Oliguria; Acute Renal Failure
William J.C. Amend, Jr., MD, & Flavio G. Vincenti, MD
Oliguria literally means “reduced” urine volume—less
than that necessary to remove endogenous solute loads
that are the end products of metabolism. If the patient
concentrates urine in a normal fashion, oliguria (for that
person) is present at urine volumes under 400 mL/day, or
approximately 6 mL/kg body weight. If the kidney con-
centration is impaired and the patient can achieve a spe-
cific gravity of only 1.010, oliguria is present at urine vol-
umes under 1000–1500 mL/day.
Acute renal failure is a condition in which the glomeru-
lar filtration rate is abruptly reduced, causing a sudden
retention of endogenous and exogenous metabolites (urea,
potassium, phosphate, sulfate, creatinine, administered
drugs) that are normally cleared by the kidneys. The urine
volume is usually low (under 400 mL/day). If renal con-
centrating mechanisms are impaired, the daily urine vol-
ume may be normal or even high (high-output or nono-
liguric renal failure). Rarely, there is no urine output at
all (anuria) in acute renal failure.
The causes of acute renal failure are listed in Table 33–1.
Prerenal renal failure is reversible if treated promptly, but a
delay in therapy may allow it to progress to a fixed intrinsic
renal failure (eg, acute tubular necrosis). The other causes of
acute renal failure are classified on the basis of their involve-
ment with vascular lesions, intrarenal disorders, or postrenal
disorders.
PRERENAL RENAL FAILURE
The term prerenal denotes inadequate renal perfusion or
lowered effective arterial circulation. The most common
cause of this form of acute renal failure is dehydration due
to renal or extrarenal fluid losses from diarrhea, vomiting,
excessive use of diuretics, and so on. Less common causes
are septic shock, “third spacing” with extravascular fluid
pooling (eg, pancreatitis), and excessive use of antihyper-
tensive drugs. Heart failure with reduced cardiac output
also can reduce effective renal blood flow. Careful clinical
assessment may identify the primary condition responsible
for prerenal renal failure, but many times several condi-
tions can coexist. In the hospital setting, these circulatory
abnormalities often lead to more fixed, acute renal failure
(acute tubular necrosis).
Acute reductions in glomerular filtration rate may also
be noted in patients with cirrhosis (hepatorenal failure) or
531
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33
in patients taking cyclosporine, tacrolimus, nonsteroidal
anti-inflammatory drugs, or angiotensin-converting enzyme
inhibitors. It is felt that these conditions represent signifi-
cant intrarenal hemodynamic functional derangements.
In these clinical circumstances, the urinary findings may
mimic prerenal renal failure, but the patient’s clinical
assessment does not demonstrate the extrarenal findings
seen in common prerenal conditions, as noted in the fol-
lowing section. Improvements in glomerular filtration rate
are usually noted after drug discontinuance or, in cases of
hepatorenal renal failure, with management of the liver
disease or liver transplantation.
Clinical Findings
A. SYMPTOMS AND SIGNS
Except for rare cases with associated cardiac or “pump”
failure, patients usually complain of thirst or of dizziness in
the upright posture (orthostatic dizziness). There may be a
history of overt fluid loss. Weight losses reflect the degree
of dehydration. Physical examination frequently reveals
decreased skin turgor, collapsed neck veins, dry mucous
membranes, and, most important, orthostatic or postural
changes in blood pressure and pulse.
B. LABORATORY FINDINGS
1. Urine—The urine volume is usually low. Accurate
assessment may require bladder catheterization followed by
hourly output measurements (which will also rule out
lower urinary tract obstruction; see discussion following).
High urine specific gravity (>1.025) and urine osmolality
>600 mOsm/kg) also are noted in this form of acute
apparent renal failure. Routine urinalysis usually shows no
abnormalities.
2. Urine and blood chemistries—The blood urea nitro-
gen-creatinine ratio, normally 10:1, is usually increased
with prerenal renal failure. Other findings are set forth in
Table 33–2. Because mannitol, radiocontrast dyes, and
diuretics affect the delivery and tubular handling of urea,
sodium, and creatinine, urine and blood chemistry tests
performed after these agents have been given to produce
misleading results.
3. Central venous pressure—A low central venous
pressure indicates hypovolemia. If severe cardiac failure is
532 / CHAPTER 33
Table 33–1. Causes of Acute Renal Failure. Table 33–2. Acute Renal Failure versus Prerenal
Azotemia.
