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M Urivetzky

Publications and source records attributed to M Urivetzky.

At least 19 recordsLinked to original sources
PubMed1995

Matrix modulates uptake of calcium oxalate crystals and cell growth of renal epithelial cells.

Handling of urinary crystals by renal epithelial and medullary interstitial cells may play an important role in the pathogenesis of renal stones and associated renal scarring. We examined the effects of calcium oxalate monohydrate (CaOM) crystals on the proliferative activity of renal tubular cells (opossum kidney) and renal medullary interstitial cells in culture. We also studied the impact of altered extracellular matrix on cell proliferation as well as on uptake of crystals by epithelial cells. Epithelial cells incubated with CaOM showed greater (p < 0.05) growth when compared with untreated cells (control, 10.5 +/- 1.1 versus CaOM, 16.6 +/- 1.6 x 10(6) cells per dish). the CaOM crystal-cell interaction also enhanced proliferation of interstitial cells (at 48 hours, control, 3.3 +/- 0.2 versus CaOM, 4.2 +/- 0.1 x 10(6) cells per dish, p < 0.02; at 72 hours, control, 3.6 +/- 0.3 versus 5.5 +/- 0.4 x 10(6) cells per dish, p < 0.01). Collagen, a constituent of extracellular matrix, inhibited (p < 0.01) proliferation of epithelial cells. Semiconfluent epithelial cells grown on collagen gels showed greater (p < 0.01) uptake of 45CaOM crystals when compared with uptake by cells grown on either uncoated (control) or albumin-coated plastic dishes (control, 979.9 +/- 51.1, albumin, 876.4 +/- 28.3, collagen gel, 1502.5 +/- 103.8 cpm per well). Epithelial cells grown to confluence on collagen gels also showed enhanced (p < 0.05) uptake of 45CaOM crystals. Reflectance microscopy as well as ultrastructural studies revealed intracellular localization of CaOM crystals. These results indicate that CaOM crystals stimulate the growth of both epithelial and interstitial cells. Enhanced growth of interstitial cells may also lead to increased synthesis of extracellular matrix. The latter may further modulate crystal uptake as well as cell growth of adjacent epithelial cells. These findings may be important in the development of nephrolithiasis and associated interstitial scarring.

Animals↗
PubMed1992

Ascorbic acid overdosing: a risk factor for calcium oxalate nephrolithiasis.

A total of 15 patients with unilateral nephrostomy tubes after extracorporeal shock wave lithotripsy received either 0 (placebo), 100, 500, 1,000 or 2,000 mg. ascorbic acid on days 2 and 3 postoperatively. Before and after administration, successive 6-hour urine specimens were collected from the nephrostomy tube and from the contralateral kidney directly into a preservative to stabilize ascorbic acid and oxalate. In 1 patient in each group preservative was omitted from the collection pouch. Urinary oxalate was then measured enzymatically after removal of ascorbic acid with sodium nitrite. Preservatives proved necessary for full recovery of analyte. At doses of 500 mg. or more of ascorbic acid there was a statistically significant increase in urinary oxalate equivalent to 1.2 to 1.8% of the millimoles of ascorbate administered. This represented an increase in urinary oxalate excretion of 6 to 13 mg. per day per 1,000 mg. ascorbic acid supplement. This amount would increase the risk of calcium oxalate urolithiasis.

Adult↗
PubMed1991

Urinary excretion of oxalate by patients with renal hypercalciuric stone disease. Effect of chronic treatment with hydrochlorothiazide.

Hydrochlorothiazide is employed to reduce calcium excretion in patients with urinary stone disease secondary to renal leak hypercalciuria. Because the drug also has been reported to be a competitive inhibitor of oxalate excretion by the renal tubules, we sought to determine whether chronic use indeed affected the amount of oxalate excreted. Patients taking hydrochlorothiazide 50 mg daily did not have a statistically significant reduction in twenty-four-hour urinary oxalate on their customary diets (pretreatment 37 +/- 3 mg/day [mean +/- S.E.M.; N = 22]; at one year 36 +/- 3 mg/day [N = 22]; at two years 37 +/- 3 mg/day [N = 16]). In 12 patients who voluntarily collected twelve-hour urine specimens after dinner on the third day of a low-oxalate diet and again the next day after a 1 g oxalate load, hydrochlorothiazide had no significant effect on oxalate excretion (19 +/- 2.3 mmol oxalate/mol creatinine on hydrochlorothiazide versus 20.6 +/- 2.6 mmol off the drug after low oxalate meal; 50 +/- 7.8 mmol/mol creatinine on hydrochlorothiazide versus 56.2 +/- 7.5 mmol off the drug after an oxalate load). As expected, there was a significant reduction in urinary calcium excretion and thus of calcium oxalate urinary saturation during hydrochlorothiazide administration. Hydrochlorothiazide by itself is not sufficient to reduce oxalate excretion in patients with renal leak hypercalciuria.

