Risk factors and outcome of Preeclampsia.

AIM: To determine differences between groups with hypertension in pregnancy and assess risk factors associated with preeclampsia. PATIENTS AND METHODS: In the period 2008-10 at the Department of Nephrology in Skopje, Macedonia, a prospective and a longitudinal study study comprising 134 pregnant women was carried out. They had regular monthly check-ups in pregnancy and after delivery (1-8), when groups were defined as gestational hypertension, pre-existing hypertension, superimposed preeclampsia, and preeclampsia. A total of 134 women were regularly controlled by 24-hour ambulatory monitoring of blood pressure (24ABPM), blood and urine, D-dimers, and a resistance index of the Doppler of the umbilical artery (RI a.umb), and a questionnaire on risk factors was filled in for every pregnant woman. RESULTS: Superimposed preeclampsia was found in 22 (16.4%) and preeclampsia was found in 20 women (14.9%). Daily diastolic blood pressure of 24-hour blood pressure monitoring at the last check-up before delivery was significantly higher in the group with superimposed preeclampsia (SP) 87.6±9.5 and in the group with preeclampsia (PE) 87.9±7.7 mm Hg. Previous preeclampsia (OR=3.28), primiparity (OR=2.35), methyldopa (OR=3.76), number of check-ups (OR=2.3), positive family history (OR=1.4) and in vitro fertilisation (OR=1.15) were found as risk factors associated with the occurrence of preeclampsia and preeclampsia superimposed on preexisting hypertension. CONCLUSIONS: Early determination of risk factors should prompt more frequent check-ups in hypertensive pregnancies in order to determine timely delivery and avoid adverse outcomes in the mother and child.

Changes of plasma fibronectin levels in pregnancy induced hypertension.

A number of laboratory tests are available for evaluation of hypertension in pregnancy. These tests can be used to either predict and/or prognosticate preeclampsia and other hypertensive disorders of pregnancy. The aim of this study was to evaluate alterations in fibronectin homeostasis in normotensive pregnancy and in hypertensive disorders of pregnancy subclassified into chronic hypertension, preeclampsia superimposed on chronic hypertension, and pregnancy induced hypertension. A prospective, longitudinal study was conducted in 115 pregnant women aged 20-39 years, divided into four groups: normotensive (n = 40), chronic hypertension (n = 18), preeclampsia superimposed on chronic hypertension (n = 20), and pregnancy induced hypertension (n = 37). Plasma concentrations of fibronectin were measured by using single radial immunodiffusion assay (RIA) in the 8th, 18th, 23rd, 28th, 32nd and 36th week of gestation. Plasma fibronectin concentration showed no significant changes in normotensive pregnancy, but was significantly elevated in the third trimester in women destined to become preeclamptic or with preeclampsia in whom it reached a mean (+/- SD) of 0.40 +/- 0.09 g/L in the 36th week of gestation. In the groups with preeclampsia superimposed on chronic hypertension and with pregnancy induced hypertension, there was a significant difference between plasma fibronectin concentrations in 32nd (p < 0.01) and 36th (p < 0.001) week of gestation compared with either other levels in the respective group (in the 8th, 18th, 23rd and 28th week of gestation) or those recorded in other groups in the same period of pregnancy. These results suggested that the measurement of plasma fibronectin might be of diagnostic value in preeclampsia but could not be considered a useful predictor for preeclampsia.

Plasma human atrial natriuretic peptide, endothelin-1, aldosterone and plasma-renin activity in pregnancy-induced hypertension.

