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Biomedical subjects

J H Parks

Publications and source records attributed to J H Parks.

At least 37 records · Page 2Linked to original sources
PubMed1996

The financial effects of kidney stone prevention.

Prevention of nephrolithiasis (NL) is now medically feasible and widely recommended. However, diagnosis and treatment of remediable causes of stones requires testing and drugs that impose a cost; this cost is balanced by the presumed reductions in stone related events and medical encounters. In order to assess the balance between these, we have analyzed results from 1092 patients with NL unselected except for having clinical follow-up during treatment. From this population, we have derived the changes in rates of new stones, hospitalizations, cystoscopies, and surgical procedures. From these changes, and assignment of a range of possible dollar costs, we estimate that medical stone prevention will result in an average saving of $2,158 +/- $500 (SEM)/patient/year, which is the difference between an expenditure of $1,068/patient on yearly drugs and testing, and a reduction of $3,226 per patient in medical costs. Medical prevention of NL seems justified on a cost saving basis quite apart from its benefits to patients in terms of reduced morbidity and risk from procedures, obstruction, and infection.

Cost of Illness↗
PubMed1996

Normal calcium oxalate crystal growth inhibition in severe calcium oxalate nephrolithiasis.

Urine from mammalian kidneys is regularly supersaturated with respect to calcium oxalate monohydrate, the most common solid phase in human nephrolithiasis, and also inhibits the nucleation, growth, and aggregation of calcium oxalate crystals. Nephrolithiasis is often associated with increased supersaturation, and it is assumed that this increase overbalances the inhibition effects, causing stones. However, some patients form stones in the absence of increased supersaturation, and in those patients, one might assume that reduced inhibition is the cause of their stones. This hypothesis was tested in 25 patients who formed at least ten stones each, yet lacked the usual metabolic abnormalities that increase supersaturation. Compared with 25 age- and sex-matched control subjects, urine supersaturation among the patients was not increased; this is an expected result of this study's selection criteria. Compared with the same age- and sex-matched control subjects, urine from the patients showed no evidence for reduced inhibition of calcium oxalate crystal growth, so low inhibition of growth did not contribute to pathogenesis of stones in our highly selected study population, despite their otherwise unexplained and active stone formation. These results do not support the hypothesis that growth inhibition defects are a cause of stone disease.

Calcium Oxalate↗
PubMed1996

Pathogenesis and treatment of calcium stones.

Calcium stones arise from imbalances between urinary excretions of insoluble salts and water. Idiopathic hypercalciuria and hyperparathyroidism are the calcium disorders usually associated with elevated levels of calcium in the urine. Renal tubular acidosis is associated with a disordered acid-base status that results in low urine citrate. Hypocitraturia itself is a cause of calcium stones because it leaves urine calcium free to complex with either oxalate or phosphate. Elevated urine oxalate is commonly associated with dietary excesses, bowel disease, and, rarely, primary hyperoxaluria. Hyperuricosuria, usually of dietary origin, when reversed can cause a fall in new calcium stones.

Allopurinol↗
PubMed1994

An increasing number of calcium oxalate stone events worsens treatment outcome.

Current practice recommends metabolic evaluation of patients who have formed multiple renal stones, but not those with one stone or temporally remote stones. This presumes that recentness and recurrence imply greater risk of new future stones. We hypothesize that number of stones reflects how long patients are permitted to form stones untreated, and that forming more stones, itself, raises risk of future stones despite treatment. Our report is a retrospective analysis of 371 male patients selected from a comprehensive clinical and laboratory data base containing 2,527 patients with nephrolithiasis. Before treatment, number of stone events rises with time of observation, and rate of stone event occurrence is constant or falls. During treatment, relapse is correlated with number of pretreatment stones. Life table analysis showed increasing relapse for patients grouped into those with one, two, and three or more stones. Even though number of stones seems controlled by the interval of observation before treatment, more stones predict higher relapse during treatment. Perhaps by leaving nuclei of crystals as residues, stones appear to promote new stones, and the practice of waiting while patients declare themselves multiple stone formers may not always be the best.

