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Year : 2021  |  Volume : 6  |  Issue : 1  |  Page : 52-55

Renovascular hypertension in a 9-year-old boy with primary vesicoureteral reflux

Department of Pediatric Nephrology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh

Date of Submission17-Sep-2021
Date of Acceptance23-Sep-2021
Date of Web Publication29-Dec-2021

Correspondence Address:
Dr. Md. Murad Chowdhury
Department Pediatric Nephrology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pnjb.pnjb_12_21

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Renovascular hypertension is an important cause of secondary hypertension in the pediatric age group. Reflux nephropathy has also been regarded as one of the most common disorders leading to secondary hypertension in children. Secondary hypertension must be appropriately diagnosed and treated. Here we report the presentation, diagnosis, and management of a case of secondary hypertension in a 9-year-old boy due to unilateral diffuse narrowing of the left renal artery along with ipsilateral grade 4 primary vesicoureteral reflux.

Keywords: Renin-angiotensin-aldosterone system (RAAS), renovascular hypertension (RVH), vesicoureteral reflux (VUR)

How to cite this article:
Chowdhury MM, Mamun AA, Jesmin T, Sharmim MS, Roy RR. Renovascular hypertension in a 9-year-old boy with primary vesicoureteral reflux. Paediatr Nephrol J Bangladesh 2021;6:52-5

How to cite this URL:
Chowdhury MM, Mamun AA, Jesmin T, Sharmim MS, Roy RR. Renovascular hypertension in a 9-year-old boy with primary vesicoureteral reflux. Paediatr Nephrol J Bangladesh [serial online] 2021 [cited 2023 Oct 4];6:52-5. Available from: http://www.pnjb-online.org/text.asp?2021/6/1/52/334114

  Background Top

Hypertension affects 1%–5% of children and adolescents.[1] Unlike adults, whose hypertension is usually primary, most childhood hypertension is secondary to an underlying cause.[2],[3],[4] Among secondary causes of hypertension, renovascular hypertension (RVH) is 5%–10%. It is characterized by segmental or diffuse narrowing of renal vessels to one or both kidneys, leading to activation of the renin-angiotensin-aldosterone system (RAAS). Activation of RAAS results in generalized vasoconstriction and increase in blood volume, contributing to hypertension, which is usually refractory to medical management.[5],[6] Among causes of RVH, fibromuscular dysplasia accounts for 60% of cases.[5]

Reflux nephropathy has been regarded as one of the most common disorders leading to hypertension during childhood.[7],[8] The prevalence of hypertension in patients with reflux nephropathy is heterogenous and the values vary (5%–27%) among series.[9],[10],[11]

Hypertension has varied presentation; it can be silent or lead to symptoms related to target organ damage (hypertensive emergency) such as heart failure, stroke, loss of vision, and chronic kidney disease.[12]

Here we report a case of a 9-year-old boy presented with the accidental finding of elevated blood pressure with no history suggestive of renal disease and uneventful clinical examination findings except raised blood pressure. After extensive evaluation, he was diagnosed as RVH due to unilateral diffuse narrowing of the left renal artery along with ipsilateral grade 4 primary vesicoureteral reflux.

  Case Report Top

A previously healthy 9-year-old boy was referred to the pediatric nephrology unit of Bangabandhu Sheikh Mujib Medical University (BSMMU) for evaluation of the cause of hypertension [Figure 1]. Regarding birth history, he was born prematurely at 33 weeks of gestation by cesarean section with a birth weight of 1400 g due to maternal pregnancy-induced hypertension and admitted in the neonatal intensive care unit for 1 week. He had no history of umbilical artery catheterization, head trauma, taking any offending drugs, urinary complaints, blurring of vision, respiratory distress, convulsion, and altered sensorium. His mother is now normotensive without any medication but his father, who is in his mid-forties, is hypertensive for the last 10 years and diabetic for the last 4 years. About 1 month back, the child took medical consultation from a pediatrician in a private clinic for recurrent episodes of headache and vomiting. He was found hypertensive, BP was 140/95 mm (both systolic and diastolic values above 99th percentile for age, sex, and height), therefore amlodipine was prescribed. As BP was not well controlled, prazosin was added along with amlodipine on subsequent visits. After admission to the inpatient department, the patient was normotensive with two antihypertensive drugs. The difference of BP among four limbs was insignificant. His height, weight, body mass index (BMI) is within the normal limit. Other systemic examination findings were normal. As his physical findings didn’t give any clue about the cause of hypertension, the patient was evaluated by considering 3 differential diagnoses including RVH, monogenic hypertension, and endocrine causes of hypertension.
Figure 1: Patients photograph

