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2371 Nephrolithiasis CHAPTER 318

Typically, helical CT reveals a ureteral stone or evidence of recent

passage (e.g., perinephric stranding or hydronephrosis), whereas

a plain abdominal radiograph (kidney/ureter/bladder [KUB]) can

miss a stone in the ureter or kidney, even if it is radiopaque, and

does not provide information on obstruction. Abdominal ultrasound offers the advantage of avoiding radiation and provides

information on hydronephrosis, but it is not as sensitive as CT and

images only the kidney and possibly the proximal segment of the

ureter; thus, most ureteral stones are not detectable by ultrasound.

Many patients who experience their first episode of colic seek

emergent medical care. Randomized trials have demonstrated that

parenterally administered nonsteroidal anti-inflammatory drugs

(such as ketorolac) are just as effective as opioids in relieving symptoms and have fewer side effects. Excessive fluid administration

has not been shown to be beneficial; therefore, the goal should be

to maintain euvolemia. If the pain can be adequately controlled

and the patient is able to take fluids orally, hospitalization can be

avoided. Use of an alpha blocker may increase the rate of spontaneous stone passage.

Urologic intervention should be postponed unless there is evidence of UTI, a low probability of spontaneous stone passage (e.g.,

a stone measuring ≥6 mm or an anatomic abnormality), or intractable pain. A ureteral stent may be placed cystoscopically, but this

procedure typically requires general anesthesia, and the stent can be

quite uncomfortable, may cause gross hematuria, and may increase

the risk of UTI.

If an intervention is indicated, the selection of the most appropriate intervention is determined by the size, location, and composition of the stone; the urinary tract anatomy; and the experience

of the urologist. Extracorporeal shockwave lithotripsy (ESWL),

the least invasive option, uses shockwaves generated outside the

body to fragment the stone, but is being used less frequently. An

endourologic approach, now more frequently used than ESWL,

can remove a stone by basket extraction or laser fragmentation. For

large upper-tract stones, percutaneous nephrostolithotomy has the

highest likelihood of rendering the patient stone-free. Advances

in urologic approaches and instruments have nearly eliminated

the need for open surgical procedures such as ureterolithotomy or

pyelolithotomy.

EVALUATION FOR STONE PREVENTION

More than half of first-time stone formers will have a recurrence

within 10 years. A careful evaluation is indicated to identify predisposing factors, which can then be modified to reduce the risk of

new stone formation. It is appropriate to proceed with an evaluation

even after the first stone if the patient is interested because recurrences are common and are usually preventable with inexpensive

lifestyle modifications or other treatments.

HISTORY

A detailed history, obtained from the patient and from a thorough

review of medical records, should include the number and frequency of episodes (distinguishing stone passage from stone formation) and previous imaging studies, interventions, evaluations,

and treatments. Inquiries about the patient’s medical history should

cover UTIs, gastric bypass surgery and other malabsorptive conditions, gout, hypertension, and diabetes mellitus. A family history of

stone disease may reveal a genetic predisposition. A complete list

of current prescription and over-the-counter medications as well as

vitamin and mineral supplements is essential. The review of systems

should focus on identifying possible etiologic factors related to

low urine volume (e.g., high insensible losses) and gastrointestinal

malabsorption as well as on ascertaining how frequently the patient

voids during the day and overnight.

A large body of compelling evidence has demonstrated the

important role of diet in stone disease. Thus, the dietary history

should encompass information on usual dietary habits (meals and

snacks), calcium intake, consumption of high-oxalate foods (spinach, rhubarb, potatoes), and fluid intake (including amount of specific beverages typically consumed). Amount and frequency of use

of vitamin and mineral supplements should be carefully assessed.

PHYSICAL EXAMINATION

The physical examination should assess weight, blood pressure,

costovertebral angle tenderness, and lower-extremity edema as well

as signs of other systemic conditions such as primary hyperparathyroidism and gout.

LABORATORY EVALUATION

If not recently measured, the following serum levels should be

determined: electrolytes (to uncover hypokalemia or renal tubular

acidosis), creatinine, calcium, and uric acid. The PTH level should

be measured if indicated by high-normal or elevated serum and

urine calcium concentrations. 25-Hydroxy vitamin D should be

measured in concert with PTH to investigate the possible role

of secondarily elevated PTH levels in the setting of vitamin D

insufficiency.

The urinalysis, including examination of the sediment, can provide useful information. In individuals with asymptomatic residual

renal stones, red and white blood cells are frequently present in

urine. If there is concern about the possibility of an infection, a

urine culture should be performed. The sediment may also reveal

crystals (Fig. 318-1), which may help identify the stone type and

also provide prognostic information, as crystalluria is a strong risk

factor for new stone formation.

The results from 24-h urine collections serve as the cornerstone on which therapeutic recommendations are based. Recommendations on lifestyle modification should be deferred until

urine collection is complete. As a baseline assessment, patients

should collect at least two 24-h urine samples while consuming

their usual diet and usual volume of fluid. The following factors

should be measured: total volume, calcium, oxalate, citrate, uric

acid, sodium, potassium, phosphorus, pH, and creatinine. When

available, the calculated supersaturation is also informative. There

is substantial day-to-day variability in the 24-h excretion of many

relevant factors; therefore, obtaining values from two collections

is important before committing a patient to long-term lifestyle

changes or medication. The interpretation of the 24-h urine results

FIGURE 318-2 Coronal noncontrast CT image from a patient who presented with

left-sided renal colic. An obstructing calculus, present in the distal left ureter

at the level of S1, measures 10 mm in maximal dimension. There is severe left

hydroureteronephrosis and associated left perinephric fat stranding. In addition,

there is a nonobstructing 6-mm left renal calculus in the interpolar region. (Image

courtesy of Dr. Stuart Silverman, Brigham and Women’s Hospital.)

2372 PART 9 Disorders of the Kidney and Urinary Tract

should take into account that the collections are usually performed

on a weekend day when the patient is staying at home; an individual’s habits may differ dramatically (beneficially or detrimentally)

at work or outside the home. Specialized testing, such as calcium

loading or restriction, is not recommended as it does not influence

clinical recommendations.

Stone composition analysis is essential if a stone or fragment is

available; patients should be encouraged to retrieve passed stones.

The stone type cannot be determined with certainty from 24-h

urine results, but pure uric acid stones can be identified by low

Hounsfield units on CT.

IMAGING

The “gold standard” diagnostic test is helical CT without contrast.

If not already performed during an acute episode, a low-dose

renal-limited CT should be considered to definitively establish the

baseline stone burden. A suboptimal imaging study may not detect

a residual stone that, if subsequently passed, would be mistaken for

a new stone. In this instance, the preventive medical regimen might

be unnecessarily changed as the result of a preexisting stone.

Recommendations for follow-up imaging should be tailored to

the individual patient. While CT provides the best information,

the radiation dose is higher than from other modalities; therefore,

CT should be performed only if the results will lead to a change in

clinical recommendations. Although less sensitive, renal ultrasound

is typically used to minimize radiation exposure, with recognition

of the limitations.