Adult↗
PubMed1994

Idiopathic hypercalciuria: the contribution of Dr. Jacob Lemann, Jr.

The original contributions of Jacob Lemann to mineral metabolism, especially calcium metabolism and idopathic hypercalciuria, are reviewed. One group of studies concern acid base balance and calcium loss, showing that acid loads increase calcium loss in the urine. Another group of studies concern the calciuria of glucose or carbohydrate ingestion, with the observation that stone patients, who as a population are enriched with hypercalciuria, respond with more exaggerated calciuria to glucose loads than do normal people. Yet another body of work shows that normal men, when given noncalcemic loads of calcitriol, exhibit two essential features of idiopathic hypercalciuria--hyperabsorptive hypercalciuria and bone mineral loss on a low-calcium diet. The final group of studies presented worked on the problem of thiazide hypocalciuric action, and where the calcium goes that does not appear in the urine, as well as the effects of potassium bicarbonate and sodium loads on mineral balance and acid base status.

Acid-Base Equilibrium↗
PubMed1994

Role of nephrocalcin in inhibition of calcium oxalate crystallization and nephrolithiasis.

Kidney cells produce at least three proteins that slow the rate of calcium oxalate crystallization. Nephrocalcin (NC), one of the three, is an acidic glycoprotein that contains gamma-carboxyglutamic acid (GLA), and inhibits nucleation, aggregation and growth of calcium oxalate crystals. Nephrocalcin is abnormal in urine of stone-forming patients, in lacking GLA. It acts by absorbing to crystal surfaces. NC is produced by cultured renal proximal tubule cells, and by some lines of renal carcinoma cells, but its regulation is not yet characterized. Its sequence is not known, nor do we known the molecular basis for the abnormal character of NC is stone-forming patients. Compared to Tamm-Horsefall protein and uropontin, the two other inhibitors, NC is very potent, and is probably of major importance in protecting kidneys against supersaturations caused by normal water conservation.

Animals↗
PubMed1992

Stone-forming potential of milk or calcium-fortified orange juice in idiopathic hypercalciuric adults.

Milk and orange juice (OJ) fortified with calcium-citrate-malate (CCM; calcium-citrate-malate salt is a coined term to describe a trademarked calcium delivery system found only in Citrus Hill Plus Calcium) were evaluated for their potential to alter urine chemistries and crystallization during the course of an eleven week, crossover study. Six male and six female, non-stone-forming, idiopathic hypercalciuric adults consumed 600 mg per day as beverage calcium for four consecutive weeks. The results show that both milk and CCM-fortified OJ (CCM-OJ) were well tolerated by male and female hypercalciurics since few significant changes occurred in overall urinary chemistry profiles. CCM-OJ did, however, significantly (P less than or equal to 0.05) increase urinary pH relative to milk in both sexes and urinary citrate concentration in women only. Both of these urinary parameters were significantly increased by CCM-OJ in both sexes relative to the basal period. The combined pH and citrate effects are recognized to protect against calcium oxalate stone formation through formation of the soluble calcium citrate salt. These data indicate that either milk or CCM-fortified orange juice can be consumed, at least within the limits tested, as a dietary source of calcium without increasing the risk of stone formation in a calcium-sensitive subpopulation. That the urine chemistries and crystallization of such calcium-sensitive individuals does not significantly change with the consumption of either beverage implies that the urine of normal individuals would be exceedingly unlikely to change as well.

Adolescent↗
PubMed1991

Inhibitors within the nephron.

Kidney-derived inhibitors of crystal growth and aggregation prevent supersaturations created by water conservation from expressing themselves in pathological soft tissue calcifications and intranephronal crystallizations. These inhibitors include nephrocalcin (NC), an acidic glycoprotein produced in proximal tubules and thick ascending limbs of Henle's loop, and the Tamm-Horsfall glycoprotein (THP), produced only in the thick ascending limb. NC inhibits growth and aggregation of calcium oxalate monohydrate (COM), the major crystalline component of human renal stones, THP inhibits only COM aggregation. Patients who form COM stones produce abnormal NC molecules that lack gamma-carboxyglutamic acid and fail to inhibit COM crystallizations normally.