OBJECTIVE: To determine the relationship between endothelin-1 (ET-1), human atrial natriuretic peptide (hANP), plasma-renin activity (PRA) and 24-h urinary excretion of aldosterone (U-Ald) in pregnancy-induced hypertension (PIH). DESIGN AND METHODS: Plasma hANP (pg/ml), ET-1 (pg/ml), PRA (ng/ml per h) and U-Ald (microg/24 h) were measured and 24 h ambulatory mean arterial pressure (MAP) was monitored in 178 normotensive subjects (NT) and 79 gravidas with PIH at the 8th, 18th, 23rd, 28th, 32nd and 36th weeks. RESULTS: The PIH group had higher MAP than the NT group from the 23rd week (91.64 +/- 8.76 versus 83.48 +/- 4.36 mmHg, P< 0.01) until the end of the pregnancy. ET-1 levels (pg/ml) in both groups were identical at the beginning of pregnancy and different in the 23rd week [(NT versus PIH) (35.11 +/- 17.42 and 40.2 +/- 19.51, respectively, P < 0.05)] and the 36th week (37.36 +/- 18.07 and 42.7 +/- 16.43, P< 0.05). hANP levels (pg/ml) in the NT group decreased insignificantly from the 8th till the 32nd week, then increased to 101.94 +/- 17.4 in the 36th (P< 0.001 versus any other week). In the PIH group, hANP increased from 104.8 +/- 26.8 pg/ml at the 8th week to 161.3 +/- 28.6 pg/ml at the 36th week (P< 0.0001). hANP correlated with MAP in the NT group (r = 0.252, P< 0.0005) but not the PIH group. U-Ald in the NT group increased from 23.52 +/- 6.83 microg/24 h at the 8th week to 54.07 +/- 19.62 microg/24 h at the 36th week (P < 0.0001) and in the PIH group it increased from 27.90 +/- 11.6 to 53.66 +/- 20.4 microg/24 h (P< 0.0001). In the PIH group, PRA was lower compared with the NT group from the 8th (2.99 +/- 1.26 versus 4.10 +/- 1.82 ng/ml per h, P< 0.05) until the 36th week (3.34 +/- 2.16 versus 4.46 +/- 2.13 ng/ml per h). In the forced multiple regression analysis model with hANP as a dependent variable, a value of P< 0.003 was found with PRA, U-Ald and MAP, which indicates an interaction between the two vasoactive and homeostatic systems: the renin-angiotensin-aldosterone system and hANP. CONCLUSIONS: In PIH, elevated hANP might be important as a counterbalance to the presence of the active vasopressors and sodium retention. By inhibiting renin release, enhancing the transcapillary fluid migration and with its action as vasodilator, it acts as a corrective factor of the imbalance between the contracted circulating fluid volume and the vasoconstricted vascular bed.

Renal dysfunction and early differences in twenty-four-hour ambulatory blood pressure monitoring in subjects predisposed for essential hypertension.

In 24 young normotensive subjects (mean age 22.25 +/- 5.65 years) with one hypertensive parent (FH(+)-), 22 subjects (mean age 23.55 +/- 5.17 years) with two hypertensive parents (FH+ +/-), and a control group of 16 age and gender matched subjects (mean age 22.50 +/- 6.00 years) with two normotensive parents (FH--), creatinine clearances and microalbuminuria (MA) were measured. Blood pressure was monitored for 24 hours and mean arterial pressure (MAP) was calculated and compared between groups. No significant differences were recorded. FH(+)- and FH++ subjects had significantly higher MAP over the sleeping period than FH-- subjects (78.63 +/- 1.71, 78.95 +/- 1.27; and 72.91 +/- 1.35 mmHg respectively; p < 0.02). Creatinine clearance was higher in FH(+)- and FH++ group compared to FH-- subjects (2.39 +/- 0.17; 2.29 +/- 0.17; and 1.66 +/- 0.11 ml/sec respectively; p < 0.01). Hyperfiltration correlated with MAP in FH++ subjects (2.29 +/- 0.17 ml/sec; 92.45 +/- 7.39 mmHg; r = 0.52 i p < 0.03). MA correlated neither with creatinine clearance nor with MAP. Our results suggest that hypertension may develop as a consequence of the long-lasting, higher GFR, which may accelerate the age-related process of sclerosis both in the small arterioles and the glomeruli.

