The genitourinary system

Kidney and urinary tract

 

Anatomy

Kidney
The kidneys (Fig. 13) are located in the retroperitoneum and measure approximately 12 cm (height), 6 cm (width) and 4-5 cm (depth). The renal surfaces are usually smooth, but fetallobulation may persist for life. The kidneys move with respiration; the cranio-caudal excursion may be as much as 10 cm. The renal pelvis is normally within the confines of the kidney, but it may also be extrarenal. The size of the pelvis depends in part on the state of hydration. At ultrasonography the parenchyma is echopoor whereas the renal pelvis and the surrounding sinus tissue (mostly fat) is echorich. The arcuate vessels when seen mark the location

	Figure 14. Relations of a transplant kidney. The graft artery may also be anastomosed end to end to the internal iliac artery.
	Figure 15. Enhanced CT of a normal renal transplant in the right iliac fossa.

of the cortico-medullary junction. At CT it is not possible to distinguish between cortex and medulla on unenhanced exposures, whereas on images taken during the first 60 seconds after the contrast medium has reached the kidney there is a clear demarcation between medulla and cortex; during the excretion phase the attenuation of the two areas is again the same. On T2-weighted MRI the renal parenchyma is bright whereas the medulla has lower signal intensity than the cortex on unenhanced T1 weighted images.

The transplanted kidney

The transplanted kidney does not differ from the kidney in situ with one exception: the location. Normally the graft artery is anastomosed end-to-end to the internal iliac artery or end-to-side to the external iliac artery (Fig. 14). The graft vein is anastomosed to the external iliac vein. It is placed in either the right or left iliac fossa just beneath the skin. Often only the upper two-third is covered by peritoneum. Its location just beneath the skin makes the allograft quite suitable for ultrasonographic examination whereas the underlying iliac bones are an obstacle to good urographic visualization. The location just under the skin makes is possible to differentiate between medulla and cortex at ultrasonography; the medulla is slightly less echogenic than the cortex. Its presentation at CT and MRI is similar to that of kidneys in situ (Fig. 15).

Ureter
The ureters course along the psoasmuscles from the renal pelvis, pass over the common iliac vessels, and enter the bladder deep in the bony pelvis dorsolaterally. Visualization of the normal ureter requires in the majority of patients intraluminal contrast.

Bladder
The urinary bladder is best examined when it is full, at which time it fills the anterior part of the pelvis. The top of a filled bladder may extend into the abdomen. Normally the bladder contains between 200 and 500 ml. The bladder wall is thicker in men than women and decreases from 2 cm to 2 mm during filling. In males the bladder is located ventral to the anterior wall of the rectum with the seminal vesicles posterior. The outlet of the bladder (e.g. neck) is separated -from the membranous urethra by the prostate. In females the uterus and vagina are located behind and underneath the bladder and the urethra, whereas the salpinges and the ovaries are located supero-laterally to the empty bladder. The upper one third of the bladder is intraperitoneal.

Urethra
The male urethra (Fig. 16) consists of four parts: pars prostatica in which the ejaculatory ducts empty on either side of the posteriorly located verumontanum; pars membranacea, the shortest part, is the part of the urethra, which transverses the urogenital diaphragm, and is followed by pars bulbosa and pars pendula. Taken together the prostatic and membranous parts are defined as the posterior urethra while the bulbous and pendular portions are known as the anterior urethra.
The female urethra is 2 to 3 cm in length and is located anterior to the vagina. It is surrounded by the internal and the external sphincter.

Physiology

The kidney has several functions including excretion of metabolic pro ducts and foreign substances ("waste products"), regulation of body fluid osmolality and volume, regulation of electrolyte balance, regulation of

Figure 16.Diagram of the male urethra and genitals.

Figure 17. The nephron. The kidney is divided into cortex, medulla and papilla. The blood enters the glomerulus (G) through the afferent arteriole and leaves for the vasa recta (VR) through the efferent arteriole. The filtered component passes through PCT (proximal convoluted tubule), PST (proximal straight tubule), tDL (thin descending limb of the loop of Henle), tAL (thin ascending limb of the loop of Henle), TAL (thick ascending limb of the loop of Henle), DCT (distal convoluted tubule), CCD (cortical collecting duct), MCD (medullary collecting duct), PCD (papillary collecting duet) and out into the calyx.

