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PubMed1991

The protective role of eicosapentaenoic acid [EPA] in the pathogenesis of nephrolithiasis.

The low incidence of atherosclerosis and other degenerative diseases including stone disease in the Greenland Eskimo has been attributed to their high consumption of oily fish with its high concentration of eicosapentaenoic acid (EPA). Man cannot synthesis EPA from the precursor essential fatty acid, linolenic acid, and can only assimilate preformed EPA present in fish and fish oil, to bring about a change in the pathway of eicosanoid metabolism from the n-6 to the n-3 series. With a westernised diet the oxygenated products of renal prostaglandin synthesis are metabolites of the n-6 series and these are known to play an important role in several pathophysiological states including stone disease. Our previous studies have shown a relationship between prostaglandin activity and urinary calcium excretion and it would seem that the initiating factor/s for stone formation trigger the mechanisms for prostaglandin synthesis resulting in the biochemical abnormalities associated with stone disease. The Eskimo may be protected from these events by possession of an eicosanoid metabolism that follows an n-3 pathway. To test this hypothesis experiments were performed using an animal model of nephrocalcinosis. The animals were divided into three groups; one group was given an intra-peritoneal injection of 10% calcium gluconate daily for 10 days to induce nephrocalcinosis; a second group was fed MaxEPA fish oil before and during the calcium gluconate injections and a third group only received an intra-peritoneal injection of N saline. A group of 12 recurrent, hypercalciuric/hyperoxaluric stone-formers were treated with fish oil for eight weeks to study the effects on solute excretion. Nephrocalcinosis, which was readily produced in the control animals, was prevented in the experimental animals by pre-treatment with fish oil and urine calcium excretion was significantly reduced. The urinary calcium and oxalate excretion in the recurrent, hypercalciuric stone-formers was significantly reduced with fish oil treatment over an eight week period. There were no untoward side-effects. These studies indicate that the incorporation of EPA in the diet as a substitute metabolic pathway could be a unique way of correcting the biochemical abnormalities of idiopathic urolithiasis.

Adult↗
PubMed1990

Triamterene nephrolithiasis: renewed attention is warranted.

Although triamterene has been known to contribute to urinary calculus formation, it has been presumed to be a rare phenomenon. Our review of stone analyses performed during the last decade by a single laboratory reveals an increasing incidence of triamterene stones. Awareness of the calculogenic potential of triamterene-containing medications should be re-emphasized.

Humans↗
PubMed1989

Clinical and laboratory approaches for evaluation of nephrolithiasis.

The initial part of this presentation deals with the sensitivity of tests commonly used in the diagnosis of primary hyperparathyroidism. Total serum calcium levels often are normal in patients with small parathyroid adenomas but levels of serum ultrafilterable and/or ionized calcium usually are elevated in these patients. The recent introduction of improved radioimmunoassays for measurement of circulating parathyroid hormone has led to greatly improved sensitivity of this test for the diagnosis of primary hyperparathyroidism. However, measurement of total urinary cyclic adenosine monophosphate, even when expressed as a function of glomerular filtration rate, is an extremely insensitive test in patients who have parathyroid adenomas weighing less than 1 gm. Consequently, this test no longer is used for diagnostic purposes in our laboratory. Data relating to the prevalence and causes of hyperoxaluria in patients with idiopathic calcium oxalate stones also are presented. Hyperoxaluria (more than 450 mumol. per 24 hours) was found in 21 of 99 consecutive untreated male patients. Approximately a third of the patients with high normal or increased urinary oxalate excretion also have increased urinary glycolate excretion, which is indicative of increased endogenous oxalate production. This metabolic abnormality was unresponsive to pyridoxine administration but preliminary findings suggest that it may be corrected by restricting dietary protein.

Calcium↗
PubMed1989

Clinical and laboratory approaches for evaluation of nephrolithiasis.

