed the 0.25% Ca diets whole-body retentions of Ca and P were lower than in the rats fed 0.50% Ca. Both increases in dietary Ca from 0.13 to 0.50% and P from 0.20 to 0.40% elevated Ca and P content of kidneys as well as the degree of nephrocalcinosis. However, after feeding the highest Ca concentration (0.75%) nephrocalcinosis was essentially absent while kidney concentrations of Ca and P were relatively low. When compared with 0.50% Ca in the diet, 0.75% Ca increased group mean whole-body retention of Ca but lowered that of P. In individual rats the degree of nephrocalcinosis and the concentrations of minerals in kidney were positively correlated.

Animals↗

PubMed1992

Inbred strains of rats have differential sensitivity to dietary phosphorus-induced nephrocalcinosis.

The degree of nephrocalcinosis after increasing the dietary phosphorus concentration from 0.2 to 0.5 g/100 g was measured in weanling female rats of 10 inbred strains. Based on kidney calcium concentrations and histological kidney calcification scores, there were considerable strain differences in nephrocalcinogenesis; 86% of the strain variability in nephrocalcinosis was attributable to genetic factors. Two strains with the most extreme nephrocalcinogenic responses were retested and the strain difference was found to be reproducible. Mean plasma phosphorus concentrations after phosphorus feeding were lower in the sensitive strain than in the insensitive strain. The high phosphorus diet produced greater urinary phosphorus concentrations, with the increase being greater in the sensitive strain. The strain difference in the response of urinary phosphorus concentrations after raising dietary phosphorus level may determine the strain difference in phosphorus-induced nephrocalcinosis. After consuming the high phosphorus diet, RP rats housed in groups in solid-floored cages had significantly higher degrees of nephrocalcinosis than their counterparts housed individually in metabolism cages with wire-mesh bases.

Animals↗

PubMed2000

Hypomagnesaemia-hypercalciuria-nephrocalcinosis: a report of nine cases and a review.

BACKGROUND: The cardinal characteristics of primary hypomagnesaemia-hypercalciuria-nephrocalcinosis include renal magnesium wasting, marked hypercalciuria, renal stones, nephrocalcinosis, a tendency towards chronic renal insufficiency and sometimes even ocular abnormalities or hearing impairment. METHODS: As very few patients with this syndrome have been described, we provide information on nine patients on follow-up at our institutions and review the 42 cases reported in the literature (33 females and 18 males). RESULTS: Urinary tract infections, polyuria-polydipsia, renal stones and tetanic convulsions were the main clinical findings at diagnosis. The clinical course was highly variable; renal failure was often reported. The concomitant occurrence of ocular involvement or hearing impairment was reported in a large subset of patients. Parental consanguinity was noted in some families. CONCLUSIONS: The results indicate an autosomal recessive inheritance. The diagnosis of primary hypomagnesaemia-hypercalciuria-nephrocalcinosis deserves consideration in any patient with nephrocalcinosis and hypercalciuria.

Adolescent↗

PubMed1993

Hypercalciuria and nephrocalcinosis in children.

Hypercalciuria has become a significant clinical focus both for pediatricians and for pediatric nephrologists after it was found that increased urinary calcium excretion is the most common abnormality in children with nonglomerular hematuria and with nephrolithiasis. The question of long-term implications of hypercalciuria in growing children, regardless of the underlying cause, remains unanswered. Whether dietary or pharmacologic therapy is warranted in children with hypercalciuria is controversial. One of the proposed consequences of hypercalciuria is nephrocalcinosis. With the availability of increasingly sensitive, noninvasive imaging techniques, nephrocalcinosis is being recognized more frequently. In some instances, concern about the risk and progression of nephrocalcinosis is provoking reevaluation of well-established metabolic therapies. New urinary inhibitors of crystal formation and aggregation have recently been identified. As the basic pathogenesis of nephrocalcinosis becomes clearer, clinical therapies will become more specific and effective.

