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Renal Hemodynamics

General Information:

Hemodynamics affect renal function and can lead to renal failure. Breaking down cardiac output into heart rate and stroke volume, and then stroke volume into preload, contractility and afterload helps show how hemodynamics can affect renal blood flow and kidney function.

 

Physiology:

Urine output relies on having a positive net filtration pressure (NFP). The NFP is what drives ultrafiltration into Bowman’s capsule and creates a glomerular filtration rate (GFR). Here is a basic drawing of the interaction between the glomerulus and Bowman’s capsule, which together is called the renal corpuscle (Figure 1).

Figure 1:

RV Cong Figure 1.png

The net filtration pressure is made of pressures that are pushing and pulling fluid between the glomerular capillaries and Bowman’s capsule. These components include the intravascular osmotic and oncotic pressure which are drawing fluid into the intravascular space and the opposing intravascular hydrostatic pressure which is pushing fluid out. The is the opposite for Bowman’s capsule where the capsular osmotic and oncotic pressures are drawing fluid into the intracapsular space and the capsular hydrostatic pressure is pushing it back into the intravascular space. The main components that contribute to the NFP are the hydrostatic and oncotic pressure of the intravascular space, and the hydrostatic pressure on the capsular side. The NFP equation typically names these as the glomerular capillary hydrostatic pressure (GCHP), Blood colloidal osmotic pressure (BCOP), and capsular hydrostatic pressure (CHP).

 

Net Filtration Pressure = Glomerular Capillary Hydrostatic Pressure – (Capsular Hydrostatic                                                Pressure + Blood Colloidal Osmotic Pressure)

 

NFP = GCHP – (CHP + BCOP)

 

The normal values are GCHP=55 mmHg, CHP=15 mmHg, BCOP= 30mmHg. Giving a positive net filtration pressure of 10 mmHg

 

NFP =  55 – (15 + 30) = 10 mmHg (Figure 2)

Figure 2:

RV Cong Figure 2.png

The more positive the NFP the better the GFR, so trying to make changes that improve the NFP will improve the patient’s urine output. The CHP is not able to be manipulated to decrease the pressure. When a patient has a kidney stone or bladder outlet obstruction it will increase CHP from back pressure and worsen NFP (3). The Intravascular oncotic pressure, or BCOP, is more difficult to navigate. According to this equation the lower the oncotic pressure the higher the NFP and 75% of oncotic pressure is albumin. This would imply a lower serum albumin would be beneficial. But, a low oncotic pressure leads to spontaneous third-spacing and decreases the intravascular hydrostatic pressure. If the oncotic pressure is too high it increases BCOP and decreases NFP and if it is too low it decreases GCHP and decreases NFP. I usually ensure the patient has an albumin >2.5g/dL to prevent spontaneous third-spacing.

 

The main focus is on GCHP when manipulating the patient’s hemodynamics to improve urine output. The hydrostatic pressure is based on the flow from the afferent arteriole to the efferent arteriole. Using a variation of Ohm’s law, we correlate flow and pressure. Ohm’s law is for electricity, V = IR. Ohm’s law can be changed to look at fluids.

 

Ohm’s Law (Fluids): Change in Pressure (P) = Flow (F)Resistance (R)

 

This formula is usually seen in hemodynamics when calculating resistance; R = â–³P/F.

 

The simplified equation for glomerular capillary hydrostatic pressure looks at the change in pressure from afferent arteriole to efferent arteriole: Pa – Pe. This is the pressure gradient that will increase NFP (Figure 3). I often think of the pressure across a dialysis filter that is helping push the ultrafiltrate out.

Figure 3:

RV Cong Figure 3.png

Abnormal Renal Hemodynamics Differential: (3 subtypes)

  1. Hypovolemic/Distributive (↓ volume/pressure - arterial)

  2. Hypervolemic                    (↑ volume/pressure - venous)

  3. Cardiogenic/Cardiorenal   (↓ flow - arterial & ↑ volume pressure - venous )

 

1. Hypovolemic/Distributive:

A decrease in blood flow to the kidney due to a lack of volume or hypotension. This is seen in hypovolemic patients with dehydration or blood loss.

 

Physiology:

The blood volume is decreased and therefore less flow. This causes a decrease in the pressure of the afferent arteriole which drops the pressure gradient. This decrease in the pressure gradient drops the NFP and decreases urine output leading to an AKI (Figure 4). This leads many providers to give fluids as I stated above. This is definitely a cause of AKI for patients in the hospital, but it is not the only cause.

Figure 4:

RV Cong Figure 4.png

2. Hypervolemic:

Hypervolemic AKI is multi-factorial as are many disease processes. The kidney is surrounded by a layer of fascia, Gerota’s fascia, that keeps the kidney from appropriately swelling if the parenchyma gets congested. If it cannot increase in size with the increased water content it gets compressed against the fascia leading to injury. Another factor is intra-abdominal pressure. When patients get volume overloaded it leads to intestinal swelling and third-spacing which causes an increase in intra-abdominal pressure. As the pressure rises, it leads to intra-abdominal hypertension (IAH) and potentially abdominal compartment syndrome. IAH causes pressure on the kidney leading to AKI.

