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J H Parks

Publications and source records attributed to J H Parks.

At least 55 records · Page 3Linked to original sources
PubMed1987

Reduced glomerular filtration rate and hypercalciuria in primary struvite nephrolithiasis.

Struvite nephrolithiasis is caused by infection with bacteria that possess the enzyme urease, and convert urea to ammonia that raises urine pH and crystallizes with magnesium and trivalent phosphate ion. Of the 75 of our 1431 stone patients with struvite stones 52 were women. Struvite stones occurred almost exclusively in women; a minority of women and most men had mixed stones of struvite and calcium oxalate. Increased serum creatinine levels and reduced creatinine clearance were common in patients with struvite stones, not in those with mixed stones; both were rare in calcium stone disease. Men and women with mixed struvite, calcium oxalate stones were hypercalciuric, but women with struvite stones were not. Patients with mixed stones usually had initial symptoms of stone passage, and were less likely to need surgery, including nephrectomy, or to form contralateral stones. Patients with struvite stones usually presented with infection or no symptom, not passage. We conclude that struvite stones occur in two forms. The struvite stone is a disease of women, presumably occurring de novo from infection. The mixed stones occur in both sexes, presumably from secondary infection in hypercalciuric patients who begin with calcium-oxalate stone disease.

Blood Pressure↗
PubMed1986

A urinary calcium-citrate index for the evaluation of nephrolithiasis.

We have performed a multivariate analysis of urine abnormalities in patients with calcium oxalate nephrolithiasis, in which effects of gender were also considered. The characteristic of patients that most clearly sets them apart from normal people is a high level of urine calcium for any given level of urine citrate. Other urine measurements cannot improve upon the separation between patients and normals provided by urine calcium and citrate, and their abnormal relationship to each other. Normal women have higher urine citrate and lower urine calcium than normal men or patients of either sex; normal men differ from stone forming men only moderately. Direct measurements of supersaturation are not helpful in distinguishing between patients and normals, once calcium and citrate have been considered. From our analysis, we have derived a new index for evaluating the significance of urine calcium and citrate levels that seems to offer a better basis for clinical diagnosis than criteria presently in use.

Calcium↗
PubMed1985

Urine glycoprotein crystal growth inhibitors. Evidence for a molecular abnormality in calcium oxalate nephrolithiasis.

One reason that some people are prone to calcium oxalate nephrolithiasis is that they produce urine that is subnormal in its ability to inhibit the growth of calcium oxalate crystals. We have identified in human urine a glycoprotein (GCI) that inhibits calcium oxalate crystal growth strongly, and at low concentrations (10(-7) M); in this study, we have isolated GCI molecules from the urine of normal people and patients with calcium oxalate stones. GCI from stone formers is abnormal in three ways: it contains no detectable gamma-carboxyglutamic acid (Gla), whereas normal GCI contains 2-3 residues of Gla per mole; about half of the GCI in urine of patients inhibits crystal growth 4-20 times less than normal GCI as judged by its performance in a kinetic growth assay, in vitro; at the air-water interface, patient GCI has a film collapse pressure approximately half of normal. GCI molecules from the urine of patients with calcium oxalate nephrolithiasis are intrinsically abnormal, and these abnormalities could play a role in the genesis of stones.

1-Carboxyglutamic Acid↗
PubMed1985

Recurrence after a single renal stone in a community practice.

The natural history of recurrence of kidney stones was studied in a community urology practice, in which treatment with agents such as thiazide, allopurinol or oral phosphate has not been consistent or widespread. Using life-table analysis, the mean interval to first recurrence was 8.8 +/- 1.2 years and was not influenced by gender, age at first occurrence, or family history of stones. The tempo of recurrence justifies an individual approach to evaluation and treatment.

Adult↗
PubMed1982

Factors that predict relapse of calcium nephrolithiasis during treatment: a prospective study.

We evaluated 522 patients with idiopathic, recurrent calcium nephrolithiasis using a comprehensive clinical and laboratory protocol, and obtained additional laboratory measurements during their subsequent years of treatment in our program. In 57 patients, a new calcium stone ultimately formed during treatment (relapse), whereas 189 others have been free of recurrence during at least two years (average 4.3 +/- 2.2 [SD] years) of follow-up. Compared with the patients who remained stone-free, the patients with relapse (1) had a shorter interval between the time they entered our program and the time their last recurrent, pretreatment stone formed; (2) excreted more calcium *in mg/kg of body weight pr 24 hours) in their urine during treatment (2.79 +/- 1.08 versus 2.39 +/- 0.98 [SD] for relapse and stone-free); and (3) increased their urine volume less during treatment compared with pretreatment values (delta in liters per 24 hours was -0.02 +/- 0.48 versus 0.23 +/- 0.54 for relapse and stone-free). The two groups were otherwise the same. All comparisons used only data obtained prior to relapse. A discriminant function using only these three characteristics correctly identified 72 percent of patients with relapse and 67 percent of those who remained stone-free.

