Medullary nephrocalcinosis associated with long‐term furosemide abuse in adults

Kim, Yoon Goo; Kim, Bohyun; Kim, Mi Kyung; Chung, Shi Jung; Han, Hyeok Jun; Ryu, Jeong Ah; Lee, Yoonha; Lee, Kyu Beck; Lee, Jee Yun; Huh, Wooseong; Oh, Ha Young

doi:10.1093/ndt/16.12.2303

Cited by 40 publications

(21 citation statements)

References 29 publications

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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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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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“…Her low urinary potassium excretion does not disprove diuretic misuse, because she was taking a potassium‐sparing diuretic (spironolactone), and her diuretic misuse may have been intermittent. Indeed, chronic use of frusemide for weight control has been associated with nephrocalcinosis in patients without anorexia nervosa 14 , 15 . Chronic diarrhoea may contribute to nephrocalcinosis by causing volume depletion.…”

mentioning

confidence: 99%

Severe renal failure and nephrocalcinosis in anorexia nervosa

Roberts

MacGregor

Paoletti

et al. 2005

Medical Journal of Australia

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“…113 Medullary nephrocalcinosis has been reported in 18 women who had long-term furosemide abuse for the purpose of slimming. 114 However, no cases of calcium nephrolithiasis have been reported in hypertensive patients treated with furosemide.…”

Section: Furosemidementioning

confidence: 99%

Drug-Induced Renal Stones

Daudon

Jungers²

2010

Urinary Tract Stone Disease

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Drug-induced stones represent about 1% of all renal stones. They involve two main mechanisms. The first one includes stones made of the drug and/or its metabolites identified by X-ray diffraction or infrared spectroscopy on the basis of their specific diagrams. Nowadays, the most commonly observed ones are antiproteases (such as indinavir) used in HIV-infected patients, high-dose sulfadiazine used for the treatment of cerebral toxoplasmosis, and abuse of ephedrine/guaifenesin-containing preparations, whereas triamterene, formerly the most often involved drug, is less frequently observed. The second one includes stones of common composition, induced by the metabolic effects of the drug on urinary pH and excretion of calcium, oxalate, phosphate, citrate, uric acid, or other purines. The most frequent causes are unsupervised calcium/vitamin D supplementation and carbonic anhydrase inhibitors, including anticonvulsants (such as topiramate). Incidence of metabolically induced stones is probably underestimated, because they are of apparently usual composition and may reveal long after drug withdrawal. Formation of iatrogenic calculi is favored by high-dose or long-lasting treatments, high renal excretion and low solubility of the drug or its metabolites, low urine output or inadequate urine pH, and is especially frequent in patients with a history of stones. Better awareness of potentially lithogenic drugs may allow more efficient prevention and reduce the incidence of drug-induced nephrolithiasis.

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Medullary nephrocalcinosis associated with long‐term furosemide abuse in adults

Cited by 40 publications

References 29 publications

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

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

Severe renal failure and nephrocalcinosis in anorexia nervosa

Drug-Induced Renal Stones

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