Alkalosis↗

PubMed1985

[Effect of calcium antagonists (nifedipine) on nephrocalcinosis and calcium excretion in the rat].

An animal model was established to test the effect of a calcium antagonist on nephrocalcinosis, which was induced by an atherogenous diet, and its effect on the excretion of calcium and other parameters relevant for stone formation. With the administration of nifedipine (Adalat), the grade of nephrocalcinosis could be significantly reduced. Furthermore, with nifedipine the excretion of calcium and sodium in the urine was raised, while phosphate and potassium levels were lowered. The excretion of magnesium and citrate, reduced by an atherogenous diet, could be raised significantly with the administration of nifedipine. The pathophysiological mechanisms underlying the effect of nifedipine on nephrocalcinosis and on the excretion of the urine parameters are discussed. Apparently hypercalciuria is the result of a reduced reabsorption of calcium in the tubulus. The inhibitory effect on the genesis of nephrocalcinosis is possibly due to the lower calcium influx into the tubular cells.

Animals↗

PubMed1990

Diet-induced nephrocalcinosis and urinary excretion of albumin in female rats.

This study was carried out to test the hypothesis that diet-induced nephrocalcinosis causes enhanced loss of albumin in urine, irrespective of the composition of the nephrocalcinogenic diet. Female rats were fed various purified diets for 28 days. There was a control diet (0.5% Ca, 0.04% Mg, 0.4% P, 15.1% protein, wt/wt), a low Mg (0.01% Mg), a high protein (30.2% protein) and a high P diet (0.6% P). The low Mg and high P diet induced nephrocalcinosis as demonstrated histologically and by markedly increased concentrations of kidney Ca. In rats fed the high protein diet, nephrocalcinosis was essentially absent. Group mean values of urinary excretion of albumin and plasma concentrations of urea were increased in rats fed either the low Mg or high P diet. The high protein diet did not affect urinary albumin but caused lysozymuria which was not seen in the other groups. Plasma urea was increased in rats fed the high protein diet. In individual rats, the concentration of Ca in kidney and urinary albumin excretion were positively correlated. It is suggested that nephrocalcinosis in female rats induced by either low Mg or high P intake causes kidney damage which in turn leads to increased concentrations of albumin in urine and urea in plasma.

Albuminuria↗

PubMed1986

[Pathological study on nephrocalcinosis in Fischer 344/Du Crj rats].

Histopathological examinations on nephlocalcinosis of the Fischer 344 (F344) rats were carried out. As the results of comparison on its appearance among F344, Wistar and SD strains of rats, F344 female rats showed the most severe nephrocalcinosis. Nephrocalcinosis developed between 4 weeks and 8 weeks and was likely to keep its appearance through 108 weeks of the survival period of the rats. Histologically, mineral deposit was always observed at cortico-medullary junction. It seemed to locate at the outer portion of the basement membrane of the tubular epithelium, adjacent to the capillary wall in the connective tissue. Four weeks after ovariectomy at 4 weeks of age, the rats showed a decrease in degree of nephrocalcinosis. In contrary, the rats treated with estorone following ovariectomy revealed an increase in degree of nephrocalcinosis. It was suggested that the oestrogen-type sex hormone appeared to give a role in nephlocalcinosis.

Animals↗

PubMed1997

High phosphorus diet rapidly induces nephrocalcinosis and proximal tubular injury in rats.

