The goal of this study was to identify the incidence of trace element and vitamin deficiencies in critically ill patients during CRRT. Limited published data suggest that CRRT may lead to depletion of water-soluble vitamins and trace elements. Kamel Amir Y,Dave Nisha J,Zhao Vivian M,Griffith Daniel P,Connor Michael J,Ziegler Thomas R Nutrition in clinical practice : official publication of the American Society for Parenteral and Enteral Nutrition BACKGROUND:Continuous renal replacement therapy (CRRT) is commonly used to provide renal replacement therapy in the intensive care unit. Micronutrient Alterations During Continuous Renal Replacement Therapy in Critically Ill Adults: A Retrospective Study. We conclude that vitamin B6 can protect against the nephrotoxicity of GM in rabbits, but that further study is needed on the possible nephrotoxicity of high doses of B6S. Unexpectedly, 1 rabbit given only 100 mg B6S/d but no GM had interstitial nephritis with focal ATN. Only a few animals given 10 mg GM/kg/d showed any renal pathology and that was minimal. At the 40 mg GM/kg/d dose, significant mild to moderate ATN was observed in the saline controls, which was prevented by either dose of B6S. After 5 d, the rabbits were euthanatized and kidneys were excised for histological evaluation by light microscopy. Blood was drawn for chemical assays on day 0 prior to any treatments and 2 h after each respective treatment on days 1, 3 and 5. All treatments were administered im once daily for 5 d. The control group only received 100 mg B6S. Three of the groups received 40 mg GM/kg with either 10 mg B6S, 100 mg B6S, or normal saline. Three of the groups received 10 mg GM/kg with either 10 mg B6S, 100 mg B6S or 0.9% saline. Twenty-one rabbits were randomly assigned to 1 of 7 treatment groups of 3 rabbits each. We have previously observed decreased plasma pyridoxal 5'-phosphate (PLP) levels in rabbits given therapeutic doses of GM and endeavor in this study to determine if vitamin B6 supplementation (B6S) could protect against the nephrotoxicity of GM. Enriquez J I,Schydlower M,O'Hair K C,Keniston R C,Nadjem M A,Delgado I Veterinary and human toxicology Therapeutic use of gentamicin (GM) in a clinical setting may result in nephrotoxicity, most commonly presenting as acute tubular necrosis (ATN). Experiments in animals support this hypothesis.Įffect of vitamin B6 supplementation on gentamicin nephrotoxicity in rabbits. Given the key role of pyridoxine in oxalate metabolism, we suggest that vitamin B6 deficiency secondary to alcoholism and denutrition could cause a rise in oxalemia leading to oxalate nephropathy. Neither intoxication nor intestinal disease could be detected. Renal function recovered spontaneously (follow-up of four years for one patient). In one patient serum oxalate level was high, and in the other urinary oxalate excretion rose above normal when diuresis resumed. Renal biopsy showed tubular epithelium alterations with marked luminal deposition of birefringent crystals consistent with calcium oxalate. Except for early lumbar and abdominal pain, the renal failure picture was without any peculiarity. Both patients had common features: chronic alcoholism and denutrition. The present report concerns two cases for which none of the known causes of oxalate nephropathy were found. Esnault V,Delcroix C,Dubigeon P,Guenel J Nephrologie Intratubular deposits of calcium oxalate crystals can be responsible for acute renal failure.

Cyclic amp signaling pathway