In contrast to other aspects of nephrology that are difficult to control (think of the inevitable slow decline of renal function in diabetic nephropathy), blood pressure is one aspect of CKD management we can fix over a realatively short period of time. It’s very satisfying to see a patient who has been battling with uncontrolled blood pressure for over a year and then easily control it over the course of a few clinic visits. When our patients ask us what their blood pressure should be, we can tell them we are shooting for a BP <130/80 in most cases (outside of the very old and frail). We should also be able to let them know how this benefits them and we should also be able to briefly communicate the evidence base to other physicians. Below is the 80/20 summary of the big 2 trials that inform our blood pressure target of 130/80.
In general, lowering blood pressure to <130/80 mmHg (referred to subsequently as intensive BP targets) as compared to <140/90 mmHg is recommended in patients with CKD and provides two major benefits. Firstly, it reduces the risk of ESRD in those with proteinuric CKD (defined in trials as a urine protein-to-creatinine ratio >0.22 g/g). Unfortunately, this benefit does not extend to those without proteinuria. Secondly, it reduces mortality whether or not the patient has proteinuria. These benefits are most evident on long-term follow up of patients.
There are three trials that inform this area – the MDRD study (1994), the AASK trial (2002), and the SPRINT trial (2015). The MDRD study showed that patients excreting more than 1 gram of protein daily had lower rates of CKD progression with an intensive BP target. Long-term follow up of MDRD participants echoed this finding. The original AASK trial showed no benefits to preservation of renal function in the original trial. On long term follow up of AASK trial participants, however, intensive BP targets slowed progression of CKD in those with proteinuria > 0.22 g/g (average daily proteinuria of 1g). The MDRD study and AASK trial show that long-term follow up is vital to seeing the benefit of intensive BP goals.
Lastly, the SPRINT trial showed that aggressive BP targets reduce mortality regardless of the presence of proteinuria. No benefit was seen for preservation of renal function. Importantly, the risk of a 30% or greater decline in renal function was higher with intensive BP targets. This finding was recently examined in more detail in a study utilizing urinary proteomic biomarkers of kidney injury. It suggested that this decline of renal function in the intensive BP arm of the SPRINT trial was not due to actual damage of the renal parenchyma, but is instead attributable to hemodynamic effects of a lower BP. Thus, targeting an intensive BP target to lower mortality is reasonable.