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

Saarela, Timo; Lanning, P; Koivisto, Maila; Paavilainen, Teemu

doi:10.1007/s004310051173

Cited by 34 publications

(20 citation statements)

References 18 publications

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“…Ultrasonographic resolution of the renal calcifications has been well documented in children with furosemideassociated NC after discontinuation of the loop diuretic [6,7,8]. In some children the resolution occurred sponta- neously, whereas in others after furosemide was replaced by thiazide diuretics [7].…”

Section: Discussionmentioning

confidence: 96%

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Resolution of medullary nephrocalcinosis in children with metabolic bone disorders

Auron

Alon

2005

Pediatr Nephrol

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Ultrasonographic resolution of nephrocalcinosis (NC) has been reported in children with furosemide-induced NC, but not in other entities. We report the cases of four children with metabolic bone disease, two with hypophosphatasia and two with X-linked hypophosphatemic rickets, in whom we observed resolution of renal calcifications. At the time of ultrasonographic resolution of NC, 3 of the patients were on anticalciuric diuretics, and all 4 had normal urinalysis, serum creatinine and electrolyte profiles, as well as estimated creatinine clearance. In 3 of the children, evidence of mild tubular dysfunction was found. It thus seems that in some children with bone and mineral disorders who develop NC, ultrasonographic resolution of the renal calcifications can be seen; however, mild tubular dysfunction may remain and require follow-up. Further studies are suggested to explore the possible role of anticalciuric diuretics in promoting the resolution of NC.

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Section: Discussionmentioning

confidence: 96%

“…Ultrasonographic resolution has been often documented in children with furosemide-associated NC after discontinuation of the loop diuretic [6,7,8,9]. However, there have been no reports of resolution of NC in other entities.…”

Section: Introductionmentioning

confidence: 96%

Resolution of medullary nephrocalcinosis in children with metabolic bone disorders

Auron

Alon

2005

Pediatr Nephrol

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“…The creatinine level would not necessarily suggest other structural abnormalities with long-term consequences. For example, the administration of frusemide is a known risk factor for the development of nephrocalcinosis [17,18,19]. The higher incidence of acute renal failure may result in the increased utilization of frusemide, which may have long-term sequelae, but neither longer-term follow-up, nor serial imaging of treatment infants and their controls were performed in this study.…”

Section: Discussionmentioning

confidence: 99%

Indomethacin and renal impairment in neonates

Akima

Kent

Reynolds

et al. 2004

Pediatric Nephrology

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Renal impairment occurs in neonates receiving indomethacin for treatment of patent ductus arteriosus. Inhibition of cyclooxygenase within the neonatal kidney results in decreased prostaglandin synthesis and consequent reduction in renal perfusion. Indomethacin has been reported to cause short-term reduction in glomerular filtration that resolves after cessation of the drug. There is little information on the long-term effects of postnatal exposure to indomethacin. The aim of this study was to determine the incidence of renal impairment in infants treated with indomethacin in a single center, to determine whether there is evidence of renal impairment on day 30 or at discharge, and to identify risk factors for renal impairment. In a retrospective study, infants of less than 30 weeks completed gestation who received indomethacin to close the ductus arteriosus were matched with infants of the same gestation, birth weight, and severity of illness. Serum creatinine and glomerular filtration rates (GFR) were obtained prior to commencing indomethacin and on days 2, 7, and 30 following indomethacin administration. Acute renal failure was defined as an increase in creatinine of greater than 25%. Of those infants who were less than 30 weeks completed gestation, 24% had acute renal failure following indomethacin administration. There was a significant elevation in serum creatinine on day 2 and day 7 ( P<0.0001, P=0.002) and a decrease in GFR on day 2 and day 7 ( P<0.0001, P=0.01) following administration of indomethacin. Renal function had normalized by day 30 or discharge. The incidence of acute renal failure in neonates treated with indomethacin is clinically significant. Renal function returns to normal by day 30. Linear regression found no statistical significance for gestational age, day of indomethacin dosing, Clinical Risk Index for Babies (CRIB) score, and presence of an umbilical artery catheter to confound the effect of indomethacin on renal function.

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“…95 Other disorders result from complications arising from the use or abuse of medicines such as dexamethasone and furosemide. 96,97 Both medicines are given to very low birth weight premature The kidney produces all components of the renin-angiotensin system (RAS), and the intrarenal RAS plays a major role in renal disease progression. [148][149] Kidneys produce both angiotensinogen and angiotensin converting enzymte (ACE), and the juxtaglomerular apparatus is the main source of circulating renin.…”

Section: Calcium Phosphate Crystalsmentioning

confidence: 99%

Crystal-induced inflammation of the kidneys: results from human studies, animal models, and tissue-culture studies

2004

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Calcium oxalate (CaOx), calcium phosphate (CaP), and uric acid or urate are the most common crystals seen in the kidneys. Most of the crystals evoke an inflammatory response leading to fibrosis, loss of nephrons, and eventually to chronic renal failure. Of the three, CaOx monohydrate is the most reactive, whereas some forms of CaP do not evoke any discernible response. Reactive oxygen species are produced during the interactions between the crystals and renal cells and are responsible for the various cellular responses. CaOx crystals generally form in the renal tubules. Exposure of renal epithelial cells to CaOx crystals results in the increased synthesis of osteopontin, bikunin, heparan sulfate, monocyte chemoattractant protein 1 (MCP-1), and prostaglandin (PG) E2, which are known to participate in inflammatory processes and in extracellular matrix production. CaOx crystal deposition in rat kidneys also activates the renin-angiotensin system. Both Ox and CaOx crystals selectively activate p38 mitogen-activated protein kinase (MAPK) in exposed tubular cells. CaP crystals can form in the tubular lumen, tubular cells, or tubular basement membrane. Renal epithelial cells exposed to brushite crystals produce MCP-1. Basic CaP and calcium pyrophosphate dihydrate induce mitogenesis in fibroblasts, stimulate production of PGE2, and up-regulate the synthesis of metalloproteinases (MMP) while down-regulating the production of inhibitors of MMPs through activation of p42/44 MAPK. Deposition of urate crystals in the kidneys becomes associated with renal tubular atrophy, interstitial fibrosis, and development of inflammatory infiltrate. Renal epithelial cells exposed to uric acid crystals synthesize MCP-1 as well as PGE2. Monocytes or neutrophils exposed to urate crystals produce tumor necrosis factor alpha, interleukin-1 (IL-1), IL-6, and IL-8. Expression of IL-8 is mediated through extracellular signal-regulated kinase 1 (ERK-1)/ERK-2 and nuclear transcription factors activated protein 1 and nuclear factor kappabeta. Urate crystals also stimulate the macrophages to produce MMPs.

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

Cited by 34 publications

References 18 publications

Resolution of medullary nephrocalcinosis in children with metabolic bone disorders

Resolution of medullary nephrocalcinosis in children with metabolic bone disorders

Indomethacin and renal impairment in neonates

Crystal-induced inflammation of the kidneys: results from human studies, animal models, and tissue-culture studies

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