Renal Parenchymal Hypertension – Secondary Hypertension

00:01 Let's talk a little bit about renal parenchymal hypertension.

00:03 This is a common feature in acute, typically glomerular or vascular disorders, and chronic kidney disease.

00:11 So, for example in acute glomerular disease, the pathogenesis is related to volume overload.

00:16 Suppression of the RAAS system.

00:18 There's actually a mechanism in the principle cell where it turns on that sodium-potassium ATPase and patients tend to reabsorb more sodium.

00:26 In acute vascular disease, it's a little bit different.

00:29 Hypertension here results from ischemic-induced activation of RAAS, much like it does in renovascular disease that we just talked about.

00:36 So, when we think about renal parenchymal hypertension due to chronic kidney disease, the pathogenesis is really multifactorial. Remember, our patients are volume expanded.

00:47 They have sodium and water retention.

00:49 They have activation of sympathetic tone or sympathetic nervous system.

00:53 Their renin-angio-aldo system is activated.

00:56 They also will have contribution from secondary hyperparathyroidism.

01:00 That means intracellular calcium is mediating vasoconstriction in those patients.

01:04 And they have endothelial dysfunction.

01:06 The treatment for CKD patients who have renal parenchymal hypertension include having an ACE inhibitor or angiotensin receptor blocker.

01:14 Those have been shown to slow decline in GFR in patients who have proteinuria.

01:20 A diuretic for volume removal and a calcium channel blocker as a third-line agent if needed.

01:26 ACE inhibitors and ARB may cause an initial fall in GFR and I want you to think about why that would happen.

01:35 Remember where ACE inhibitors and ARBs work.

01:37 They're, again, at that efferent arteriole and if they're causing vasodilation or keeping it from being constricted, remember what happens.

01:45 That's going to drop the hydrostatic pressure in the glomerulus and therefore, decrease GFR potentially.

01:51 But we typically tolerate an increase in serum creatinine.

01:55 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.