Let's talk a little bit about renal parenchymal hypertension.
This is a common feature in acute, typically glomerular or vascular disorders, and chronic kidney disease.
So, for example in acute glomerular disease, the pathogenesis is related to volume overload.
Suppression of the RAAS system.
There's actually a mechanism in the principle cell where it turns on that sodium-potassium ATPase
and patients tend to reabsorb more sodium.
In acute vascular disease, it's a little bit different.
Hypertension here results from ischemic-induced activation of RAAS,
much like it does in renovascular disease that we just talked about.
So, when we think about renal parenchymal hypertension due to chronic kidney disease,
the pathogenesis is really multifactorial. Remember, our patients are volume expanded.
They have sodium and water retention.
They have activation of sympathetic tone or sympathetic nervous system.
Their renin-angio-aldo system is activated.
They also will have contribution from secondary hyperparathyroidism.
That means intracellular calcium is mediating vasoconstriction in those patients.
And they have endothelial dysfunction.
The treatment for CKD patients who have renal parenchymal hypertension
include having an ACE inhibitor or angiotensin receptor blocker.
Those have been shown to slow decline in GFR in patients who have proteinuria.
A diuretic for volume removal and a calcium channel blocker as a third-line agent if needed.
ACE inhibitors and ARB may cause an initial fall in GFR
and I want you to think about why that would happen.
Remember where ACE inhibitors and ARBs work.
They're, again, at that efferent arteriole
and if they're causing vasodilation or keeping it from being constricted, remember what happens.
That's going to drop the hydrostatic pressure in the glomerulus
and therefore, decrease GFR potentially.
But we typically tolerate an increase in serum creatinine.
If it's less than 30-35%, we tolerate that and we don't want to discontinue therapy
because it's vital in that patient population.