Animals↗
PubMed1991

Molecular abnormality of Tamm-Horsfall glycoprotein in calcium oxalate nephrolithiasis.

Tamm-Horsfall glycoprotein (THP) inhibits self-aggregation of calcium oxalate monohydrate (COM) crystals and may therefore be part of the natural defenses against deposition of COM in the kidney in the form of stones or nephrocalcinosis. We have studied THP from six patients with severe nephrolithiasis and have found that their THP inhibits COM self-aggregation less than normal THP under conditions of NaCl and THP concentration and pH similar to those of human urine. The reason for the reduced inhibition of COM crystal aggregation seems to be an enhanced self-aggregation of patient THP, which removes it from effective interactions with the COM crystals. In one family, the father and the oldest son both excreted THP that behaved abnormally and in similar ways, whereas THP from the other son and from the wife behaved normally.

Adult↗
PubMed1989

Gestational hypercalciuria causes pathological urine calcium oxalate supersaturations.

Although normal pregnant women are more hypercalciuric than women with calcium oxalate nephrolithiasis (243 +/- 23 mg/day vs. 194 +/- 5 mg/day), pregnancy is not an established stone-forming state and pregnant women do not exhibit pathological crystalluria. One hypothesis to explain their lack of overt stone formation and pathological crystalluria is that pregnancy does not raise urine supersaturation with respect to stone forming salts such as calcium oxalate or calcium monohydrogen phosphate (brushite) to levels as high as in stone forming women. To test this hypothesis, we studied eleven normal women during each trimester of pregnancy, and between six and eight weeks post-partum. During pregnancy, hypercalciuria occurs with unchanged urine volume, citrate and magnesium excretions do not increase proportionally with calcium excretion, and urine pH increases. Supersaturations with respect to calcium oxalate (CaOx) and brushite (Br) are as high as those of women with calcium nephrolithiasis. The lack of pathological crystalluria and stones during pregnancy is not due to a failure of supersaturations to increase; urinary potential for crystallization is as high as in patients with established stone disease.

Adult↗
PubMed1988

Chlorthalidone promotes mineral retention in patients with idiopathic hypercalciuria.

In seven patients with severe idiopathic hypercalciuria and recurrent calcium oxalate nephrolithiasis, we have determined the effects on mineral balance of chronic treatment with chlorthalidone or trichlormethiazide, drugs that are widely used to lower urine calcium losses and reduce stone recurrence. Each person excreted above 350 mg of calcium daily while untreated, and was studied twice, before and after three to six months of treatment. Compared to pretreatment, the drugs reduced intestinal calcium absorption; but they reduced urine calcium loss even more, so calcium retention increased. Phosphate retention also increased. Serum levels of calcitriol, parathyroid hormone, calcium, phosphate, and magnesium were unchanged. At least in patients of this type, chlorthalidone and trichlormethiazide seem ideal treatments, that lower urine calcium yet increase calcium and phosphate retention. Whether patients with less severe hypercalciuria respond this way is unknown.

Adult↗
PubMed1987

Nephrolithiasis and gestation.

Although both anatomical and physiological changes in pregnancy may predispose to kidney stone formation, it still remains an uncommon occurrence. Correct diagnosis is often difficult. Ultrasound has become the primary diagnostic tool, and a limited study excretory urogram is only necessary for complicated cases. Nephrolithiasis during pregnancy occurs more frequently during the later stages of gestation in multiparas, and without a difference in laterality. Conservative management with bed rest, hydration and analgesia can result in spontaneous passage of the majority of stones in gravidas. Past experience indicates that cystoscopy and/or surgery can usually be done safely when absolutely necessary. Pre-existing stone disease can increase the incidence of maternal urinary tract infections by 10-20%. The most common obstetric complication of stones during gestation is the precipitation of premature labour by renal colic. Unfortunately, most drugs used to treat stone disease are contraindicated in gestation. Experimental evidence suggests that known inhibitors of stone formation are present in gestation, and may help to explain why the incidence of stones is not increased in this particularly hypercalciuric state.

Female↗