A case of nephrogenic diabetes insipidus caused by partial bilateral ureteral obstruction due to advanced stage ovarian carcinoma.

Nephrogenic diabetes insipidus (NDI) secondary to chronic urinary tract obstruction is a rare condition. The exact cause is unknown; it is likely that increased collecting duct pressures cause damage to the tubular epithelium, resulting in insensitivity to the antidiuretic hormone (ADH). We report a case of NDI associated with ureteral obstruction caused by advanced stage ovarian carcioma in a 20-year-old girl. After debulcking surgery, massive polyuria continued. Several administrations of an ADH analog were ineffective in reducing urine output, suggesting a possible relationship of massive polyuria with NDI. Following oral administration of a thiazide diuretic, known to exert antidiuretic action in NDI, the urine output was dramatically reduced. This case suggests that ureteral obstruction due to ovarian mass may cause NDI and after the surgery thiazide diuretics are effective in reducing urine output in NDI with ureteral obstruction.

Plasma homocysteine, vitamin B12 and folate levels in hydatidiform moles and histopathological subtypes.

OBJECTIVE: To investigate the association of mole hydatidiform with plasma homocysteine, vitamin B(12), and folate levels. METHODS: Sixty-eight patients diagnosed with mole hydatidiform at our clinic between February and October 2007 were assessed in a case-control study. Plasma homocysteine, vitamin B12, and folate levels, taken before evacuation of patients with hydatidiform mole, were compared with the results of 100 healthy normal pregnants of first trimester; and also plasma homocysteine, vitamin B12, and folate levels were compared according to histopathological types of mole hydatidiforms. SPSS 14.0 package program was used to analyze the data. Logarithmic transformation was applied for variables. Parameters were expressed as mean+/-standard deviation. RESULTS: The mean of plasma homocysteine levels was higher in molar group (0.8+/-0.13) than in normal pregnant group (0.7+/-0.13) and the difference was statistically significant (P<0.001). The mean of plasma vitamin B12 levels was found to be similar both in normal pregnant women (2.4+/-0.17) and in the molars (2.4+/-0.15) (P=0.272). The mean of plasma folate levels was lower in molar group (1.0+/-0.15) than in normal pregnant women (1.2+/-0.17) and the difference was statistically significant (P<0.001). The hydatidiform moles of 68 patients were divided into two groups according to histopathological examination: 36 patients were partial moles and the others were complete. The difference of plasma mean homocysteine, vitamin B12, and folate levels in these two groups was not statistically significant. There were statistically significant differences of plasma mean homocysteine and folate levels one by one in complete and in partial moles when compared with the normal pregnants. The mean of plasma folate levels were lower (1.0+/-0.17 for partials, 1.0+/-0.13 for completes) and the homocysteine levels were higher (0.9+/-0.14 for partials, 0.8+/-0.12 for completes) than the levels of normal group. CONCLUSION: This study suggests that there may be an association between plasma folate and homocysteine levels with hydatidiform moles. Folate may play a protective role in preventing molar pregnancy. Further controlled prospective studies are needed to investigate the possible effect of homocysteine, vitamin B12, and folate in molar pregnancies.

Alterations in the 'local umbilical cord blood renin-angiotensin system' during pre-eclampsia.

BACKGROUND: Local autocrine-paracrine renin-angiotensin system (RAS), independently functioning from the circulating RAS, is present in major organs of the female reproductive tract. We have previously demonstrated 'a local RAS in human umbilical cord' via verifying the corresponding ACE, renin, and angiotensinogen mRNAs. The aim of this study is to search alterations of the local umbilical cord RAS during pre-eclampsia. METHODS: Cord blood samples were obtained from 19 patients with pre-eclampsia (aged mean 26.6 ± 5.83 (range 18-42) years) and 20 women with normal pregnancy (aged mean 28.26 ± 7.30 (range 19-37) years). Women with uncomplicated pregnancy formed the control group. Real time quantitative PCR analysis for ACE, renin and angiotensinogen gene expressions were carried out using a LightCycler™ instrument. RESULTS: The mean expression ratios were 0.0029 ± 0.0015 for renin, 0.153 ± 0.166 for angiotensinogen, and 0.220 ± 0.294 for ACE, in control samples. The mean expression ratios of pre-eclamptic patients were 0.0061 ± 0.00068, 0.035 ± 0.008, and 0.030 ± 0.006 for renin, angiotensinogen and ACE genes, respectively. While renin expressions increased in the local cord blood of pre-eclampsia in comparison to the normal cord blood, unpredictable decrements in the angiotensinogen and ACE expressions were observed within the same pre-eclamptic samples. There were no statistically significant differences between intrauterine growth restriction (IUGR) and appropriate for gestational age (AGA) newborns in respect to renin, angiotensinogen and ACE gene expressions. CONCLUSIONS: These findings indicate that the gene expression in the major components of the local RAS does not represent a constant mathematical model, but is affected from the ongoing pathobiological events associated with the disease course. Local umbilical cord blood RAS alterations at the basis of genetic expression are evident in pre-eclampsia.