Allopurinol↗
PubMed1982

Effects of low-calcium diet on urine calcium excretion, parathyroid function and serum 1,25(OH)2D3 levels in patients with idiopathic hypercalciuria and in normal subjects.

We have used a low-calcium diet providing only 2 mg/kg (body weight) per 24 hours of calcium to distinguish between "renal" and "absorptive" idiopathic hypercalciuria. Sixteen of 27 hypercalciuric subjects excreted calcium in excess of intake during days seven, eight and nine of he diet, suggesting some element of renal hypercalciuria; however, all patients had low or normal serum PTH and urine cAMP levels. In general, fasting urine calcium was elevated in these 16 subjects and normal in the remaining 11, who conserved calcium more normally. SErum 1,25(OH)2D3 levels were the same in patients and normal subjects, even though PTH levels of the patients were below those of he normal subjects. Urine magnesium excretion and phosphorus excretion were both increased in the patients who excreted calcium in excess of intake. Our findings suggest that renal and absorptive hypercalciuria may not be distinct entities but rather the two extremes of a continuum of behavior. A uniform elevation of intestinal calcium absorption and a variable defect of renal calcium reabsorption could explain our results far better than the hypothesis of distinct absorptive and renal forms of hypercalciuria.

Calcitriol↗
PubMed1982

Pathogenesis and clinical course of mixed calcium oxalate and uric acid nephrolithiasis.

By direct measurement, urine from patients who form calcium oxalate stones was supersaturated abnormally with respect to calcium oxalate monohydrate but not supersaturated with respect to undissociated uric acid. Urine from patients who form uric acid stones was supersaturated excessively with undissociated uric acid but not calcium oxalate. Patients who form both calcium oxalate and uric acid stones, however, produce urine that is supersaturated with respect to both solid phases. Low urine pH was the primary factor that increased supersaturation with respect to undissociated uric acid. The formation of both calcium oxalate and uric acid stones appears to be explained by a dual abnormality of urine supersaturation.

Calcium Oxalate↗
PubMed1982

Formation of a single calcium stone of renal origin. Clinical and laboratory characteristics of patients.

Of 859 consecutive patients with calcium renal stones, 182 had formed only one stone before entering our program. Ninety-three (51.1%) had idiopathic hypercalciuria or hyperuricosuria; 36 (19.8%) others had a systemic disorder producing stones. The remainder, 53 (29.1%) patients, had no metabolic disorder. The frequency of hypercalciuria was lower than among patients with multiple stones. Compared with recurrent stone formers, patients with single stones were older when they passed their stones, suffered higher rates of complication such as surgery, cystoscopy, and urinary tract infection, and had a lower frequency of idiopathic hypercalciuria. During treatment, 11% formed a new stone in an average follow-up period of three years, a relapse rate similar to that of multiple stone formers; however, those patients with single stones who did relapse formed new stones at lower rates than multiple stone formers. Compared with recurrent stone formers, patients with solitary stones were more often treated with diet alone. Since there were no substantial differences between solitary and recurrent stone disease, patients who have formed a single stone should be evaluated and they should be treated no differently from other patients with stone disease.

Adult↗
PubMed1979

Familial idiopathic hypercalciuria.

The frequency of hypercalciuria was determined in the families of nine hypercalciuric patients with idiopathic hypercaliuria who formed recurrent calcium oxalate renal stones. Idiopathic hypercalciuria occurred in 26 of 73 relatives, in three consecutive generations of two families and in two successive generations of four other families. Multiple siblings or children of the probands were affected in three families. Nineteen of 44 first-degree relatives (43 per cent) had idiopathic hypercalciuria, as compared to seven of 29 (29 per cent) other relatives; there was no relation to age or sex. Renal stones were formed by 19 of the 44 first-degree relatives but by none of the others; nine of the 19 were women. We conclude that there is a familial form of hypercalciuria, which appears to be transmitted as an autosomal dominant trait. Stone disease is frequent in first-degree relatives, and affects both sexes equally.

Adult↗
PubMed1979

Urinary saturation measurements in calcium nephrolithiasis.

Urinary saturation with respect to calcium oxalate monohydrate was measured in 111 consecutive patients with calcium nephrolithiasis. Each patient also was evaluated by a detailed conventional metabolic protocol. Patients with idiopathic hypercalciuria produced abnormally oversaturated urine more frequently than normal subjects and normocalciuric patients, but normocalciuric patients had unexpectedly high levels of urine saturation. Measuring levels of calcium concentration, oxalate concentration, or the chemical concentration product of calcium and oxalate in urine did not predict oversaturation. During thiazide treatment, saturation level tended to fall if it was initially elevated, whether the patient was hypercalciuric or not. Patients whose urine was not remarkably oversaturated showed no tendency to elaborate even less saturated urine during thiazide treatment; instead, the average calcium oxalate saturation level remained constant. Direct urine saturation measurements can detect a small but significant number of normocalciuric patients who have marked oversaturation with respect to calcium oxalate and appear to benefit from treatment.

Calcium↗