PREVENTION OF NEW STONE FORMATION

Recommendations for preventing stone formation depend on the

stone type and the results of metabolic evaluation. After remediable

secondary causes of stone formation (e.g., primary hyperparathyroidism) are excluded, the focus should turn to modification of the

urine composition to reduce the risk of new stone formation. The

urinary constituents and calculated urine supersaturation are continuous variables, and the associated risk is continuous; thus, there

are no definitive thresholds. Dichotomization into “normal” and

“abnormal” can be misleading and should be avoided.

For all stone types, consistently diluted urine reduces the likelihood of crystal formation. The urine volume should be at least

2 L/d. Because of differences in insensible fluid losses and fluid

intake from food sources, the required total fluid intake will vary

from person to person. Rather than specify how much to drink, it

is more helpful to educate patients about how much more they need

to drink in light of their 24-h urine volume. For example, if the daily

urine volume is 1.5 L, then the patient should be advised to drink

at least 0.5 L more per day in order to increase the urine volume to

the goal of 2 L/d.

■ RECOMMENDATIONS FOR SPECIFIC STONE TYPES

Calcium Oxalate Risk factors for calcium oxalate stones include

higher urine calcium, higher urine oxalate, and lower urine citrate.

This stone type is insensitive to pH in the physiologic range.

Individuals with higher urine calcium excretion tend to absorb a

higher percentage of ingested calcium. Nevertheless, dietary calcium

restriction is not beneficial and, in fact, is likely to be harmful (see

“Dietary Risk Factors,” above). In a randomized trial in men with high

urine calcium and recurrent calcium oxalate stones, a diet containing

1200 mg of calcium and a low intake of sodium and animal protein

significantly reduced subsequent stone formation compared with a

low-calcium diet (400 mg/d). Excessive calcium intake (>1200 mg/d)

should be avoided.

A thiazide diuretic, in doses higher than those used to treat hypertension, can substantially lower urine calcium excretion. Several randomized controlled trials have demonstrated that thiazide diuretics,

most commonly chlorthalidone, can reduce calcium oxalate stone

recurrence by ~50%. When a thiazide is prescribed, dietary sodium

restriction is essential to obtain the desired reduction in urinary

calcium excretion and minimize urinary potassium losses. While bisphosphonates may reduce urine calcium excretion in some individuals,

there are only observational data to suggest whether this class of medication can reduce stone formation; therefore, bisphosphonates cannot

be recommended solely for stone prevention at present, but they can be

used to treat those individuals with low bone density.

A reduction in urine oxalate will in turn reduce the supersaturation

of calcium oxalate. In patients with the common form of nephrolithiasis, avoiding high-dose vitamin C supplements is the only known

strategy that reduces endogenous oxalate production.

Oxalate is a metabolic end product; therefore, any dietary oxalate

that is absorbed will be excreted in the urine. Reducing absorption

of exogenous oxalate involves two approaches. First, the avoidance

of foods that contain high amounts of oxalate, such as spinach, rhubarb, almonds, and potatoes, is prudent. However, extreme oxalate

restriction has not been demonstrated to reduce stone recurrence

and could be harmful to overall health, given other health benefits

of many foods that are erroneously considered to be high in oxalate.

Controversy exists regarding the most clinically relevant measure of the

oxalate content of foods (e.g., bioavailability). Second, the absorption

of oxalate is reduced by higher calcium intake; therefore, individuals

with higher-than-desired urinary oxalate should be counseled to consume adequate calcium. Oxalate absorption can be influenced by the

intestinal microbiota, depending on the presence of oxalate-degrading

bacteria. Currently, however, there are no available therapies to alter

the microbiota that beneficially affect urinary oxalate excretion over

the long term.

Citrate is a natural inhibitor of calcium oxalate and calcium phosphate stones. Higher-level consumption of foods rich in alkali (i.e.,

fruits and vegetables) can increase urine citrate. For patients with

lower urine citrate in whom dietary modification does not adequately

increase urine citrate, the addition of supplemental alkali (typically

potassium citrate or bicarbonate) will lead to an increase in urinary

citrate excretion. Sodium salts, such as sodium bicarbonate, while

successful in raising urine citrate, are typically avoided due to the

adverse effects of sodium on urine calcium excretion. Urine pH in the

physiologic range does not influence calcium oxalate stone formation.

Past reports suggested that higher levels of urine uric acid may

increase the risk of calcium oxalate stones, but more recent studies do

not support this association. However, allopurinol reduced stone recurrence in one randomized controlled trial in patients with calcium oxalate

stones and high urine uric acid levels. The lack of association between

urine uric acid level and calcium oxalate stones suggests that a different

mechanism underlies the observed beneficial effect of allopurinol.

Additional dietary modifications may be beneficial in reducing

stone recurrence. Restriction of nondairy animal protein (e.g., meat,

chicken, seafood) is a reasonable approach and may result in higher

excretion of citrate and lower excretion of calcium. In addition, reducing sodium intake to <2.5 g/d may decrease urinary excretion of calcium.

Sucrose and fructose intake should be minimized.

For adherence to a dietary pattern that is more manageable for

patients than manipulating individual nutrients, the DASH (Dietary

Approaches to Stop Hypertension) diet provides an appropriate and

readily available option. Randomized trials have conclusively shown

the DASH diet to reduce blood pressure. At present, only data from

observational studies are available, but these demonstrate a strong and

consistent inverse association between the DASH diet and risk of stone

formation.

Calcium Phosphate Calcium phosphate stones share risk factors

with calcium oxalate stones, including higher concentrations of urine

calcium and lower concentrations of urine citrate, but additional factors deserve attention. Higher urine phosphate levels and higher urine

pH (typically ≥6.5) are associated with an increased likelihood of calcium phosphate stone formation. Calcium phosphate stones are more

common in patients with distal renal tubular acidosis and primary

hyperparathyroidism.

There are no randomized trials on which to base preventive recommendations for calcium phosphate stone formers, so the interventions

2373 Urinary Tract Obstruction CHAPTER 319

are focused on modification of the recognized risk factors. Thiazide

diuretics (with sodium restriction) may be used to reduce urine calcium, as described above for calcium oxalate stones. In patients with

low urine citrate levels, alkali supplements (e.g., potassium citrate or

bicarbonate) may be used to increase urine citrate. However, the urine

pH of these patients should be monitored initially because supplemental alkali can raise urine pH, thereby potentially increasing the

risk of stone formation. Because these patients tend to have a urinary

acidification defect, reducing the urine pH is not an option. Reduction

of dietary phosphate may be beneficial by reducing urine phosphate

excretion.