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His electrocardiogram (ECG) revealed sinus rhythm, heart rate was 80 bpm, P wave was normal, PR interval was 0.12 s, QRS duration was 0.10 s, and T wave was also normal. The conclusion was sinus rhythm electrocardiogram. Urine examination showed normal findings (RBC: nil; pus cell: 1–2/HPF; albumin: nil) and urine culture and sensitivity (C/S) revealed no growth of bacteria. Complete blood count revealed normal findings (hemoglobin 13 gm/dL, total leukocyte 7800/cmm, platelet 215,000/cmm). Serum creatinine was 0.69 mg/dL (ref. value 0.3–1 mg/dL) and serum electrolytes report was normal (sodium-137mmol/l, potassium-3.5mmol/l, chloride- 106mmol/l, T-co2 24.3 mmol/L and pH 7.39). 24 h urine vanillylmandelic acid (VMA) was also normal (9.4 mg/day, ref. value <13). His anti-nuclear antibody (ANA) was negative (0.5 IU/mL, ref. value <1.5 IU/mL) and serum C3 was normal (1.27 g/L, ref. value 0.9–1.8 g/L). His thyroid function status was normal (TSH 3.6 microIU/mL, FT4 8.24 µg/dL) and fasting blood glucose was also normal (5 mmol/L, ref. value 3.5–6 mmol/l). Fasting lipid profile was normal (total cholesterol 167 mg/dL, HDL 57 mg/dL, LDL 94 mg/dL, triglyceride 79 mg/dL). His serum aldosterone (308.05 pg/mL, reference value 20–180 pg/mL) and plasma renin level (43.25 pg/mL, ref. value 4–37.52 pg/mL) were high, indicating underlying RVH.

Abdominal ultrasound revealed poorly defined small (5 cm) lobulated left kidney with ill-defined corticomedullary junction and moderate dilatation of the pelvicalyceal system (mid pelvic diameter 8.2 mm). The right kidney was normal in size (10.1 cm) with well-defined corticomedullary differentiation. The right and the left suprarenal areas appear free of any hyperplastic changes, any mass or cysts. Renal Doppler ultrasound was compatible with RVH at three levels in left side (intralobar resistive index 0.77, hilum resistive index 0.74, origin resistive index 0.71, peak systolic velocity 173 cm/s). CT angiogram of the aorta and its branches revealed normal aortogram and mild diffuse narrowing of left renal artery with smaller left kidney. CT renal angiogram revealed diffuse narrowing of left renal artery and smaller left kidney with mild nephropathy [Figure 2]. Micturating cystourethrogram revealed left-sided grade 4 vesicoureteral reflux. Retrograde urethrogram was normal [Figure 3]. Renal scintigraphy with Tc-99m DTPA was also performed, which revealed poor parenchyma function of the left kidney. Differential kidney function was 83.4% (right kidney) vs. 16.6% (left kidney) [Figure 4]. Magnetic resonance imaging of the brain was normal. Echocardiography revealed good biventricular function with normal pulmonary arterial pressure (ejection fraction 69%). Urethrocystoscopy was performed, which revealed a left-sided wide open ureteric orifice at its insertion into the urinary bladder.
Figure 2: CT angiogram showing narrow left renal artery

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Figure 3: MCU showing left-sided VUR

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Figure 4: DTPA renogram showing poor parenchyma function of left kidney

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Patients’ blood pressure was well controlled with two oral antihypertensive drugs. The patient was discharged with follow-up advice and we also taught him double voiding technique for primary VUR. Further plan is to preserve the residual function of the left kidney with optimum control of blood pressure and other necessary measures.