The development of nephrocalcinosis and the time course of changes in kidney function, especially proximal tubular function, were studied in young male rats fed a high-phosphorus diet. The animals were fed a purified diet with a phosphorus content of either 0.5% (normal phosphorus diet) or 1.5% (high-phosphorus diet). In the group fed the high-phosphorus diet, nephrocalcinosis was found in 4 of 42 rats after 1 d of feeding and in all rats of this group at 3 d. The degree of nephrocalcinosis gradually increased with time. Upon histological observation by electron microscopy, vacuoles, lysosomes and swelling of microvilli in the proximal tubules were observed in rats fed the high-phosphorus diet after 1 d of feeding. Giant lysosomes with deposition of calcium and deposition of hydroxyapatite in mitochondria were observed in the proximal tubules of rats fed the high-phosphorus diet at 3 d. Albumin concentration in the urine of these rats was significantly increased at 3 d. The activity of N-acetyl-beta-D-glucosaminidase in the urine was also significantly increased after 1 d of feeding the high-phosphorus diet, and then reached a plateau. The beta 2-microglobulin concentration in the urine of rats fed the high-phosphorus diet was significantly increased at 14 d, and increased more toward 21 d. We concluded that nephrocalcinosis and injury to the proximal tubules are rapidly induced in rats fed a high-phosphorus diet.

Animals↗

PubMed1994

Nephrocalcinosis in very low birth weight neonates: sonographic patterns, histologic characteristics, and clinical risk factors.

Fifty infants weighing less than 1200 grams at birth who survived at least 3 weeks were enrolled in this study, of whom 14 (28%) developed sonographic evidence of nephrocalcinosis by 9 weeks, despite median total furosemide dose of only 2 mg/kg. Risk factors for development of neonatal nephrocalcinosis were white race (P < 0.01) and positive family history of kidney stones (P < 0.001). Sonography demonstrated echogenic foci measuring 2 to 9 mm near the papillary tips in most infants with nephrocalcinosis even though the kidneys apparently had not progressed through the stages of diffuse medullary echogenicity that Patriquin and Robitaille postulated are the sonographic correlates of the Anderson-Carr-Randall progression, a leading theory of renal calculus formation. The presence of intratubular calcifications in the two patients studied post mortem also is contrary to the Anderson-Carr-Randall theories that center on interstitial calcium deposition. Although neonatal nephrocalcinosis shares some clinical risk factors (white race and positive family history of renal calculi) with renal calcium deposition in older children and adults, the prevalent theories of renal calcium deposition do not account for its sonographic or histologic manifestations.

Adult↗

PubMed1992

[Vitamin D poisoning in infants: a preventable cause of hypercalciuria and nephrocalcinosis].

The established prophylaxis for vitamin D-deficient rickets today is 400 IU vitamin D3 given daily during the first year of life. With this regimen, vitamin D intoxication is a rare event. Nevertheless, we have recently seen 4 infants with vitamin D intoxication after a so called "stoss" prophylaxis, i.e. twice 300,000 units (7.5 mg) vitamin D3 orally within 4 weeks. One patient presented with failure to thrive due to marked hypercalcemia (3.9 mmol/l) and nephrocalcinosis, 2 patients showed medullary nephrocalcinosis on ultrasonography and one patient had gross hematuria and spontaneous passage of a calculus. Three patients had massive hypercalciuria (calcium/creatinine ratio 1.8-4.8 mol/mol, normal less than 1). The 25 (OH) vitamin D3 plasma levels, measured only in 2 patients, were strikingly increased (270 and 158 nmol/l, respectively, normal 25-80). Urinary calcium excretion slowly decreased to normal values on a low calcium diet and high fluid intake. Nephrocalcinosis, however, persisted in 2 patients and showed a slight progression ultrasonographically in one patient. The short time interval between vitamin D administration and onset of symptoms and the subsequent clinical course provide strong evidence that hypercalciuria and nephrocalcinosis were due to vitamin D "stoss" prophylaxis in all four cases. In conclusion, there is no indication for vitamin D "stoss" prophylaxis for vitamin D-deficient rickets in infants. Vitamin D intoxication still has to be considered as a possible cause of hypercalciuria.

Calcifediol↗

PubMed1985

Prognosis of urolithiasis and nephrocalcinosis in hypomagnesemia.

