Clinical Note

Urinary Tract Calculi (Kidney Stones)

The formation of kidney stones is a relatively common and potentially serious renal disorder. Kidney stones are crystalline precipitates of solutes that are present in the urine, and they usually form in the calyces because the urine is the most concentrated there. However, the presence of high concentrations of ions with low solubility products, such as calcium and phosphate, is not the sole reason for the formation of calculi. A normal individual may have even higher average concentrations of such solutes in his or her urine than an individual who is susceptible to kidney stones, and yet never have kidney stones. Although the biochemistry of the processes remains poorly understood, it is thought that endogenous substances are produced by renal epithelia that inhibit crystallization from supersaturated urine. Stone formers may be deficient in these agents. In other cases, such as the formation of oxalate, uric acid, or cystine stones, the underlying cause may be a metabolic disturbance that leads to abnormally high concentrations of these solutes in the urine.

Infection is also a frequent cause of stone formation, especially in women with frequent urinary tract infections (UTIs). Some bacteria, especially Proteus, metabolize urea and increase the urine concentration of ammonium ion, which can result in the formation of a triple phosphate stone, calcium magnesium ammonium phosphate.

Kidney stones can remain in the renal calyxes, or they may be small enough that they produce no symptoms when excreted. However, when larger stones are passed through the ureters to the bladder, extreme acute pain can result that brings most patients to the emergency room. The danger of stone formation is that persistent occlusion of the ureter may lead to deterioration of renal function and eventual destruction of the renal parenchyma. Kidney stones are diagnosed by severe pain, usually extending from the loin to the groin, and accompanied by microscopic hematuria and often crystals in the urine sediment. These crystals can be recognized by appearance or chemically analyzed, and include (in order of most to least frequent) calcium oxalate, calcium oxalate and phosphate, triple phosphate, uric acid, and cystine.

In many cases, kidney stones can be passed without intervention other than pain medication and fluids to increase urine flow. When the stones are too large, extracorporeal shockwave litho-tripsy has proved to be very effective. Shockwaves from, for example, a shock generator or electromagnetic plate generator, are concentrated under x-ray visualization through the skin and tissues on the stone, and are used to break the stone into pieces small enough to be passed in the urine. In the extreme, kidney stones can be too large for even this treatment. For example, "staghorn" calculi, so-called because of a shape that conforms to the shape of the calyxes, usually have to be removed surgically.

Neural Regulation of Micturition

Bladder function is normally regulated by a coordinated switching between two states: a storage phase and an emptying phase. As shown in Fig. 6, during the storage phase the volume of urine in the bladder can increase to 200-300 mL with little rise in pressure due to the remarkably high compliance of the bladder wall. The bladder wall is made up of an extracellular fibrous matrix of collagen and elastin, and the detrusor muscle fibers, which can lengthen more than threefold during bladder filling. Nevertheless, as the radius of the bladder increases, the wall tension increases and activates stretch receptors. The resulting afferent firing is conveyed to the lumbar spinal cord via the hypogastric nerve. When the pressure in the bladder increases above about 10 cm H2O, this afferent input causes reflex firing of para-sympathetic cholinergic efferent fibers that run from the sacral cord via the pelvic nerves to the detrusor muscle. This efferent input causes the muscle to contract, resulting in transient pressure waves and heightened afferent firing that, when conveyed to higher brain centers, gives the sensation of bladder fullness and the urge to urinate.

When the bladder is only partially filled, these pressure waves relax spontaneously, the detrusor muscle ceases to contract, and the pressure falls back to the baseline, as shown by the spikes of pressure (dashed lines) in Fig. 6. In the storage phase, continence is maintained by the influence of descending fibers from

FIGURE 6 Relationship between pressure in the bladder and bladder volume. As filling of the bladder progresses beyond 200 mL, pressure waves begin to appear. These transient contractions of the bladder detrusor muscle are shown by the vertical dotted lines superimposed on the smooth pressure curve. These waves of contraction contribute to the sensation of bladder fullness and increase in frequency and intensity as the bladder continues to fill.

FIGURE 6 Relationship between pressure in the bladder and bladder volume. As filling of the bladder progresses beyond 200 mL, pressure waves begin to appear. These transient contractions of the bladder detrusor muscle are shown by the vertical dotted lines superimposed on the smooth pressure curve. These waves of contraction contribute to the sensation of bladder fullness and increase in frequency and intensity as the bladder continues to fill.

the pons that suppress the firing of parasympathetic efferents to the detrusor muscle while augmenting the output of parasympathetic efferents to the internal urethral sphincter. The pressure of the filling bladder on the pelvic floor also activates reflex arcs that increase the tension of the external sphincter via cholinergic efferents in the pudendal nerves. Contraction of the external sphincter is an important part of the ''guarding reflex" that prevents urinary leakage during the bladder pressure waves. The voluntary augmentation of this reflex and constriction of other muscle groups in the pelvic floor are important for maintaining continence when the bladder is filled and afferent output is high or when other regulatory pathways are defective.

In the absence of any input from higher nervous centers as occurs, for example, after spinal cord transection, the bladder can fill and empty spontaneously, a condition referred to as an automatic bladder. When the bladder reaches a certain volume, the reflex contraction of the detrusor muscle becomes sufficiently strong to force open the internal sphincter and urine distends the bladder neck, initiating a reflex inhibition of the external sphincter. However, voiding that occurs in the absence of input from the pons is sporadic and incomplete because the afferent output from the bladder drives parasympathetic output that constricts both the detrusor muscle and the internal sphincter muscle.

Even in infants and unconscious adults, the emptying phase of the bladder is usually coordinated by input from the micturition center in the pons. When afferent output from the bladder due to distension reaches some threshold, the pontine center reverses its influence on the spinal reflexes by decreasing efferent output to the internal and external sphincters and augmenting the output to the detrusor muscle. However, the decrease in urethral outflow resistance precedes contraction of the detrusor muscle by a few seconds, thereby decreasing the pressure necessary to expel the urine from the bladder. When urine enters the urethra, afferent output acts to maintain detrusor contraction and sphincter relaxation until the bladder has completely emptied and flow ceases.

During development of the nervous system in the toddler, voluntary control of voiding is established by input to the pontine center primarily from the right frontal cerebral cortex. Older children and adults can voluntarily stop voiding with a partially emptied bladder. It has been found that such voluntary stoppage is accomplished by constriction of the internal and external sphincters followed by detrusor muscle relaxation. When voiding is reinitiated voluntarily, detrusor muscle contraction is preceded by relaxation of the sphincters. Thus, the voluntary regulation and timing of urination is exerted by facilitory or inhibitory input to

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