  Discussion Top

In approximately 90% of cases, pediatric hypertension has underlying secondary causes; therefore, an age-based approach of evaluation is necessary based on differential diagnosis. When hypertension is confirmed clinically, every patient should be evaluated for etiology according to history and physical examination findings. The most common cause of secondary hypertension in adolescent age is renal disease.[13]

This patient had no history suggestive of renal disease and clinical examination findings were also normal except hypertension. His renal function status was also normal. This finding leads to more investigations, considering some differential diagnosis in mind including RVH, endocrine causes of hypertension, and monogenic hypertension.

Renal artery stenosis or narrowing limits blood flow to one or more kidneys leads to increased production of renin. Hence, plasma renin level was found elevated in patients with RVH. Subsequently angiotensin II is produced, which is a potent vasoconstrictor. Angiotensin II stimulates adrenal cortex to produce aldosterone. Hence serum aldosterone level is also found elevated in RVH. Angiotensin II-induced vasoconstriction and aldosterone-induced salt and water retention are responsible for hypertension in patients with RVH. So raised plasma renin and aldosterone is an important clue of RVH. This patient’s plasma renin activity and serum aldosterone were raised, which was compatible with RVH.

The literature reports limitations of renal Doppler ultrasound scanning in diagnosing RVH.[14] For diagnosis of RVH CT angiogram and MR angiogram are useful to visualize renal artery. This patient’s CT angiogram revealed mild diffuse narrowing of the left renal artery with a smaller left kidney.

Renal angiography is the gold standard for diagnosis of renal artery stenosis.[15] During angiography blood samples can be collected from the renal vein for plasma renin and aldosterone measurement, which also helps in diagnosis of RVH. If the selective vein renin concentration is at least 1.5 times greater than concentration in the contralateral kidney, the result is diagnostic for renin-mediated hypertension from that kidney.[16] We consulted with the pediatric cardiology department and vascular surgery department regarding renal angiography in this patient, but the respective department deferred it due to poor parenchymal function on the left side.

Computed tomographic angiography (CTA) and magnetic resonance angiography (MRA) are 80%–90% accurate alternative to renal angiogram.[17]

This patient’s diffuse narrowing of left renal artery and poorly defined small left kidney raised suspicion of congenital abnormality of kidney and urinary tract (CAKUT). MCU revealed left-sided grade 4 VUR. Urethrocystoscopy was performed in the pediatric urology department, which revealed a left-sided wide open ureteric orifice at its insertion into the urinary bladder, consistent with left-sided primary vesicoureteral reflux.

Some cohort studies of patients with primary VUR have shown a relatively low incidence of hypertension during childhood, but the tendency of hypertension increases with age, that’s why long follow-up is advised. It is estimated that 50% of patients with unilateral and bilateral VUR would develop sustained hypertension by the age of 30 and 22 years, respectively, due to renal damage with scar formation.[18] This patient’s hypertension was detected at 9 years of age.

Blood pressure in RVH is usually resistant to medical management, but will respond to surgical intervention. Percutaneous renal angioplasty is the first-line intervention in childhood RVH, with a cure rate between 22% and 59%. Angioplasty results are not as satisfactory in children as adults, due to small vessel diameter and higher sensitivity of immature vessels to vascular growth factors. Renal artery stenting is another surgical modality but is controversial in children.[19]

If unilateral renal artery is involved, the contralateral normal kidney may compensate for the salt and water retention and hypertension can be managed with anti-hypertensives.[20] In this patient, only left renal artery was involved with normal right kidney and his hypertension was well controlled with two anti-hypertensive drugs including amlodipine and prazosin.

Regarding pharmacological therapy, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers must be carefully used as they provoke efferent arteriolar dilatation, thus reducing filtration pressure. In cases with bilateral stenosis, they can induce an important decline in glomerular filtration rate with subsequent acute renal failure.[21] We discharged our patient with calcium channel blocker (amlodipine) and alpha-receptor blocker (prazosin), which can be used safely in the case of RVH.

