Urinary kallikrein in hypertension secondary to hemolytic uremic syndrome: response to diuretic stimulus

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The International Journal of Pediatric Nephrology
|December 1, 1984
PubMed

Insights

Children with a history of hemolytic uremic syndrome (HUS) showed varied urinary kallikrein responses to diuretics. Normotensive children experienced a significant increase, unlike hypertensive children, suggesting altered vasodilator system reactivity.

Area of Science:

  • Pediatric Nephrology
  • Hypertension Research
  • Urology

Background:

  • Hemolytic uremic syndrome (HUS) can lead to long-term renal complications, including hypertension.
  • The kallikrein-kinin system plays a role in regulating blood pressure and vascular tone.
  • Investigating vasodilator system function in HUS survivors is crucial for understanding post-HUS hypertension.

Purpose of the Study:

  • To assess urinary kallikrein excretion in children with a history of HUS.
  • To compare kallikrein excretion between normotensive and hypertensive HUS survivors.
  • To evaluate the effect of diuretic administration on kallikrein excretion in these children.

Main Methods:

  • Urinary kallikrein excretion was measured in 43 children with a history of HUS (mean age 8 years).
  • Children were categorized into normotensive (n=28) and hypertensive (n=15) groups.
  • A subset of 23 children received hydrochlorothiazide and amiloride for ten days to assess diuretic response.

Main Results:

  • No significant difference in baseline urinary kallikrein excretion was observed between normotensive and hypertensive HUS survivors.
  • Administration of hydrochlorothiazide plus amiloride resulted in a threefold increase in urinary kallikrein excretion in normotensive children.
  • Urinary kallikrein excretion remained unchanged in hypertensive children following diuretic administration.

Conclusions:

  • Diuretic administration reveals distinct responses in the kallikrein-kinin system between normotensive and hypertensive children with a history of HUS.
  • These differential responses may indicate altered reactive capabilities of the vasodilator system in HUS-associated hypertension.
  • Further research is warranted to elucidate the role of the kallikrein-kinin system in the pathogenesis of hypertension post-HUS.

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