This lecture discussed the basic physiologic mechanisms behind hepatorenal syndrome (HRS). The main take home point is understanding that HRS occurs at the end-stage of chronic liver disease, after cirrhosis, portal hypertension, ascites (and usually hyponatremia) have already occurred. The syndrome must be recognized and diagnosed quickly because prognosis is only 2-4 weeks if left untreated.
In the late stages of chronic liver disease, when the hyperdynamic circulatory state is in full swing, the proximal convoluted tubule is very sodium avid, as the nephron does everything in its power to refill the vasodilated periphery. In addition, the nephron’s afferent arteriole is constricted in order to decrease GFR (again, the body wants to produce less urine and reabsorb more water into the body). This intense vasoconstriction essentially deprives a healthy kidney of the needed blood flow, and a rising creatinine ensues.
Treatment of HRS therefore is predicated on vasoactive substances, in attempt to cut down on peripheral and splanchnic vasodilation and shift volume to the “relatively ischemic” nephrons. Midodrine is a vasoconstrictor, octreotide prevents vasodilation, and albumin adds oncotic potential.
For more information on hepatorenal syndrome, click on the link below to this review article: