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Among the medications investigated, the injectables are the most significant source of aluminium for patients with renal insufficiency. This extra aluminium intake is reflected in higher aluminium levels in the patients' blood.

Preterm neonates receiving parenteral nutrition are at risk of aluminum (Al) overload because of the presence of Al as a contaminant in parenteral formulations. Despite US Food and Drug Administration regulation, commercial products continue to present Al contamination. To reassess Al exposure in the premature neonatal population, the present study evaluated the Al balance (intake vs urinary excretion) in a group of preterm neonates during the period in which they stayed in the intensive care unit (NICU) under total parenteral nutrition. For the 10 patients selected, daily infusion solutions (nutrition and medication) were collected and the level of Al contamination was measured. From the urine collected daily, an aliquot was taken for Al determination. Blood was also collected for Al determination on the first and last day in the NICU. The measurements were carried out by atomic absorption spectrometry. The difference between Al administered and excreted revealed that 56.2% +/- 22.7% of the Al intake was not eliminated. The mean serum Al levels from the first to the last day decreased from 41.2 +/- 23.3 to 23.5 +/- 11.2 microg/L. The resulting mean Al daily intake of the 10 patients was 15.2 +/- 8.0 microg x kg(-1) x day(-1). Because Al intake was higher than that excreted and Al in serum decreased to practically half during the period in the NICU (+/-7.3 days), some amount of Al deposition occurred. Moreover, premature neonates were receiving, on average, 3 times the amount of 5 microg x kg(-1) x day(-1), considered by the Food and Drug Administration as a safe limit.

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Background/Aims: The effects of cigarette smoke (CS) on cyclosporine (CsA)-induced nephrotoxicity are poorly studied. This study aims to assess the effects of previous exposure to CS on CsA nephrotoxicity. Methods: Rats were either exposed to CS or sham (S) procedures for 10 min twice a day for 20 weeks. From the 16th to the 20th week, they received a low-salt diet. Beginning with the 17th week, they were given 2.5 mg/day CsA or vehicle (VH) for 3 weeks. The final groups were VH/CS, CsA/CS, VH/S, and CsA/S. On day 141, glomerular filtration rate (GFR), renal blood flow (RBF), renal vascular resistance (RVR), tubulointerstitial fibrosis, and CsA blood levels were measured and immunohistochemistry was analyzed for renal α-smooth muscle actin (SMA), nitrotyrosine, and vimentin. Results: CsA decrease in GFR was enhanced by CS exposure. CsA associated with CS induced higher periglomerular α-SMA and renal nitrotyrosine expression. CsA decreased RBF, but increased RVR, tubulointerstitial fibrosis, and α-SMA and renal vimentin expression. These changes and the CsA blood levels were not affected by CS exposure. Conclusion: CS aggravated the CsA-induced impairment of GFR and CS associated with CsA caused the development of periglomerular structural lesions and oxidative stress in a rat model of CsA nephrotoxicity.