Urolithiasis in pediatric patients with acute lymphoblastic leukemia

Sc, Howard; Sd, Kaplan; Razzouk, Bassem I.; Rivera, GK; Jt, Sandlund; Rc, Ribeiro; Rubnitz, Jeffrey E.; Aj, Gajjar; Ke, Wei; Ml, Hancock; Jp, Skoch; S, Roy; Hudson, Melissa M.; Ch, Pui

doi:10.1038/sj.leu.2402852

Cited by 29 publications

(51 citation statements)

References 30 publications

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“…Howard et al suggested glucocorticoids as a cause of urolithiasis in children with ALL [14]; however, urolithiasis was never observed in our study group throughout the follow-up period although we used a high-dose methylprednisolone protocol. Other factors such as ethnicity or small sample size might have affected the urolithiasis incidence in our group.…”

Section: Discussionmentioning

confidence: 63%

Evaluation of kidney damage in patients with acute lymphoblastic leukemia in long‐term follow‐up: Value of renal scan

Yetgin

Olgar

Aras³

et al. 2004

American J Hematol

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In order to evaluate potential long-term kidney damage of childhood leukemia and risk factors affecting renal damage, we studied 116 children treated for acute lymphoblastic leukemia (ALL) using the St. Jude Total XI and XIII protocols in 1991-1998. The median follow-up period after the completion of treatment was 35 months. The following parameters were examined: urinalysis, urinary creatinine (Cr), calcium (Ca), phosphorus, b 2 -microglobulin, glomerular filtration rate (GFR), tubular phosphorus reabsorption (TPR), and renal function tests. Radiological evaluation included renal ultrasonography (US), and renal scans with DMSA or MAG-3 were performed. Blood chemistry and renal US patients were normal in all patients except two. GFR, TPR, urinary Ca/Cr, b 2 -microglobulin, and renal scan were abnormal in 19.0%, 16.4%, 13.8%, 6.0%, and 40.5% of patients, respectively. The abnormality rate in GFR was significantly higher in patients<2 years of age. TPR abnormality was found to be significantly higher in patients who did not have G-CSF. An abnormal renal scan was associated with Hb< 10 g/dL, kidney infiltration, or hypertension at presentation and also occurred patients who underwent methotrexate treatment with frequent intervals during the follow-up period. Patients should be followed-up after cessation of therapy with the conventional tests mentioned above. In case of any abnormality, further detailed tests should be performed; renal scan seems to be more predictive for renal damage. Am.

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Section: Discussionmentioning

confidence: 63%

Evaluation of kidney damage in patients with acute lymphoblastic leukemia in long‐term follow‐up: Value of renal scan

Yetgin

Olgar

Aras³

et al. 2004

American J Hematol

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“…Previous extensive reports demonstrating this include a pediatric study of over 2,000 children treated for ALL and a Korean study of over 900 adults who were treated for both lymphoproliferative and myeloproliferative disorders (5,8). Both investigations demonstrated that the incidence of nephrolithiasis in these populations was significantly higher than in the general population.…”

Section: Discussionmentioning

confidence: 99%

“…Steroids are used in multiple contexts for lymphoproliferative diseases and can increase the risk of nephrolithiasis by decreasing renal calcium absorption. The authors cited the predominance of calcium-based stones as opposed to uric acid stones as evidence supporting the steroid-nephrolithiasis hypothesis (8). However, almost half of stone analyses in the Korean adult study showed uric acid stones despite the common use of glucocorticoid therapy (5).…”

Section: Discussionmentioning

confidence: 99%

“…There are case reports documenting nephrolithiasis among patients receiving chemotherapy for these disorders (5-7), and a single study examined a larger cohort (5). Moreover, risk factors for nephrolithiasis in patients undergoing chemotherapy have been identified in the pediatric literature but not in an adult chemotherapy population (8). We therefore sought to identify the incidence and risk factors of de novo nephrolithiasis after chemotherapy in adult patients with lymphoproliferative or myeloproliferative disorders.…”

Section: Introductionmentioning

confidence: 99%

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What is the Incidence of Kidney Stones after Chemotherapy in Patients with Lymphoproliferative or Myeloproliferative Disorders?

et al. 2014

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ARTICLE INFO ______________________________________________________________ ______________________Introduction: This study describes the incidence and risk factors of de novo nephrolithiasis among patients with lymphoproliferative or myeloproliferative diseases who have undergone chemotherapy. Materials and Methods: From 2001 to 2011, patients with lymphoproliferative or myeloproliferative disorders treated with chemotherapy were retrospectively identified. The incidence of image proven nephrolithiasis after chemotherapy was determined. Demographic and clinical variables were recorded. Patients with a history of nephrolithiasis prior to chemotherapy were excluded. The primary outcome was incidence of nephrolithiasis, and secondary outcomes were risk factors predictive of de novo stone. Comparative statistics were used to compare demographic and disease specific variables for patients who developed de novo stones versus those who did not.Results: A total of 1,316 patients were identified and the incidence of de novo nephrolithiasis was 5.5% (72/1316; symptomatic stones 1.8% 24/1316). Among patients with nephrolithiasis, 72.2% had lymphoproliferative disorders, 27.8% had myeloproliferative disorders, and 25% utilized allopurinol. The median urinary pH was 5.5, and the mean serum uric acid, calcium, potassium and phosphorus levels were 7.5, 9.6, 4.3, and 3.8 mg/dL, respectively. In univariate analysis, mean uric acid (p=0.013), calcium (p<0.001)), and potassium (p=0.039) levels were higher in stone formers. Diabetes mellitus (p<0.001), hypertension (p=0.003), and hyperlipidemia (p<0.001) were more common in stone formers. In multivariate analysis, diabetes mellitus, hyperuricemia, and hypercalcemia predicted stone. Conclusions: We report the incidence of de novo nephrolithiasis in patients who have undergone chemotherapy. Diabetes mellitus, hyperuricemia, and hypercalcemia are patient--specific risk factors that increase the odds of developing an upper tract stone following chemotherapy.

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“…1 Corticosteroid therapy induces hypercalciuria and hyperphosphaturia, although formation of urinary calculi is infrequent. 123,124 Ascorbic acid (vitamin C) overdosing increases urinary oxalate excretion 125,126 and therefore may result in calcium oxalate nephrolithiasis. 127 However, epidemiological studies failed to observe an association between high vitamin C ingestion and incidence of stones, both in men 128 and in women.…”

Section: Other Drugsmentioning

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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Urolithiasis in pediatric patients with acute lymphoblastic leukemia

Cited by 29 publications

References 30 publications

Evaluation of kidney damage in patients with acute lymphoblastic leukemia in long‐term follow‐up: Value of renal scan

Evaluation of kidney damage in patients with acute lymphoblastic leukemia in long‐term follow‐up: Value of renal scan

What is the Incidence of Kidney Stones after Chemotherapy in Patients with Lymphoproliferative or Myeloproliferative Disorders?

Drug-Induced Renal Stones

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