The kidneys concern us when drugs or their products of biotransformation need to be eliminated in urine. For this route out of the body, the substances need to be non-protein-bound so that they make it through the glomeruli and are then ionized so as to escape tubular reabsorption.
Impaired renal function becomes relevant with advancing years (creatinine clearance declines with age), with low cardiac output and decreased glomerular filtration, and with renal disease. The elimination of some drugs can be affected by decreased renal function. Of greatest interest to the anesthesiologist are a number of muscle relaxants such as pancuronium and doxacurium and their antagon-ist, neostigmine. Thus for patients in renal failure, we might elect atracurium or cisatracurium, muscle relaxants that undergo hydrolysis in plasma making them independent of renal excretion.
Patients in renal failure present special challenges not only because they cannot eliminate drugs in urine, but also because their water and electrolyte balance goes through roller coaster swings with intermittent dialysis. Ideally, the patient should have undergone dialysis within 24 hours before the anesthetic. Intra-operatively, the intravenous fluids need to be managed carefully, as the patient has no mech-anism to eliminate excess water or electrolytes. These patients tend to be ane-mic with a reduced oxygen-carrying capacity, which puts an extra burden on the heart should it be called on to increase cardiac output in order to compensate for reduced delivery of oxygen to the tissues. Vascular access is often a problem in patients with arteriovenous fistulas.
In patients at risk of major changes of renal perfusion (operations with antici-pated great blood loss, cardiac insufficiency, vascular procedures affecting renal blood flow or ureteral function), we often monitor urine production by collecting urine with the help of an indwelling urinary catheter (Foley). The gold standard of normal function calls for urine flow of around 0.5 ml/kg/h, though renal fail-ure may occur at even higher rates of urine output, and often enough, patients make less urine intra-operatively without sliding into acute renal failure or tubular necrosis. After all, complex physiologic mechanisms enable the kidney to reduce urine production and to conserve blood volume. ADH (antidiuretic hormone, also known as vasopressin), whose job it is to retain fluid in the face of hypovolemia, is secreted during anesthesia even without the normal triggers. Regardless, if fluid deficits cannot account for reduced urine production, and there is no reason to assume reduced kidney blood flow e.g., secondary to hypotension, low car-diac output or because of mechanical interference with renal blood flow, and we confirm the Foley catheter is intact (not kinked or compressed), we begin to worry about acute tubular damage, for which a number of direct or indirect acting toxins (including antibiotics, chemotherapeutic agents and contrast dyes) can be responsible. Acute tubular damage, if not too severe, can undergo spontaneous repair over days to weeks.
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