acid-base balance, and production and secretion of hormones, The kidney forms concentrated urine as a mechanism for relieving the body of waste materials (Fig, 17). This is accomplished by filtration of the blood at the glomerulus, resulting in a protein-free ultrafiltrate of plasma. The kidneys are perfused by one-fourth of the cardiac output, resulting in a renal blood flow of 1,250 ml per min. The glomerular filtrate averages 125 ml per min, which then through reabsorption of water is reduced to the normal urine output of about l ml per min. Approximately two-thirds of the ultrafiltrate volume is reabsorbed by the proximal tubule by a process linked to the active secretion of hydrogen ions and the active reabsorption of sodium, glucose, amino acids, and other solutes ("obligatory" reabsorption). Isotonicity of the fluid in the proximal tubule with the plasma is maintained as the cells of the proximal tubule are freely permeable to water. The counter-current multiplier system of the loop of HenIe then acts to create a high solute concentration in the medulla by active transport of sodium out of the ascending limb of the loop, resulting in a high osmotic gradient between the medulla and the collecting ducts descending through it. The cells in the descending limb have a high permeability for water, whereas the cells in the ascending limb are impermeable to water. The gradient, in conjunction with antidiuretic hormone secreted by the posterior lobe of the pituitary, allows water to diffuse from the collecting ducts into the medulla and results in a concentrated - so called mature - urine. From the collecting ducts the final 15 % of water absorption is achieved (“facultative” reabsorption). Body acid-base balance is maintained by the ability of the kidney to secrete hydrogen by the formation of titrable acid and excretion of ammonium and its ability to reabsorb bicarbonate selectively in exchange for hydrogen. The kidney is also instrumental in erythropoiesis, being the chief site of either the activation or production of erythropoietin. It also produces renin and 1,25-dihydroxyvitamin D3' Parathyroid hormone also acts on the distal tubule to conserve calcium.

After formation by the kidney, urine is delivered to the bladder by the collecting system and ureter. The calyces function independently and asynchronously in transmitting urine to the renal pelvis. While the location of a pacemaker for coordinated peristalsis is not precisely known, it is felt that the first propagating wave begins in response to urine distending the renal pelvis, although in some kidneys the activity can originate in the upper infundibulum. This wave then passes down the ureter in a coordinated fashion via an electrical impulse that passes through connecting smooth muscle cells in the ureteral wall. As one segment of the ureter contracts to propel the urine bolus caudad, another immediately below relaxes to accept the bolus, this sequence repeating until the bolus reaches the bladder into which it is expelled as a jet (Fig. 18). Peristaltic waves are inhibited as pressure in the bladder rises and by ureteral distension.

Figure 18. CT of the bladder demonstrating a jet (arrow) of contrast medium entering the bladder from the ureter (arrowhead).

The micturition reflex are is parasympathetic and derived from the second through fourth sacral cord segments. The external sphincter has a somatic innervation. Receptors in the bladder wall initiate the micturition reflex via afferent fibers in the arc in response to bladder distention. This voiding reflex can then be inhibited or facilitated by activity originating in the cerebral cortex and extending down the spinal cord to the sacral level. During voiding, the bladder detrusor contracts and actively funnels the bladder neck; the sphincters surrounding the membranous urethra then relax, allowing complete expulsion of the bladder content. Between voiding, the intravesical pressure normally remains at a low level because of the reflex arc by the inhibitory effect of the central nervous system as well as the elastic properties of the bladder smooth muscle. Urinary continence is maintained by the internal and intrinsic sphincters combined.

Pathology

Prerenal pathology
The kidneys are commonly affected by disorders of the aorta, renal arteries, and renal veins. Hypertension is a frequent concomitant of renal artery disease - both as a cause and as an effect. Disorders that affect the renal artery and its major branches include atherosclerosis, fibromuscular

	Figure 19.Arteriosclerosis. Arteriogram demonstrating arteriosclerosis in the lower abdominal aorta and a stenosis (arrow) of the left renal artery dose to the aorta.
	Figure 20. Fibromuscular dysplasia. Arteriogram demonstrating several narrowings in the right renal artery of a young woman.

hyperplasia, arteritis, neurofibromatosis, aneurysms, arteriovenous malformations, embolic disease, and thrombosis.

Renal artery stenosis
In atherosclerosis deposition of lipid material on the intimal surface leads to a secondary reaction within the intima. Arteriosclerosis is primarily a problem of the elderly (Fig. 19). Fibromuscular hyperplasia is term that encompasses several' disorders characterized by multiple fibrosing lesions in main and segmental vessels. It typically occurs in young females (Fig. 20). Among the protean manifestations of neurofibromatosis are renal artery stenosis and renovascular hypertension. Two characteristic lesions are seen in patients with neurofibromatosis: 1) stenosis of one or both renal arteries, and 2) unilateral or bilateral aneurysms in the renal artery or its branches. The aorta and renal arteries may be involved in inflammatory processes that result in marked narrowing. One such disorder, Takayasu's arteritis, occurs most frequently in young females.