Adult↗
PubMed1990

Absence of effect of allopurinol on oxalate excretion by stone patients on random and controlled diets.

After 1 year of allopurinol treatment in 36 patients with a history of uric acid and/or calcium oxalate lithiasis and hyperuricosuria, we observed that in addition to the desired decreases in uric acid there were apparently significant decreases in urinary oxalate levels: 37 +/- 3 mg. per day (mean +/- standard error) before therapy and 31 +/- 4 mg. per day after a mean decrease of 16% (p less than 0.05) with an equivalent decrease in the supersaturation (calcium oxalate) of the urine. However, the decrease in oxalate could have been related to changes in dietary habits rather than to any specific effects of allopurinol on oxalate metabolism. Therefore, we recruited 26 of the patients for a study in which dietary factors were controlled. Each participant was assigned to 1 of 3 diet groups: low or high protein, or a customary diet. Each patient collected a urine specimen while on allopurinol and again after the medication was discontinued. With analytical procedures that we ascertained to be free of any significant methodological bias, we observed no significant changes in urinary oxalate excretion that could be attributed to allopurinol. There were significant differences in oxalate excretion on versus off allopurinol between the low and high protein groups, with higher oxalate levels found for the latter group. Our results indicate that allopurinol does not have a specific effect on oxalate metabolism or oxaluria.

Adult↗
PubMed1990

Biochemical evaluation of calcium stone patients: how soon can it be done after stone surgery/passage?

Biochemical evaluations were done two times for 29 outpatients with calcium stone disease, the first time within one month after surgical extraction or passage of stones and the second time two months or more later. Classification of the etiologic basis for the stone disease was the same after both tests in 27 patients. In the other 2 patients the diagnosis was changed from renal to absorptive hypercalciuria. Both of these patients had creatinine clearance rates less than 60 percent of normal during the first test. One also had multiple residual stones during both evaluations, and the second had a urinary tract infection during the first test that resolved with a normal creatinine clearance by the second test period. When nephrogenous cyclic adenosine monophosphate (cAMPn) assays were done on fasting specimens in these patients, the results were consistent with absorptive hypercalciuria. Almost all patients can be evaluated and placed in management programs within a few weeks after surgery. If cAMPn assays are not done, patients with decreased renal function secondary to residual stones or infection can be tested at a later time.

Adolescent↗
PubMed1988

Plasma osteocalcin levels in stone disease. A potential aid in the differential diagnosis of calcium nephrolithiasis.

Plasma osteocalcin levels were measured by radioimmunoassay in 70 consecutive patients with recurrent calcium (sterile) nephrolithiasis during diagnostic evaluation for the cause of the disease. Nephrogenous cyclic adenosine 3,5'-monophosphate levels also were measured in most of the subjects. Included in the sampling, as determined by standard diagnostic criteria, were 12 patients with absorptive hypercalciuria type I, 15 with absorptive hypercalciuria type II, 22 with renal leak hypercalciuria, 11 with normocalciuria, 6 with primary hyperparathyroidism, 3 with renal tubular acidosis and 1 with Paget's disease, as well as 12 control subjects. The observed plasma osteocalcin levels (ng. per ml. mean +/- standard error) were absorptive hypercalciuria I 2.6 +/- 0.20, absorptive hypercalciuria II 3.1 +/- 0.21, renal hypercalciuria 8.7 +/- 0.45, normocalciuric nephrolithiasis 3.3 +/- 0.25, primary hyperparathyroidism 13.2 +/- 0.91, renal tubular acidosis (range) 5.2 to 10.6, Paget's disease 18.0 and control 3.1 +/- 0.20. There were significant differences between the plasma osteocalcin levels of renal hypercalciuria versus primary hyperparathyroidism and renal hypercalciuria/primary hyperparathyroidism versus any other group. There was good correlation between plasma osteocalcin and cyclic adenosine 3,5'-monophosphate data (correlation coefficient 0.72, p less than 0.005). Plasma osteocalcin levels are a potential differential diagnostic tool for patients with stone disease. The diagnostic value compares favorably with that of cyclic adenosine 3,5'-monophosphate, with the advantage that the determination of plasma osteocalcin requires only a single test.