Uric Acid The two main risk factors for uric acid stones are persistently low urine pH and higher uric acid excretion. Urine pH is the

predominant influence on uric acid solubility; therefore, the mainstay

of prevention of uric acid stone formation entails increasing urine

pH. Alkalinizing the urine can be readily achieved by increasing the

intake of foods rich in alkali (e.g., fruits and vegetables) and reducing

the intake of foods that produce acid (e.g., animal flesh). If necessary,

supplementation with bicarbonate or citrate salts (preferably potassium-based) can be used to reach the recommended pH goal of 6.5

throughout the day and night.

Urine uric acid excretion is determined by uric acid generation. Uric

acid is the end product of purine metabolism; thus, reduced consumption of purine-containing foods can lower urine uric acid excretion. It

is noteworthy that the serum uric acid level is dependent on the fractional excretion of uric acid and therefore does not provide information on urine uric acid excretion. For example, an individual with high

uric acid generation and concurrent high fractional excretion of uric

acid will have high urine uric acid excretion with a normal (or even

low) serum uric acid level. If alkalinization of the urine alone is not

successful and if dietary modifications do not reduce urine uric acid

sufficiently, then the use of a xanthine oxidase inhibitor, such as allopurinol or febuxostat, can reduce urine uric acid excretion by 40–50%.

Cystine Cystine excretion is not easily modified. Long-term dietary

cystine restriction is not feasible and is unlikely to be successful; thus,

the focus for cystine stone prevention is on increasing cystine solubility. This goal may be achieved by treatment with medication that

covalently binds to cystine (tiopronin or penicillamine) and a medication that raises urine pH. Tiopronin is the preferred choice due to its

better adverse event profile. The preferred alkalinizing agent to achieve

a urine pH of 7.5 is potassium citrate or bicarbonate as sodium salts

may increase cystine excretion. As with all stone types, and especially

in patients with cystinuria, maintaining a high urine volume is an

essential component of the preventive regimen.

Struvite Struvite stones, also known as infection stones or triplephosphate stones, form only when the upper urinary tract is infected

with urease-producing bacteria such as Proteus mirabilis, Klebsiella

pneumoniae, or Providencia species. Urease produced by these bacteria

hydrolyzes urea and may elevate the urine pH to a supraphysiologic

level (>8.0). Struvite stones may grow quickly and fill the renal pelvis

(staghorn calculi).

Struvite stones require complete removal by a urologist. New stone

formation can be avoided by the prevention of UTIs. In patients with

recurrent upper UTIs (e.g., some individuals with surgically altered

urinary drainage or spinal cord injury), the urease inhibitor acetohydroxamic acid can be considered; however, this agent should be used

with caution because of potential side effects.

■ LONG-TERM FOLLOW-UP

In general, the preventive regimens described above do not cure the

underlying pathophysiologic process. Thus, these recommendations

typically need to be followed for the patient’s lifetime, and it is essential

to tailor recommendations in a way that is acceptable to the patient.

Because the memory of the acute stone event fades and patients often

return to old habits (e.g., insufficient fluid intake), long-term follow-up,

including repeat 24-h urine collections typically annually, is important

to ensure that the preventive regimen has been implemented and has

resulted in the desired reduction in the risk of new stone formation.

Follow-up imaging should be planned thoughtfully. Many patients

with recurrent episodes of renal colic that lead to emergency room

visits often undergo repeat CT studies. While CT does provide the best

information, the radiation dose is substantially higher than that with

plain abdominal radiography (KUB). Small stones may be missed by

KUB, and ultrasound has a limited ability to determine the size and

number of stones. Minimizing radiation exposure should be a goal of

the long-term follow-up plan and must be balanced against the gain in

diagnostic information.

■ FURTHER READING

Pearle MS et al: Medical management of kidney stones: AUA guideline. J Urol 192:316, 2014.

Prochaska ML et al: Insights into nephrolithiasis from the Nurses’

Health Studies. Am J Public Health 106:1638, 2016.

Obstruction to the flow of urine, with attendant stasis and elevation

in urinary tract pressure, impairs renal and urinary conduit functions

and is a common cause of acute and chronic kidney disease (obstructive nephropathy). Early recognition and prompt treatment of urinary

tract obstruction (UTO) can prevent or reverse devastating effects on

kidney structure and function, and decrease susceptibility to hypertension, infection, and stone formation. Chronic obstruction may lead to

permanent loss of renal mass (renal atrophy) and excretory capability.

Because obstructive disease may be secondary to serious underlying

inflammatory, vascular, or malignant disease, familiarity with clinical

findings, appropriate diagnostic testing, and therapeutic approach is of

great importance to the clinician.

■ ETIOLOGY

Obstruction to urine flow can result from intrinsic or extrinsic mechanical

blockade as well as from functional defects not associated with fixed

occlusion of the urinary drainage system. Mechanical obstruction can

occur at any level of the urinary tract, from within the renal tubules,

or the renal calyces to the external urethral meatus (obstructive uropathy). Normal points of narrowing, such as the ureteropelvic and ureterovesical junctions, bladder neck, and urethral meatus, are common

sites of obstruction. When lower UTO is above the level of the bladder,

unilateral dilatation of the ureter (hydroureter) and renal pyelocalyceal

system (hydronephrosis) occurs; lesions at or below the level of the

bladder cause bilateral involvement.

Common forms of obstruction are listed in Table 319-1. Childhood

causes include congenital malformations, such as narrowing of the ureteropelvic junction (UPJ) and abnormal insertion of the ureter into the

bladder, the most common cause. Vesicoureteral reflux in the absence

of urinary tract infection or bladder neck obstruction often resolves

with age. Reinsertion of the ureter into the bladder is indicated if reflux

is severe and unlikely to improve spontaneously, if renal function deteriorates, or if urinary tract infections recur despite chronic antimicrobial therapy. Vesicoureteral reflux may cause prenatal hydronephrosis

and, if severe, can lead to recurrent urinary infections, hypertension,

and renal scarring in childhood. Posterior urethral valves are the most

common cause of bilateral hydronephrosis in boys. In adults, UTO

is due mainly to acquired defects. Pelvic tumors, calculi, and urethral

stricture predominate. Ligation of, or injury to, the ureter during pelvic or colonic surgery can lead to hydronephrosis which, if unilateral,

may remain undetected. Obstructive uropathy may also result from

extrinsic neoplastic (carcinoma of cervix or colon) or inflammatory

disorders. Lymphomas, particularly follicular, and pelvic or colonic

neoplasms with retroperitoneal involvement are causes of ureteral

319 Urinary Tract Obstruction

Julian L. Seifter

2374 PART 9 Disorders of the Kidney and Urinary Tract

may be useful in evaluating incomplete emptying and bladder neck and

urethral pathology.

