What is the case of primary high uric acid?

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Abstract: primary urinary oxalate is a congenital autosomal recessive disorder, which is divided into two types (Table 8).(1) I before that

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Abstract: primary urinary oxalate is a congenital autosomal recessive disorder, which is divided into two types (Table 8).

(1) I before that of primary hyperoxaluria type I is due to lack of alpha ketoglutarate: glyoxylate carboligase, it is clear that due to the peroxisomal enzyme alanine exists in peroxidase in vivo: glyoxylate aminotransferase deficiency, the glyoxylate metabolism disorder, resulting in increased production of glycolic acid and oxalic acid therefore, in the urine of patients with type I in oxalate excretion increased, and glycolic acid, glyoxylic acid excretion is increased, so the I type called glycolic acid in urine;

(2) type II D- glycerol dehydrogenase deficiency due to acid, the hydroxyl pyruvate accumulation, followed by lactate dehydrogenase and nicotinamide adenine dinucleotide under the action of glycerol into L- acid and oxalic acid. Therefore, D- glycerol acid dehydrogenase deficiency to hydroxyl pyruvate metabolism disorders, in addition to the increase in urinary oxalate excretion, urinary acid excretion and L- glycerol increased, so also known as type II L- glycerol acid in urine.

Table 8 the difference between the two types of primary high urinary oxalate

Type I (glycolic acid)

Type II (L-)

Defective enzyme

Alanine: glyoxylate aminotransferase

Glycerate dehydrogenase.

Metabolic disorder

The enzyme is deficient, the glyoxylate can not be converted into alpha hydroxy - beta - keto acid, glyoxylic acid increased, resulting in increased glycolic acid and oxalic acid production.

The enzyme is deficient, resulting in the accumulation of pyruvic acid, followed by the conversion of L- to glycerol and oxalic acid.

Change in urine

Glycolic acid and oxalic acid increased

L- acid and oxalic acid increased

What are the hazards of the primary high urinary oxalate?

Children with onset, recurrent kidney stones, renal calcinosis, renal function damage, often need dialysis or kidney transplantation in teens. Because despite the high oxalate excretion of the most easy to form stones but stones to some extent self perpetuating, and other related reasons such as water and urinary tract infection, so the recurrence rate and the degree of renal damage varies greatly. The patient's response to vitamin B6 is also important. Calcium oxalate crystals can be formed in many organs (oxalosis, oxalosis), the occurrence of advanced disease, when the glomerular filtration rate reduced to 25 ml/min/1.73m3 under the calm danger calcium increased rapidly. The infant cases showed the discharge of sand and stones, urinary tract infection, obstructive urinary tract disease or advanced renal failure. 65% of the patients had symptoms before the age of 5, and died of renal failure before the age of 80% in 20. Calcinosis and calcium oxalate deposition are characteristic pathological features of the disease. The intestinal absorption of oxalate is no exception, 24h in urinary oxalate 1140 mol (100 mg) or more, even up to 4560 mol (400 mg).

 

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