  Declaration of patient consent Top

The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given his consent for images and other clinical information to be reported in the journal. The guardian understands that names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

  Conclusion Top

Hypertension can lead to severe target organ damage. Secondary hypertension is the most common form of hypertension in childhood. Renovascular disease is an important cause of severe childhood hypertension. Appropriate tests are essential to reach the diagnosis. Optimum control of hypertension either by pharmacotherapy or surgical intervention is essential to prevent target organ damage.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Norwood VF Hypertension. Pediatr Rev 2002;23:197-208.  Back to cited text no. 1
Bayazit AK, Yalcinkaya F, Cakar N, Duzova A, Bircan Z, Bakkaloglu A, et al. Reno-vascular hypertension in childhood: A nationwide survey. Pediatr Nephrol 2007;22:1327-33.  Back to cited text no. 2
Sorof JM, Lai D, Turner J, Poffenbarger T, Portman RJ Overweight, ethnicity, and the prevalence of hypertension in school aged children. Paediatrics 2004;113:475-82.  Back to cited text no. 3
Flynn JT, Tullus K Severe hypertension in children and adolescents: Pathophysiology and treatment. Pediatr Nephrol 2009;24:1101-12.  Back to cited text no. 4
Tullus K, Brennan E, Hamilton G, Lord R, Mclaren CA, Marks SD, et al. Renovascular hypertension in children. Lancet 2008;371:1153-63.  Back to cited text no. 5
Srinivasan A, Krishnamurthy G, Fontalvo-Herazo L, Nija E, Keller MS, Meyers K, et al. Angioplasty for renal artery stenosis in paediatric patients: An 11-year retrospective experience. J Vascular Interview Radiol 2010;21:1672-80.  Back to cited text no. 6
Goonasekera CD, Dillon MJ Hypertension in reflux nephropathy. BJU Int 1999;83:1-12.  Back to cited text no. 7
Farnham SB, Adams MC, Brock JW, Pope JC Paediatric urological causes of hypertension. J Urol 2005;173:697-704.  Back to cited text no. 8
Blumenthal I Vesicoureteric reflux and urinary tract infection in children. Postgrad Med J 2006;82:31-5.  Back to cited text no. 9
Heale WF Hypertension and reflux nephropathy. Aust Pediatr J 1977;13:56.  Back to cited text no. 10
Wallace DM, Rothwell DL, Williams DI The long-term follow-up of surgically treated vesicoureteric reflux. Br J Urol 1978;50:479-84.  Back to cited text no. 11
Deshpande PV, Gilbert RD, Williams J, Hulton SA, Milford DV Hypertension: A cause of growth impairment. J Hum Hypertens 2002;16:363-6.  Back to cited text no. 12
Viera AJ, Neutze DM Diagnosis of secondary hypertension: An age-based approach. Am Fam Physician 2010;82:1471-8.  Back to cited text no. 13
Ellis D, Shapiro R, Scantlebury VP, Simmons R, Towbin R Evaluation and management of bilateral renal artery stenosis in children: A case series and review. Pediatr Nephrol 1995;9:259-67.  Back to cited text no. 14
Kaplan NM Renovascular Hypertension. In: Kaplan NM, editor. Kaplan’s Clinical Hypertension. vol. 9; 9th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006. p. 683-733.  Back to cited text no. 15
Goonasekera CD, Shah V, Wade AM, Dillon MJ The usefulness of renal vein renin studies in hypertensive children: A 25 year experience. Paediatric Nephrol 2002;17:943-9.  Back to cited text no. 16
Kurian J, Edelman M, Darge K, et al. The role of CT angiography in the evaluation of pediatric Reno vascular hypertension. Paediatric Radiol 2013;43:490-302.  Back to cited text no. 17
Zhang Y, Bailey RR A long term follow up of adults with reflux nephropathy. N Z Med J 1995;108:142-4.  Back to cited text no. 18
Zhu G, He F, Gu Y, Yu H, Chen B, Hu Z, et al. Angioplasty for paediatric renovascular hypertension: A 13 year experience. Diagn Interv Radiol 2004;20:285-92.  Back to cited text no. 19
Jaff MR Hypertension and renal artery stenosis: A complex clinical scenario. J Am Osteopath Assoc 2000;100:S5-9.  Back to cited text no. 20
Meyers KE, Cahill AM, Sethna C Interventions for paediatric reno vascular hypertension. Curr Hypertens Rep 2014;16:422.  Back to cited text no. 21


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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