Catheter-based renal denervation as a novel treatment for loin pain haematuria syndrome

Abstract

Renal denervation using a catheter delivering radiofrequency energy to the renal artery vessel wall has recently emerged as a promising new treatment for difficult-to-treat hypertension. The beneficial effect of this intervention, attributable to sympathetic nerves interruption, has been coherently demonstrated in both an observational study [1, 2] and a controlled trial [3, 4]. Of note, according to the available follow-up studies, the hypotensive effect of renal denervation has been shown to last for up to 2–3 years. The European Society of Hypertension has published a position paper with recommendations for the application of this new technique including the eligibility criteria and issues that need to be addressed in further trials [5]. Several other conditions associated with sympathetic overactivity as diverse as heart failure, atrial fibrillation, insulin resistance [6], sleep apnoea [7] and polycystic ovary syndrome [8] have been described as being responsive to renal denervation and/or are being subjected to further study. Renal denervation has become a hot topic as illustrated by the large number of ongoing and planned trials of the technique [9]. In this issue, Gambaro et al. describe the use of catheterbased renal denervation for yet another indication, namely pain control in loin pain haematuria syndrome (LPHS). LPHS is a rare condition of uncertain aetiology and definition. Over 100 papers on LPHS have been cited in PubMed (accessed on 18 March 2013) so far, but many nephrologists agree that the actual number of cases is probably far larger. First described in 1967, LPHS is still a poorly understood condition consisting of recurrent flank pain often accompanied by nonvisible or visible haematuria. Women are more often affected (about three-fourths of cases described so far) than men and patients are typically young at onset. The pain is often unilateral, but recurrences on the contralateral side after invasive treatment are the rule rather than the exception. Pain exacerbations may be accompanied by low-grade fever and sometimes urinary symptoms mimicking urinary tract infection [10]. Episodes of (particularly) visible or non-visible haematuria very often accompany exacerbation of loin/flank pain. The duration of such episodes is variable but in some cases symptoms persist for months and cause serious disability. Pain may be severe and associated with nausea and vomiting, mimicking renal colic. Often, opioid analgesics are eventually prescribed in the most severe cases. Kidney function remains normal and development of hypertension is not associated with the syndrome. Although spontaneous disappearance of symptoms can occur after years, many patients remain symptomatic long-term [11]. A diagnosis of LPHS can only be made after a thorough evaluation for, and exclusion of other causes of loin pain and/or haematuria. Interestingly, many patients report a history of nephrolithiasis [12]. A kidney biopsy shows no glomerular abnormalities, but intratubular erythrocytes are seen more often than in healthy controls (7.2 versus 1.6%), suggesting a glomerular origin of haematuria [12]. Disparate structural abnormalities of the glomerular basement membrane, from excessive thickening to excessive thinning, may be the explanation [12]. Several other hypotheses for the cause of LPHS have been proposed including microvascular abnormalities, abnormal platelet function, intra-tubular microcrystal formation and complement activation [10, 13]. The complexity of this disorder is underscored by the fact that many patients meet the criteria for somatoform disorder on the basis of other physical complaints preceding the onset of LPHS [14].