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I Petrů

Publications and source records attributed to I Petrů.

7 recordsLinked to original sources
PubMed1991

[The effect of decreased thromboxane synthesis on proliferative glomerulonephritis].

The authors investigated in 19 patients with chronic proliferative glomerulonephritis the effect of 100 mg acetylsalicylic acid (ACA) administered for 12 months and the effect of 50 mg ACA administered for the same period. They evaluated the effect of the two doses on the urinary excretion of PGI and TXA2 metabolites as well as the effect on proteinuria and glomerular filtraction (GF). The authors provided evidence that small and very small amounts of ACA did not affect the excretion of the PGI metabolite, while they reduced significantly the excretion of the TXA2 metabolite and of proteinuria, and significantly increased GF.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

[Treatment of chronic glomerulonephritis with small doses of acetylsalicylic acid].

The purpose of the investigation was to evaluate the long-term administration of 100 mg acetylsalicylic acid in patients with chronic proliferative glomerulonephritis. Two 12-month periods are compared in the same patients (n = 19) without and with treatment. Glomerular filtration and quantitative proteinuria did not change significantly one year prior to treatment. During treatment glomerular filtration increased from 1.22 +/- 0.37 to 1.70 + 0.55 ml/s (p less than 0.01) and proteinuria declined from 2.6 + 1.1 to 1.6 +/- 1.0 g/24 h (p less than 0.01). Treatment did not influence the excretion of the metabolite prostacyclin 186 +/- 56 and 189 + 75 ng/24 h resp., and significantly reduced the thromboxane excretion from 565 +/- 267 to 348 + 123 ng/24 h, p less than 0.01). The authors assume that long-term treatment could influence in a favourable way the course of chronic proliferative glomerulonephritis.

Adult↗
PubMed1990

[The effect of acetylsalicylic acid and dipyridamole on glomerular filtration and proteinuria in chronic glomerulonephritis].

The authors treated 14 patients with chronic proliferative glomerulonephritis for one year with acetylsalicylic acid--400 mg/day--and dipyridamole--225 mg/day. They investigated changes of glomerular filtration and proteinuria before treatment, during treatment and one year after its completion. They found that in the course of treatment proteinuria did not change and glomerular filtration declined insignificantly. During the subsequent year proteinuria and glomerular filtration declined significantly. The above findings can be partly explained by changes in the synthesis of renal prostacyclin and thromboxane. The combination of acetylsalicylic acid and dipyridamole in the amounts used did not have a favourable effect on glomerular filtration in patients with chronic proliferative glomerulonephritis.

Adult↗
PubMed1989

[Treatment of chronic proliferative glomerulonephritis using acetylsalicylic acid and dipyridamole].

Fourteen patients with chronic proliferative glomerulonephritis were given for the period of one year 400 mg acetylsalicylic acid and 225 mg dipyridamole per day. During this treatment the thrombocyte aggregation became normal, however, the mean reduction of antiheparin plasma activity was not statistically significant. Normal synthesis of renal prostacyclin declined significantly as a result of treatment, while the renal thromboxane A2 synthesis remained normal even during treatment. Treatment did not influence proteinuria. The mean annual decline of glomerular filtration was greater during the investigation period than the mean annual decline in previous years, the difference was, however, only at the borderline of statistical significance. The authors did not prove a favourable effect of this treatment in patients with chronic proliferative glomerulonephritis.

Adult↗
PubMed1989

[Prostaglandins and chronic proliferative glomerulonephritis].

In 14 patients with chronic proliferative glomerulonephritis, corrected arterial hypertension and normal or marginal glomerular filtration the authors assessed plasmatic and urinary metabolites of PGI2 and TXA2. They found that the production of both PGI2 and TXA2 was raised in the organism and they assume that in the stimulated synthesis hypertension and its treatment participated. The production of both prostaglandins in the kidneys was, however, normal.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

[Cryoglobulinemia].

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Cryoglobulinemia↗