■ CLINICAL FEATURES AND PATHOPHYSIOLOGY

The pathophysiology and clinical features of UTO are summarized in

Table 319-2. Flank pain, the symptom that most commonly leads to

medical attention, is due to distention of the collecting system or renal

capsule. Pain severity is influenced more by the rate at which distention

develops than by the degree of distention. Acute supravesical obstruction, as from a stone lodged in a ureter (Chap. 318), is associated with

excruciating, sometimes intermittent, pain, known as renal colic. This

pain often radiates to the lower abdomen, testes, or labia. By contrast,

more insidious causes of obstruction, such as chronic narrowing of the

UPJ, may produce little or no pain and yet result in total destruction

of the affected kidney. Flank pain that occurs only with micturition is

pathognomonic of vesicoureteral reflux.

Obstruction of urine flow results in an increase in hydrostatic pressures proximal to the site of obstruction. It is this buildup of pressure

that leads to the accompanying pain, the distention of the collecting

system in the kidney, and elevated intratubular pressures that initiate

tubular dysfunction. In the first days of obstruction, the dilatation

of the poorly compliant collecting system may be minimal. As the

increased hydrostatic pressure is expressed in the urinary space of the

glomeruli, further filtration decreases or stops completely.

Azotemia develops when overall excretory function is impaired,

often in the setting of bladder outlet obstruction, bilateral renal pelvic

or ureteric obstruction, or unilateral disease in a patient with a solitary

functioning kidney. Complete bilateral obstruction should be suspected when acute renal failure is accompanied by anuria. Any patient

with renal failure otherwise unexplained, or with a history of nephrolithiasis, hematuria, diabetes mellitus, prostatic enlargement, pelvic

surgery, trauma, or tumor should be evaluated for UTO.

In the acute setting, partial, bilateral obstruction may mimic prerenal azotemia with a high blood urea nitrogen-to-creatinine ratio,

concentrated urine, and sodium retention. Renal vascular resistance

may be increased. However, with more prolonged obstruction, symptoms of polyuria and nocturia commonly accompany partial UTO and

result from loss of medullary hypertonicity with diminished renal concentrating ability. Failure to produce urine free of salt (natriuresis) is

due to downregulation of salt reabsorption in the proximal tubule and

TABLE 319-1 Common Mechanical Causes of Urinary Tract

Obstruction

URETER BLADDER OUTLET URETHRA

Congenital

Ureteropelvic junction

narrowing or obstruction

Ureterovesical junction

narrowing or obstruction and

reflux

Ureterocele

Retrocaval ureter

Bladder neck obstruction

Ureterocele

Posterior urethral

valves

Anterior urethral

valves

Stricture

Meatal stenosis

Phimosis

Acquired Intrinsic Defects

Calculi

Inflammation

Infection

Trauma

Sloughed papillae

Tumor

Blood clots

Benign prostatic

hyperplasia

Cancer of prostate

Cancer of bladder

Calculi

Diabetic neuropathy

Spinal cord disease

Anticholinergic drugs

and α-adrenergic

agonists

Stricture

Tumor

Calculi

Trauma

Phimosis

Acquired Extrinsic Defects

Pregnant uterus

Retroperitoneal fibrosis

Aortic aneurysm

Uterine leiomyomata

Carcinoma of uterus, prostate,

bladder, colon, rectum

Lymphoma

Pelvic inflammatory disease,

endometriosis

Accidental surgical ligation

Carcinoma of cervix,

colon

Trauma

obstruction. As many as 50% of men aged >40 years may have lower

urinary tract symptoms associated with benign prostatic hypertrophy,

but these symptoms may occur without bladder outlet obstruction.

Functional impairment of urine flow occurs when voiding is altered

by abnormal pontine or sacral centers of micturition control. It

may be asymptomatic or associated with lower urinary tract symptoms such as frequency, urgency, and postmicturition incontinence,

nocturia, straining to void, slow stream, hesitancy, or a feeling of

incomplete emptying. A history should be sought for trauma, back

injury, surgery, diabetes, neurologic or psychiatric conditions, and

medications. Causes include neurogenic bladder, often with adynamic ureter, and vesicoureteral reflux. Reflux in children may result

in severe unilateral or bilateral hydroureter and hydronephrosis.

Overflow urinary incontinence combined with sudden-onset fecal

incontinence, severe lower back pain, and saddle anesthesia, requires

emergency evaluation for possible cauda equina syndrome. Urinary

retention may be the consequence of α-adrenergic and anticholinergic agents, as well as opiates. Hydronephrosis in pregnancy is due to

relaxational effects of progesterone on smooth muscle of the renal

pelvis, as well as ureteral compression by the enlarged uterus, more

often on the right side.

Diagnostic tools to identify anatomic obstruction include urinary

flow measurements and a postvoid residual. Bladder volume may

be readily assessed by bedside ultrasound. Cystourethroscopy and

urodynamic studies may be reserved for the symptomatic patient to

assess the filling phase (cystometry), pressure-volume relationship of

the bladder, bladder compliance, and capacity. Pressure-flow analysis

evaluates bladder contractility and bladder outlet resistance during

voiding. Bladder obstruction is characterized by high pressures in

women, whereas in men, a diagnosis of bladder outlet obstruction is

based on flow rate and voiding pressures. A voiding cystourethrogram

TABLE 319-2 Pathophysiology of Bilateral Ureteral Obstruction

HEMODYNAMIC

EFFECTS TUBULE EFFECTS CLINICAL FEATURES

Acute

↑ Renal blood flow

↓ GFR

↓ Medullary blood flow

↑ Vasodilator

prostaglandins, nitric

oxide

↑ Ureteral and tubule

pressures

↑ Reabsorption of Na+

urea, water

Pain (capsule distention)

Azotemia, oliguria, or

anuria

Chronic

↓ Renal blood flow

↓↓ GFR

↑ Vasoconstrictor

prostaglandins

↑ Renin-angiotensin

production

↓ Medullary osmolarity

↓ Concentrating ability

Structural damage;

parenchymal atrophy

↓ Transport functions for

Na+

, K+

, H+

Azotemia

Hypertension

AVP-insensitive polyuria

Natriuresis

Hyperkalemic,

hyperchloremic acidosis

Release of Obstruction

Slow ↑ in GFR (variable) ↓ Tubule pressure

↑ Solute load per

nephron (urea, NaCl)

Natriuretic factors

present

Postobstructive diuresis

Potential for volume

depletion and electrolyte

imbalance due to losses

of Na+

, K+

, PO4

2–, Mg2+,

and water

Abbreviations: AVP, arginine vasopressin; GFR, glomerular filtration rate.

2375 Urinary Tract Obstruction CHAPTER 319

of transport proteins including the Na+, K+ adenosine triphosphatase

(ATPase), Na:K:2Cl cotransporter (NKCC2) in the thick ascending

limb, and the epithelial Na+ channel (ENaC) in collecting duct cells.

In addition to direct effects on renal transport mechanisms, increased

prostaglandin E2

(PGE2

) (due to induction of cyclooxygenase-2 [COX-2]),

angiotensin II (with its downregulation of Na+ transporters), and atrial

or B-type natriuretic peptides (ANP or BNP) due to volume expansion

in the azotemic patient contribute to decreased salt reabsorption along

the nephron. Nitric oxide synthases (NOS) in ureteral smooth muscle

and urothelial tissues have been found to oppose the high ureteral

pressure in unilateral obstruction.

