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Results for “NEPHROCALCINOSIS”

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PubMed2005

Preconditioning of the distal tubular epithelium of the human kidney precedes nephrocalcinosis.

BACKGROUND: Preterm neonates and renal transplant patients frequently develop nephrocalcinosis. Experimental studies revealed that crystal retention in the distal nephron, a process that may lead to nephrocalcinosis, is limited to proliferating/regenerating tubular cells expressing hyaluronan and osteopontin at their luminal surface. Fetal and transplant kidneys contain proliferating and/or regenerating cells since nephrogenesis is not completed until 36 weeks of gestation, while ischemia and nephrotoxic immunosuppressants may lead to injury and repair in renal transplants. This prompted us to investigate the expression of hyaluronan and osteopontin and to correlate this to the appearance of tubular calcifications both in fetal/preterm and transplanted kidneys. METHODS: Sections of fetal/preterm kidneys and protocol biopsies of transplanted kidneys (12 and 24 weeks posttransplantation from the same patients) were stained for osteopontin, hyaluronan, and calcifications (von Kossa). RESULTS: Hyaluronan and osteopontin were expressed at the luminal surface of the epithelial cells lining the distal tubules of all fetal kidneys at birth and in all kidney graft protocol biopsies 12 and 24 weeks posttransplantation. In 7 out of 18 surviving (at least 4 days) preterm neonates crystal retention developed. In renal allografts a striking increase (from 2/10 to 6/10) in tubular crystal retention between 12 and 24 weeks posttransplantation was observed. In addition, crystals were selectively retained in distal renal tubules containing cells with hyaluronan and osteopontin at their luminal surface. CONCLUSION: The results of this study show that luminal expression of hyaluronan and osteopontin preceded renal distal tubular retention of crystals in preterm neonates and renal transplant patients. We propose that the presence of this crystal binding phenotype may play a general role in renal calcification processes.

Cell Division↗

PubMedDate not supplied

Nephrocalcinosis, hypercalciuria and elevated serum levels of 1,25-dihydroxyvitamin D in children. Possible link to vitamin D toxicity.

Ten children age 1 1/2 to 14 years, had bilateral nephrocalcinosis and hypercalciuria, but normal serum calcium (Ca) and phosphate (P) concentrations. Patients with hypercalciuria were divided into absorptive (n = 4) and renal (n = 6) subgroups, and in the latter four patients had a primary Ca-leak and two had a P-leak. All the children had received intermittent high dose vitamin D prophylaxis during infancy. At the time of investigation all had normal serum levels of 25-hydroxyvitamin D, yet all but one had elevated values of 1,25-(OH)2D. Although the hypercalciuria was indistinguishable from the various known forms of idiopathic hypercalciuria, the previous clinical course and the pattern of bone mineral homeostasis suggest that both clinical features, namely nephrocalcinosis and hypercalciuria were related to vitamin D toxicity through various pathogenetic pathways.

Adolescent↗

PubMed1993

Renal function in hyperparathyroidism with complicating nephrocalcinosis.

Primary hyperparathyroidism in childhood is rare. Long-standing hypercalcaemia is reported to result in severe and irreversible renal damage. However, renal complications of hyperparathyroidism, particularly nephrocalcinosis are uncommon. We report a 12-year-old girl presenting after three years with extensive nephrocalcinosis and with rapid recovery of renal function.

Adenoma↗

PubMed1989

Nephrocalcinosis in Shwachman's syndrome.

Nephrocalcinosis has been reported only infrequently in Shwachman's syndrome. We describe a case in which nephrocalcinosis occurred and speculate that this may be due to increased urinary oxalate excretion.

Bone Marrow Diseases↗

PubMed1989

Diffuse nephrocalcinosis and idiopathic renal hypercalciuria.

A 12 year old boy presented with primary nocturnal enuresis. Investigation showed extensive bilateral nephrocalcinosis of no obvious or recognised cause. Persistent severe renal hypercalciuria was confirmed by an intravenous calcium infusion. Idiopathic hypercalciuria is not a common cause of nephrocalcinosis and has not previously been described in a child.

Calcium↗

PubMed2000

Urinary oxalate excretion in urolithiasis and nephrocalcinosis.

AIMS: To investigate urinary oxalate excretion in children with urolithiasis and/or nephrocalcinosis and to classify hyperoxaluria (HyOx). METHODS: A total of 106 patients were screened. In those in whom the oxalate: creatinine ratio was increased, 24 hour urinary oxalate excretion was measured. Liver biopsy and/or genomic analysis was performed if primary hyperoxaluria (PH) was suspected. Stool specimens were examined for Oxalobacter formigenes in HyOx not related to PH type 1 or 2 (PH1, PH2) and in controls. RESULTS: A total of 21 patients screened had HyOx (>0.5 mmol/24 h per 1.73 m(2)); they were classified into five groups. Eleven had PH (PH1 in nine and neither PH1 nor PH2 in two). Six had secondary HyOx: two enteric and four dietary. Four could not be classified. Seven patients had concomitant hypercalciuria. Only one of 12 patients was colonised with O formigenes compared to six of 13 controls. CONCLUSIONS: HyOx is an important risk factor for urolithiasis and nephrocalcinosis in children, and can coexist with hypercalciuria. A novel type of PH is proposed. Absence of O formigenes may contribute to HyOx not related to PH1.

