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Malignant hypertension in children secondary to chronic pyelonephritis: laboratory and radiologic indications for
Insights
Vesicoureteral reflux can cause severe renin-mediated hypertension in children years later. Treating damaged kidney segments, even after reflux correction, can significantly reduce hypertension and renin levels.
Area of Science:
- Pediatric Nephrology
- Hypertension Research
- Renal Pathophysiology
Background:
- Vesicoureteral reflux (VUR) is a common condition in children that can lead to kidney damage.
- Late-onset hypertension has been observed in individuals with a history of VUR, even after successful surgical correction.
- The renin-angiotensin-aldosterone system plays a crucial role in blood pressure regulation.
Observation:
- Two pediatric cases presented with severe renin-mediated hypertension.
- Hypertension developed years after VUR had been surgically corrected.
- Renal damage, including segmental scarring from chronic pyelonephritis and calicectasis, was identified.
Findings:
- Nephrectomy of a unilaterally damaged kidney led to immediate hypertension relief.
- Partial nephrectomy (atrophied lower pole) in the second case improved hypertension and reduced excessive renin output.
- The mechanism involves ischemia in scarred renal cortex, leading to renin overproduction.
Implications:
- Segmental renal scarring from chronic pyelonephritis can cause late-onset renin-mediated hypertension.
- Surgical intervention targeting damaged renal segments can effectively manage hypertension in these cases.
- Understanding the pathophysiology of renin-mediated hypertension in scarred kidneys is crucial for pediatric care.
Abstract:
Severe renin-mediated hypertension was noted in 2 children as a result of selective renal damage from vesicoureteral reflux during the early years of life. In each case the reflux had been corrected successfully long before hypertension developed. In 1 case the late damage involved only 1 kidney and nephrectomy resulted in immediate relief of the hypertension. In the second case, even though both kidneys showed segmental scarring from calicectasis and chronic pyelonephritis, removal of the atrophied lower pole of 1 kidney made hypertension amenable to medical treatment and reduced excessive renin output to a fraction of the original high levels. The mechanism of renin-mediated hypertension in kidneys with segmental scars of chronic pyelonephritis is believed to be ischemia of the relatively normal renal cortex in proximity to areas of interstitial fibrosis, within which are tortuous interlobular and smaller arterioles with severe intimal thickening. Hypertrophy of normal renal segment occurs in young patients with segmental chronic pyelonephritis. To accommodate this enlargement the original calix develops an extension or elongation readily distinguishable from other dilated calices.