Complex equilibrium involving aldosterone underlies the pathophysiology of renovascular hypertension.

Masanori Adachi, Takanari Fujii, Ayako Ochi, Tatsuyuki Ishida, Sakura Motegi, Keiko Nagahara, Katsumi Mizuno
Author Information
  1. Masanori Adachi: Department of Pediatrics, Showa University School of Medicine, Tokyo, Japan.
  2. Takanari Fujii: Pediatric Heart Disease and Adult Congenital Heart Disease Center, Showa University Hospital, Tokyo, Japan.
  3. Ayako Ochi: Department of Pediatrics, Showa University School of Medicine, Tokyo, Japan.
  4. Tatsuyuki Ishida: Department of Pediatrics, Showa University School of Medicine, Tokyo, Japan.
  5. Sakura Motegi: Department of Pediatrics, Showa University School of Medicine, Tokyo, Japan.
  6. Keiko Nagahara: Department of Pediatrics, Showa University School of Medicine, Tokyo, Japan.
  7. Katsumi Mizuno: Department of Pediatrics, Showa University School of Medicine, Tokyo, Japan.

Abstract

The mechanisms underlying the maintenance of hypertension in renovascular hypertension (RVH) are not well understood. To test the current concept of RVH pathophysiology, circulating aldosterone levels in clinical cases were investigated through a literature survey of pediatric cases. Fifty-four patients with documented aldosterone levels were identified. Of these, 42 patients (78%) were assigned to the high renin (HR) group and the rest to the low-normal renin (LR) group. Patients in the HR group were more likely to have unilateral lesions (35/42) than those in the LR group (6/12). In the LR group (corresponding to volume-dependent RVH), 50% (6/12) of patients had elevated aldosterone levels, indicating that the equilibrium between renin and aldosterone shifted towards aldosterone dominance. In the HR group (corresponding to renin-dependent RVH), aldosterone levels were much higher, with 76% (32/42) of patients exceeding the reference range and 14 patients developing hypokalemia. These results are consistent with the notion that pressure natriuresis allows continuous aldosterone action in renin-dependent RVH. In conclusion, the aldosterone status observed in the clinical cases is in agreement with the current understanding of the pathophysiology of RVH, in which a complex equilibrium state involving renin, angiotensin-II, pressure natriuresis, and aldosterone exists.

Keywords

References

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