Renal Function In Heart Failure

About 20% of the cardiac output is normally delivered to the kidneys and virtually all of the renal blood flow (>98%) passes first through the glomeruli. Hydrostatic pressures within glomerular capillaries are regulated by constriction, or dilation, of preglomerular afferent arterioles and postglomerular efferent arterioles and by contraction or relaxation of periglomerular capillary mesangial cells. The hydrostatic pressures, surface area, and epithelial hydraulic permeability of glomerular capillaries determine the fraction of blood plasma perfusing the glomeruli which is filtered.

The filtration fraction (FF) represents the ratio of the rates of glomerular filtration (GFR) to renal plasma flow (RPF):

The magnitude of the FF has a major impact on solute and water reabsorption by the proximal renal tubules. The capillaries which surround the proximal tubules are principally supplied by the postglomerular efferent arterioles (Figs. 4 and 5). Changes in the FF alter the oncotic and hydrostatic pressures in these vessels and these parameters affect renal tubule backleak. Backleak refers to the reverse movement of reabsorbed solute and water across the tubule epithelium to return into the lumen.

Net proximal tubule salt and fluid reabsorption is equal to total reabsorption minus the rate of backleak. Therefore, regulation of backleak magnitude is an important control mechanism. The oncotic and hydrostatic pressures in the peritubule capillaries are major regulators of the backleak rate. A high oncotic pressure and low hydrostatic pressure in these capillaries increases the reabsorption of solute and fluid by reducing backleak. Low oncotic and high hydrostatic pressures have the opposite effect.

The plasma oncotic pressure within the postglomerular arterioles and the peritubular capillaries is a function of the plasma protein concentration and the glomerular filtration fraction. A high FF increases the protein concentration and oncotic pressure in these vessels (Figs. 5 and 6). Usually, a high FF is produced by increased efferent arteriolar resistance which markedly reduces the downstream hydrostatic pressures in the peritubular capillaries.

Cardiac failure due to ventricular dysfunction reduces cardiac output, EABV, and renal perfusion. The low EABV elicits the vasoconstricting neurohormonal cascades described above. They increase afferent and efferent arteriolar resistances and contract glomerular mesangial cells. However, differential sensitivity of the efferent and afferent arterioles to vasoconstricting and vasodilating stimuli causes relatively greater contraction of the efferent vessels. This pattern

Glomerular Capillary

Peritubular Capillary figure 4. The renal microcirculation showing the relationship of the major resistance vessels (the afferent and efferent arterioles) to the glomerular and peritubular capillary beds. (Adapted from Marsh, D. J. (1983). Renal Physiology. Raven Press, New York, p. 62.)

Glomerular Capillary

Peritubular Capillary

Renal Artery

Renal Vein figure 4. The renal microcirculation showing the relationship of the major resistance vessels (the afferent and efferent arterioles) to the glomerular and peritubular capillary beds. (Adapted from Marsh, D. J. (1983). Renal Physiology. Raven Press, New York, p. 62.)

Efferent Arteriole

Bowman's Capsule

Bowman's Capsule

Efferent Arteriole

FIGURE 5. (A) The vascular supply of the glomerulus and proximal tubule. (Adapted from Marsh, D. J. (1983). Renal Physiology. Raven Press, New York, p. 74.) (B) The effect of filtration fraction (FF) on peritubular capillary hydrostatic and oncotic pressures. High effective arterial blood volume (EABV) reduces the FF by causing dilation of the efferent arteriole. Backleak increases (reabsorption falls) because high peritubule hydrostatic (Pc) and low oncotic (7rc) pressures develop. A low EABV increases the FF because of relatively greater constriction of the efferent arteriole compared with the afferent arteriole. Backleak decreases (net reabsorption increases) because hydrostatic pressure (Pc) falls and oncotic pressures (ttc) increase in the peritubule capillaries. GFR, glomerular filtration rate; RPF, renal plasma flow; Pt, interstitial hydrostatic pressure. See text for details.

