A 16-month-old boy with severe hypertension, metabolic alkalosis, hyponatremia and hypokalemia: a case report and literature review

Introduction

Background

Renovascular hypertension (RVH) results from kidney hypoperfusion, often due to anatomical stenosis of the renal artery, which activates the renin-angiotensin-aldosterone system (RAAS) (1). RVH accounts for 3–25% of secondary hypertension cases in children (1-4). It is often asymptomatic and incidentally discovered in 26–70% of cases (2). RVH should be suspected in children with severe, treatment-resistant hypertension, particularly when associated with hyperaldosteronism or hyperreninemia (2). Younger children may also present with severe neurological symptoms related to high blood pressure, such as seizures, and cardiac manifestations like left ventricular hypertrophy and congestive heart failure (1).

Hyponatremic hypertensive syndrome (HHS) is a rare complication of unilateral renal artery stenosis. It typically presents with severe hypertension, hyponatremia, hypokalemia, polydipsia, polyuria, proteinuria and neurological symptoms such as seizures or altered consciousness. Prompt recognition is essential for effective management and for preventing complications involving the nervous system, eyes, and heart (1).

Rationale and knowledge gap

Although cases of pediatric HHS have been reported, data in children under 2 years are limited (5), especially regarding long-term outcomes following revascularization. In most published reports, follow-up is either short or incompletely documented, and diagnostic and management strategies vary considerably, particularly in complex presentations.

Objective

We report the case of a toddler with HHS due to unilateral renal artery stenosis, successfully treated with percutaneous transluminal renal angioplasty (PTRA), with a 3-year follow-up. This report outlines the full clinical course from presentation to long-term recovery, emphasizing diagnostic and therapeutic challenges and the resolution of both renal and cardiac involvement. Our aim is to increase awareness of HHS in pediatric practice and highlight the importance of early diagnosis and timely referral to specialized care. We present this article in accordance with the CARE reporting checklist (available at https://pm.amegroups.com/article/view/10.21037/pm-24-84/rc).

Case presentation

A 16-month-old boy presented with a one-week history of vomiting, diarrhea and abdominal pain. On admission, his blood pressure was 145/75 mmHg, significantly above the 95th percentile for age and gender (normal systolic <100 mmHg; diastolic <54 mmHg) (6), while heart rate (99 beats/min) and body temperature (36 ℃) were within normal limits. Baseline clinical and laboratory investigations, including serum and urinary electrolytes, proteinuria, glycosuria, and other metabolic parameters, are summarized in Figure 1. Clinical examination revealed signs of dehydration, including lethargy and poor peripheral perfusion. In addition, biochemical indicators of dehydration included, elevated serum urea, mildly increased lactate (2.2 mmol/L; normal range 0.5–2.2 mmol/L), and slightly elevated serum creatinine (0.5 mg/dL; normal range 0.2–0.4 mg/dL), with an estimated glomerular filtration rate (eGFR) of 66 mL/min/1.73 m² (normal >90 mL/min/1.73 m²). These findings, along with marked polyuria and excessive urinary solute loss, prompted the immediate initiation of intravenous fluid therapy, which was subsequently adjusted based on urine output and evolving laboratory parameters (Figure 1). Amlodipine was initiated at 1.25 mg/day (0.125 mg/kg/day). After 36 hours, urine output tripled, and blood pressure remained consistently elevated (>150/90 mmHg). The child became lethargic again, exhibiting signs of worsening dehydration. Repeat laboratory tests revealed further deterioration, including hyponatremia (123 mEq/L; normal range 135–145 mEq/L), hypochloremia (87 mEq/L; normal range 98–105 mEq/L) and hypokalemia (2.8 mEq/L; normal range 3.5–5.5 mEq/L), along with increased proteinuria and worsening urinary solute losses, including elevated fractional excretion of sodium and potassium, glycosuria, hypercalciuria, and phosphaturia (Figure 1). This acute deterioration was managed with a 3% NaCl bolus (2 mL/kg), followed by continuous infusion with potassium and sodium supplementation, titrated according to serum electrolyte levels and urine output (ranging from 20 to 150 mL/h) (Figure 1). The results of plasma renin (30 ng/mL/h; normal 1.4–7.8 ng/mL/h) and aldosterone (>100 ng/dL; normal <40 ng/dL), although tested at admission, became available only after the patient’s clinical and biochemical deterioration, and were consistent with HHS due to right renal artery stenosis. Echocardiogram showed mild posterolateral left ventricular hypertrophy (0.55 cm, z-score +1.86). The sweat test for cystic fibrosis was negative, and fundoscopy was normal. Due to persistent hypertension, the dose of amlodipine was increased to 0.5 mg/kg/day, and ramipril 1.25 mg/day (2.5 mg/m²) was added due to inadequate blood pressure control. Over the following days, the patient’s clinical status improved, with stabilization of fluid and electrolyte balance, although polyuria, polydipsia and severe hypertension persisted (Figure 1). Renal ultrasound revealed a small right kidney (−3.3 standard deviation) with a normal left kidney (Figure 1). Spectral Doppler analysis demonstrated a reduced resistance index (=0.45) with increased acceleration time (parvus and tardus pattern) in the right interlobar artery, and an elevated peak systolic velocity (approximately 170 cm/s) with increased resistance index in the right renal artery (Figure 2A). Computed tomography angiography and arteriography, performed under sedation, confirmed a focal stenosis in the middle third of right renal artery. The patient underwent PTRA under general anaesthesia. A few days later, technetium-99m mercaptoacetyltriglycine (Tc^99m-MAG3) scintigraphy revealed reduced split renal function of 26% in the right kidney. Due to persistent hypertension, losartan (0.77 mg/kg/day) was added one week after PTRA to achieve double blockade of the RAAS (Figure 1). Progressive clinical improvement and blood pressure normalization were observed, with complete resolution of initial symptoms. Plasma renin activity and aldosterone levels were reassessed during follow-up and showed a gradual decline and normalization by 4 months, consistent with the resolution of RAAS activation (Figure 1). These findings supported a sustained improvement in the patient’s clinical condition and quality of life. Amlodipine and ramipril were discontinued at two and four months post-PTRA, respectively (Figure 1). Losartan was maintained longer and successfully withdrawn 2 years post-procedure. At two months post-PTRA, renal ultrasound with color Doppler study showed improved size (up to 63.4 mm), trophism and vascularization of the right kidney (Figure 1; Figure 2B,2C). A repeat Tc99m-MAG3 scintigraphy demonstrated improved split function of 40.9%. Three years after PTRA, the patient remained normotensive without antihypertensive medications, with normal kidney function, no proteinuria and normal kidney ultrasound findings (Figure 1; Figure 2D). Follow-up echocardiogram confirmed the complete resolution of the previously reported left ventricular hypertrophy, consistent with the normalization of blood pressure. No adverse or unanticipated events occurred during the treatment and follow-up period.