In 78 patients with hypomagnesemia in urolithiasis the clinical course of disease was established in relation to therapy and dynamics of changes of serum magnesium levels. Almost 70% of patients had multiple, bilateral or recurrent nephrolithiasis or nephrocalcinosis. 70% of patients had Ca-oxalate stones or bilateral nephrocalcinosis. In 52% of patients a long-term magnesium supplementation was necessary. Significant progress of nephrolithiasis and nephrocalcinosis was observed in 80% of patients with permanent hypomagnesemia and in 4% of patients with normalization of serum magnesium level. Three of 15 patients with hypomagnesemia and progress of disease were transplanted a kidney and two were treated by hemodialysis. All five patients with renal failure had bilateral nephrocalcinosis, in three of them familiar occurrence of nephrolithiasis and hypomagnesemia was found.

Adolescent↗

PubMed1983

Phosphate and the development of nephrocalcinosis in rats fed diets containing alpha protein.

It has been suggested that nephrocalcinosis in rats fed diets containing alkali-treated soy protein may be due to a high availability of phosphate in the diet. In the present study, the development of nephrocalcinosis in rats fed a diet containing 20% alpha protein (an alkali-treated soy protein) was compared with that in rats fed the same diet supplemented with additional phosphate. Phosphate supplementation of the alpha protein diet produced a form of nephrocalcinosis that was morphologically different, at both the light- and electronmicroscopic level, from that obtained with the unsupplemented diet but was quite similar to that obtained with a phosphate-supplemented standard commercial laboratory diet. Levels of serum and urinary calcium and phosphorus and urinary cyclic AMP suggested that a phosphate-induced secondary hyperparathyroidism was present in the rats fed either of the phosphate-supplemented diets, but not in the rats fed the unsupplemented alpha protein diet. The results of this study suggest that nephrocalcinosis in rats fed a diet containing 20% alpha protein, without additional phosphate, is not typically phosphate-induced.

Animals↗

PubMed1994

Nephrocalcinosis in X-linked hypophosphataemic rickets: its relationship to treatment, kidney function, and growth.

We studied 25 patients treated with oral phosphate and 1,25(OH)2 vitamin D for 0.5-15 y (mean, 7 y) to determine the incidence of nephrocalcinosis and its relationship to treatment, renal function, and growth. During the follow-up period, 3 hypercalcaemic and 13 random hypercalciuric episodes were documented. Creatinine clearances and urine concentration tests were normal in all patients. One patient's 24-h urine specimen indicated hypercalciuria. Kidney ultrasonography revealed nephrocalcinosis in 80% of the patients, but its severity was not significantly related to the dose of calcitriol or of phosphate, the duration of treatment, the age at which treatment was started, or growth. None of the 9 untreated affected family members had nephrocalcinosis. Longitudinal studies revealed that the greatest loss in height velocity occurred during the first 2 y of life. Our study shows that nephrocalcinosis is a common complication of phosphate and 1,25(OH)2D3 treatment, but it is not necessarily associated with impaired renal function. Although the treatment failed to prevent a decrease in height velocity during infancy, it effectively maintained height velocity after 2 y of age.

Adolescent↗

PubMed1988

Nephrocalcinosis in Bartter's syndrome.

Nephrocalcinosis was demonstrated by computerized tomography (CT) in all five children with Bartter's syndrome followed at our institution. In three of these five patients, nephrocalcinosis was also noted on ultrasound examination. Hypercalciuria was present in only one case. The mechanism leading to renal calcification remains unclear in this disease. It is noteworthy, however, that Bartter's syndrome is associated with such a high incidence of nephrocalcinosis.

Adolescent↗

PubMed1984

Nephrocalcinosis in Bartter's syndrome. Demonstration by ultrasonography.

Nephrocalcinosis in Bartter's syndrome has been recognized since 1962, but has not previously been shown in an infant with the syndrome. Ultrasonography shows striking echogenicity of the renal pyramids which appears to be a specific finding in medullary nephrocalcinosis. We suspect nephrocalcinosis will be found in many infants with Bartter's syndrome if ultrasonography is used to examine their kidneys.

Bartter Syndrome↗