FIGURE 5. (A) The vascular supply of the glomerulus and proximal tubule. (Adapted from Marsh, D. J. (1983). Renal Physiology. Raven Press, New York, p. 74.) (B) The effect of filtration fraction (FF) on peritubular capillary hydrostatic and oncotic pressures. High effective arterial blood volume (EABV) reduces the FF by causing dilation of the efferent arteriole. Backleak increases (reabsorption falls) because high peritubule hydrostatic (Pc) and low oncotic (7rc) pressures develop. A low EABV increases the FF because of relatively greater constriction of the efferent arteriole compared with the afferent arteriole. Backleak decreases (net reabsorption increases) because hydrostatic pressure (Pc) falls and oncotic pressures (ttc) increase in the peritubule capillaries. GFR, glomerular filtration rate; RPF, renal plasma flow; Pt, interstitial hydrostatic pressure. See text for details.

of sequential resistances will increase intraglomerular hydrostatic pressure and thereby partially counteract the fall in glomerular filtration produced by renal underperfusion. Disproportionate efferent arteriolar constriction also elevates

0 Glomerular 1 0 Peritubular 1 0 Glomerular 1 0 Peritubular 1 Capillary Capillary Capillary Capillary

Dimensionless Distances Along Capillary Segments

FIGURE 6. Representation of the changes in net hydrostatic pressure (AP) and net oncotic pressure (Ait) over the length of an idealized glomerular and idealized peritubular capillary. The pressures expected in normal subjects are shown on the left and in subjects with congestive heart failure on the right. 0 represents the afferent end and 1 the efferent portion of these capillaries. Air increases along the length of the glomerular capillary as the result of ultrafiltration of protein-free fluid and AP decreases slightly. The net driving force for ultrafiltration, AP-A7t, falls mainly because of the increasing Act. When AP = Act, the driving force for filtration is zero and filtration ceases. Hydrostatic pressures in the peritubular capillary are much lower as a result of the resistance to flow through the postglomerular arteriole. AP is reduced below Act so that AP-Act becomes negative and the gradient will favor solute and fluid reabsorption from the proximal tubule. In this example, the patient with heart failure has much higher glomerular capillary hydrostatic pressures. This results from intense efferent postglomerular arteriolar constriction. Note that the increase in Act is much greater than in normals, reflecting the higher filtration fraction characteristic of CHF. Marked efferent arteriolar vasoconstriction also causes a greater reduction in hydrostatic pressures within the peritubular capillaries. The lower hydrostatic and higher oncotic peritubule capillary in patients with heart failure reduces their backleak and increases tubular reabsorption of salt and water. (Adapted from Brenner, B. M. (1978). The kidney in congestive heart failure. In "Sodium and Water Homeostasis" (B. M. Brenner and J. H. Stein, eds.) p. 54, Longman, New York.

the FF, which increases efferent arteriolar and peritubular capillary protein concentration and also reduces hydrostatic pressures in the postglomerular arterioles and peritubular capillaries. The net effect of these changes in pressure on proximal tubule transport is less backleak and therefore increased reabsorption of fluid and solute from the proximal tubule.

Proximal tubule reabsorption of sodium salts is also enhanced by high levels of angiotensin II, catecholamines, and sympathetic nerve activity, which de velop in response to EABV contraction. These neurohormonal mediators activate Na/H antiporters in the apical membrane of the proximal tubule cells which directly increases NaHC03 reabsorption and also indirectly increases NaCl reabsorption by raising the chloride concentration in tubule fluid which increases passive outward diffusion of chloride [19,36].

ADH stimulates sodium reabsorption in the TALH and aldosterone stimulates sodium reabsorption in the distal renal tubules and collecting ducts. Beyond the TALH, ADH also increases water reabsorption. ANP, prostaglandins E2 and F2a, prostacyclin, nitric oxide, bradykinin, and dopamine oppose sodium and water reabsorption, but the net effect of all of these factors favors reabsorption of sodium and water.

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