In our cohort, we studied the impact of guidelines-targeted BP control in patients with emergency HTN on their renal outcome. We found that patients with positive hs-troponin on admission have worse outcomes regarding renal dysfunction as well as mortality.

Resultant pressure overload due to severe HTN may result in subclinical myocardial wall remodeling and potential ischemic cardiomyocyte injury [16].

Severe hypertension exerts very high-pressure overload that causes relative ischemia and necrosis or minute damage to myocytes, and thus troponin release. This effect similarly occurs in any other cause of increased pressure loads [17, 18]. In addition, activation of the sympatho-adrenal system in hypertensive patients leads to increased catecholamine release and subsequent myocyte injury [19].

Optimal SBP targets from ACCORD [20], INVEST [21], and ONTARGET [14] seem to be between 120 and 140 mmHg. A comprehensive meta-analysis [22] of 17 trials including SPRINT, aiming at assessing optimal BP targets, found that the balanced efficacy and safety could be achieved at 130 mmHg.

More consideration was given to the results from SPRINT, suggesting reduced CV risk with SBP treatment target at 120 mmHg [23].

The concept of “the lower the better” in case of hypertension in diabetic, renal, or CAD patients should be revised. The guidelines-targeted BP reduction in case of severe hypertension could be changed if we found an increased risk of morbidity and mortality by applying this strategy.

In the current study, we found that emergency hypertensive patients with initially raised hs-TNT had higher in-hospital mortality and morbidity (renal dysfunction) than those with normal hs-TNT when we applied the guidelines in controlling their BP. They developed deterioration of their renal function if their BP was controlled to the guideline level. In addition, the degree of deterioration of s.creat was positively correlated with the initial level of hs-TNT. However, those with initial normal hs-TNT levels would get benefit of guideline-targeted BP control.

Hypertension-induced TOD may affect the kidneys in its early stages. The risk of albuminuria progression was assessed in meta-analysis and found to be significantly reduced after intensive BP control [24].

Another study found that greater proteinuria and reduced eGFR in the general population are associated with masked hypertension [25]. This may suggest that the damaging effect of hypertension might affect the kidney earlier than other organs, causing TOD for the kidney even before the diagnosis of HTN or the occurrence of any symptoms.

In our study, there was a significant difference between both groups with and without elevated hs-TNT regarding initial s-creat, with higher values in group B with elevated initial hs-TNT. This may indicate that the kidney has been already affected by HTN in those patients to a subclinical degree. Therefore, the relatively marked reduction of BP (according to the guidelines target) may disturb the renal autoregulation that seems to be developed with time in those patients.

Our conclusion was supported by another study conducted by Seccia et al. They found that a relatively high proportion of hypertensive patients develop mild-to-moderate hypertensive nephrosclerosis. This pathology was found to progress into end-stage renal disease only in a relatively small percentage, especially those with prolonged uncontrolled SBP [26].

In this context, a more personalized, biomarker-guided, approach to BP treatment in this group with severe HTN may be a preferred alternative.

We hypothesize that target BP should not be a solid figure and should be individualized. It depends on the degree of TOD. Elevated hs-TNT, as an indicator of TOD, could be used to guide BP control. When hs-TNT is not elevated, intense BP control to the guideline-targeted BP could be applied. However, if hs-TNT is elevated during the sitting of severe HTN, more caution should be exerted not to reduce BP markedly or over a short time. In this condition, the reduction of BP just to the level making the hs-TNT value return to normal seems to be appropriate in the first days. Longer duration may be better needed before returning the BP to normal.

Patients with positive hs-troponin on admission may benefit from closer monitoring, cautious blood pressure control over a longer period and potentially more frequent assessment of renal function. These individuals may be at higher risk for renal dysfunction and mortality, so tailoring their treatment approach to address these risks could be beneficial. A multidisciplinary approach involving cardiologists, nephrologists, and intensivists may be considered to optimize the management of these high-risk patients.

In a study done on isolated systolic hypertension in older adults [27], the authors concluded that cardiac biomarkers hs-cTnT and NT-proBNP might be used to identify older adults who would benefit from more intensive BP therapy to reduce systolic hypertension. They thought that high biomarker levels might identify older patients who could benefit from intensive BP treatment. This conclusion may conflict with our findings that intense BP control increases the risk of mortality and renal failure in patients with high hs-TNT. This controversy may be due to the difference in studied populations. Those in our study had severe or emergency HTN, which might differ in their myocardial tolerance to pressure overload and in TOD risk at lower cTnT thresholds.

Cardiac troponins may be elevated in asymptomatic end-stage renal patients [28]. The mechanisms causing such biomarker elevation in renal patients are not clear. There is emerging evidence that troponin elevation in asymptomatic renal patients indicates subclinical myocardial necrosis or minute injury [29].

In a trial aiming to determine the independent risk factors of CKD progression, higher hs-TNT was significantly associated with 1.5-fold of the composite outcome of CKD deterioration. This association was similar to or stronger than that of high systolic BP [30].

The association between cardiac biomarkers such as hs-TNT and NT-proBNP and CKD may indicate their value as markers of cardiorenal syndrome [30, 31].

None of our patients took nephrotoxic drugs over the past 3 months prior to admission. While certain medications, such as ACE inhibitors and angiotensin receptor blockers, can decrease GFR by impacting renal hemodynamics. Drugs that affect kidney perfusion and haemodynamics may safeguard nephrons against hyperfiltration, which can lead to CKD progression [32].

The decrease in all-cause mortality with more intensive blood pressure lowering was also demonstrated in the SPRINT trial; however, in the subgroup of chronic kidney disease, there was not any significant reduction in risk for the primary composite endpoint of cardiovascular morbidity and mortality in those treated with more intensive therapy [33]. Post hoc analysis of some studies demonstrated higher mortality associated with more systolic hypotension [34].