Hypertension
Hypertension is reported to affect from 7% to 20% of the adult population. An exact prevalence is, however, unknown, mainly because of differences in the study populations and the diagnostic criteria. Among the rare secondary causes of hypertension renovascular disorder is the most frequent. The prevalence depends not only on the source of the study population but also on the definition of hypertension in that population and on its severity. The prevalence of renovascular hypertension in a hypertensive population with diastolic pressure between 90 and 104 mmHg is probably less than 1%, whereas in a population with a diastolic pressure above 125 mmHg the prevalence is reported to about 30%. With such a low prevalence in the largest group of patients, screening of all hypertensive patients for renovascular hypertension with either scintigraphy, intravenous urography, or digital angiography is not advisable owing to the low number of true positives, the cost and the unacceptably high false-positive rate. Before the patient is referred for an imaging examination, some selection must take place. Patients with a diastolic pressure above 110 mm Hg, young patients, those with a sudden rise in blood pressure independent of age, and patients with a poor response to therapy should be examined further. The captopril-enalpril renogram appears to be the most cost-effective procedure for screening those patients. Understanding the effects of angiotensin-converting enzyme inhibition on the kidney distal to a stenosis and appreciating the potential effect of sodium balance or antihypertensive medications are crucial in anticipating the putative changes in the radionuclide studies of the renovascular bed following angiotensin-converting enzyme inhibition (Fig. 21).

 

Figure 21. The effect of angiotensin converting enzyme inhibition on glomerular perfusion and filtration rate in renal artery stenoses.

Normally, renin secretion is stimulated by extracellular fluid volume contraction, reduced pressure in the baroreceptor of the afferent arteriole, diminished sodium delivery to the macula densa, and influence of cathecholamines or prostaglandins. A negative feed back loop also exists such that angiotensin II itself, reduces the production of renin. Renovascular hypertension appears to be dependent on renin secretion from the juxtaglomerular apparatus from the underperfused stenotic kidney and is partially maintained by participation of the contralateral kidney, which demonstrates an abnormal pressure-natriuresis relationship in which a new set-point of sodium homeostasis is attained at a higher level of arterial pressure. Angiotensin-converting enzyme inhibition acts to interrupt the renin-angiotensin-aldosterone system pathway by preventing the conversion of the decapeptide angiotensin I to the octapeptide angiotensin II such that both the vasoconstrictor-hemodynamic and aldosterone-stimulating effects of angiotensin II are blocked. Hence, angiotensin-converting enzyme inhibition acts as a pharmacological probe for investigating the role of angiotensin II in the pathophysiology of renovascular hypertension. In addition, the converting enzyme also serves to degrade vasodilatory prostaglandins and bradykinins, such that enzyme inhibition may result in the enhancement of the tissue levels of these vasodilatory substances. The rationale for captopril- and enalpril-stimulated radionuclide

Figure 22. Captopril scintigraphy. a) Without captopril. b) With captopril. Captopril abolishes the uptake of99mTc DMSA in the right kidney (arrowheads) (PA-image) causing so-called medical nephrectomy. Subsequent angiography showed a stenosis of the right renal artery.

studies is that the angiotensin-converting enzyme inhibitor removes the angiotensin Il -dependent efferent arteriolar resistance, which results in a reduction in transcapillary forces and, therefore, reduces renal function in the kidney distal to stenosis. When renal perfusion is reduced, as seen in patients with renal artery stenosis, the transcapillary pressures that maintain the forces to drive glomerular filtration are sustained by a preferential increase in efferent arteriolar resistance. The increased efferent arteriolar resistance is maintained via angiotensin Il. Captopril and enalpril act to block the formation of angiotensin Il and consequently remove postglomerular forces maintaining filtration; thus, the glomerular filtration rate of the affected kidney decreases. The decrement in individual kidney function may then be noninvasively assessed using conventional radionuclide studies (Fig. 22). The hippuran renogram after captopril or enalpril has been reported to be highly predictive of the blood pressure response to angioplasty or reconstructive surgery with a sensitivity of 96 % and specificity of 95 %. In the 1970's intravenous urography and simple renography were popular for screening a hypertensive patient, but these modalities are no longer used due to poor sensitivity and specificity. Doppler ultrasonography demonstrating hemodynamic changes may be useful in very experienced hands, but as a routine examination the sensitivity and specificity are less than that for captoprilenalpril renography. In some places central vein renin assay is used for the diagnosis of renal artery stenosis. The role of MR angiography is

Figure 23. Wedge-shaped photon deficient area in the left kidney due to an infarct demonstrated during 99mTc DMSA scintigram.

promising, but unsettled regarding screening. A major drawback is the expense. Conventional or digital radiographic angiography is still needed for definitive demonstration of the lesion. However, it should be kept in mind that only after correction of the stenosis is achieved and the blood pressure has become normal, can the diagnosis of renovascular hypertension be made with certainty.