[Serum levels of uric acid, lipids and glucose in essential hypertension]. / Nivo uricne kiseline, lipida i glikoze u serumu i esencijalna arterijska hipertenzija.

In 48 men, 42, 1 +/- 8.8 yrs old, with untreated mild essential hypertension, serum uric acid, total cholesterol triglycerides and glucose were examined at 8 a.m after 16 hour overnight fasting. All patients were overweight, with body mass index: 26.9 +/- 2.4 kg/m2, (normal value: 19-24.9); serum uric acid 293.1 +/- 89.3 mmol/l; cholesterol 6.3 +/- 1.4; triglycerides 2.0 +/- 1.3 and glucose 5.4 +/- 0.9 mmol/l. File out of 48 (10.4%) patients had hyperuricemia, nine (18.7%) had hypercholesterolemia, twenty (41.7%) had hypertriglyceridemia and 19 (39.6%) had hyperglycemia. Significant correlation between serum uric acid and triglycerides only (r = 0.35; p < 0.01), was found. A correlation exists between the diastolic blood pressure and cholesterol (r = 0.35; p < 0.01); as well as, between mean arterial blood pressure and cholesterol (r = 0.34; p < 0.02). Only three out of 48 (6.2%) patients with hypertension had all four biochemical parameters above normal levels. Our results suggest that interrelation of all these metabolic disorders are important in essential hypertension, and especially the association of high serum uric acid and triglyceride level.

Primary disseminated form of Ewing sarcoma in association with hypercalcemia and acute renal failure.

We present a case of an extremely rare form of Ewing sarcoma--primary disseminated, with fulminating course, severe hypercalcemia, extensive calcium deposition in parenchymatous organs, including kidneys, and acute renal failure as a clinical consequence. Correction of hypercalcemia was followed by prompt restoration of the glomerular filtration rate (GFR), suggesting that hypercalcemia had a direct effect on its regulation independent of the renal tubular damage. The effectiveness of the treatment with indomethacin indirectly supports the possibility of prostaglandin-mediated humoral hypercalcemia of malignancy.

Urinary excretion of three specific renal tubular enzymes in patients treated with nonsteroidal anti-inflammatory drugs (NSAID).

Ten patients, mean age 51.50 +/- 3.03 years, with degenerative rheumatism on NSAID treatment without any sign of renal disease, and 11 control subjects, mean age 43.50 +/- 1.51 years, were studied. NSAID treatment was of 11.30 +/- 5.60 weeks duration in average, with ibuprofen, naproxen, or indomethacin. Urinary excretion of three specific renal tubular enzymes--AAP: alanine-amino-peptidase, GGT: gamma-glutamyl-transpeptidase, and beta-NAG: beta-N-acetyl-glucosaminidase, were determined in 8-h overnight urine samples, as well as GFR creatinine clearance/1.73 m2, urinary volume/8 h, specific gravity of the urine, proteinuria and glucosuria. In the group treated with NSAIDs, urinary excretion of the enzymes was significantly higher than in the control group--AAP: 1414.20 +/- 317.60, 864.20 +/- 94.42, p < 0.00001; GGT: 8034.6 +/- 1378.55, 5095.64 +/- 614.40, p < 0.00001, and beta-NAG: 1644.60 +/- 299.97, 964.82 +/- 142.00, p < 0.00001. Patients on NSAID treatment showed abnormal urinary excretion of AAP in 7/10 cases, of GGT in 6/10, and of beta-NAG in 7/10 cases. Duration of the treatment did not correlate with the urinary excretion of the enzymes. Age was in correlation with the urinary excretion of the enzymes only in the control group, r = 0.52, p < 0.005 for AAP, r = -0.43, p < 0.02 for GGT, and r = -0.23, p < 0.05 for beta-NAG.(ABSTRACT TRUNCATED AT 250 WORDS)