Adolescent↗

PubMed1998

Effect of age on furosemide-induced nephrocalcinosis in the rat.

Furosemide (F)-induced nephrocalcinosis (NC) has been traditionally described in low birth weight premature infants. To investigate the role of age on F-induced nephrocalcinosis we studied 24 Sprague-Dawley male rats grouped by age and F therapy vs. control as follows: A (4-week-old control), B (4-week-old + F), C (6-week-old control), D (6-week-old + F), E (10-week-old control), F (10-week-old + F). The rats were placed in metabolic cages for measurement of urine output, food and water intake. At day 14 they were anesthetized, exsanguinated and their kidneys harvested. Renal calcium deposition was assessed using NC score (scale 0-4) and quantitative calcium analysis in the contralateral kidney. Treated animals gained less weight and had higher urine output and fluid intake than the age-matched controls demonstrating the diuretic effect of furosemide. Control groups A, C, and E scored 0 histologically compared with B 2.75 +/- 0.50, D 2.00 +/- 0.58, and F 3.00 +/- 0.82 (p < 0.05 in all three paired groups). Kidney calcium content (micrograms/g dry weight) in B was 2,815.68 +/- 1,553.77 vs. A 202.58 +/- 32.02 (p = 0.04); D 1,574.05 +/- 540.21 vs. C 212.22 +/- 30.91 (p = 0.02); F 2,591.40 +/- 1,269.80 vs. E 210.38 +/- 26.79 (p = 0.02). There was no difference in the magnitude of NC among the three treated groups themselves. To determine the possible effect of age on timing of onset of NC additional 30 4-week-old and 30 10-week-old rats were studied. All 60 rats received furosemide. Six rats from each group were sacrificed on days 1, 3, 5, 7 and 11. In both groups, significant calcifications were seen already on day 3 and maximum calcification noted between days 3 and 5. We conclude that in this model the development of NC occurs within a few days of furosemide administration and that this phenomenon is not age dependent but rather reflects a property of the loop diuretic itself.

Aging↗

PubMed2006

Ibandronate for the treatment of hypercalcemia or nephrocalcinosis in patients with multiple myeloma and acute renal failure: Case reports.

Multiple myeloma disrupts calcium homeostasis by a variety of mechanisms, including bone destruction and resorption. This causes hypercalcemia. When left untreated, hypercalcemia leads to nephrocalcinosis, impairment of kidney function, and eventually renal failure. Some degree of renal dysfunction is common in myeloma patients. Here, we report case studies showing the efficacy and renal safety of the single-nitrogen bisphosphonate, ibandronate, for the treatment of hypercalcemia and/or nephrocalcinosis in multiple myeloma patients hospitalized with acute renal failure. Patients (n = 7) received either one or two intravenous infusions of ibandronate (2-6 mg). Ibandronate was well tolerated in all patients and returned elevated blood calcium levels to normal. Renal function improved for all patients and normalized in 3/7 patients. We conclude that ibandronate is involved in rapidly improving or restoring acute renal function and calcium levels to within the normal range in this patient population. To clarify the exact value of ibandronate, further investigation is warranted in randomized prospective trials.

Acute Kidney Injury↗

PubMed1985

Distal renal tubular acidosis and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism. Report of 1 case without nephrocalcinosis.

In a 33-year-old woman concurrence of a complete distal renal tubular acidosis (RTA) and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism was observed. Until recently, the rare association of RTA and hyperthyroidism had been thought to be governed by nephrocalcinosis, via hypercalcemia and hypercalciuria. However, in this case, nephrocalcinosis was not present, but there were histological signs of renal interstitial mononuclear cell infiltration, and the RTA persisted despite the resolution of the hyperthyroidism. This observation supports the idea that immunological mechanisms may relate RTA and hyperthyroidism when the latter has an autoimmune origin.

Acidosis, Renal Tubular↗

PubMed1983

X-ray microanalysis of uremic nephrocalcinosis.

The nature of uremic nephrocalcinosis was studied by means of X-ray microanalysis in 5/6 nephrectomized rats. The data show that calcified deposits in the renal parenchyma of uremic rats contained substantial amounts of calcium, magnesium, aluminum and silicon. Since calcificates did not reveal a uniform composition they were arbitrarily divided into 3 categories: 'high-calcium' with Mg:Al:Si: Ca molar ratios 7:3:8:37; 'low-calcium' particles were characterized by Fe:Mg:Al:Ca:Si molar ratios 7:3:5:6:13; while 'intermediate-calcium' particles showed Al:Mg:Si:Ca molar ratios equivalent to 2:4:6:7. The variability of calcified deposits in the renal parenchyma of 5/6 nephrectomized rats might be due to different sources, different environmental conditions along the nephron and different stages of calcification process. It is suggested that aluminum and silicon content of deposits may be of value in further characterization of uremic nephrocalcinosis.