Emboli and thrombi
Emboli or in situ thrombosis can result in acute obstruction of the renal artery or its branches. Failure to restore renal blood flow within a few hours after renal artery occlusion usually results in infarction and loss of function. Intravenous urography and nuclear medicine will show absent function or delayed function if the obstruction is incomplete (Fig. 23). A rim-like nephrogram ("cortical rim-sign") may be seen on enhanced CT or angiography due to collateral circulation. However the cortical rim sign may also be seen in renal vein obstruction, acute tubular necrosis (vasomotor nephropathy) and cortical necrosis. Ultrasonography is often normal in the acute stage; in the ensuing days the size decreases and the kidney becomes more echogenic. Both Doppler ultrasonography and angiography (Fig. 24) will show absence of flow.

Renal artery aneurysm
Renal artery aneurysm may impress the renal pelvis and mimic a parapelvic cyst on intravenous urography and ultrasonography. Color

Figure 24. Multiple infarcts in a transplanted kidney shown at arteriography. Estimated original outline of the graft (---).

Doppler ultrasonography, enhanced CT and angiography will confirm the diagnosis.

Renal arteriovenous fistula
A renal arteriovenous fistula may be congenital (arteriovenous malformation) or acquired. Causes of the latter include rupture of a renal artery aneurysm, blunt trauma, penetrating injuries (e.g. renal biopsy). The typical presenting sign are a bruit, hypertension, hematuria, and signs of high output congestive heart failure. Intravenous urography and ultrasonography are rarely helpful, although pyeloureteral "notching" from collaterals is sometimes noted on the urogram. Dynamic CT, nuclear medical angiography (first passage scintigraphy) and Doppler ultrasonography may be diagnostic. Selective renal arteriography is definitive and demonstrates early venous filling with dilatation of each feeding artery and draining vein. Embolization may be attempted at the time of angiography. MRI will demonstrate signal void on both T1-and T2-weighted spin-echo images due to fIowing blood, but MRA is much more sensitive and graphic, and the vascular images can be projected in any plane as well as in 3D.

Renal vein thrombosis
The patient with acute renal vein thrombosis typically presents with flank pain, hematuria, fever, and proteinuria. Signs of the nephrotic syndrome may appear in the subacute phase. Renal enlargement is detected by many imaging studies. Whether there is opacification at intravenous urography and accumulation of radioactivity on scintigrams depends on the degree of obstruction and the extent of collateral venous circulation, which is usually better in the left kidney. Intravenous urography and direct pyelography may show notching of the ureter by periureteric collaterals. CT may demonstrate a thrombus in the renal vein and/or inferior vena cava and perinephric venous engagement ("cobwebbing"). Ultrasonography will show nephromegaly and decreased echogenicity due to edema. Renal arteriography demonstrates prolongation of arterial and capillary flow, stretched vessels, a decreased nephrogram, and non-visualization of the renal vein. Clot visualization with renal phlebography is superior, but invasive procedures are no longer called for in renal vein thrombosis unless thrombolysis is attempted, which is unusual. At present, MRA is probably the most sensitive, accurate and best test, but lack of availability is a major drawback.

Renal pathology

Anomalies
Renal agenesis is often an incidental radiological finding. A major clue is the characteristic compensatory hypertrophy of the contralateral kidney. If this is lacking one should search for an ectopic kidney. A nonvisualizing kidney on urography caused by renal agenesis can be confirmed by ultrasound or CT. Ultrasonography can evaluate the renal fossae, but CT is more effective in evaluating the lower abdomen for a small ectopic kidney (Fig. 25). Renal anomalies, especially agenesis, are associated with a significant incidence of seminal vesicle anomalies, and in the female, with utero-vaginal anomalies. This should be kept in mind during ultrasonographic examination.

Fusion anomalies of the kidney are often asymptomatic. Intravenous urography will show the abnormal axis of fusion and delineate the ureters

	Figure 25. Normal sized ectopic kidney above os sacrum. The kidney is also rotated.
	Figure 26.