The diagnosis of Hydrops fetalis still carries a grave prognosis with reported mortality ranging from 50 to 100%. With the advent of more aggressive therapy, improvement of survival is undetermined. The study population of this outcome case series was gathered from all cases of hydrops fetalis admitted to our Loyola University Medical Center Neonatal Intensive Care Unit (NICU) from 1990 to 1997. Forty-one patients were eligible for inclusion. Only four had a diagnosis of immune hydrops fetalis, while the remainder had varied nonimmune causes. Models predicting survival were constructed with various neonatal and maternal factors as explanatory variables using Cox proportional Hazards technique. Kaplan-Meier estimates of median survival times for different stratifying variables were likewise computed. The overall mortality rate was 49% with an overall median survival time of 15 days (95% CI 8-38). Median survival time estimates differed significantly between patients who had (a) proven infection or not and (b) had less than or greater than two fluid-filled cavities. The use of steroids, surfactant, or high-frequency ventilation did not improve survival. Stratifying the study base into those treated in early or late 1990s likewise failed to show difference in survival times. Infection remains a significant problem (46%). In our series of 41 infants with hydrops fetalis, survival rates remain comparable to those reported in the literature, despite aggressive therapy. Although the use of surfactant, steroids, and high-frequency ventilation appear to prolong survival times, these treatments failed to alter overall survival outcome.
We examined the effect of acute systemic blockade of nitric oxide synthesis on blood pressure and renal function in the monogenetically hypertensive TGR(mRen2)27 rat strain. Untreated conscious transgenic rats had significantly (p < 0.01) higher systolic blood pressures (185 +/- 9 versus 130 +/- 5 mm Hg) and urinary albumin excretion (32 +/- 5 versus 6 +/- 2 mg/day) than did control animals without evidence of renal insufficiency. Plasma and urinary nitric oxide metabolite levels did not differ between transgenic and control rats. i.v. administration of NG-nitro-L-arginine methyl ester (10 mg/kg) to both groups caused similar elevations in systemic blood pressure (transgenic 25 +/- 3 versus control 24 +/- 3 mm Hg). NG-Nitro-L-arginine methyl ester induced reductions in whole kidney (1.4 +/- 0.2 versus 0.7 +/- 0.1 mL/min), and single nephron (23 +/- 3 versus 11 +/- 2 nL/min) glomerular filtration rates were significantly (p < 0.05) larger in transgenic than in control rats. This greater loss of GFR in transgenic animals was caused by a larger reduction in glomerular ultrafiltration coefficient (1.8 +/- 0.2 versus 1.1 +/- 0.1 nL x min[-1] x mmHg[-1], p < 0.05), a larger increase in afferent arteriole resistance (3.4 +/- 0.2 versus 1.4 +/- 0.1 dyne x s x cm[-5], p < 0.05), and a subsequently smaller rise in glomerular transcapillary pressure (10 +/- 1 versus 5 +/- 1 mmHg, p < 0.05). These results indicate that the renal microvasculature and glomerular hydraulic conductivity or surface area of transgenic rats are more sensitive to nitric oxide inhibition and are consistent with an important role for nitric oxide in TGR(mRen2)27 kidney function.
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