Severe hypertension (HTN) may cause target organ damage (TOD). Kidney can tolerate severe HTN to very high levels. Cardiac remodeling as TOD could be detected by elevation of biomarker Troponin. Aim We aim to detect the response of organs (heart & kidney) to tight control of severe HTN. Patients & Methods Patients admitted due to severe hypertension (BP> 180/120) associated with any symptoms were enrolled. All patients were managed according to the European guidelines to the target BP. Cardiac biomarker Hs-Troponin T (hs-TNT) and serum creatinine (s.creat) were measured for all patients on admission and 24hours later. Results Ninty five patients with hypertensive crisis were treated to target BP. Forty six patients had initially high hs-TNT (Group A) and 49 patients had initially normal hs-TNT (Group B). There was a highly significant difference between both groups regarding initial and follow-up s.creat with higher values in Group B (P= 0.03 and 0.004 respectively).There was high significant difference between initial and follow up s.creat values in Group B with higher values in the follow up measurements after BP control to the target (P= 0.03), while this difference is insignificant in Group A (P=0.26). Five patients in Group B developed renal failure after tight BP control. There was a significant positive correlation between hs-TNT and the follow-up s.creat (P=0.018) with more deterioration of s.creat in those having initial high hs-TNT. Conclusion In severe HTN, hs-TNT may be elevated due to marked afterload. Renalaffection and TOD occurs before cardiac remodeling and damage due to severe HTN. Renal autoregulation occurs in chronic elevation of BP. Acute control of severe HTN leads to disrruption of renal autoregulation and renal shut down. European guidelines regarding severe HTN control should be revised. In hypertensive patients with high hs-TNT, BP should not be well controlled on the short term not to disrupt renal autoregulation.