dinoprost and Pyelonephritis

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Child; Child, Preschool; Chronic Disease; Dinoprost; Dinoprostone; Female; Humans; Hydronephrosis; Male; Prostaglandins; Pyelonephritis; Reference Values; Renin; Sodium; Thromboxane B2; Vesico-Ureteral Reflux

Eighteen patients with senile pyelonephritis and nephrogenic arterial hypertension were examined for the effect of trental monotherapy (600 mg/day) on intrarenal hemodynamics, the rate of glomerular filtration (effective renal blood flow, the intensity of blood flow in the medullary layer of the kidney), activity of the renin-angiotensin-aldosterone system (plasma renin activity, plasma and urine aldosterone), prostaglandin synthetic capacity of the kidneys (PGE and PGF2 alpha), water-electrolyte balance (circulating blood volume, sodium content in the serum and its excretion with urine), and on arterial pressure and general vascular peripheral resistance. Prolonged administration of the drug (from 3 weeks to 6 months) led to a significant improvement of the medullary blood flow, increase (p less than or equal to 0.05) of excretion of natriuretic PGE [correction of RGE] and lowering (p less than or equal to 0.05) of diurnal excretion of PGF2 alpha, which was accompanied by a rise of natriuresis (p less than or equal to 0.05) and diuresis.

Topics: Dinoprost; Drug Evaluation; Female; Hemodynamics; Humans; Hypertension; Male; Middle Aged; Pentoxifylline; Prostaglandins E; Pyelonephritis; Renin-Angiotensin System; Time Factors; Water-Electrolyte Balance

Topics: Adolescent; Child; Child, Preschool; Chronic Disease; Dinoprost; Dinoprostone; Humans; Prostaglandins E; Prostaglandins F; Pyelonephritis

The state of the renal prostaglandins (PG) system was assessed in 54 patients with essential hypertension, stage IB-IIA, as compared to that of patients with symptomatic arterial hypertensions. A decrease in renal PGE2 production, noted in all hypertensive patients and determined on the basis of its diurnal excretion, was particularly pronounced in essential hypertension. Diurnal PGE2 excretion decreased as hypertension progressed in patients with essential hypertension, and renal PGF2 alpha production became prevalent. Renal function is dependent on the level of PG production by the kidney. As renal concentration capacity decreases and renographic findings become less satisfactory, PGE2 excretion decreases as well. Salt loads can bring out functional insufficiency of the renal PG system in essential hypertension, as reflected in a much smaller increase in PGE2 excretion, as compared to the control values, at early stages of salt loading and a considerable increase in PGF2 alpha excretion. In essential hypertension, inadequate renal prostaglandin response to salt loading is, to a certain degree, related to changed renal PGE-9-ketoreductase activity.

Topics: Dinoprost; Dinoprostone; Humans; Hypertension; Hypertension, Renal; Hypertension, Renovascular; Kidney; Prostaglandins; Prostaglandins E; Prostaglandins F; Pyelonephritis; Sodium Chloride

Levels of PGE2, PGF2 alpha and renin activity were measured in renal venous blood of 29 patients with essential hypertension (EH), 23 patients with renovascular hypertension (RVH) and 10 patients with unilateral pyelonephritis and high arterial hypertension. The pattern of change in renal venous PG content was found to be related to the type of renal lesion: the level of PGE2 was lowered and PGF2 alpha/PGF2 ratio increased in the blood outflow from the kidneys of EH patients and from ischemized kidneys of RVH patients as compared to similar parameters in the outflow from contralateral kidneys of patients with RVH and pyelonephritis. Venous levels of both PGs were the highest in pyelonephritis-affected kidneys. Renal venous PG levels go down in all cases as the disease grows older. An acute drop in arterial pressure is accompanied with increased withdrawal of PGF2 alpha from the kidneys and enhanced renin activity in renal veins, while PGE2 drops simultaneously. PGF2 and PGE2 showing different trends of change in response to falling arterial pressure suggests increased transition of PGE2 to PGF2 alpha under the effect of enhanced PG-9-ketodehydrogenase activity. In the abdominal aorta, the scope of drop in arterial pressure correlates to the change in PGF2 alpha level, that is an evidence of PG direct involvement in the autoregulation of renal blood flow.

Topics: Dinoprost; Dinoprostone; Humans; Hypertension; Hypertension, Renal; Hypertension, Renovascular; Kidney; Prostaglandins E; Prostaglandins F; Pyelonephritis; Renal Artery; Renal Veins; Renin

The values of PGf2 alpha were studied in 20 renal patients with renal hypertension, with and without chronic renal insufficiency via a radioimmunologic method. A control group of 10 healthy volunteers wer used without data from arterial hypertension. Values (672.0 +/- 99.5 pg/ml), being, with statistically significant difference, increased as compared with the healthy volunteers (347.13 +/- 49.9 pg/ml) were found in renal patients with chronic renal insufficiency. With the advancement of CRI in patients with renal hypertension, PG concentration was also increased (505.5 +/- 77.6 pg/ml) but it was not significant as in the patients without CRI. The elevated values of PGF2+ alpha suggest their participation in the pathogenesis of renal hypertension.

Topics: Adult; Chronic Disease; Dinoprost; Female; Humans; Hypertension, Renal; Kidney Failure, Chronic; Male; Prostaglandins F; Pyelonephritis