This case illustrates the importance of prompt management of the underlying secondary cause of a hypertensive crisis. In this case, the patient had an acute bilateral UPJ obstruction causing hydronephrosis secondary to bilateral nephrolithiasis.
UPJ obstruction is an anatomical distortion causing the impediment of urinary flow from the renal pelvis to the ureter, increasing back pressure to the kidneys and eventually leading to hydronephrosis. It is most often congenital and is diagnosed during childhood as part of the workup for secondary hypertension . In contrast, acquired UPJ obstruction causing hydronephrosis is more common in adults secondary to nephrolithiasis, previous surgery, or malignancy. Although the incidence of nephroliths causing bilateral obstruction simultaneously is lower, it can still occur and is a plausible cause of secondary hypertensive crisis. Hydronephrosis as a cause of secondary hypertension has been evident in several studies [5,6,7,8], although most of these studies described unilateral hydronephrosis. Based on these limited studies, it was concluded that even unilateral obstruction causing hydronephrosis is enough to cause secondary hypertension [5, 7, 8]. On the other hand, there are even limited reports citing acquired bilateral hydronephrosis from bilateral UPJ obstruction as a secondary cause of hypertension. It is postulated that relief of the obstruction causes resolution of the hypertensive crisis. One case report describes rapid resolution of hypertension after bilateral nephrostomy insertion in a patient with bilateral hydronephrosis secondary to a pelvic malignancy. This now leads to the notion that different intrarenal mechanisms play a significant role in causing the elevation of blood pressure in hydronephrotic kidneys .
Although the exact mechanisms of hypertension among patients with hydronephrosis are still unknown, two mechanisms are implicated in the development of hypertension in hydronephrotic kidneys. These include increased tubuloglomerular feedback (TGF) activity and activation of the renin–angiotensin–aldosterone system (RAAS) .
The RAAS plays a role in the development of hypertension among patients with hydronephrotic kidneys, as evidenced by increased plasma renin activity . In the setting of an obstruction, the urine returns to the renal system, causing stasis and increasing back pressure, leading to hydronephrosis. Although the exact mechanism of increased activity of the RAAS in hydronephrotic kidneys is still unknown, it is postulated that it may be related to reduced renal blood flow because of increased TGF. TGF is a physiological mechanism involving the regulation of glomerular blood flow. With high glomerular flow rates, such as in the setting of volume overload, there is increased sodium delivery to the macula densa, causing release of the afferent arteriolar vasoconstrictor adenosine, leading to decreased glomerular blood flow. Nitric oxide, a modulator of TGF, is downregulated in hydronephrotic kidneys. This causes unrestricted vasoconstriction of the afferent arteriole, decreasing sodium delivery to the macula densa, and thereby activating the RAAS and its downstream effects . The improvement of hypertension after relief of the obstruction suggests that humorally mediated vasoconstriction plays a significant role in the mechanism by which hydronephrosis causes hypertension [9, 10].
The patient in this case developed bilateral nephrolithiasis, which was asymptomatic, eventually causing acute UPJ obstruction and subsequent hydronephrosis. This simultaneous acute bilateral obstruction caused the rapid development of hydronephrosis leading to downstream effects that culminated in a hypertensive crisis. The elevated blood pressure led to target organ damage, including flash pulmonary edema, because of the increased hydrostatic pressure. There was rapid resolution of the elevated blood pressure after relief of the obstruction using bilateral nephrostomy tubes. The patient’s serum creatinine level also greatly improved after relief of the obstruction.
Among patients presenting with acute bilateral UPJ obstruction complicated by a hypertensive crisis, prompt treatment is necessary to ameliorate target end-organ damage. According to the American Urological Association (AUA), an obstructed renal system is a urological emergency, and thus immediate intervention is needed . Recommendations include either ureteric stenting or percutaneous nephrostomy for alleviating the obstruction and have been deemed equally effective in achieving decompression. If sepsis or infection is involved, definitive treatment should be postponed until it is resolved [11, 12]. Although this is true for unilateral ureteral obstruction, the same principle could also be applied for bilateral obstruction. Therefore, regardless of whether the obstruction is unilateral or bilateral, prompt treatment is necessary to decompress the obstruction and alleviate the elevated blood pressure to ameliorate further damage to organs. We report this case of acute bilateral UPJ obstruction due to bilateral obstructing nephrolithiasis causing hypertensive crisis to emphasize the importance of prompt recognition and treatment to mitigate the deleterious effects of elevated blood pressure on target organs.