Glomerular filtration rate and prevalence of chronic kidney disease in Wilms’ tumour survivors

Glomerular filtration rate (GFR) was evaluated in 32 Wilms’ tumour survivors (WTs) in a cross-sectional study using 99 Tc-diethylene triamine pentaacetic acid (99 Tc-DTPA) clearance, the Schwartz formula, the new Schwartz equation for chronic kidney disease (CKD), cystatin C serum concentration and the Filler formula. Kidney damage was established by beta-2-microglobulin (B-2-M) and albumin urine excretion, urine sediment and ultrasound examination. Blood pressure was measured. No differences were found between the mean GFR in 99 Tc-DTPA and the new Schwartz equation for CKD (91.8 ± 11.3 vs. 94.3 ± 10.2 ml/min/1.73 m2 [p = 0.55] respectively). No differences were observed between estimated glomerular filtration rate (eGFR) using the Schwartz formula and the Filler formula either (122.3 ± 19.9 vs. 129.8 ± 23.9 ml/min/1.73 m2 [p = 0.28] respectively). Increased urine albumin and B-2-M excretion, which are signs of kidney damage, were found in 7 (22%) and 3 (9.4%) WTs respectively. Ultrasound signs of kidney damage were found in 14 patients (43%). Five patients (15.6%) had more than one sign of kidney damage. Eighteen individuals (56.25%) had CKD stage I (10 with signs of kidney damage; 8 without). Fourteen individuals (43.75%) had CKD stage II (6 with signs of kidney damage; 8 without). The new Schwartz equation for CKD better estimated GFR in comparison to the Schwartz formula and the Filler formula. Furthermore, the WT survivors had signs of kidney damage despite the fact that GFR was not decreased below 90 ml/min/1.73 m2 with 99 Tc- DTPA

Kidney Disease in Childhood Cancer Survivors

Chronic glomerular and tubular nephrotoxicity has been reported in up to 50% and 25%, respectively, of children and adolescents treated with ifosfamide and up to 60% and 30% of those given cisplatin. Up to 35% of children have proteinuria and microalbuminuria, implying chronic glomerular damage, after unilateral nephrectomy for a renal tumour. We are still learning about nephrotoxicity due to the new targeted anticancer drugs. Overall, childhood cancer survivors have nine times greater risk of developing renal failure than their siblings. Such chronic nephrotoxicity may have multiple causes including certain chemotherapy agents (especially ifosfamide and platinum agents), radiotherapy to the kidneys, renal surgery, supportive care drugs and tumour-related factors. These cause a wide range of chronic glomerular and tubular toxicity, often with potentially severe clinical sequelae. Although many risk factors for developing nephrotoxicity, mostly patient and treatment-related, have been described, they do not predict all children who subsequently develop chronic renal damage. This suggests that other factors may be involved, such as genetic polymorphisms influencing drug metabolism. Further research is necessary to enable prediction or early detection of nephrotoxicity, whilst greater understanding of the pathogenesis of nephrotoxicity is needed to allow us to prevent its occurrence in the future