I. Prerenal renal failure:
1. Dehydration Acute Renal Prerenal
2. Vascular collapse due to sepsis, antihypertensive Failure Azotemia
drug therapy, “third spacing”
3. Reduced cardiac output Urine osmolarity (mOsm/L) < 350 > 500
II. Functional–hemodynamic: Urine/plasma urea < 10 > 20
1. Angiotensin-converting enzyme inhibitor drugs Urine/plasma creatinine < 20 > 40
2. Nonsteroidal anti-inflammatory drugs Urine Na (mEq/L) > 40 < 20
3. Cyclosporine; tacrolimus Renal failure index* =
4. Hepatorenal syndrome >1 <1
U Na
III. Vascular: --------------
1. Atheroembolism U ⁄ P cr
2. Dissecting arterial aneurysms >1 <1
U ⁄ P Na
3. Malignant hypertension - × 100
FE Na = ---------------
IV. Parenchymal (intrarenal): U ⁄ P cr
1. Specific: *Excreted fraction of filtered sodium. See Espinel CH: JAMA
a. Glomerulonephritis 1976;236:579; and Miller TR et al: Ann Intern Med 1978; 89:47.
b. Interstitial nephritis
c. Toxin, dye-induced
d. Hemolytic uremic syndrome
2. Nonspecific:
sis; see discussion following). If oliguria and hypotension
a. Acute tubular necrosis persist in a well-hydrated patient, vasopressor drugs are
b. Acute cortical necrosis indicated in an effort to correct the hypotension associated
V. Postrenal: with sepsis or cardiogenic shock. Pressor agents that restore
1. Calculus in patients with solitary kidney systemic blood pressure while maintaining renal blood
2. Bilateral ureteral obstruction flow and renal function are most useful. Dopamine, 1–5
3. Outlet obstruction µg/kg/min, may increase renal blood flow without sys-
4. Leak, posttraumatic temic pressor responses. Higher doses of 5–20 µg/kg may
be necessary if systemic hypotension persists after volume
correction. Discontinuance of antihypertensive medica-
tions or diuretics can, by itself, cure the apparent acute
the principal cause of prerenal renal failure (it is rarely the renal failure resulting from prerenal conditions.
sole cause), reduced cardiac output and high central
venous pressure are apparent. VASCULAR RENAL FAILURE
4. Fluid challenge—An increase in urine output in
response to a carefully administered fluid challenge is both Common causes of acute renal failure due to vascular dis-
diagnostic and therapeutic in cases of prerenal renal failure. ease include atheroembolic disease, dissecting arterial aneu-
Rapid intravenous administration of 300–500 mL of rysms, and malignant hypertension. Atheroembolic disease
physiologic saline is the usual initial treatment. Urine out- is rare before age 60 and in patients who have not under-
put is measured over the subsequent 1–3 hours. A urine gone vascular procedures or angiographic studies. Dissect-
volume increase of more than 50 mL/h is considered a ing arterial aneurysms and malignant hypertension are
favorable response that warrants continued intravenous usually clinically evident.
infusion. If the urine volume does not increase, the physi- Rapid assessment of the arterial blood supply to the
cian should carefully review the results of blood and urine kidney requires arteriography or other noncontrast blood
chemistry tests, reassess the patient’s fluid status, and flow studies (eg, magnetic resonance imaging or Doppler
repeat the physical examination to determine whether an ultrasound). The cause of malignant hypertension may be
additional fluid challenge (with or without furosemide) identified on physical examination (eg, scleroderma). Pri-
might be worthwhile. mary management of the vascular process is necessary to
affect the course of these forms of acute renal failure.
Treatment
INTRARENAL DISEASE STATES;
In states of dehydration, fluid losses must be rapidly cor- INTRARENAL ACUTE RENAL FAILURE
rected to treat oliguria. Inadequate fluid management may
cause further renal hemodynamic deterioration and even- Diseases in this category can be divided into specific and
tual renal tubular ischemia (with fixed acute tubular necro- nonspecific parenchymal processes.

1. Specific Intrarenal Disease States
The most common causes of intrarenal acute renal failure
are acute or rapidly progressive glomerulonephritis, acute
interstitial nephritis, toxic nephropathies, and hemolytic
uremic syndrome.
Clinical Findings
A. SYMPTOMS AND SIGNS
Usually the history shows some salient data such as sore
throat or upper respiratory infection, diarrheal illness, use
of antibiotics, or intravenous use of drugs (often illicit
types). Bilateral back pain, at times severe, is occasionally
noted. Gross hematuria may be present. It is unusual for
pyelonephritis to present as acute renal failure unless there
is associated sepsis, obstruction, or involvement of a soli-
tary kidney. Systemic diseases in which acute renal failure
occurs include Henoch-Schönlein purpura, systemic lupus
erythematosus, and scleroderma. Human immunodefi-
ciency virus (HIV) infection may present with acute renal
failure from HIV nephropathy.