Figure 1 Clinical evolution of the patient. Clinical and biochemical data, 24-hour diuresis, renal longitudinal diameter on ultrasound, split renal function on MAG3 scintigraphy at diagnosis and post-PTRA, and volume depletion/hypertension management. Over 3 years, we noted optimal blood pressure without medication, and enhanced kidney function/dimensions. The timeline illustrates examination timing. eGFR, estimated glomerular filtration rate; FEK, fractional excretion of potassium; FENa, fractional excretion of sodium; PTRA, percutaneous transluminal renal angioplasty; TRP, tubular reabsorption of phosphate; UCa/UCr, urinary calcium/urinary creatinine ratio; UPr/UCr, urinary protein/urinary creatinine ratio.

Figure 2 Ultrasound evaluation of the right kidney and renal artery at diagnosis and during follow-up. (A) Color-Doppler ultrasound at diagnosis showed a reduced resistance index (=0.45) and a parvus and tardus pattern in the right interlobar artery. (B,C) Two months after PTRA, follow-up ultrasound revealed a normalization of the resistive index and acceleration time (B), along with improved vascularization of the right kidney (C). (D) Ultrasound at 3-year follow-up demonstrated restored growth of the right kidney (=72.7 mm). PTRA, percutaneous transluminal renal angioplasty.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the parent of the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

We present the case of a toddler diagnosed with HHS due to right renal artery stenosis. The main clinical features included severe hypertension, polyuria, dehydration, proteinuria with normal serum albumin, and metabolic alkalosis associated with hyponatremia, hypokalemia, and hypercalciuria. Tubular solute losses were evident, as demonstrated by elevated urinary sodium and potassium excretion, hypercalciuria, reduced tubular phosphate reabsorption, glycosuria, and elevated urinary beta-2-microglobulin levels. Following PTRA, the patient experienced complete recovery of renal and cardiac function, with sustained drug-free normotension during a 3-year follow-up.

Strengths and limitations

Although cases of HHS have been previously reported in young children, this case stands out due to the early age of onset and the detailed documentation of the entire clinical course, including a long-term follow-up. To our knowledge, it is among the few reports providing comprehensive data extending over 3 years period following PTRA. However, as a single case report, its findings may not be generalizable, and the long-term outcomes may not apply to all infants with HHS or renal artery stenosis.

Comparison with similar research

A literature search on PubMed using the terms “hyponatremic hypertensive syndrome”, “polyuria”, “polydipsia”, and “hypertension” identified 39 pediatric cases of HHS, 12 of which involved children aged ≤2 years (excluding newborns) and were attributed to isolated or idiopathic unilateral renal artery stenosis (3,7-15). Other cases were associated with conditions such as Moyamoya disease, Wilms tumor, neuroblastoma, and polyarteritis nodosa. The main features of these 12 patients are summarized in Table 1. In this group, the most common presenting features were hypertension, polyuria, and polydipsia. Persistent hypertension was not reported at initial evaluation in only four cases (7,9,16,17). Seizures occurred in three patients. The left kidney was most frequently affected, although both sides were represented. Cardiac and ophthalmologic complications were also observed, including left ventricular hypertrophy in 10 cases and funduscopic abnormalities in 2. In our case, left ventricular hypertrophy was present at diagnosis and resolved completely after treatment. Regarding treatment, various antihypertensive drugs were used across the cases, but medical therapy alone was insufficient to control blood pressure. Therefore, corrective intervention for renal artery stenosis was required: 5 patients underwent PTRA, 2 received stents, and 5 required surgery, including 2 nephrectomies. Overall, outcomes were favorable, with normalization of blood pressure and no major complications reported during follow-up.

Explanation of findings

The main causes of RVH in children include genetic, inflammatory, compressive, and idiopathic conditions (1,2,18). Although fibromuscular dysplasia has historically been considered the most common cause, many cases, especially in young children, are now classified as idiopathic renal artery stenosis, given that histological confirmation is rarely obtained and the diagnosis remains largely presumptive (1). In our patient, the young age, absence of systemic or inflammatory features, and unilateral involvement with associated renal hypoplasia suggest that the most plausible cause of the renal artery stenosis was a congenital, idiopathic hypoplastic process affecting the right renal artery.

The metabolic and tubular abnormalities observed are consistent with HHS pathophysiology (Figure 3). Renal ischemia activates the RAAS cascade, leading to hypertension and hyperaldosteronism with hypokalemia and metabolic alkalosis. The contralateral healthy kidney responds with pressure natriuresis and diuresis, causing sodium loss, polyuria, and volume depletion, which further stimulates RAAS and anti-diuretic hormone secretion, exacerbating hyponatremia and thirst (8-10,19). Secretion of atrial and brain natriuretic peptides contributes to salt and protein loss (8). Hyperfiltration in the non-stenotic kidney may lead to tubulointerstitial injury, manifesting as proteinuria, glycosuria, hypercalciuria, and hyperuricosuria (8-10,19). In the differential diagnosis, HHS should be considered in infants presenting with hypokalemic metabolic alkalosis, especially when associated with hypertension and tubular signs. Measurement of blood pressure, plasma renin activity, and aldosterone levels is helpful (Figure 4) (20). The sweat test was performed in our patient to exclude cystic fibrosis, which may present as pseudo-Bartter syndrome, with similar electrolyte abnormalities (21).

Figure 3 Pathophysiological mechanisms underlying HHS. Renal hypoperfusion activates RAAS. Hyperaldosteronism induces hypokalemia. Angiotensin II-induced hypertension causes hyperfiltration, ANP and BNP release, natriuresis, proteinuria, hypercalciuria, hyperuricosuria, tubular injury and volume depletion. Proteinuria stems from hyperfiltration and tubular damage. Hyponatremia worsens due to natriuresis, ADH, thirst, and direct renal angiotensin II action. Polyuria results from natriuresis, thirst, and exacerbating volume depletion. ADH, anti-diuretic hormone; ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; GFR, glomerular filtration rate; HHS, hyponatremic hypertensive syndrome; RAAS, renin-angiotensin-aldosterone system.

Figure 4 Flow-chart showing differential diagnosis of hypokalemic metabolic alkalosis. Hypokalemic metabolic alkalosis with normal/low BP may stem from renal (Bartter/Gitelman syndromes, diuretics) or extra-renal causes (cystic fibrosis, vomiting). High BP with low renin/aldosterone suggests genetic (Liddle syndrome, apparent mineralocorticoid excess) or acquired conditions (Cushing syndrome, licorice abuse). High renin/aldosterone levels indicate artery stenosis or renin-secreting tumors. BP, blood pressure.

