Nephrocalcinosis

Adams, Nancy D.; Rowe, Jonelle

doi:10.1016/s0095-5108(18)30481-0

Cited by 54 publications

(44 citation statements)

References 49 publications

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“…Although the etiological factors leading to NC and nephrolithiasis may be similar, it is unclear which factors favor the occurrence of calcifications in one or the other [2, 3] and some patients may present both NC and nephrolithiasis. However, the frequency of medullary sponge kidney, primary hyperparathyroidism, distal renal tubular acidosis and hyperoxaluria is higher among NC patients [4]. …”

Section: Introductionmentioning

confidence: 99%

A Critical Appraisal of the Radiological Evaluation of Nephrocalcinosis

et al. 2007

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Background/Aim: The level of agreement concerning the diagnosis of nephrocalcinosis (NC) based on ultrasonography (US), computed tomography (CT) or kidney/ureter/bladder (KUB) X-ray was assessed. Methods: Sequences of KUB+US+CT from 62 patients, 48 with at least one exam suggesting NC and 14 with pelvicalyceal calcifications (nephrolithiasis) were reviewed twice by 3 radiologists (firstly randomized and secondly presenting KUB+US+CT of each patient together). Results: The intraobserver concordance varied from 76 to 90% for KUB, 77 to 85% for US and 82 to 89% for CT. There was a significant change in diagnosis between the 1st and 2nd reviews for observer 1 in KUB and CT, for observer 2 in US, but not for observer 3. Evaluating patients’ exams together did not provide a better agreement. The highest sensitivity and specificity (92 and 89%, respectively) were only attained when 2 exams suggested NC diagnosis, being CT one of them. These enabled us to suggest that 33 out of 48 (62.5%) patients had NC (evidenced in US+CT+KUB (81.8%), US+CT (12.1%) or KUB+CT (6.1%). Conclusion: The low level of concordance renders the radiological diagnosis of NC difficult. Nephrocalcinosis should be confirmed by CT combined with either US or KUB.

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Section: Introductionmentioning

confidence: 99%

A Critical Appraisal of the Radiological Evaluation of Nephrocalcinosis

et al. 2007

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“…It has been estimated that between 20 and 60% of this patient population develops nephrocalcinosis and nephrolithiasis secondary to the treatment with the loop diuretic [3,4,6]. In 1994, Alon et al [7] reported a small series of older infants who developed nephrocalcinosis in association with furosemide treatment for congestive heart failure.…”

Section: Introductionmentioning

confidence: 99%

Effect of Age on Furosemide-Induced Nephrocalcinosis in the Rat

Osorio

Alon²,

Nichols³

et al. 1998

Neonatology

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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 (µg/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.

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“…10 Supersaturation of urine with calcium results in intratubular crystal formation at the tip of the renal papilla. 7 Increased urinary calcium excretion is a common complication of vitamin D and oral phosphate therapy, and it is associated with nephrocalcinosis. 3,4 HCTZ decreases urinary calcium excretion both by direct tubular effect and by volume depletion, leading to increased distal tubular sodium and calcium resorption.…”

Section: Discussionmentioning

confidence: 99%

“…4 -6 Hypercalcuria also has been shown to be associated with nephrocalcinosis in distal renal tubular acidosis, hyperparathyroidism, prolonged immobilization, Bartter's syndrome, hypophosphatasia, certain tumors, high-dose vitamin D therapy, and idiopathic and drug-induced hypercalcuria. [7][8][9][10][11][12][13] Hydrochlorothiazide (HCTZ) decreases urinary calcium excretion. The effect of HCTZ on nephrocalcinosis in children with XLH is not known.…”

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confidence: 99%

Thiazide Diuretics Arrest the Progression of Nephrocalcinosis in Children With X-Linked Hypophosphatemia

Seikaly

Baum

2001

Pediatrics

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ABSTRACT. Objective. X-linked hypophosphatemia (XLH) is characterized clinically by rickets, hypophosphatemia, and hyperphosphaturia. Conventional treatment of XLH with oral phosphate and vitamin D is associated with increased urinary calcium excretion and nephrocalcinosis. Thiazide diuretics decrease urinary calcium excretion. The objective of this study was to determine the effect of thiazide diuretics on the clinical and radiologic course of nephrocalcinosis in children with XLH.Methods. The effect of hydrochlorothiazide (HCTZ) on clinical and radiologic progression of nephrocalcinosis was evaluated in 11 children with XLH. All patients had been treated previously with vitamin D and oral phosphate and had radiologic evidence of nephrocalcinosis. The average age of the patients at the start of HCTZ was 6.6 ؎ 1.0 years. The effect of oral HCTZ at 0.8 ؎ 0.1 mg/kg body weight per day given for 3.3 ؎ 0.6 years on the progression of nephrocalcinosis and urinary calcium excretion was evaluated.Results. There was no change in serum phosphorous, calcium, potassium, and chloride after HCTZ therapy. HCTZ therapy increased serum bicarbonate and decreased urinary calcium excretion. The grade of nephrocalcinosis increased from 0.4 ؎ 0.2 to 1.5 ؎ 0.3 in the 2.3 ؎ 0.3 years before initiation of HCTZ therapy, whereas the degree of nephrocalcinosis was stable after 3.3 ؎ 0.6 years of HCTZ therapy (1.5 ؎ 0.3 vs 3.0 ؎ 0.3).Conclusion. HCTZ decreased urinary calcium excretion but did not result in the resolution of nephrocalcinosis. However, when compared with the control period, HCTZ prevented the progression of nephrocalcinosis in children with XLH. Pediatrics 2001;108(1). URL: http:// www.pediatrics.org/cgi/content/full/108/1/e6; X-linked hypophosphatemia, rickets, nephrocalcinosis, thiazide diuretics.ABBREVIATIONS. XLH, X-linked hypophosphatemia; HCTZ, hydrochlorothiazide; TmP/GFR, tubular maximum reabsorption of phosphate per deciliter of glomerular filtration; SEM, standard error of the mean. X -linked hypophosphatemia (XLH) is the most common inherited cause of rickets. It is characterized by hypophosphatemia caused by impaired proximal tubular reabsorption of phosphorous and an inappropriately normal serum level of 1,25(OH) 2 vitamin D. The resulting hypophosphatemia leads to defective bone mineralization. 1 Current therapy includes administration of 1,25(OH) 2 vitamin D (calcitriol) and phosphate to replete urinary phosphate losses without stimulating parathyroid hormone release. 2 Such therapy often leads to hypercalcuria and nephrocalcinosis. 3,4 Nephrocalcinosis can lead to renal tubular acidosis and possibly renal insufficiency. 4 -6 Hypercalcuria also has been shown to be associated with nephrocalcinosis in distal renal tubular acidosis, hyperparathyroidism, prolonged immobilization, Bartter's syndrome, hypophosphatasia, certain tumors, high-dose vitamin D therapy, and idiopathic and drug-induced hypercalcuria. 7-13 Hydrochlorothiazide (HCTZ) decreases urinary calcium excretion. The effect of HCTZ on nephrocalcino...

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Nephrocalcinosis

Cited by 54 publications

References 49 publications

A Critical Appraisal of the Radiological Evaluation of Nephrocalcinosis

A Critical Appraisal of the Radiological Evaluation of Nephrocalcinosis

Effect of Age on Furosemide-Induced Nephrocalcinosis in the Rat

Thiazide Diuretics Arrest the Progression of Nephrocalcinosis in Children With X-Linked Hypophosphatemia

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