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Chapter: Clinical Anesthesiology: Anesthetic Management: Renal Physiology & Anesthesia

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Renal Blood Flow & Glomerular Filtration

Renal Blood Flow & Glomerular Filtration
The concept of clearance is frequently used in mea-surements of RBF and the glomerular filtration rate (GFR).

RENAL BLOOD FLOW & GLOMERULAR FILTRATION

Clearance

The concept of clearance is frequently used in mea-surements of RBF and the glomerular filtration rate (GFR). The renal clearance of a substance is defined as the volume of blood that is completely cleared of that substance per unit of time (usually, per minute).

Renal Blood Flow

Renal plasma flow (RPF) is most commonly mea-sured by p-aminohippurate (PAH) clearance. PAH at low plasma concentrations can be assumed to be completely cleared from plasma by f ltration and secretion in one passage through the kidneys. Consequently,


where [PAH]U= urinary concentration of PAH and [PAH]P= plasma PAH concentration.

If the hematocrit (measured as a decimal rather than as a percent) is known, then


RPF and RBF are normally about 660 and 1200 mL/min, respectively.

Glomerular Filtration Rate

The GFR, the volume of fluid filtered from the glo-merular capillaries into Bowman’s capsule per unit time, is normally about 20% of RPF. Clearance of inulin, a fructose polysaccharide that is completely filtered but is neither secreted nor reabsorbed, is a good measure of GFR. Normal values for GFR are about 120 ± 25 mL/min in men and 95 ± 20 mL/ min in women. Although less accurate than measur-ing inulin clearance, creatinine clearance is a much more practical measurement of GFR . Creatinine clearance tends to overestimate GFR because some creatinine is normally secreted by renal tubules. Creatinine is a product of phospho-creatine breakdown in muscle. Creatinine clearance is calculated as follows:


where [creatinine]U= creatinine concentration in urine and [creatinine]P= creatinine concentration in plasma.

The ratio of GFR to RPF is called the filtrationfraction (FF) and is normally 20%. GFR is dependenton the relative tones of both the afferent and efferent arterioles (see above). Afferent arteriolar dilation or efferent arteriolar vasoconstriction can increase the and maintain GFR, even when RPF decreases. Afferent arteriolar tone appears to be responsible for maintaining a relatively constant GFR over a wide range of blood pressures.

Control Mechanisms

Regulation of RBF represents a complex interplay between intrinsic autoregulation, tubuloglomerular balance, and hormonal and neuronal influences.

A. Intrinsic Regulation

Autoregulation of RBF normally occurs between mean arterial blood pressures of 80and 180 mm Hg and is principally due to intrinsic myogenic responses of the afferent glomerular arte-rioles to blood pressure changes. Within these lim-its, RBF (and GFR) can be kept relatively constant by afferent arteriolar vasoconstriction or vasodilation. Outside the autoregulation limits, RBF becomes pressure dependent. Glomerular filtration generally ceases when mean systemic arterial pressure is less than 40–50 mm Hg.

B. Tubuloglomerular Balance and Feedback

Tubuloglomerular feedback plays an important rolein maintaining constant GFR over a wide range of perfusion pressures. Increased tubular flow tends to result in reduced GFR; conversely, decreased tubular flow tends to result in increased GFR. Although the mechanism is poorly understood, the macula densa appears to be responsible for tubuloglomerular feed-back by inducing reflex changes in afferent arteriolar tone and possibly glomerular capillary permeability. Angiotensin II probably plays a permissive role in this mechanism. Local release of adenosine, which occurs in response to volume expansion, may inhibit renin release and dilate the afferent arteriole.

C. Hormonal Regulation

Increases in afferent glomerular arteriolar pressure stimulate renin release and formation of angiotensinAngiotensin II causes generalized arterial vaso-constriction and secondarily reduces RBF. Both afferent and efferent glomerular arterioles are con-stricted, but because the efferent arteriole is smaller, its resistance becomes greater than that of the affer-ent arteriole; GFR therefore tends to be relatively preserved. Very high levels of angiotensin II con-strict both arterioles and can markedly decrease GFR. Adrenal catecholamines (epinephrine and norepinephrine) directly and preferentially increase afferent arteriolar tone but usually do not cause marked decreases in GFR because these agents also increase renin release and angiotensin II formation. Relative preservation of GFR during increased aldo-sterone or catecholamine secretion appears at least partly to be mediated by angiotensin-induced pros-taglandin synthesis because it can be blocked by inhibitors of prostaglandin synthesis such as nonste- roidal antiinflammatory drugs (NSAIDs). Renal synthesis of vasodilating prostaglandins

(PGD2, PGE2, and PGI2) is an important protective mechanism during periods of systemic hypotension and renal ischemia.

ANP is released from atrial myocytes in response to atrial distention. ANP is a direct smooth muscle dilator and antagonizes the vasoconstric-tive action of norepinephrine and angiotensin II. It preferentially dilates the afferent glomerular arteri-ole, constricts the efferent glomerular arteriole, and relaxes mesangial cells, effectively increasing GFR . ANP also inhibits both the release of renin and angiotensin-induced secretion of aldo-sterone, and antagonizes the action of aldosterone in the distal and collecting tubules.

D. Neuronal and Paracrine Regulation

Sympathetic outflow from the spinal cord at the level of T4–L1 reaches the kidneys via the celiac and renal plexuses. Sympathetic nerves innervate the juxtaglo-merular apparatus (β1) as well as the renal vasculature (α1). This innervation is largely responsible for stress-induced reductions in RBF (below). α1-Adrenergic receptors enhance sodium reabsorption in proximal tubules, whereas α2 receptors decrease such reabsorp-tion and promote water excretion. Dopamine and fenoldopam dilate afferent and efferent

 

arterioles via D1-receptor activation. Unlike dopa-mine, fenoldopam is selective for the D1-receptor. Fenoldopam and low-dose dopamine infusion can at least partially reverse norepinephrine-induced renal vasoconstriction. Activation of D2-receptors on pre-synaptic postganglionic sympathetic neurons can also vasodilate arterioles through inhibition of nor-epinephrine secretion (negative feedback). Dopamine is formed extraneuronally in the proximal tubule cells from circulating L-3,4-dihydroxyphenylalanine (L-dopa). Dopamine is released into the tubule where it can bind dopaminergic receptors to reduce proxi-mal reabsorption of Na+

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