Adult↗
PubMed1987

Dietary protein levels affect the excretion of oxalate and calcium in patients with absorptive hypercalciuria type II.

A total of 12 patients with absorptive hypercalciuria type II and 11 normal controls participated in a study to evaluate the effects of dietary protein levels on urinary calcium and oxalate excretion before and after a 1 gm. dose of oxalate. Two test periods were used during which calcium (less than 400 mg. per day) and oxalate were restricted. The first test was done under conditions of low dietary protein (12 per cent total caloric intake, 60 gm.) and the second test was done at a high protein level (25 per cent, 125 gm. protein). Twelve-hour urine specimens were obtained after dinner on day 3 of each diet (low and high protein) and again on day 4 when 1 gm. oxalate (spinach) was added to the dinner meal. The specimens were analyzed for calcium, oxalate and relative calcium oxalate saturation (concentration product ratio). There were no significant differences between the controls and subjects with absorptive hypercalciuria type II in oxalate excretion before the oxalate load on the low protein (controls 31.4 +/- 4.2 standard error, expressed as mmol. oxalate per mol. creatinine, and absorptive hypercalciuria type II 23.1 +/- 3.1) and high protein (controls 30.4 +/- 4.2 and absorptive hypercalciuria type II 28.8 +/- 5.9) diets. After the oxalate bolus the positive changes in oxalate excretion were 11.8 +/- 4.8 (low protein) and 17.8 +/- 4.7 (high protein) for controls, and 11.4 +/- 4.4 (low protein) and 31.8 +/- 5.2 (high protein) for patients with absorptive hypercalciuria type II. Thus, the increases in post-load urinary oxalate levels observed for controls and patients were greater on the high protein than on the low protein diets. After the oxalate load the increases in urinary oxalate and calcium oxalate supersaturation were significantly greater for patients with absorptive hypercalciuria type II than for control subjects for the high protein but not the low protein diets (p less than 0.05).

Adult↗
PubMed1976

Rat polyvinyl sponge model for the study of infections: initial investigations.

Polyvinyl sponges were implanted subcutaneously on both sides of young female rats. One sponge was infected with 10(8) of either Escherichia coli K-12 F-, Staphylococcus aureus ATCC 25923, or Pseudomonas aeruginosa CDC 7725. P. aeruginosa remained at the inoculum level and S. aureus declined by 1 log, whereas E. coli was reduced 1,000-fold. Only P. aeruginosa was recovered from the blood in 36% of the animals in 24 h and in 20% of the rats in 48 h. The nutrient potential of rat inflammatory fluid was compared to nutrient broth by growth of each bacterium in untreated and heat-inactivated sponge fluids and Trypticase soy broth.

Animals↗
PubMed1976

Rat polyvinyl sponge model for the study of infections: host factors and microbial proliferation.

Female rats were treated with several administration regimens of methylprednisolone, cobra venom anti-complementary factor, and cyclophosphamide in conjunction with polyvinyl sponge implantations. The effect of these drugs on host factors active against bacteria was evaluated with Staphylococcus aureus ATCC 25933, Escherichia coli K-12, and Pseudomonas aeruginosa CDC 7725. One of two implants in each animal was infected with 10(8) of one of the three bacteria, and bacterial and granulocyte content was determined in the infected and control sponges after 48 h. The single large dose of methylprednisolone decreased staphylococcal and E. coli clearance while promoting dissemination of P. aeruginosa. A low chronic dose of the steroid inhibited E. coli chemotaxis only. A higher dose of the steroid administered chronically interfered markedly with S. aureus and E. coli curtailment by the host while leading to enhanced dissemination of P. aeruginosa, accompanied by a precipitous decline in granulocytes. Results with cobra factor resembled the higher chronic dose of steroid enhancing, especially the dissemination of the pseudomonad and its anti-granulocytic propensity. Cyclophosphamide depression of granulocytes revealed the rat's ability to curtail the proliferation of particular S. aureus and E.coli strains even in the absence of leukocytes. This treatment resulted in the rapid spread of P. aeruginosa, leading to the death of some experimental animals. These experiments underline the versatility of this animal model in the study of host and microbial factors influential in infectious disease.

