Antibiotic treatment-induced tubular dysfunction as a risk factor for renal stone formation in cystic fibrosis

Böhles, Hansjosef; Gebhardt, Boris; Beeg, T.; Sewell, A. C.; Solem, Eivind; Posselt, G.

doi:10.1067/mpd.2002.120694

Cited by 23 publications

(9 citation statements)

References 14 publications

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“…In the present study, an increased urinary calcium excretion was observed in 18% of patients. These results are similar to those reported by other studies (12-20%) [5,29]. Hypercalciuria may be explained by mild intermittent hyperparathyroidism due to a lack of vitamin D [28] or to proximal tubule antibiotic toxicity leading to renal loss of phosphorus [29].…”

Section: Discussionsupporting

confidence: 92%

“…These results are similar to those reported by other studies (12-20%) [5,29]. Hypercalciuria may be explained by mild intermittent hyperparathyroidism due to a lack of vitamin D [28] or to proximal tubule antibiotic toxicity leading to renal loss of phosphorus [29]. Moreover, increased sodium excretion (due to oral supplementation) in the proximal tubule induces parallel urinary calcium excretion [32].…”

Section: Discussionsupporting

confidence: 91%

“…The early onset of lithiasis, within the first year of life for both our patients, contrasts with previous studies in which the first urolithiasic episode occurred in adolescents or young adults, and in only one five-year old child [28,29]. In the present study, one patient presented with multiple bilateral microlithiases at the age of 3 months, with the only risk factor identified being isolated hypocitraturia.…”

Section: Discussioncontrasting

confidence: 85%

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Renal impairment in children with cystic fibrosis

Andrieux

Harambat

Bui

et al. 2010

Journal of Cystic Fibrosis

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Section: Discussioncontrasting

confidence: 85%

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Renal impairment in children with cystic fibrosis

Andrieux

Harambat

Bui

et al. 2010

Journal of Cystic Fibrosis

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“…115,116 Most patients with cystic fibrosis exhibit hyperoxaluria and hypocitraturia, these anomalies being more marked in those affected by stone formation or nephrocalcinosis. [117][118][119][120] Absence of Oxalobacter formigenes in the gut may also be a favoring lithogenic factor in idiopathic calcium stone formers.…”

Section: Antibacterial Agents In Cystic Fibrosismentioning

confidence: 95%

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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“…Renal transplant recipients are at increased risk of infection stones in the setting of concomitant hyperparathyroidism, hypercalciuria, recurrent UTI, hypocitraturia, or urinary tract obstruction [11]. Patients with cystic fibrosis were reported to be at increased risk of infection stones as a result of renal tubular dysfunction caused by chronic antibiotic exposure [12].…”

Section: Infection Stonesmentioning

confidence: 99%

Management of Urinary Tract Infections Associated with Nephrolithiasis

Brown

2010

Curr Infect Dis Rep

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Nephrolithiasis is a common clinical entity, and the incidence of renal stones appears to be increasing in the United States. Infection with uropathogens that produce urease can lead to the development of stones (infection stones), which serve as a continued source of recurrent infection and can lead to chronic kidney disease. Other than treating infection, medical management has little role in the treatment of infection stones; complete eradication of the stones with percutaneous nephrolithotomy or extracorporeal shock wave lithotripsy is required. Stones of metabolic origin can cause obstruction in the ureter and predispose to the development of urinary tract infection (UTI). Recognizing obstruction and initiating prompt drainage of the collecting system is important in the successful management of nephrolithiasis complicated by UTI. These patients are often at high risk of infection with an antimicrobial-resistant pathogen, so careful consideration of antimicrobial therapy is required, especially for patients who present with severe sepsis.

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Antibiotic treatment-induced tubular dysfunction as a risk factor for renal stone formation in cystic fibrosis

Cited by 23 publications

References 14 publications

Renal impairment in children with cystic fibrosis

Renal impairment in children with cystic fibrosis

Drug-Induced Renal Stones

Management of Urinary Tract Infections Associated with Nephrolithiasis

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