Dysregulation of aquaporin-2 water channels in the collecting duct

contributes to the polyuria. The defect usually does not improve with

administration of vasopressin and is therefore a form of acquired nephrogenic diabetes insipidus.

Wide fluctuations in urine output in a patient with azotemia

should always raise the possibility of intermittent or partial UTO.

If fluid intake is inadequate, severe dehydration and hypernatremia

may develop. However, as with other causes of poor renal function, excesses of salt and water intake may result in edema and

hyponatremia.

Partial bilateral UTO often results in acquired distal renal tubular

acidosis, hyperkalemia, and renal salt wasting. The H+-ATPase, situated on the apical membrane of the intercalated cells of the collecting

duct, is critical for distal H+ secretion. The trafficking of intracellular

H+ pumps from the cytoplasm to the cell membrane is disrupted in

UTO. The decreased function of the ENaC, in the apical membrane of

neighboring collecting duct principal cells, contributes to decreased

Na+ reabsorption (salt-wasting), and, therefore, decreased K+ secretion via K+ channels. Ammonium (NH4

+) excretion important to the

elimination of H+ is impaired. These defects in tubule function are

often accompanied by renal tubulointerstitial damage. Azotemia with

hyperkalemia and metabolic acidosis should prompt consideration

of UTO.

The renal interstitium becomes edematous and infiltrated with

mononuclear inflammatory cells early in UTO. Later, interstitial fibrosis and atrophy of the papillae and medulla occur and precede these

processes in the cortex. The increase in angiotensin II noted in UTO

contributes to the inflammatory response and fibroblast accumulation

through mechanisms involving profibrotic cytokines. With time, this

process leads to chronic kidney damage.

UTO must always be considered in patients with urinary tract

infections or urolithiasis. Urinary stasis encourages the growth of

organisms. Urea-splitting bacteria are associated with magnesium

ammonium phosphate (struvite) calculi that may take on a staghorn

appearance. Hypertension is frequent in acute and subacute unilateral

obstruction and is usually a consequence of increased release of renin

by the involved kidney. Chronic kidney disease from bilateral UTO,

often associated with extracellular volume expansion, may result in

significant hypertension. Erythrocytosis, an infrequent complication

of obstructive uropathy, is secondary to increased erythropoietin

production.

■ DIAGNOSIS

A history of difficulty in voiding, pain, infection, or change in urinary

volume is common. Evidence for distention of the kidney or urinary

bladder can often be obtained by palpation and percussion of the abdomen. A careful rectal and genital examination may reveal enlargement

or nodularity of the prostate, abnormal rectal sphincter tone, or a rectal

or pelvic mass.

Urinalysis may reveal hematuria, pyuria, and bacteriuria. The urine

sediment is often normal, even when obstruction leads to marked

azotemia and extensive structural damage. An abdominal scout film,

although insensitive, may detect nephrocalcinosis or a radiopaque

stone. As indicated in Fig. 319-1, if UTO is suspected, a bladder

catheter should be inserted. Abdominal ultrasonography should be

performed to evaluate renal and bladder size, as well as pyelocalyceal

contour. Ultrasonography is ~90% specific and sensitive for detection

of hydronephrosis. False-positive results are associated with diuresis,

renal cysts, or the presence of an extrarenal pelvis, a normal congenital variant. Congenital UPJ obstruction may be mistaken for renal

cystic disease. Hydronephrosis may be absent on ultrasound when

obstruction is <48 h in duration or associated with volume contraction,

staghorn calculi, retroperitoneal fibrosis, or infiltrative renal disease.

Duplex Doppler ultrasonography may detect an increased resistive

index in urinary obstruction.

Urologic

evaluation

Unexplained renal failure

Insert bladder catheter

Do CT scan to identify

site and etiology of

obstruction

Negative

Diuresis

Obstruction below

bladder neck

High suspicion Low suspicion

Hydronephrosis

No diuresis: do

ultrasound

Retrograde urography

and ureteral stent

considered

Antegrade urography

and percutaneous

nephrostomy considered

No further workup

for obstruction

hydronephrosis

Positive or negative

but still high suspicion

FIGURE 319-1 Diagnostic approach for urinary tract obstruction in unexplained renal failure. CT, computed tomography.

2376 PART 9 Disorders of the Kidney and Urinary Tract

Recent advances in technology have led to alternatives and have

replaced the once standard intravenous urogram in the further evaluation of UTO. The high-resolution multidetector row computed

tomography (CT) scan in particular has the advantages of visualizing

the retroperitoneum, as well as identifying both intrinsic and extrinsic sites of obstruction. Noncontrast CT scans improve visualization

of the urinary tract in the patient with renal impairment and are safer

for patients at risk for contrast nephropathy. Magnetic resonance

urography is not at this time superior to the CT scan and certain

gadolinium agents carry a risk of systemic sclerosis in patients with

renal insufficiency. Recently, promising alternatives to gadolinium

have emerged. CT scanning may define the site of obstruction, identify and characterize kidney stones, and demonstrate dilatation of

the calyces, renal pelvis, and ureter above the obstruction. The ureter

may be tortuous in chronic obstruction. Though radionuclide scans

give less anatomic detail than CT scans, they are able to give differential renal function. In the case of asymmetric renal function, the

clinician may decide on a preferable kidney to decompress in the case

of bilateral obstruction. Furosemide is sometimes given to increase

detection with imaging, and to distinguish functional from anatomic

obstruction. The increase in urinary flow may bring out the pain of

an acute obstructive process.

To facilitate visualization of a suspected lesion in a ureter or renal

pelvis, retrograde or antegrade urography should be attempted. These

procedures do not carry risk of contrast-induced acute kidney injury

in patients with renal insufficiency. The retrograde approach involves

catheterization of the involved ureter under cystoscopic control,

whereas the antegrade technique necessitates percutaneous placement

of a catheter into the renal pelvis. Although the antegrade approach

may provide immediate decompression of a unilateral obstructing

lesion, many urologists initially attempt the retrograde approach unless

the catheterization is unsuccessful.

Voiding cystourethrography is of value in the diagnosis of vesicoureteral reflux and bladder neck and urethral obstructions. Postvoiding films reveal residual urine. Endoscopic visualization by the

urologist often permits precise identification of lesions involving the

urethra, prostate, bladder, and ureteral orifices.

TREATMENT

Urinary Tract Obstruction

UTO complicated by infection requires immediate relief of obstruction to prevent development of generalized sepsis and progressive

renal damage. Sepsis necessitates prompt urologic intervention.