B. LABORATORY FINDINGS
1. Urine—Urinalysis discloses variably active sediments:
many red or white cells and multiple types of cellular and
granular casts. Phase contrast microscopy usually reveals
dysmorphic red cells in the urine. In allergic interstitial
nephritis, eosinophils may be noted. The urine sodium
concentration may range from 10 to 40 mEq/L.
2. Blood test—Components of serum complement are
often diminished. In a few conditions, circulating immune
complexes can be identified. Other tests may disclose sys-
temic diseases such as lupus erythematosus. Thrombocyto-
penia and altered red cell morphologic structure are noted
in peripheral blood smears in the hemolytic uremic syn-
drome. Rapidly progressive glomerulonephritis can be
evaluated with tests for ANCA (antineutrophil cytoplas-
mic antibodies) and anti-GBM titers (anti-glomerular
basement membrane antibodies).
3. Renal biopsy—Biopsy examination shows characteris-
tic changes of glomerulonephritis, acute interstitial nephri-
tis, or glomerular capillary thrombi (in hemolytic uremic
syndrome). There may be extensive crescents involving
Bowman’s space.
C. X-RAY FINDINGS
Dye studies should be avoided because of the risk of dye-
induced renal injury. For this reason, sonography is prefer-
able to rule out obstruction.
Treatment
Therapy is directed toward eradication of infection,
removal of antigen, elimination of toxic materials and
OLIGURIA; ACUTE RENAL FAILURE / 533
drugs, suppression of autoimmune mechanisms, removal
of autoimmune antibodies, or a reduction in effector-
inflammatory responses. Immunotherapy may involve
drugs or the temporary use of plasmapheresis. Initiation
of supportive dialysis may be required (see discussion
below).
2. Nonspecific Intrarenal States
Nonspecific intrarenal causes of acute renal failure include
acute tubular necrosis and acute cortical necrosis. The lat-
ter is associated with intrarenal intravascular coagulation
and has a poorer prognosis than the former. These forms
of acute renal failure usually occur in hospital settings. Var-
ious morbid conditions leading to septic syndrome–like
physiologic disturbances are often present.
Degenerative changes of the distal tubules (lower neph-
ron nephrosis) are believed to be due to ischemia. With
dialysis, most of these patients recover—usually com-
pletely—provided intrarenal intravascular coagulation and
cortical necrosis does not occur.
Elderly patients, who are more prone to have this form
of oliguric acute renal failure, develop following hypoten-
sive episodes. It appears that exposure to some drugs such
as nonsteroidal anti-inflammatory agents may increase the
risk of acute tubular necrosis. Although the classic picture
of lower nephron nephrosis may not develop, a similar
nonspecific acute renal failure is noted in some cases of
mercury (especially mercuric chloride) poisoning and fol-
lowing exposure to radiocontrast agents, especially in
patients with diabetes mellitus or myeloma.
Clinical Findings
A. SYMPTOMS AND SIGNS
Usually the clinical picture is that of the associated clinical
state. Dehydration and shock may be present concur-
rently, but the urine output and acute renal failure fail to
improve following administration of intravenous fluids, in
contrast to patients who have prerenal renal failure (see
preceding discussion). On the other hand, there may be
signs of excessive fluid retention in patients with acute
renal failure following radiocontrast exposure. Symptoms
of uremia per se (eg, altered mentation or gastrointestinal
symptoms) are unusual in acute renal failure (in contrast to
chronic renal failure).
B. LABORATORY FINDINGS
(See also Table 33–2.)
1. Urine—The specific gravity is usually low or fixed in
the 1.005–1.015 range. Urine osmolality is also low (<450
mOsm/kg and U/P osmolal ratio <1.5:1). Urinalysis often
discloses tubular cells and granular casts; the urine may be
muddy brown. If the test for occult blood is positive, one
must be concerned about the presence of myoglobin or
534 / CHAPTER 33
hemoglobin. Tests for differentiating myoglobin pigment
are available.
2. Central venous pressure—This is usually normal to
slightly elevated.
3. Fluid challenges—There is no increase in urine vol-
ume following intravenous administration of mannitol or
physiologic saline. Occasionally, following the use of furo-
semide or “renal doses” of dopamine (1–5 µg/kg/min), a
low urine output is converted to a high fixed urine output
(low-output renal failure to high-output renal failure).
Treatment
If there is no response to the initial fluid or mannitol chal-
lenge, the volume of administered fluid must be sharply
curtailed to noted losses. An assessment of serum creati-
nine and blood urea nitrogen and of the concentrations of
electrolytes is necessary to predict the possible use of dialy-
sis. With appropriate regulation of the volume of fluid
administered, solutions of glucose and essential amino
acids to provide 30–35 kcal/kg are used to correct or
reduce the severity of the catabolic state accompanying
acute tubular necrosis.