Aluminum↗

PubMed1993

Hypercalciuria and nephrocalcinosis, a feature of Wilson's disease.

Hypercalciuria and nephrocalcinosis are not uncommon in patients with Wilson's disease but have only once been reported as the presenting sign. We diagnosed Wilson's disease in a 17-year-old male patient 6 years after his first episode of gross hematuria and 2 years after detection of hypercalciuria and nephrocalcinosis. Therapy with penicillamine resulted only in a moderate reduction of urinary calcium excretion but oxalate excretion increased.

Adolescent↗

PubMed1995

Nephrocalcinosis and prematurity: importance of urate and oxalate excretion.

Nephrocalcinosis was described in preterm infants by several authors who tried to determine its association with hypercalciuria and furosemide therapy. We evaluated these potential mechanisms along with other lithogenic factors not previously studied in 10 premature babies. Hypercalciuria was an inconsistent finding like in other reports; elevated uric acid excretion and hyperoxaluria were observed in 5 and 6 cases, respectively. The aminocid excretion was normal in all infants. Our data suggest that in addition to hypercalciuria, other lithogenic factors may play a role in the pathophysiology of nephrocalcinosis of premature infants.

Glycosuria↗

PubMed1987

Extensive glomerular immaturity associated with renal tubular acidosis, nephrogenic diabetes insipidus and nephrocalcinosis.

Neonatal renal failure and glomerular immaturity have been described in 1983. The present paper describes 3 cases with the same histological features. However, follow-up of the patients during 14, 18 and 4 years, respectively, showed the following: The histologic immaturity may be followed by maturation. Thus, late maturation may be a term more suitable to designate this constellation. Renal failure may not necessarily ensue, at least not during early infancy. In the 3 cases presented in this report, the histological finding is associated with renal tubular acidosis, renal diabetes insipidus and nephrocalcinosis. The association of transient glomerular immaturity (or late glomerular maturation) and renal tubular acidosis may enhance the development of nephrocalcinosis.

Acidosis, Renal Tubular↗

PubMed1981

The ultrastructure of nephrocalcinosis induced in chicks by Cestrum diurnum leaves.

Powdered Cestrum diurnum leaves, mixed with two diets differing in calcium and phosphorus contents, produced nephrocalcinosis in young chicks regardless of serum calcium elevation. The calcific deposits, found in both proximal and distal portions of cortical tubules, began either in the cytoplasm or in lysosomal bodies as a unilaminar spheroid structure containing apatite crystals. The ultrastructural characteristics of intraluminal concretions suggested that they were formed intracellularly but later were extruded into the lumen. The extent of calcific deposits increased with duration and with hypercalcemia. Although Cestrum contains an analog of 1,25-dihydroxycholecalciferol, neither mitochondria nor basal lamina contained calcific deposits described in nephrocalcinosis secondary to hypervitaminosis D.

Animals↗

PubMed1980

Nephrocalcinosis in 2 young rats: a case report.

Nephrocalcinosis was diagnosed as an incidental histopathological finding in 2 Sprague-Dawley rats of 150 g bodyweight. The calcified material was located along the entire corticomedullary junction. Dietary and other causes of nephrocalcinosis are discussed.

Animal Nutritional Physiological Phenomena↗

PubMed1991

In-vivo monitoring of corticomedullary nephrocalcinosis in rats using computerized tomography.

An in-vivo method, computerized tomography (CT), was used to monitor nephrocalcinosis in female rats. CT density data correlated well with renal Ca content measured by atomic absorption spectrophotometry. In-vivo CT measurements revealed that the severity of nephrocalcinosis may change spontaneously with time. Manifest calcifications may exhibit spontaneous regression and are probably affected positively by high dietary Mg, in contrast to increased Ca. It is concluded that CT is a suitable and reliable non-invasive in vivo method to follow up time-dependent alterations in kidney calcifications in rats.

Animals↗

PubMed1997

Medullary nephrocalcinosis associated with vesicoureteral reflux.

A case of medullary nephrocalcinosis developing in the course of vesicoureteral reflux is described. It is suggested that the probable mechanism of nephrocalcinosis was the stagnation of urine in collecting tubules favouring precipitation of calcium salts.

Child, Preschool↗

PubMed2006

Oral alendronate therapy for severe vitamin D intoxication of the infant with nephrocalcinosis.

Vitamin D intoxication is a well-known cause of hypercalcemia in children. We report here the use of oral alendronate for the treatment of hypercalcemia due to vitamin D intoxication in a 7 month-old infant with nephrocalcinosis. The serum calcium levels were normalized without complications. Oral alendronate therapy may be safely used in hypercalcemia due to vitamin. D intoxication in pediatric patients with nephrocalcinosis resistant to hydration, diuretics or corticosteroids.

Administration, Oral↗