A medical history and laboratory investigation of patients with recurrent stones serve as the cornerstone for preventive and therapeutic treatment. Identifiable risk factors can be discovered in 90 per cent of the patients. More sophisticated analyses of urinary supersaturation can be helpful in resistant cases.

Calcium↗
PubMed1988

Gouty diathesis and sarcoidosis in patient with recurrent calcium nephrolithiasis.

We describe a patient who initially formed calcium-containing renal stones owing to gouty diathesis and hypocitraturia. On therapy with 300 mg. allopurinol and 60 mEq. potassium citrate daily serum uric acid decreased from 9.2 to 5.8 mg. per dl., urinary pH increased from less than 5.5 to 6.6 and urinary citrate increased from 223 to 1,005 mg. per day. Four months later while still on this medical regimen, the patient presented with hypercalcemia (13.4 mg. per dl.), high serum 1,25-dihydroxyvitamin D (65 pg. per ml.) and hypercalciuria (598 mg. per day), which subsequently were found to result from sarcoidosis. Prednisone therapy normalized the disturbances in calcium metabolism. During 33 months of combined treatment with 7.5 to 10 mg. prednisone a day, allopurinol and potassium citrate, the patient was free of stones and he had normal urinary calcium, pH and citrate. However, a calcium stone formed 1 month after discontinuation of prednisone therapy, although treatment with allopurinol and potassium citrate was continued. The patient had marked hypercalciuria of 447 to 465 mg. per day, despite normal urinary pH, citrate and uric acid. This case represents calcium stone formation in a patient with 2 separate etiologies for stone disease, that is gouty diathesis and sarcoidosis. Therapeutic regimens directed at the correction of both metabolic disturbances were required to control renal stone formation.

Allopurinol↗
PubMed1986

Management of cystine nephrolithiasis with alpha-mercaptopropionylglycine.

The effect of long-term treatment with alpha-mercaptopropionylglycine was examined in 66 patients with cystinuria. Of the patients 49 took D-penicillamine before therapy, whereas 17 did not. Over-all side effects to alpha-mercaptopropionylglycine were common, and occurred in 75.5 per cent of the patients with and 64.7 per cent without a history of D-penicillamine treatment, compared to 83.7 per cent who suffered toxicity to D-penicillamine. Serious adverse reactions requiring cessation of therapy were less common with alpha-mercaptopropionylglycine. Among the patients who took both drugs 30.6 per cent had to stop taking alpha-mercaptopropionylglycine, whereas 69.4 per cent could not tolerate D-penicillamine. Of the latter group with toxicity to D-penicillamine before therapy, whereas 17 did therapy only 5.9 per cent had side effects to alpha-mercaptopropionylglycine of sufficient severity to require withdrawal. Alpha-mercaptopropionylglycine was equally as effective as D-penicillamine in reducing cystine excretion. During long-term treatment with alpha-mercaptopropionylglycine (average dose 1,193 mg. per day) urinary cystine levels were maintained at 350 to 560 mg. per day and urinary cystine was kept at undersaturated levels. Commensurate with these changes, alpha-mercaptopropionylglycine produced remission of stone formation in 63 to 71 per cent of the patients and reduced individual stone formation rate in 81 to 94 per cent. Thus, alpha-mercaptopropionylglycine has a definite therapeutic role in cystinuric patients with toxicity to D-penicillamine.

Adolescent↗
PubMed1985

Comparative efficacy of "specific" potassium citrate therapy versus conservative management in nephrolithiasis of mild to moderate severity.