Drainage may be achieved by nephrostomy, ureterostomy, or ureteral, urethral, or suprapubic catheterization. Prolonged antibiotic

treatment may be necessary. Chronic or recurrent infections in a

poorly functioning obstructed kidney may necessitate nephrectomy. When infection is not present, surgery is often delayed until

acid-base, fluid, and electrolyte status is restored. Nevertheless, the

site of obstruction should be ascertained as soon as feasible. Elective

relief of obstruction is usually recommended in patients with urinary

retention, recurrent urinary tract infections, persistent pain, or progressive loss of renal function. Benign prostatic hypertrophy may

be treated medically with α-adrenergic blockers and 5α-reductase

inhibitors. Renal colic may be treated with anti-inflammatory medication as edema often contributes to an obstructing ureteral stone,

and α-adrenergic blockers may also be of benefit. The clinician

should be aware of the risk of intraoperative floppy iris syndrome

associated with cataract surgery in patients taking α-adrenergic blockers. Use of nonsteroidal anti-inflammatory medication must take

into account the potential for renal harm, and opiates in patients

with decreased renal function may be dangerous and should be

used with caution. Functional obstruction secondary to neurogenic

bladder may be decreased with the combination of frequent voiding

and cholinergic drugs.

■ PROGNOSIS

With relief of obstruction, the prognosis regarding return of renal

function depends largely on whether irreversible renal damage has

occurred. When obstruction is not relieved, the course will depend

mainly on whether the obstruction is complete or incomplete and

bilateral or unilateral, as well as whether or not urinary tract infection

is also present. Complete obstruction with infection can lead to total

destruction of the kidney within days. Partial return of glomerular filtration rate may follow relief of complete obstruction of 1 and 2 weeks’

duration, but after 8 weeks of obstruction, recovery is unlikely. In the

absence of definitive evidence of irreversibility, every effort should be

made to decompress the obstruction in the hope of restoring renal

function at least partially. A renal radionuclide scan, performed after a

prolonged period of decompression, may be used to predict the reversibility of renal dysfunction.

■ POSTOBSTRUCTIVE DIURESIS

Relief of bilateral, but not unilateral, complete obstruction commonly

results in polyuria, which may be massive. The urine is usually hypotonic

and may contain large amounts of sodium chloride, potassium, phosphate, and magnesium. The natriuresis is due in part to the correction

of extracellular volume expansion, the increase in natriuretic factors

accumulated during the period of renal failure, and depressed salt and

water reabsorption when urine flow is reestablished. The retained urea

is excreted with improved GFR, resulting in an osmotic diuresis that

increases the urine volume of electrolyte-free water. Electrolyte-free water

excretion (hypotonic urine) is recognized as being present when the sum

of the urinary concentrations of sodium and potassium, is lower than the

serum sodium concentration. Causes include suppression of antidiuretic

hormone at arterial baroreceptor sites or elevation of atrial peptides, and

nephrogenic diabetes insidpidus due to obstructive tubular injury. In the

majority of patients, this diuresis results in the appropriate excretion of

the excesses of retained salt and water. When extracellular volume and

composition return to normal, the diuresis usually abates spontaneously.

Occasionally, iatrogenic expansion of extracellular volume is responsible

for, or sustains, the diuresis observed in the postobstructive period.

Replacement with intravenous fluids in amounts less than urinary losses

usually prevents this complication. More aggressive fluid management is

required in the setting of hypovolemia, hypotension, or disturbances in

serum electrolyte concentrations.

The loss of electrolyte-free water with urea may result in hypernatremia. Measured urinary output and serum and urine sodium,

potassium, and osmolal concentrations should guide the use of appropriate intravenous replacement. Often replacement with 0.45% saline

is required. Relief of obstruction may be followed by urinary salt and

water losses severe enough to provoke profound dehydration and vascular collapse. In these patients, decreased tubule reabsorptive capacity

is probably responsible for the marked diuresis. Appropriate therapy in

such patients includes intravenous administration of salt-containing

solutions to replace sodium and volume deficits.

■ FURTHER READING

Frokiaer J: Urinary tract obstruction, in Brenner and Rector’s The

Kidney, 10th ed. K Skorecki et al (eds). Philadelphia, W.B. Saunders

& Company, 2016, pp 1257–1282.

Meldrum KK: Pathophysiology of urinary tract obstruction, in

Campbell Walsh Wein Urology, AW Partin, CA Peters, LR Kavoussi,

R Dmochowski, AJ Wein (eds). Philadelphia, Elsevier; 2020, Chapter 48.

Smith-Bindman R et al: Ultrasonography versus computed tomography for suspected nephrolithiasis. N Engl J Med 371:1100, 2014.

Stoller ML: Urinary obstruction and stasis, in Smith and Tanagho’s

General Urology, 18th ed. JW McAninch, TF Lue (eds). New York,

McGraw-Hill, 2013, pp 170–182.

Tanagho EA, Nguyen HT: Vesicoureteral reflux, in Smith and

Tanagho’s General Urology, 18th ed. WJ McAninch, TF Lue (eds).

New York, McGraw-Hill, 2013, pp 182–197.

Vollman DE et al: Intraoperative floppy iris and prevalence of intraoperative complications: Results from ophthalmic surgery outcomes

database. Am J Ophthalmol 157:1130, 2014.

2377 Interventional Nephrology CHAPTER 320

Interventional nephrology is a procedure-oriented subspecialty with

a focus on dialysis access for peritoneal and hemodialysis, typically

performed under fluoroscopy. Ultrasound (US) evaluation of dialysis

access is common and some practitioners perform renal and renal

artery US evaluation as well as renal biopsies. Endovascular creation

of arteriovenous fistulas (AVFs) is a recent addition to the procedural

spectrum; (open) surgical access creation by nephrologists is limited

to very few centers in the United States, while common in China,

Germany, India, and Italy.

Interventional nephrologists (INs) usually provide patient care in

multidisciplinary teams that include clinical nephrologists; access

surgeons with vascular, transplant, or general surgery background;

other interventionalists (with radiology or cardiology training); and

dialysis unit access coordinators, nurses, and technicians involved in

needle placement. Long-term preservation of venous and arterial vascular access options is one tenet of chronic kidney disease (CKD) care,

leading INs to advocate for specific vascular access options (tunneled

small-diameter catheters over peripherally inserted central catheters

[PICCs]) and cardiac devices (epicardial rather than endovascular lead

passage).

■ HISTORY

The history of vascular access for hemodialysis is closely tied to the

history of dialysis. The first hemodialysis treatments in humans were

performed in 1924 using glass needles to access the radial artery and

return blood into the cubital vein. In 1943 a “rotating drum kidney”

was used to dialyze a 29-year-old housemaid with CKD by surgical

exposure of different arteries until she ran out of access sites after 12

treatments. The challenge of repetitive vascular access prevented dialysis from becoming a routine method for the treatment of CKD until

the development of an arteriovenous Teflon shunt and then the development of an autogenous arterial-venous access (arteriovenous fistula,

AVF) by side-to-side-anastomoses between the radial artery and the

cephalic vein at the wrist (Cimino fistula). Catheter-based approaches

for chronic renal replacement therapy (RRT) were designed initially in

1961 for hemodialysis and in 1968 for peritoneal dialysis, both using

Dacron felt cuffs to protect against infection.

