Renal structure and function

The kidneys are paired retroperitoneal organs found on either side of the spinal cord at the level of the umbilicus. In an adult, each kidney weighs approximately 160 to 175 g and is 10 to 12 cm long. The renal artery provides perfusion to the kidneys. Kidneys receive the highest blood flow per gram of organ weight in the body. Approximately 22% of the cardiac output, or about 1.1 L/min in a normal 70-kg adult, flows through the kidneys. Similar to the heart and brain, the kidney is an active organ (not a passive filter) with high oxygen consumption. For this reason, impaired circulation can cause renal failure or damage.

Figure 19-1 illustrates the kidney and a nephron, which is the functional unit of the kidney, similar to the alveolus in the lung. The nephron is composed of the glomerulus, proximal tubule, loop of Henle, distal tubule, and collecting duct. Almost 75% of the almost 1 million nephrons may need to be compromised before renal disease is apparent. The renal artery branches into the afferent arteriole, which enters and forms the capillary tuft of the glomerulus. This blood flow leaves in the efferent arteriole, which forms the capillary network around the tubules and loop of Henle. This capillary network rejoins to form the renal vein.

The glomerulus is supported and surrounded by an epithelial-lined capsule named Bowman capsule. The glomerular capsule is actually the beginning of the proximal tubule, and filtration of fluid from the blood to the tubule occurs in the glomerulus. This fluid is the glomerular filtrate, which empties into the proximal tubule, goes through the descending and ascending loops of Henle, goes into the distal tubule, and later goes into the collecting duct. Each of the nearly 250 collecting ducts collects urine from about 4000 nephrons. The collecting ducts merge to form larger ducts that eventually empty into the renal papillae and finally empty into the ureter to be stored in the bladder.

The principal function of the nephron is to maintain homeostasis or equilibrium between the internal volume and electrolyte status and the influences of the environment, diet and intake. This mission is accomplished by almost 2 million nephrons through the processes of glomerular ultrafiltration, tubular reabsorption, and tubular secretion. The kidney cannot regenerate new nephrons.

Renal injury, disease, and aging are associated with a gradual decrease in nephron number. The body maintains blood pressure at the expense of extracellular fluid volume (ECFV). Control of ECFV is achieved by adjusting sodium chloride (NaCl) and water (H₂O) excretion.

Acid-base balance

Because a fundamental function of the kidney is the control of buffering substances, especially HCO₃⁻, diuretics may cause acid-base imbalances to occur as they increase water loss. Figure 19-2 illustrates the hydrogen and bicarbonate pathways that regulate pH. The filtration and reabsorption of Na⁺, Cl⁻, and HCO₃⁻, described previously, can be seen in Figure 19-2.

The important exchange for acid-base balance is that of Na⁺. Na⁺ is reabsorbed in the tubules by several means, as follows:

• Reabsorption with chloride to preserve electrical neutrality

• Exchange of Na⁺ for H⁺ or K⁺, also to preserve neutrality

Either low chloride (hypochloremia) or low potassium (hypokalemia) forces Na⁺ to exchange for H⁺, producing a loss of H⁺ and metabolic alkalosis:

< ?xml:namespace prefix = "mml" />HypochloremiaHypokalemia]→Metabolic alkalosis

Finally, preventing HCO₃⁻ in the filtrate from forming CO₂ and water leads to a loss of bicarbonate buffer in the urine and metabolic acidosis.

Diuretic groups

The primary therapeutic goal of diuretic use is to reduce the ECFV. NaCl output must exceed NaCl intake. Diuretics primarily prevent Na⁺ entry into the tubule cell. Diuretics need to access the tubule fluid to exert their action. Once in the tubule fluid, the nephron site at which the diuretic acts determines its effect. The site of action also determines which electrolytes, other than Na⁺, are affected. All diuretics except spironolactone exert their effects from the luminal side of the nephron.¹

Five major groups of diuretics are described in this chapter. Figure 19-3 illustrates the site of action, and Table 19-1 summarizes the mechanism of action and the indications for use of each of the five major groups of diuretics.^2–5

Because hypertension affects one-third of adults in the United States,⁶ the diuretics of most immediate relevance to respiratory and critical care clinicians are those used to treat hypertension and congestive heart failure (CHF). There is evidence that diuretic-based therapy is effective in reducing morbidity and mortality among elderly hypertensive patients.^7–10 Diuretics are also used to aid in the treatment of other conditions associated with fluid retention, such as corticosteroid therapy and certain renal and liver diseases.