It generally is believed that conservative measures of high fluid intake and dietary modification in the setting of a stone clinic could favorably influence the course of renal stone disease. To establish the effect of specific medical treatment from the stone clinic effect, we compared the results of potassium citrate therapy to those of 11 reported conservative or placebo trials. The 54 patients receiving potassium citrate chosen for this comparison had mild to moderately severe stone disease (less than 1 stone per patient per year), similar to that encountered in conservative placebo trials (mean 0.54 stones per patient per year). New stone formation was virtually eliminated by potassium citrate therapy (a decrease from 0.52 to 0.02 stones per patient per year, a remission rate of 96 per cent, p less than 0.001), whereas it continued in 39 per cent of the patients during conservative or placebo trials. However, in patients participating in conservative or placebo trials new stone formation decreased by only 54 per cent (from 0.54 to 0.25 stones per patient per year). The superior response to potassium citrate suggested that this specific medical treatment exerted an additional favorable effect on the course of stone disease above the stone clinic effect.

Citrates↗
PubMed1984

Five years of experience with selective therapy in recurrent calcium nephrolithiasis.

We evaluated the efficacy of selective treatment in 126 patients with recurrent calcium urolithiasis who were chosen on the basis of ability to correct underlying physiochemical disturbances. Patients with hyperparathyroidism underwent an operation. Patients with renal hypercalciuria were treated with thiazide and those with absorptive hypercalciuria were given a low calcium, low oxalate diet with or without thiazide. The only treatment for normocalciuric patients was high fluid intake, which was suggested also to the other groups. A significant individual mean reduction in stone formation was observed in all groups after 5 years of treatment. However, only 48 per cent of the normocalciuric patients were in remission after 5 years of high fluid intake therapy and 45 per cent of those with absorptive hypercalciuria were free of recurrence with diet only. Thiazide treatment seemed to be effective despite the type of hypercalciuria. The effect of the treatment on stone formation was mediated through reduction of risk factors in the urine. Conversely, a high level of risk factors commonly predicted stone recurrence.

Adult↗
PubMed1983

Increased urinary excretion of renal enzymes in idiopathic calcium oxalate nephrolithiasis.

Urinary excretion of gamma-glutamyl transpeptidase, angiotensin I converting enzyme, beta-galactosidase and N-acetyl-beta-glucosaminidase was evaluated in 30 patients with idiopathic calcium oxalate urolithiasis. Higher than normal values were observed and the excretory enzyme pattern suggested tubular damage in patients with stones. A parallel study in the rat showed that an oxalate surcharge can promote increased urinary excretion of these enzymes. It is known that urothelium injury may enhance crystal adhesion. If the damage is primary it may be viewed as a promoting factor. If it is secondary it may be considered a factor capable of increasing salt precipitation.

Acetylglucosaminidase↗
PubMed1976

Nephrolithiasis and nephrocalcinosis after renal transplantation: a case report and review of the literature.

Stone formation in renal allografts is rare. Although infection or renal tubular acidosis can predispose to calcium deposition in a renal allograft, hyperparathyroidism is usually an accompanying factor. Parathyroidectomy is recommended as the treatment of choice when stone deposition or nephrocalcinosis occurs after transplantation. The reported case demonstrates that aggressive therapy is also necessary to eliminate calculi from the urinary system to avoid mechanical obstruction, continued infection or renal paraenchymal damage.

Adult↗
PubMed1997

Medical management of nephrolithiasis.

About 1 out of 14 males and 1 out of 30 females are afflicted with kidney stones. In many of these patients, the disease is recurrent. Fortunately, our understanding of the disease and ability to treat renal stone disease has increased in the last decade. Parenteral NSAIDs have been shown to be as effective as narcotics in treating renal colic. Dietary and drug therapy after proper metabolic evaluation of patients with recurrent stones is beneficial in reducing the recurrence rate. New understanding of the role of diet and many organic inhibitors of crystallization in urine will further broaden the scope of management of this common disease.

Benzothiadiazines↗
PubMed1984

Medical evaluation and management of calcium nephrolithiasis.

Stone disease is a common medical problem, frequently recurs, and is associated with significant morbidity. Because appropriate medical therapy significantly decreases stone recurrence, this disorder must not be ignored by nonurologists. Even the single stone-former should be offered a metabolic evaluation.

Acidosis, Renal Tubular↗