RESUMEN
BACKGROUND: In obstetrical service it is frequent to find women with acute renal failure during second trimester of pregnancy. Main causes are related to hypertensive alterations, hemorrhage, sepsis, intrinsic renal disease and some rare disorders that produce high maternal morbidity and mortality. OBJECTIVE: [corrected] To evaluate changes of adrenal function in pregnancy as well as its associated repercussions in diabetic and preeclamsic patients. PATIENTS AND METHODS: Prospective study in 56 patients. Groups included women with normal pregnancy, patients with diabetes type 2, and women with preeclampsia. It was requested basic exams and samples from urine of 24 h for catecholamines determinations; as well as after two months of delivery. Catecholamines were measured with Bertler immune-fluorescent procedure. RESULTS: Levels of catecholamines has statistically significant difference in all groups of study during the gestation. There was high quantity in the group of patients that developed preeclampsia 4535.5 +/- 356.4 microg/24 h (p < 0.05), compared with 31.2 +/- 9.2 microg/24 h in normal pregnancy; however, those with diabetes has a trend to increas 45.6 +/- 3.7 microg/24 h, without statistical differences. Two months after pregnancy levels shown 17.1 +/- 4.9 microg/24 h in normal pregnancy group, with preeclampsia 17.2 +/- 8.7 microg/24 h, and mild permanent increase 33.8 +/- 4.7 microg/24 h in the group with diabetes (p = 0.537). CONCLUSIONS: An important catecholamines elevation is related with progress or severity of preeclampsia, and could be due to less adrenal injury associated with pregnancy, and contribute to renal failure. Longer studies are necessary to evaluate this approach in renal function.
Asunto(s)
Catecolaminas/orina , Preeclampsia/orina , Embarazo en Diabéticas/orina , Adulto , Femenino , Humanos , Embarazo , Estudios ProspectivosRESUMEN
Diabetic nephropathy is associated with increased urinary albumin and reduce kallikrein excretion. Increased activity of the renal kallikrein-kinin system has been suggested as one of the possible mechanisms underlying diabetic hyperfiltration. The present study shown that the Kallikrein-kinin system is progressively increased in the diabetic-pregnant rats at 7, 14, 21 days; 48 and 7 days after pregnancy (P < 0.05 vs Control). However, this increase during diabetic pregnancy did not reached the levels of control pregnancy. On the other hand albumin excretion shown a significant and progressive renal damage in the diabetic state. These findings suggest that the diabetic pregnancy could impair the renal hemodynamic, but, on the other side could modulate the vasodilator system at pregnancy in the attempt to protect the fetus.