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Hyperoxaluria And Oxalosis

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  • Hyperoxaluria and oxalosis

    Hyperoxaluria and oxalosis
    Hyperoxaluria occurs when you have too much oxalate in your urine. Oxalate is a natural chemical in your body, and it's also found in certain types of food. But too much oxalate in your urine can cause serious problems.Hyperoxaluria can be caused by inherited (genetic) disorders, an intestinal disease or eating too many oxalate-rich foods. Quick diagnosis and treatment of hyperoxaluria is important to the long-term health of your kidneys.Oxalosis happens after the kidneys fail in people who have primary and intestinal causes of hyperoxaluria, and excess oxalate builds up in the blood. This can lead to oxalate deposits in blood vessels, bones and body organs.

  • Hyperoxaluria and oxalosis

    Disease Symptoms
    Commonly, kidney stones are the first sign of hyperoxaluria. Kidney stones are uncommon in childhood. Kidney stones that form in children and teenagers are likely to be caused by an underlying condition, such as hyperoxaluria. For this reason, all young people with kidney stones should have a thorough evaluation, including measurement of oxalate in the urine. Adults with recurrent kidney stones also should be evaluated for oxalate in the urine.Symptoms of a kidney stone can include the following:Severe or sudden abdominal or flank pain,Blood in the urine,Frequent urge to urinate,Pain when urinating,Fever and chills.Primary hyperoxaluria (PH) that goes untreated can eventually damage your kidneys. Over time your kidneys may stop working. For some people, this is the first sign of the disease.

  • Hyperoxaluria and oxalosis

    Disease Treatment
    Treatment will depend on the type, symptoms and severity of hyperoxaluria and how well you respond to treatment.Medications. Prescription doses of vitamin B-6 can be effective in reducing oxalate in the urine in some people with primary hyperoxaluria. Oral preparations of phosphates and citrate help prevent the formation of calcium oxalate crystals. Other medications, such as thiazide diuretics, also may be considered, depending on which other abnormalities are present in your urine.High fluid intake. If your kidneys are still functioning normally, your doctor will likely tell you to drink more water or other fluids. This flushes the kidneys, prevents oxalate crystal buildup and helps keep kidney stones from forming.Dietary changes. The effectiveness of diet will depend on the cause of increased levels of oxalate. Diet may include restricting foods high in oxalates, limiting salt, and decreasing animal protein and sugar (high fructose corn syrup). This may help to lower urinary oxalate in people with enteric hyperoxaluria or excess dietary intake. Dietary restrictions may not be as important for all people with primary hyperoxaluria. Follow the advice of your doctor.
       

  • Hyperoxaluria and oxalosis

    Statistics
    Hyperoxaluria causes crystal deposition in the kidney, which leads to oxidative stress and to injury and damage of the renal epithelium. Sodium thiosulfate (STS, Na2S2O3) is an anti-oxidant, which has been used in human medicine for decades. The effect of STS on hyperoxaluria-induced renal damage is not known. Methods Hyperoxaluria and renal injury were induced in healthy male Wistar rats by chronic exposure to ethylene glycol (EG, 0.75%) in the drinking water for 4 weeks. The treatment effects of STS, NaCl or Na2SO4 were compared. Furthermore, the effects of STS on oxalate-induced oxidative stress were investigated in vitro in renal LLC-PK1 cells. Results Chronic EG exposure led to hyperoxaluria, oxidative stress, calcium oxalate crystalluria and crystal deposition in the kidneys. Whereas all tested compounds significantly reduced crystal load, only STS-treatment maintained tissue superoxide dismutase activity and urine 8-isoprostaglandin levels in vivo and preserved renal function. In in vitro studies, STS showed the ability to scavenge oxalate-induced ROS accumulation dose dependently, reduced cell-released hydrogen peroxide and preserved superoxide dismutase activity. As a mechanism explaining this finding, STS was able to directly inactivate hydrogen peroxide in cell-free experiments. Conclusions STS is an antioxidant, which preserves renal function in a chronic EG rat model. Its therapeutic use in oxidative-stress induced renal-failure should be considered.

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