Kidneys perform a number of essential physiologic functions, including water management, electrolyte homeostasis, acid–base balance, and several neurohumoral and hormonal functions. Anesthesiologists are often called upon to (1) assess and manage perioperative oliguria (Table 18–1); (2) provide renal protection; and (3) use renal function to achieve goals not directly related to urine output, such as decreasing brain swelling or decreasing accumulation of fluid in lung alveoli.
Sources of perioperative oliguria.
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Table 18–1 Sources of perioperative oliguria.
|Category ||Description |
|Preexisting renal insufficiency || |
Decreased glomerular filtration ratea
Decreased renal reserve
Increased sensitivity to any renal insult
|Conditions associated with chronic renal insufficiency || |
Coronary artery disease
Congestive heart failure
Peripheral vascular disease
|Nephrotoxic drugs || |
Angiotensin-converting enzyme Inhibitors
Nonsteroidal anti-inflammatory drugs
|Procedures associated with acute renal failure || |
Organ transplant surgery
Vascular surgery (especially with a suprarenal aortic cross-clamp)
Prolonged intraoperative hypovolemia
|Anesthetic effects || |
Decreased glomerular filtration rate
Hypoperfusion (MABP < 70–80 mm Hg in healthy adults)
|Mechanical causes ||Kinked or obstructed urinary catheter |
This chapter will briefly discuss drugs used to preserve or manipulate renal function. In general, several drugs are effective diuretics but less effective at providing renal protection.
Furosemide was first approved for human use in the United States by the Food and Drug Administration, in July of 1982. It subsequently became a common treatment for congestive heart failure in the late 1980s. Its most common uses are in the treatment of hypertension; mobilization of edema fluid due to renal, hepatic, or cardiac dysfunction; treatment of increased intracranial pressure; and in the differential diagnosis of acute oliguria. Interestingly, furosemide has also long been used in veterinary medicine to prevent thoroughbred racehorses from bleeding through the nose during races.
Furosemide exerts its diuretic effect by inhibiting the reabsorption of sodium and chloride, primarily in the medullary portions of the ascending limb of the loop of Henle. Protein-bound drug is secreted into the renal tubules and specifically acts on the sodium-chloride-potassium cotransporters on the intraluminal side of the loops of Henle (Figure 18–1). The accumulation of ions inside the lumen of renal tubules that occurs after furosemide administration inhibits the passive reabsorption of potassium, calcium, and magnesium. This results in urinary losses of these ions. Furosemide also stimulates renal production of prostaglandins, resulting in renal vasodilation and increased renal blood flow.
Location and mechanisms of action for furosemide, mannitol, and fenoldopam. The image shown represents the renal artery, glomerulus, and the descending and ascending loop of Henle. Each box shows a magnified representation of the underlying structure. DA1, dopaminergic receptor.
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