Animals↗
PubMed1976

Fibroblast DNA synthesis activation in sponge induced granulation tissue. The effect of antineutrophil serum and cyclophosphamide.

DNA synthesis in rat and rabbit polyvinyl sponge induced granulation tissue has been studied using thymidine (methyl-3H). Synthesis was determined by measurement of thymidine incorporation into cold trichloroacetic acid insoluble material and by autoradiography. Granulation tissue was removed and immediately incubated in vitro in the presence of thymidine (methyl-3H) for three hours. The label was incorporated into the nuclei of fibroblasts and, to a lesser extent, of endothelial cells. The labeled material was 93% lysable by DNase and its synthesis was inhibited by hydroxyurea and bleomycin. In this system synthesis was linear for two hours and then ceased. A marked increase in DNA synthesis occurred in tissue harvested at 44 hours after sponge implantation. This rise was confirmed by autoradiographic studies which showed an increase in nuclear labeling at two days after implantation. Neutropenia produced by injections of antineutrophil serum or cyclophosphamide failed to inhibit activation of DNA synthesis in fibroblasts or endothelial cells. Amonocytosis also had no effect on this process. Rates of thymidine incorporation into DNA and thymidine phosphates in vivo were similar to those found during in vitro incubations of granulation tissue.

Animals↗
PubMed1975

The mechanism of action of a single dose of methylprednisolone on acute inflammation in vivo.

A model system for the study of inflammation in vivo has been developed using the 16-h polyvinyl sponge implant in the rat. This system allows for simultaneous measurement of in vivo chemotaxis, volume of fluid influx, and fluid concentrations of lysosomal and lactic dehydrogenase (LDH) enzymes. In addition, the enzyme content of inflammatory fluid neutrophils may also be determined. A parallel time course of neutrophil and lysosomal enzyme influx into sponge implants was observed. This was characterized by an initial lag phase and a rapid increase between 5 and 16 h. The origin of supernatant LDH and lysosomal enzymes was studied with anti-neutrophil serum to produce agranulocytic rats. Inflammatory fluid in these rats was almost acellular and contained decreased concentrations of beta glucuronidase (-96%) and LDH (-74%). In control rats all of the supernatant beta glucuronidase could be accounted for by cell death and lysis, as estimated from measurements of soluble DNA. Only 15-20% of the LDH activity could be accounted for on the basis of cell lysis. The remainder was derived from neutrophil-mediated injury to connective tissue cells. Large intravascular doses of methylprednisolone markedly inhibited neutrophil influx into sponges and adjacent connective tissue. Secondary to decreased neutrophil influx, fewer neutrophils were available for lysis, and lysosomal enzyme levels in inflammatory fluid decreased. No evidence for intracellular or extracellular stabilization of neutrophil lysosomal granules by methylprenisolone was found.

Animals↗
PubMed1975

The need for modification of the polyvinyl sponge model of connective tissue growth. Histoligic and biochemical studies in the rabbit.

Quantitative histopathologic and biochemical comparisons were made between polyvinyl sponge capsular and sponge tissue in the rabbit on different days after subcutaneous implantation. Up to 9 days the predominant cell type in the capsular tissue is the fibroblast and in the sponge it is the neutrophil. During this time period the sponge tissue shows lower rates of (14C) proline and (14C) cytidine incorporation and lower rates of total (14C) collagen synthesis than the surrounding capsule. Different gel electrophoretic patterns of isolated radioactive proteins are found in sponge and capsule at 6 days. These biochemical differences appear to be related to the small number of fibroblasts, relative to granulocytes present in sponges during the first 9 days after implantation. It is suggested that future biochemical investigations of the early phase of connective tissue reactions (first 9 days) in this model utilize sponge capsular tissue within 1 cm of the sponge edge instead of the sponge and its contents.

Animals↗
PubMed1975

Kinetic study of neutrophil and inflammatory fluid beta glucuronidase.

Beta glucuronidase obtained from rat inflammatory fluid and granulocytes was studied kinetically. Linear increases in activity occurred with time and enzyme concentration. No evidence of enzyme degradation during incubation was obtained. Supernatant and granulocyte enzyme activity was identical in relation to Km, and pH optima and resistance to high NaCl concentration. Minimal contributions to supernatant activity occur from plasma and red cells.

Animals↗