 

Physiology:

Renal venous congestion increases the efferent arteriole pressure and decreases the pressure gradient (Figure 5). The end result of a decreased pressure gradient is the same as for hypovolemic/distributive, but it is due to venous pressure problems.

Figure 5:

RV Cong Figure 5.png

3. Heart Failure/Cardiorenal:

Cardiorenal is a combination of the previous two which explains why decompensated heart failure patients with an AKI are so difficult to treat. These patients are in a low-flow state (low cardiac output) which decreases afferent arteriole pressure and they also have significant renal venous congestion which increases efferent arteriole pressure. This is a double insult and causes a more significant decrease in the pressure gradient (Figure 6). In a study looking at decompensated heart failure patients it was found that the venous congestion played a bigger role than decreased flow (4).

Figure 6:

RV Cong Figure 6.png

Work-up:

Volume assessment:

Bedside echocardiogram with IVC evaluation is the best way to differentiate between the different subtypes.  Echo can determine cardiac function and IVC can help determine volume status. The extremes are very helpful. If the IVC collapses completely with normal work of breathing I can safely say it is not renal venous congestion. If the IVC is dilated and non-variable I can say they do not need more fluids, they need either diuresis or better hemodynamics.

 

Treatment:

Hypovolemic/Distributive:

Treating a decreased pressure gradient due to hypovolemia or distributive shock is treated IV fluids and vasopressors (Figure 7). This will ensure appropriate blood flow and pressure.

Figure 7:

RV Cong Figure 7.png

Hypervolemic/Renal Venous Congestion:

For a decreased pressure due to renal venous congestion, the treatment is to decrease the renal venous pressure. This can be done by decreasing absolute volume with diuresis or by decreasing the venous pressure with venodilators (Figure 8). Diuretics are first-line and decreasing the volume should be the top priority. This can be difficult if the renal venous pressures are extremely elevated. When diuretics are initiated there can be an increase in creatinine before the appropriate decrease. It is important to just hold steady and continue diuresis. If diuretics alone are not working, adding a venodilator like nitroglycerin can work really well. As long as the patient has enough blood pressure to tolerated a nitrate, there should be a significant increase in UOP.

Figure 8:

RV Cong Figure 8.png

Cardiogenic/Cardiorenal:

Cardiorenal is the most difficult to treat. Both sides of the pressure equation have to be addressed to appropriately treat the patient. Often these patients are started on diuretics, which will help the venous congestion, but is not enough to increase the afferent arteriole pressure. These patients need an increase in flow to the kidney. If the patient has low blood pressure, inotropes should be initiated to help increase flow. If the patient is normotensive to hypertensive afterload reduction with hydralazine, ACE inhibitors, or even nitroprusside will help (Figure 9).

Figure 9:

RV Cong Figure 9.png

Resources:

  1. Blogs/Podcasts/Videos:

  2. Lectures/Handouts:

  3. References:

References:

  1. Messmer AS, Zingg C, Müller M, Gerber JL, Schefold JC, Pfortmueller CA. Fluid Overload and Mortality in Adult Critical Care Patients-A Systematic Review and Meta-Analysis of Observational Studies. Crit Care Med. 2020 Dec;48(12):1862-1870. doi: 10.1097/CCM.0000000000004617. PMID: 33009098.

  2. Wang N, Jiang L, Zhu B, Wen Y, Xi XM; Beijing Acute Kidney Injury Trial (BAKIT) Workgroup. Fluid balance and mortality in critically ill patients with acute kidney injury: a multicenter prospective epidemiological study. Crit Care. 2015 Oct 23;19:371. doi: 10.1186/s13054-015-1085-4. PMID: 26494153; PMCID: PMC4619072.

  3. Austin Peay State University. https://www.apsubiology.org/anatomy/2020/2020_Exam_Reviews/Exam_4/CH25_Physiology_of_Glomerular_Filtration.htm, 2020, accessed 3/20/21.

  4. Wilfried Mullens, Zuheir Abrahams, Gary S. Francis, George Sokos, David O. Taylor, Randall C. Starling, James B. Young, W.H. Wilson Tang. Importance of Venous Congestion for Worsening of Renal Function in Advanced Decompensated Heart Failure. Journal of the American College of Cardiology. 2009 53;7:589-596,

  5. Beaubien-Souligny, W., Rola, P., Haycock, K. et al. Quantifying systemic congestion with Point-Of-Care ultrasound: development of the venous excess ultrasound grading system. Ultrasound J 12, 16 (2020). https://doi.org/10.1186/s13089-020-00163-w

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