Material sciences have continued to evolve the development of grafts

for use in hemodialysis. A modified bovine carotid artery biological

graft was introduced in 1972, followed by the use of expanded polytetrafluoroethylene (ePTFE) grafts in 1976, and, most recently in 2016,

tissue-engineered blood vessels from human fibroblasts and endothelial cells. Some ePTFE grafts are modified with a silicone layer to allow

for early cannulation within days of insertion. Ultra-high-pressure (up

to 40 atm) angioplasty balloons are a mainstay of peripheral and central

venous therapy, and Nitinol self-expanding stents and stent grafts serve

as rescue tools for unsuccessful angioplasty as well as vessel rupture

with extravasation.

■ PHYSIOLOGY AND PATHOPHYSIOLOGY OF

DIALYSIS ACCESS

Peritoneal Dialysis Peritoneal dialysis (PD) catheters can be

placed fluoroscopically, peritoneoscopically, laparoscopically, and open

surgically. Procedural success is typically linked to provider experience

and procedural planning to optimize positioning of the PD catheter

coil as this improves function and decreases drain pain and other

complications. The internal cuff is placed within the rectus sheath just

laterally to the linea alba, while the external PD catheter cuff should be

located 2–4 cm from the skin exit site. Ingrowth of both cuffs ensures

secure positioning of the catheter and allows water emersion. Over

time the peritoneal catheter can become encased in a fibrous sheath,

which, if limiting fluid flow during exchanges, can be disrupted by

320 Interventional Nephrology

Dirk M. Hentschel

guidewire manipulation. Omental entrapment of the catheter often

requires laparoscopic intervention; omentopexy at the time of PD

catheter placement can prevent later entrapment. Repeated infections

affect the permeability of the peritoneal membrane, as does long-term

exposure to glucose-containing exchange solutions. Encapsulating

peritoneal sclerosis is a late-stage complication of PD thought to be

triggered by repeated peritonitis.

Hemodialysis Catheters Dialysis catheters are typically made

of polyurethane that softens at body temperature but is sufficiently

strong to allow for blood flow rates of 400–500 mL/min in each of

two channels inside a 14.5–16 French design without collapse of the

catheter lumen. Tunneled catheters have a cuff that creates a barrier

between skin flora at the exit site and the sterile catheter tunnel leading

into the fibrous sheath covering the catheter from the vessel insertion

point to its tip. The fibrous sheath can extend too far, impeding catheter flow and necessitating exchange of the catheter with disruption of

the sheath by balloon angioplasty. Catheter-related bacteremia is best

treated with exchange of the catheter and disruption of any fibrous

sheath, although removal of the catheter and delayed reinsertion after

several days is also successful. Thrombotic occlusion and later sclerotic

scarring of the vein at catheter insertion sites is common, however,

and removal of a catheter may lead to loss of this access site. Catheter

wall contact points are thought to lead to central vein stenosis, which

is more commonly observed in patients with catheter contact times of

longer duration (>3 months). Catheter tip position in the large central

veins instead of the right atrium causes additional injury from dynamic

blood movement during dialysis treatments and should be corrected. A

thrombus is commonly found attached to the catheter, often tethering

the catheter to the vessel wall and right atrium. While some thrombi

are mobile and dissolve with anticoagulation, a wall-tethered thrombus

is often well organized with cellular components and quite resistant to

pharmacologic lysis. Clinically significant pulmonary embolism from

catheter-associated thrombus is rare, and it may be that only intra-atrial

thrombus >2 cm in diameter deserves active intervention.

■ ARTERIOVENOUS GRAFTS AND FISTULAS

During the first decades of hemodialysis for loss of renal function,

US patients were relatively young and without long-term systemic

vascular disease. Creation of forearm Cimino AVFs was common, and

access failure usually led to creation of a second AVF slightly higher

up on the arm. As diabetes and hypertension with associated systemic

arterial and venous vascular disease became more prevalent in the

CKD population, placement of nonautogenous accesses (arteriovenous

grafts [AVGs]) increased. In the mid-1990s, 65% of prevalent dialysis

patients used an AVG for access. The US was an international outlier

in this regard, and studies associated increased mortality in US dialysis

patients with lower AVF prevalence. In the context of “Fistula First”

and then “Fistula First, Catheter Last” campaigns, AVG prevalence

decreased to its current value of less than 20%, while AVFs increased

to near 65% prevalence. However, most centers still struggle with the

challenging conditions of arteries and veins in these patients requiring

that 75% of AVFs are now created in the upper arm, where the veins a

priori are larger in diameter, and arteries can deliver higher blood flow

rates due to large vessel diameter (see Fig. 320-1).

To provide successful dialysis, an AVF or AVG has to provide at least

the desired blood pump speed (see Chap. 312) plus 100–200 mL/min

to minimize recirculation and prevent collapse of the access. In the

United States, this usually means flow in the 600–800 mL/min range.

After creation of the arterial-venous anastomosis (or insertion of the

AVG), blood flow increases significantly: brachial artery flow at rest

is typically <50 mL/min, but after access creation flow volume in AVFs

increases within weeks to 800 mL/min, while flow volume in AVGs

increases within minutes to 1000 mL/min. The increased flow changes

the arterial shear stress profile and leads to enlargement of the artery

over time. In AVGs, this process is limited by the graft itself, which

typically is 6 mm in diameter and 35–40 cm long, and access flows are

1200–1800 mL/min. The access vein in AVFs in the right shear stress

environment enlarges over time, often to >10 mm in diameter in the

2378 PART 9 Disorders of the Kidney and Urinary Tract

upper arm such that the artery continues to enlarge until a narrow

segment in the venous conduit becomes flow limiting. Flow volumes

in these mature upper arm AVFs are usually 1400–1800 mL/min, but

after a few years can be as high as 2000–4000 mL/min. Forearm AVFs

usually have lower flow volumes (600–800 mL/min) as the feeding

radial artery is of smaller diameter, and in the context of systemic

vascular disease in the United States, only increases in diameter over

many years.

Increased flows and pressure in the venous segment of the access

circuit combine to lead to “chronic dialysis access disease” that manifests differently for each type of the common long-term accesses in

predetermined segments particularly prone to shear stress and needle

insertion-related injury. AVGs develop venous anastomotic stenoses

that recur with very short periodicity in the 3- to 4-month range. Stent

grafts can effectively be deployed to extend patency for usually 1 year

at the site, after which the buildup of pauci-cellular fibrous depositions

at the stent edges requires re-angioplasty one to three times per year.

