The pathophysiology of
ovarian hyperstimulation syndrome (OHSS) remains unclear. Several lines of evidence indicate that OHSS is associated with a stimulation of the renin-angiotensin system (RAS), but its functional significance as well as its role in the pathogenesis of the syndrome are not yet determined. OHSS is associated with high plasma and ascitic concentrations of total
renin,
renin activity (RA) and
angiotensin II (Ang II). Their ovarian or renal origin is, however, still a matter of debate. To clarify these issues further, total
renin, active
renin,
prorenin, RA and
aldosterone were measured in plasma and
ascites of nine patients who developed severe OHSS after in-vitro fertilization. Blood and
ascites were sampled simultaneously during therapeutic paracentesis. Total
renin and
prorenin concentrations were significantly higher in the
ascites (mean concentration +/- SE respectively of 5920 +/- 1430 mIU/l and 5250 +/- 1350 mIU/l) than in the plasma (respectively 3060 +/- 740 mIU/l and 2000 +/- 460 mIU/l) (P = 0.020 and 0.017 respectively). Conversely, active
renin and RA concentrations tended to be lower, although not statistically significantly so in the
ascites (respectively 670 +/- 190 mIU/l and 47 +/- 11 ng Ang I/ml/h) than in the plasma (respectively 1060 +/- 370 mIU/l and 75 +/- 21 ng Ang I/ml/h).
Aldosterone concentrations were significantly higher in the serum (2609 +/- 374 pg/ml) than in the
ascites (2025 +/- 347 pg/ml) (P = 0.015). The concentration gradient between plasma and
ascites for total
renin and
prorenin supports the hypothesis of their ovarian origin in
ascites and, to a large extent, in plasma, while it is likely that the high plasma active
renin and RA concentrations reflect a peripheral activation of the RAS. In conclusion, the present findings are consistent with a marked stimulation of both ovarian and renal RAS during OHSS.