Acute Cardio-renal Syndrome: Progression from Congestive Heart Failure to Congestive Kidney Failure in the Journal Curr Heart Fail Rep.
Few interesting points that the article discusses.
1. Creatinine 0.3mg/dl over baseline and BUN greater than 50mg/dl is the strongest predictor of in hospital mortality in cardio renal syndrome( acute kind). The article seems to talk more of the Type I CRS.
2. One potential cause of acute cardio-renal syndrome is worsening intrinsic
kidney disease (eg, diabetic or hypertensive nephropathy) which could trigger the cascade of activation of the renin–angiotensin-II–aldosterone system, volume retention, and heart failure exacerbation.
3.Other potential causes for acute cardio-renal syndrome include drugs that can be nephrotoxic or decrease GFR. Prior history of renal dysfunction and/or heart failure is a risk factor for developing acute cardio-renal syndrome.4. We always think of acute cardio renal as hypoperfusion of the kidney explained by hypotension or hypovolemia. But majority of the patients are clinically “warm and wet.” Hypervolemia is far more common in these patients then hypovolemia.
5. Hypertension is a more marked predictor of CRS than hypotension
6. If the above are true, what is causing the presumed pre renal like state in the kidney. The article argues that this is due to high central venous pressure transmitted to the renal veins and kidneys.Two prior studies ( one in mammals in 1931 and another in humans in 1988) are cited as evidence in this review article.
Hypervolemia and acute increase in renal vein pressure leads to profound azotemia combined with reduced glomerular fitration rate, urine output and sodium retention.
7. Apparently the threshold renal vein pressure before azotemia ensues is 18-20mmHg.
Many other studies have shown that renal vein constriction results in reduced sodium excretion. This is a possible mechanism in intraabdominal pressure - compartment syndrome associated renal disease perhaps?
8. Congestion of the kidney combined with elevated renal interstitial pressure might be the mechanism by which tubular dysfunction, azotemia and renal failure occurs in CRS rather than presumed hypovolemic state in CRS.
So is renal venous pressure more important then hypovolemia in decompensated heart failure. The above review thinks so and few recent papers as well. The 1931 paper mentioned above says that you stop making urine after pressure of 20-25mmHg.
Take a look at few recent RFN blog posts on this topic
Image source: http://chfc.uk-wuerzburg.de/en/research/projects/project-area-e.html