Implications and actions needed

Non-invasive imaging and appropriate diagnostic strategies are essential for identifying secondary hypertension in children (2,22). Doppler ultrasonography is an effective screening tool for renal artery stenosis, detecting abnormal waveform patterns or flow parameters suggestive of vascular narrowing (1,18). It also helps exclude non-vascular causes of hypertension (e.g., neuroblastoma or pheochromocytoma) and identify structural kidney abnormalities (18). A kidney length discrepancy of ≥1 cm may indirectly suggest renal artery stenosis (23), as seen in our patient, who had a significantly smaller right kidney with poor perfusion. This finding must be interpreted with caution, as similar discrepancies can occur in patients with vesico-ureteral reflux-associated nephropathy, a condition also associated with pediatric hypertension (24). Computed tomographic angiography and magnetic resonance angiography can confirm renal artery stenosis based on reduced intraluminal diameter or the presence of collateral vessels (18,23). Moreover, echocardiography and fundoscopy should be included in the diagnostic workup of HHS to assess for organ damage (2).

The treatment of renal artery stenosis with HHS includes restoring intravascular volume, correcting electrolyte disturbances, managing severe hypertension, and treating the underlying stenosis. Volume depletion must be corrected early to prevent further renal injury (1). In our case, fluid therapy initially followed calculations of sodium and fluid losses, and maintenance requirements were based on Holliday-Segar’s rule (25). However, due to the patient’s significant polyuria, it was successfully adjusted and tailored to the urine output and electrolyte abnormalities.

Calcium channel blockers are recommended as first-line agents for severe hypertension (1). In cases of HHS, angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers are required to suppress the overactive RAAS in unilateral renal artery stenosis (19). However, ACE inhibitors are generally contraindicated as first-line agents in children with suspected RVH due to the risk of renal impairment in cases of bilateral renal artery stenosis (1,2). In patients with RAAS-driven hypertension unresponsive to monotherapy, dual RAAS inhibition (ACE inhibitors and angiotensin II receptor blockers) has been proposed to overcome mechanisms such as aldosterone breakthrough and angiotensin II escape (26). Although pediatric data are limited, adult studies support the use of dual blockade for its additional cardiovascular and renal benefits, including improved blood pressure control, reduced proteinuria, and delayed progression of chronic kidney disease (26). In our patient, the decision to add an angiotensin receptor blocker to ongoing ACE-inhibitor therapy was prompted by persistent hypertension following PTRA. The dual therapy was well tolerated and associated with a progressive decline in proteinuria and regression of left ventricular hypertrophy. Nonetheless, pharmacologic therapy alone may be insufficient to maintain blood pressure control in RVH (7). Therefore, corrective intervention of renal artery stenosis, such as revascularization with PTRA or surgery, becomes essential when hypertension is refractory to medical treatment or with significant adverse effects (2). Surgery is reserved for cases with unsuccessful angioplasty and poor renal function (4). PTRA is often preferred over surgery due to its lower complication rate, although restenosis is more common (1). Endovascular treatment normalizes or improves blood pressure in more than 50% of cases (2). Better outcomes are more likely in short-segment stenosis (<10 mm), residual stenosis <10–20% after intervention, younger age, and recent RVH diagnosis (18). In contrast, poor outcomes are associated with ostial, multi-vessel, or intrarenal involvement (5,27). HHS seems to develop in children with severe artery stenosis, where PTRA may be more technically challenging (28). Angioplasty has proven safe and effective treatment in infants ≤2 years with RVH (5). Post-revascularization follow-up should include monitoring of hypertension and kidney vascular patency using Doppler ultrasonography (27), and scintigraphy to monitor functional recovery (2,9). In our case, the patient showed significant improvement and sustained normalization of renal function and blood pressure following PTRA, without recurrence of hypertension or need for antihypertensive therapy during the 3-year follow-up.

Conclusions

We report the case of a toddler with HHS due to unilateral renal artery stenosis, presenting with hypertension, polyuria, polydipsia, metabolic alkalosis with hyponatremia, hypokalemia, and hypochloremia. Prompt clinical suspicion, early diagnosis, and effective management, including volume repletion, pharmacologic blood pressure control, and angioplasty, led to complete resolution of symptoms. At three years of follow-up, the child remained normotensive, medication-free, and with normal renal and cardiac function. This case underscores that, despite overlapping features with other childhood illnesses, blood pressure measurement remains a key diagnostic tool in raising suspicion for renal artery stenosis in general, and HHS in particular. Therefore, blood pressure should be routinely assessed in children with unexplained biochemical imbalances. Finally, this case supports the safety and long-term efficacy of angioplasty in a toddler with renal artery stenosis, contributing valuable insight to the limited pediatric literature on long-term outcomes after revascularization.

Acknowledgments

During the preparation of this work, we used ChatGPT 4.0 in October 2024 in order to improve the fluency of the written English.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://pm.amegroups.com/article/view/10.21037/pm-24-84/rc

Peer Review File: Available at https://pm.amegroups.com/article/view/10.21037/pm-24-84/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://pm.amegroups.com/article/view/10.21037/pm-24-84/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. Written informed consent was obtained from the parent of the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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