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[Diagnostic markers in calcium nephrolithiasis--current and traditional ideas with a new look].

About 80% of all renal stones contain calcium oxalate and/or calcium phosphate as their main crystalline components. The most important risk factors for increases in calcium oxalate crystallization are low urine volume, hyperoxaluria and hypocitraturia. Hypercalciuria, however, is of secondary importance as a cause of increased crystallization: whereas calcium and oxalate crystallize in a 1:1 ratio, the molar concentration ratio in urine amounts to about 10:1 in favor of calcium. Therefore, increases in urinary calcium will not be followed by a rise in crystallization as long as oxalate remains constant, whereas even the slightest increases in urinary oxalate immediately cause more crystals to precipitate. Thus, low calcium diet is not only unnecessary but is contraindicated since it may cause secondary hyperoxaluria (increased intestinal oxalate absorption) and osteopenia (negative calcium balance). On the other hand, overconsumption of animal protein (meat, poultry, fish) induces more pronounced hyperoxaluria and hypocitraturia and contributes to an overall negative calcium balance. It is, however, only by the interplay of "bad" dietary habits with underlying abnormalities such as up-regulation of calcitriol production, incomplete renal tubular acidosis or defective macromolecular crystallization inhibitors, that people become recurrent calcium renal stone formers.

Adult↗

[The morphofunctional changes in the kidneys of patients with staghorn nephrolithiasis operated on using a block of the renal blood flow].

A study was made of morphofunctional changes in the kidneys depending on duration of ischemia and use of the drug combination proposed by the contributors to the article, for pharmacological protection of the kidney. The examination of intraoperative renal biopsy specimens revealed the hystological structure of the kidney to be more intact, with its functional capacity tending to restore more readily than in control, in those patients in whom pharmacological protection had been embarked on. Constricting the renal artery and carrying on pharmacological protection of kidney we succeeded in effecting a complete elimination of the coral-like calculus fragments in favourable conditions on a "dry" organ, being able to manage with almost non-traumatic nephrotomy associated with minimum loss of blood, which fact resulted in the reduction of the lithogenesis recurrence rate by 17 %.

Animals↗

[Nephrolithiasis in children].

We reevaluated the medical records of 112 children with urolithiasis. The prevalence of this condition was 1/4.500 children admitted to our hospital. The mean age was 8.2 years and 54.4% of the afflicted patients were males. Fifty percent of the patients studied had a family history of urolithiasis. The two most frequent etiologies were urinary tract infections and metabolic disorders (hypercalciuria states, distal renal tubular acidosis and cystinuria). The etiology of the urolithiasis was unknown in 15% of our patients. The levels of magnesium and citrate, inhibitors of crystallization, were moderately low in some of the cases in which it was determined. Fifty percent of the children with urolithiasis showed urinary or renal complications. The extracorporeal lithotripsy was an effective treatment of urolithiasis in the patients in which it was performed. The recurrence rate was 8%. In one third of the urolithiasis associated with urinary infections and/or urinary tract malformations we found chronic pyelonephritis.

Child↗

[Animal-experiment studies on the effect of magnesium and vitamin B 6 on calcium-oxalate nephrolithiasis].

By chronic intoxication with ethylene glycol or acute intoxication by Na-glyoxalate in the animal experiment a Ca-oxalatenephrolithiasis could be produced. At this model the influence of magnesium, pyridoxine and phosphate was studied. The combination therapy of magnesium and vitamin B6 can completely prevent the formation of Ca-oxalate-microliths in the kidney. The production of a preparation with 200 mg MgO and 10 mg pyridoxine per tablet for the metaphylaxis of oxalate calculi is recommended.

Animals↗

Nephrolithiasis.

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Humans↗

Nephrolithiasis: recent advances in therapy.

The stone-forming process includes crystal formation, crystal aggregation, and retention time to allow growth. The crystal-forming process, in turn, is influenced by the pH of the urine, the solute load, and inhibitors of crystallization. Idiopathic stone disease is characterized by recurrent formation of calcium oxalate, calcium phosphate, and hydroxyapatite stones without an apparent underlying cause. Treatment of idiopathic stone disease has been aimed at decreasing the solute concentration, increasing the solubility of calcium phosphate, or interfering with extension of the crystal lattice.

Allopurinol↗

Effect of vitamin E and mannitol on renal calcium oxalate retention in experimental nephrolithiasis.

The calcium oxalate stone formation is induced in rats by a single injection of sodium oxalate (i.p., 7 mg/100 g body weight). There was increase in kidney oxalate concentration and kidney mitochondrial oxalate binding activity with increased lipid peroxidation. Histopathological observations showed larger aggregates of calcium oxalate crystals in the renal tubules. At 12 hours after oxalate administration a maximal crystal deposition in the renal tubule with denuded epithelium, lymphocytic infiltration and blood were observed. Increased blood urea and creatinine indicated kidney failure after oxalate administration. Calcium oxalate crystalluria, hematuria, and proteinuria with casts were observed. Renal antioxidants vitamin E, ascorbic acid and glutathione were significantly decreased on oxalate challenge. Pretreatment with vitamin E provided only partial protection from calcium oxalate deposition. Pretreatment with vitamin E and mannitol together protected the renal tubules completely from calcium oxalate deposition by normalizing the tissue oxalate concentration and mitochondrial oxalate binding activity and increasing the concentration of antioxidants on oxalate challenge.

Animals↗