Transient Hypertension with Urinary Tract Infection in Congenital Hydronephrosis

Abstract

Introduction: Hypertension is occasionally associated with congenital hydronephrosis. Case report: The authors report a four-month-old boy with severe left congenital hydronephrosis and transient hypertension triggered by his first urinary tract infection (UTI). Despite the satisfactory UTI clinical course, he suddenly developed severe hypertension (130/80 mmHg) on the ninth day of UTI. His aldosterone level was within the reference range and his plasma renin activity was slightly elevated. Although his hypertension was refractory to calcium channel blockers, an angiotensin-converting enzyme inhibitor was effective for hypertension. On day 24, he was able to discontinue the antihypertensive without organ damage. Conclusions: Although the precise cause of hypertension was unclear in our case, we considered it to be temporary renin-associated hypertension due to decreasing renal blood flow due to UTI in a patient with severe congenital hydronephrosis. In pediatric UTI, particularly in patients with unilateral hydronephrosis, blood pressure monitoring is very important.

Introduction

Hypertension is a complication in 5-10% of patients with congenital hydronephrosis [1], and is more likely to occur in severe hydronephrosis [2]. Pediatric hypertension with hydronephrosis is often associated with stimulated renin-angiotensin-aldosterone (RAA) systems, enhanced renal sympathetic nerve activities, oxidative stress, and nitric oxide deficiency in the distressed kidney [3]. Hypertension can induce life-threatening symptoms or target-organ damage, including hypertensive encephalopathy or heart failure. In particular, hypertension is even less noticeable in infants.

Here we report a case of severe left congenital hydronephrosis with transient hypertension that was triggered by acute urinary tract infection (UTI), and suggest the necessity of monitoring of blood pressure during treatment of UTI in patients with severe congenital hydronephrosis.

Case report

A four-month-old boy with left congenital hydronephrosis of grade 4 in the Society for Fetal Urology (SFU) classification was admitted to our hospital with a diagnosis of UTI. He had been diagnosed with congenital hydronephrosis at 8 months of gestation, and was born at term. He had no past episode of UTI, and there was no other urological anomaly before. On admission, his blood pressure was 108/66 mmHg. Blood tests exhibited 19,570/µL WBC and 9.0 mg/dL CRP. Renal function was normal. Urinalysis revealed + nitrites, + bacteria, and 3+ protein, 50 to 99 white cells and 20 to 29 red cells per high-power field. Urine culture showed Gram-positive cocci, Gram-negative bacilli, and eventually Klebsiella pneumoniae 10⁵ CFU/mL. Blood cultures were negative.

Intravenous ampicillin (200 mg/kg/day) and cefotaxime (200 mg/kg/day) were initiated for complex UTI in accordance with our hospital’s protocol on hospital day one. The fever resolved the next day and the clinical course of UTI was satisfactory. This antibiotic treatment was continued for 14 days. The abdominal ultrasonogram had shown left hydronephrosis of grade 4 in the SFU classification with the left dilated anterior-posterior dimeter of 33 mm and no abnormalities of his ureters or bladder, which did not change since before the onset of UTI (Figure 1). Sudden severe hypertension of 130/80 mmHg (95^th percentile 110/68 mmHg) occurred on day nine, and he did not have any other clinical changes by hypertension. Although we started amlodipine, hypertension did not improve. An additional blood examination showed aldosterone level 38.6 ng/dL (reference range 10–50 ng/dL) and plasma renin activity 6.5 ng/mL/h (reference range 2–6 ng/mL/h). Electrolyte abnormalities including potassium were unremarkable. The values of serum catecholamines were within normal range: adrenaline 90 pg/mL (reference range ≤464 pg/mL); noradrenaline 654 pg/mL (reference range ≤1251 pg/mL); dopamine 16 pg/mL (reference range ≤60 pg/mL). As the hypertension was refractory to the maximum dose of amlodipine (0.6 mg/kg/day), lisinopril (0.1 mg/kg/day), an angiotensin-converting enzyme (ACE) inhibitor was added from day 12. Thereafter, hypertension improved and the antihypertensive medications were eventually discontinued on day 24. His renal function and urine output were maintained during the hospitalization and organ damage due to hypertension was not observed. He was discharged on day 27. Plasma renin activity was monitored for 11 months after discharge and ranged 4.9-8.7 ng/mL/h. His blood pressure remained normal for two years after discharge.

Discussion

We reported a case of severe left congenital hydronephrosis with transient hypertension triggered by UTI. We speculated that the temporary renin-associated hypertension might have been induced by decreasing renal blood flow due to the UTI in a patient with severe hydronephrosis. The monitoring of blood pressure is important after the onset of UTI in patients with severe congenital hydronephrosis.

Sudden hypertension occurred on hospital day nine in the present case despite the satisfactory UTI clinical course. The timing of the onset was atypical. In general, hypertension in UTI occurs in the chronic phase from renal scarring [4]. It is possible that, in other cases of UTI with hydronephrosis, hypertension might be missed, particularly in the late phase of UTI treatment, because blood pressure is often measured only in the acute phase of treatment in pediatric cases. Therefore, monitoring blood pressure continuously and closely is important to treat it appropriately to avoid its complications, such as hypertension emergency.

Although the precise cause of hypertension was unclear in our case, we considered it to be temporary renin-associated hypertension due to decreasing renal blood flow due to UTI in a patient with severe congenital hydronephrosis. The renin elevation during UTI could be associated with the UTI itself [5], transient exacerbation of hydronephrosis [6], or systemic sympathetic activation. In hydronephrosis, the dilation of the renal pelvis can cause decreased renal blood flow (functional ischemia) and increased renin production from the diseased kidney, leading to hypertension [6]. Exacerbation of dilation of the renal pelvis was not observed in our case. In addition, the values of plasma renin activity and aldosterone were near the upper reference ranges in our case. However, the hypertension responded well to ACE inhibitor. Transient pseudohypoaldosteronism was ruled out based on his clinical presentation. In a previous report of patients with unilateral hydronephrosis, even when peripheral plasma renin activity was normal, renin production in the diseased kidney increased and that in the healthy kidney was suppressed, resulting in renin-associated hypertension [7]. In these patients, the RAA system seems to play an important role in sustaining hypertension.

Conclusions

Blood pressure monitoring is important in pediatric UTI, particularly in patients with severe congenital hydronephrosis, to prevent organ damage due to hypertension.