Forearm radial-cephalic autogenous accesses are most prone to low

flow due to juxta-anastomotic stenoses. Over time, these stenoses can

stabilize, and with enlargement of the inflow artery, they effectively

provide protection against excessive flows and their sequelae. Upper

arm brachial-cephalic autogenous accesses typically develop stenoses

in the cephalic arch, which recur in accelerated fashion after each

angioplasty. Flexible stent grafts in the cephalic arch extend intraprocedural intervals usually to 9–12 months. Upper arm transposed

brachial-basilic autogenous accesses develop stenoses in the swing

point where the basilic vein is curved to provide a location more

lateral and closer to the skin to facilitate ready cannulation. Angioplasty and stent graft placement approaches extend patency. In both

types of upper arm accesses, there are often prolonged periods with

increased intra-access pressures due to outflow stenoses, which lead

to enlargement of needle insertion site aneurysm as the skin heals in

a pressurized, stretched state. Continued use of pressurized accesses

leads to enlargement of needle sites, then thinning of the skin, scab

formation, and, finally, full thickness ulceration with often significant

bleeding events. Recognizing the occurrence of outflow stenoses early

is an important skill for nurses and technologists working in dialysis

units to learn in order to avoid irreversible loss of skin coverage, which

can result in loss of the access.

High-access flow can lead to systemic complications, such as heart

failure and pulmonary hypertension. Fistula inflow higher than outflow capacity leads to accelerated aneurysm formation and breakdown

of skin coverage as intra-access pressures are increased over the ideal

pressure of 20–35 mmHg. High-access flows are also associated with

steal syndrome, typically ischemia of the hand. A variety of procedures

have been described to reduce access flows, the most common being

“banding,” where a 2-0 Prolene suture is guided around the inflow and

a 3- or 4-mm spacer once or twice and is tied snugly over the spacer.

APPROACH TO THE PATIENT

Physical Examination of Dialysis Access

The 2019 KDOQI vascular access guidelines were developed under

the tenet, “[t]he right access for the right patient at the right time.”

Progression of CKD is highly variable, many patients die from other

causes before reaching end-stage renal disease (ESRD), and some

AVFs require 6–12 months to mature to usability in patients with

HTN and diabetes leading to uncertainty as to when to create AVFs.

The more common need of upper arm accesses for interventions

to maintain patency favors the creation of forearm accesses during

the pre-ESRD period. The processes of care from vein mapping,

surgery, follow-up visits after access creation, to availability and

timing of open surgical or endovascular interventions have profound effects on the overall success rate needed to achieve mature

and usable accesses, and appear to be key factor with highly variable

outcomes across the United States.

A central skill in dialysis access evaluation is the physical examination. Five aspects capture all aspects of possible pathology:

Pulsatility reflects the force of access expansion during systole and

the degree of softening during diastole. Very high blood pressures

will suggest increased pulsatility, but the access softens remarkably

during diastole. An outflow stenosis will lead to increased pulsatility and reduced softening during diastole. An inflow stenosis will

blunt with the systolic component and create the impression of an

“empty” access during diastole unless there is a coexisting outflow

stenosis. The audible flow murmur can be characterized by pitch

A C

B D

FIGURE 320-1 Dialysis access health depends on intra-access pressures and needle insertions. A. A right upper arm brachial-cephalic arteriovenous fistula (AVF) with

two recurrences of clinically relevant inflow stenosis in 4 years has low-normal intra-access pressure before and after angioplasty; there is only minimal needle insertion

site enlargement. B. In contrast, a right upper arm brachial-cephalic AVF with seven recurrences of cephalic arch outflow stenosis in 4-year cycles between states of highnormal to high intra-access pressures with notable needle insertion site enlargement. C. Focal needle insertions despite available graft segments led to penetrating

skin ulcers over 3 years. D. Segmental needle rotation preserves skin integrity even after 7 years of arteriovenous graft (AVG) use.

2379 Interventional Nephrology CHAPTER 320

and continuity (Video 320-1). A change in pitch toward higher

frequency is typical at the site of a stenosis due to accelerated flow

velocity at this site. A discontinuous flow murmur indicates that

during diastole flow is so low that no audible shear force is created;

this is the sign of a severe inflow or outflow stenosis. Typically, the

stenotic inflow murmur is faint (like a whistle), whereas the stenotic

outflow murmur can be coarse and loud (akin to a handsaw)

(Video 320-2). A thrill is palpable through the skin when the vessel

is close enough to the surface and the flow high enough in relation

to the diameter of the vessel to create vibration of the vessel wall. A

continuous thrill can be a sign of a well-developed access, usually

in the inflow segment, dissipating as the access vessel branches

and takes a deeper course. In contrast, a discontinuous thrill is

found with severe stenosis. An isolated thrill is also found focally

immediately after a stenosis. The differentiation from a “healthy”

thrill can be made by documenting a change in pulsatility at the

site of the focal thrill, increased retrograde (inflow) and decreased

antegrade (outflow). Augmentation is the engorgement of the

body of the access (where needles are inserted) with occlusion of

the outflow necessary for safe and successful needle insertions. An

inflow stenosis will impair augmentation as will side-branches and

collaterals between the occluding finger/tourniquet and the inflow.

The location of side-branches can be elucidated by moving the

occluding finger closer toward the anastomosis until augmentation

is achieved. With several collaterals, this may be a staged phenomenon. Collapse of the access with arm elevation (against gravity)

is a measure of inflow and outflow capacity match or mismatch. A

forearm access typically displays complete collapse while upper arm

accesses typically show only partial collapse. An outflow stenosis

or very high inflow will decrease the degree of collapse; banding of

an upper arm access or a natural flow limiting stenosis may lead to

complete collapse of an upper arm access.

Enlarged needle insertion sites (and any sites of suspected skin

thinning) are best examined while occluding inflow: the completely

empty access allows palpation of a firm, layered thrombus inside

aneurysms as well as a better appreciation of the thickness of the

overlying skin by rolling it between thumb and index finger. The

chest wall and neck should be inspected for the presence of skin

veins and venous distention, which are associated with central

venous stenosis or occlusion, as is ipsilateral arm edema.

PRESERVATION OF VENOUS “REAL ESTATE”

Preserving access is a key care component for the patient with

advancing CKD. Approximately 8–10% of this population has the

need for cardiac rhythm management devices (CRMDs) that can

VIDEO 320-1 Flow murmur of an upper arm brachial-cephalic autogenous access

(AVF) with a juxta-anastomotic stenosis. The sound is discontinuous as the stenosis

is severe enough that only during systole is the flow volume high enough to create

audible turbulence. There also is a high-pitch component of the murmur due to the

high flow velocity during the peak of the flow cycle.

VIDEO 320-2 Flow murmur of an upper arm brachial-cephalic autogenous access

(AVF) with a juxta-anastomotic stenosis after angioplasty. The sound is now

continuous with systolic-diastolic modulation. There is an even pitch, overall lower

than the pitch associated with peak flow in the setting of an untreated stenosis.

lead to loss of the upper arm cephalic vein as well as central venous

stenoses and occlusions around device leads. Planning for which

side a future autogenous access is to be placed an