The incidence of stroke in this study was 7.4 per 1000 patient-months. This observation corroborates data from the literature reporting a higher incidence of stroke in chronic hemodialysis compared to the general population [
3‐
8]. Indeed, the incidence of stroke observed in this study is higher than that of 1.123 per 1000 patient-years reported in a meta-analysis of some available African studies [
12]. This incidence is also higher than that of 0.8 per 1000 patient-years in African hospital settings and those in chronic hemodialysis patients in Europe and Asia who varied between 17 and 74 per 1000 patient-years [
3‐
8]. The propensity of chronic hemodialysis patients to develop more strokes relies mainly upon the acceleration of the dynamic process of atherosclerosis already initiated by uremia and its underlying cause [
13]. Indeed, hemodialysis accelerates, through oxidative stress and subsequent inflammation, pre-existing remodeling of all vascular beds especially cerebral vessels [
13,
14]. The particular vulnerability of brain vessels to the deleterious effects of uremia and hemodialysis is related to the structural and functional similarities between renal glomerular microcirculation and cerebral microcirculation [
15,
16]. Indeed, the large extra-cerebral arterial trunks (aorta and carotids) play an important role of shock absorber (“Windkessel effect”) to modulate hemodynamic stress from the heart to the brain [
15,
16]. Similar to renal glomerular microcirculation, the peculiar nature of cerebral microcirculation, characterized by high blood flow and low vascular resistance, makes the brain vulnerable to pulsatory hemodynamic stress during each cardiac cycle [
15,
16]. With the acceleration of atherosclerosis through uremia and hemodialysis, the wall of the central elastic arteries (aorta and carotid arteries) loses its elasticity and becomes rigid, resulting in loss of shock function and direct transmission from hemodynamic stress to cerebral microcirculation [
15,
16]. This will result in structural and functional lesions responsible for a wide range of subclinical and clinical conditions including stroke [
15,
16]. Apart from these structural similarities, the high incidence of stroke in chronic hemodialysis patients can also be explained by several other factors including the coexistence of uremic (anemia, hyperphosphorémie, ADMA retention and NO inhibitor) and traditional risk factors as well as the passive selection by hemodialysis of an elderly population with multiple comorbidities [
4,
6].
In the present study, non-hypertensive patients are at increased risk of stroke suggesting a paradoxical protective effect of elevated blood pressure in chronic hemodialysis. This observation disagrees with the high risk of stroke conferred by elevated blood pressure in the general population. Indeed, INTERSTROKE Study shows that hypertension is the main risk factor for all stroke subtypes, particularly among young Africans who develop stroke while ignoring their hypertensive status [
17]. The apparent paradoxical protection afforded by elevated blood pressure against stroke observed in the present study can be partly explained by the phenomenon of reverse epidemiology of traditional risk factors reported both in ESRD and chronic dialysis [
18,
19]. This inverse relationship does not necessarily mean that the principles of vascular physiopathology of atherosclerosis are different in patients with ESRD under dialysis; It seems rather to indicate the existence of additional and more powerful risk factors such as inflammation and malnutrition which apparently alter the relationship between traditional risk factors and outcomes in dialysis patients [
18,
19]. This phenomenon, not specific to chronic kidney disease and dialysis, is also reported in chronic conditions such as chronic heart failure, cancer and chronic infections like HIV/AIDS [
18,
19]. Another plausible explanation of the apparent paradox can be systolic cardiac dysfunction [
18,
19]. Indeed, hypertension-induced cardiac failure is associated with low blood pressure or hypotension that is both a marker of cardiac disease severity and a powerful predictor of morbidity and mortality [
18,
19]. Low blood pressure in uremic patients can also be a reflection of autonomic neuropathy that, in turn, is a marker for more severe uremic complications [
18,
19]. Apart from the aforementioned mechanisms underlying reverse epidemiology of hypertension, more recent studies have suggested this phenomenon to be mainly due to inadequacy of peridialytic BP recordings per se to describe the true BP load, rather than a true U-shaped relationship of BP with cardiovascular morbidity and mortality [
20]. Indeed, peridialytic BP recordings are not made for diagnostic reasons but to exploit a major hemodynamic metric like BP in order to assess cardiovascular stability before, during and immediately after the dialysis procedure. Thus, using these readings to diagnose hypertension, assess the success of antihypertensive treatment or examine future cardiovascular risk could be inherently hazardous [
20].In contrast to the unclear association of peridialytic BP recordings with all-cause and cardiovascular mortality, recent prospective studies have shown that interdialytic BP recorded either at home or by ambulatory BP monitoring (ABPM) associates more closely with mortality and cardiovascular events, as it is documented for the general population [
20]. In practice, these data suggest that there is probably no benefit to recommended achieving normal BP in dialysis. Reverse epidemiology has misleading relevance on dialysis management. The high early mortality universally associated with low baseline BP figures does not contradict the need to achieve normal BP in dialysis patients to reduce long-term cardiovascular mortality. Besides, the eventual noxious/beneficial role of antihypertensive medications in dialysis patients needs to be investigated.