Acute Perioperative Urinary and Renal Dysfunction

Michael Hermann

Sheri Berg

EPIDEMIOLOGY

The exact percentage of patients who suffer from some degree of acute kidney injury (AKI) is difficult to assess, because the number will vary depending upon which definition for AKI is used for determining whether or not AKI is present. The incidence varies depending on the type of procedure that was performed; however, about 25% of all hospital-acquired AKI occurs in the surgical setting.

There are known preoperative risk factors that will increase the patient’s chance of developing AKI. These include:

Age > 55 years
Male sex
Active congestive heart failure
Presence of ascites
Diabetes requiring oral therapy or insulin therapy
Hypertension
Mild or moderate perioperative renal insufficiency
Nephrotoxic agents (contrast dyes)

With regard to intraoperative risk factors, procedures that are performed emergently involve cardiopulmonary bypass, and many vascular surgical procedures all carry an increased risk of developing AKI, likely secondary to relative intraoperative hypovolemia and renal ischemia.

Inadequate hydration, perioperative hypotension, and urinary obstruction can instigate possible postoperative AKI.

PATHOPHYSIOLOGY

The etiology of AKI is conventionally separated into prerenal, intrinsic renal, and postrenal considerations (Table 20.1).

Kidney dysfunction in the perioperative period is frequently multifactorial, with acute tubular necrosis (ATN) as the most common cause, given preoperative risks of hypotension and hypovolemia.

Perioperative kidney hypoxia that occurs intraoperatively is a result of anesthetic-induced decreases in kidney perfusion and function; this is usually reversible and without permanent damage.

Prerenal injury to the kidneys can be caused by decreased perfusion, which is a known common complication of hypotension and hypovolemia. In addition, increased intra-abdominal pressure during surgery (laparoscopy) can create a hypotensive state to the kidneys.

Normally renal blood flow (RBF) is 20% of the cardiac output, and 90% of RBF supplies the renal cortex. The kidney is very sensitive to hypoperfusion, because the medulla extracts ˜80% of the delivered oxygen. Blood flow to the kidney is autoregulated between a blood pressure of 80 and 160 mm Hg. Medullary blood flow is normally controlled by vasodilators (nitric oxide,
prostaglandins, adenosine, dopamine), vasoconstrictors (endothelia, angiotensin II, antidiuretic hormone), and tubuloglomerular feedback (reflex mechanism from insufficient sodium reabsorption causing glomerular afferent vasoconstriction, thus reducing filtration). Blood flow and glomerular filtration rate (GFR) are maintained to a mean arterial pressure (MAP) as low as 60. Autoregulation is maintained by decreasing afferent glomerular arteriolar resistance with prostaglandins as well as increasing efferent
arteriolar resistance with angiotensin II. Below the autoregulatory range, endogenous vasoconstrictors increase afferent arteriolar resistance, which in turn decreases GFR, causing prerenal azotemia.

TABLE 20.1 Causes of Acute Kidney Injury

Prerenal	Intrinsic Renal	Postrenal (Obstructive)
Intravascular volume depletion GI fluid loss (e.g., vomiting, diarrhea, EC fistula) Renal fluid loss (e.g., diuretics) Burns Blood loss Redistribution of fluid (e.g., “third spacing,” pancreatitis, cirrhosis)	Acute tubular necrosis Ischemic Toxin induced Drugs IV contrast Rhabdomyolysis Massive hemolysis Tumor lysis syndrome	Upper urinary tract obstruction Nephrolithiasis Hematoma Aortic aneurysm Neoplasm
Decreased renal perfusion pressure Shock (e.g., sepsis) Vasodilatory drugs Preglomerular (afferent) Postglomerular (efferent) arteriolar vasodilation	Acute interstitial nephritis Drug induced Infection related Systemic diseases (e.g., SLE) Malignancy	Lower urinary tract obstruction Urethral stricture Hematoma Benign prostatic hypertrophy Neurogenic bladder Malpositioned urethral catheter Neoplasm
Decreased cardiac output Congestive heart failure Myocardial ischemia	Acute glomerulonephritis Postinfectious Systemic vasculitis TTP/HUS Rapidly progressive GN
	Vascular Atheroembolic disease Renal artery or vein thrombosis Renal artery dissection Malignant hypertension
	Hepatorenal syndrome
	Increased intra-abdominal pressure
GI, gastrointestinal; EC, enterocutaneous; IV, intravenous; SLE, systemic lupus erythematosus; TTP, thrombotic thrombocytopenic purpura; HUS, hemolytic uremic syndrome; GN, glomerulonephritis.

Hypoxia disrupts several pathways in cellular metabolism coalescing in cytoskeletal disruption. This mechanism can result in the sloughing of cells and can possibly lead to tubular obstruction. Further oxidant injury causes an increased amount of vasoconstriction and propagates the cycle of further damage, ultimately culminating in ATN, see below. Vasoconstrictors can cause significant renal ischemia, because α₁ activation is unopposed given the absent β₂ receptors in the renal vascular bed. Cardiopulmonary bypass produces ischemia repercussion injury secondary to hypovolemia and low cardiac output. Aortic surgery, with cross-clamping, decreases RBF by up to 40%, causing renal vascular resistance to increase by 75%.

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