Uric Acid Stone Disease Research Articles

Uric acid stone disease.

The trend in uric acid stone formation appears to be on the rise again throughout much of the world. This is thought secondary to diet, body habitus, and social reasons. Uric acid stone disease has a rich and fascinating medical history and probably is the oldest known stone disease. Uric acid stone disease is strongly linked to the purine metabolic pathway, and its treatment is primarily medical. Uric acid stone disease can be prevented and these are one of the few urinary tract stones that can be dissolved successfully. Surgical intervention with uric acid stone disease represents a failure of medical therapy and a whole host of modern, minimally invasive methods are available for treating patients with this disease. Finally, uric acid nephrolithiasis is associated with a variety of inborn errors of metabolism based on mutations of key enzymes in the purine metabolic pathways. This review of uric acid stone formation will start with historical consideration, review basic biochemistry, and physiology and then focus upon specific clinical scenarios. The discussions will be heavily referenced for those interested in greater details.

Effect of blackcurrant-, cranberry- and plum juice consumption on risk factors associated with kidney stone formation.

To evaluate the influence of plum-, cranberry- and blackcurrant juice on urinary stone risk factors. Investigations were carried out in 12 healthy male subjects aged 18-38 y. All subjects received a standardized diet formulated according to the dietary recommendations of the German Society of Nutrition. The subjects provided 24 h urine collections in a control, three loading phases. In each loading phase a neutral mineral water was substituted for 330 ml of the particular juice. Cranberry juice decreased the urinary pH, whereas the excretion of oxalic acid and the relative supersaturation for uric acid were increased. Blackcurrant juice increased the urinary pH and the excretion of citric acid. The excretion of oxalic acid was increased too. All changes were statistically significant. The plum juice had no significant effect on the urinary composition. It is concluded that blackcurrant juice could support the treatment and metaphylaxis of uric acid stone disease because of its alkalizing effect. Since cranberry juice acidifies urine it could be useful in the treatment of brushite and struvite stones as well as urinary tract infection. Funded by our own Division respectively the University.

URIC ACID–RELATED NEPHROLITHIASIS

Abnormalities in uric acid metabolism are associated with uric acid and calcium oxalate urolithiasis. Clinical stone formation depends on multiple identifiable risk factors that affect uric acid and calcium oxalate solubility. The understanding of urinary pH is critical to direct appropriate treatment of uric acid-related nephrolithiasis. Understanding uric acid metabolism and the pathophysiology of uric acid and calcium oxalate stone formation leads to a rational treatment approach to uric acid and hyperuricosuric calcium oxalate stone disease.

Management of uric acid calculi in the elderly patient

Uric acid stones are more common in older patients. Their formation usually requires a persistently acid urine. Conversely, they can be dissolved and their re-formation prevented by the use of alkaline salt therapy. This paper discusses the spectrum of uric acid stone disease including the frequent presentation as a recurrent gravel/colic syndrome. It reviews the clinical situations in which uric acid stones often form and outlines an approach to dissolution of stones using either oral therapy or urinary tract irrigation. Prophylaxis of further stone formation is often possible with only alternate day, single dose treatment with alkaline potassium salts.

Prophylaxis of uric acid and cystine stones

Although they are two very distinct entities, uric acid and cystine stone disease share a common physico-chemical background, i.e. urinary supersaturation with respect to a compound that is poorly soluble in an acid milieu. Therefore, high-fluid intake and urine alkalinization, preferably by potassium citrate, are of utmost importance for prophylaxis. Urinary excretion of uric acid and cystine may be reduced by dietary measures as well as by drug therapy (allopurinol and thiols, respectively).

Pharmacologic Treatment of Uric Acid Calculi

Uric acid stone disease is dependent on three pathogenetic factors: acid urine pH, low urine volume, and hyperuricosuria. The management of nonobstructing uric acid calculi should include maintenance of an alkaline urine, an increase in urine volume, and reduction in urinary uric acid excretion. It appears that potassium alkali may avoid the complication of calcium stone formation in patients with uric acid stones. In patients with obstructing uric acid calculi, more rapid dissolution may be accomplished with intravenous alkalinization or direct irrigation of the stone with an alkaline solution.

Management of the Choked Ureter in Obstructive Renal failure Due to Uric Acid Lithiasis

We report on 8 azotemic patients with anuria or progressive oliguria owing to bilateral uric acid lithiasis. In 7 patients the precipitating cause of acute obstructive renal insufficiency was choking of at least 1 distal ureter with numerous small uric acid stones. In 6 of these ureters contrast retrograde ureterography showed relief of obstruction, which was believed to be owing to the stone dissolution properties of the contrast medium used. In situ alkalization via nephrostomy catheters achieved dissolution of obstructing stones in 3 tracts and systemic alkalization dissolved the stones in 3 others. An operation was necessary in 4 cases of large calculi, all of which showed some radiodensity, either because of super added calcification or phosphatic incrustation, rendering dissolution unfeasible. Methods of management of the obstructed tract caused by uric acid stone disease are evaluated and discussed.

Biochemical evidence for a distinct type of primary gout.

IN recent years several reports1–3 have called attention to a disorder occurring in the paediatric age group which is characterized by marked over-production of uric acid. The clinical features include haematuria and uric acid stone disease, and often, but not always, mental retardation, neurological signs, and self-mutilation. Intravenous injection of glycine-14C into such patients results in a rapid incorporation1 of isotope into urinary uric acid, signifying the presence of a shunt pathway whereby precursor is incorporated into uric acid without previous incorporation into nucleic acid purines.

HYPERPARATHYROIDISM AND URIC ACID LITHIASIS: A REPORT OF TWO CASES.

SUMMARY Two patients suffering from hyperparathyroidism and idiopathic uric acid lithiasis are described. A correct diagnosis of uric acid stone disease in a patient with hyperparathyroidism is important in establishing therapy after parathyroidectomy. There is no evidence in the patient material of our metabolic clinic that the association of hyperparathyroidism with uric acid lithiasis is other than fortuitous.