Serum potassium must be closely monitored to ensure
early recognition of hyperkalemia. This condition can be
treated with (1) intravenous sodium bicarbonate adminis-
tration, (2) Kayexalate, 25–50 g (with sorbitol) orally or by
enema, (3) intravenous glucose and insulin, and (4) intra-
venous calcium preparations to prevent cardiac irritability.
Peritoneal dialysis or hemodialysis should be used as
necessary to avoid or correct uremia, hypokalemia, or fluid
overload. Hemodialysis in patients with acute renal failure
can be either intermittent or continuous (with arteriove-
nous or venovenous hemofiltration techniques). Vascular
access is obtained with percutaneous catheters. The contin-
uous dialysis techniques allow for easier management in
many hemodynamically unstable patients in intensive care
units.
Prognosis
Most cases are reversible within 7–14 days. Residual renal
damage may be noted, particularly in elderly patients.
POSTRENAL ACUTE RENAL FAILURE
The conditions listed in Table 33–1 involve primarily the
need for urologic diagnostic and therapeutic interven-
tions. Following lower abdominal surgery, urethral or ure-
teral obstruction should be considered as a cause of acute
renal failure. The causes of bilateral ureteral obstruction are
(1) peritoneal or retroperitoneal neoplastic involvement,
with masses or nodes; (2) retroperitoneal fibrosis; (3) calcu-
lous disease; and (4) postsurgical or traumatic interruption.
With a solitary kidney, ureteral stones can produce total
urinary tract obstruction and acute renal failure. Urethral
or bladder neck obstruction is a frequent cause of renal
failure, especially in elderly men. Posttraumatic urethral
tears are discussed in Chapter 17.
Clinical Findings
A. SYMPTOMS AND SIGNS
Renal pain and renal tenderness often are present. If there
has been an operative ureteral injury with associated urine
extravasation, urine may leak through a wound. Edema
from overhydration may be noted. Ileus is often present
along with associated abdominal distention and vomiting.
B. LABORATORY FINDINGS
Urinalysis is usually not helpful. A large volume of urine
obtained by catheterization may be both diagnostic and
therapeutic for lower tract obstruction.
C. X-RAY FINDINGS
Radionuclide renal scans may show a urine leak or, in cases
of obstruction, retention of the isotope in the renal pelvis.
Ultrasound examination often reveals a dilated upper col-
lecting system with deformities characteristic of hydrone-
phrosis.
D. INSTRUMENTAL EXAMINATION
Cystoscopy and retrograde ureteral catheterization demon-
strate ureteral obstruction.
Treatment
For further discussion of ureteral injuries, see Chapter 17.
REFERENCES
Forni LG, Hilton PJ: Continuous hemofiltration in the treatment of
acute renal failure. N Engl J Med 1997;336:1303.
Gines P, Arroyo V: Hepatorenal syndrome. J Am Soc Nephrol 1999;
10:1833.
Intensive care nephrology. J Am Soc Nephrol 2001;12(suppl 17):S1.
Marik PE et al: Low-dose dopamine does not prevent acute renal fail-
ure in patients with septic shock and oliguria. Am J Med
1999;107:387.
Murphy SW et al: Contrast nephropathy. J Am Soc Nephrol 2000;11:
177.
Nolan CR, Anderson RJ: Hospital-acquired acute renal failure. J Am
Soc Nephrol 1998;9:710.
Schiffl H et al: Daily hemodialysis and the outcome of acute renal fail-
ure. N Engl J Med 2002;346:305.
Schor N: Acute renal failure and the sepsis syndrome. Kidney Int
2002;61:764.
Star RA: Treatment of acute renal failure. Kidney Int 1998;54:1817.
Tepel M et al: Prevention of radiographic-contrast-agent-induced re-
ductions in renal function by acetylcysteine. N Engl J Med
2000;343:180.
 Chronic Renal Failure & Dialysis
William J.C. Amend, Jr., MD, & Flavio G. Vincenti, MD
Overview
In chronic renal failure, reduced clearance of certain sol-
utes principally excreted by the kidney results in their
retention in the body fluids. The solutes are end products
of endogenous metabolism as well as exogenous substances
(eg, drugs). The most commonly used indicators of renal
failure are blood urea nitrogen and serum creatinine. The
clearance of creatinine can be used as a reasonable measure
of glomerular filtration rate (GFR).
Renal failure may be classified as acute or chronic
depending on the rapidity of onset and the subsequent
course of azotemia. An analysis of the acute or chronic
development of renal failure is important in understanding
physiologic adaptations, disease mechanisms, and ultimate
therapy. In individual cases, it is often difficult to establish
the duration of renal failure. Historical clues such as pre-
ceding hypertension or radiologic findings such as small,
shrunken kidneys tend to indicate a more chronic process.
Acute renal failure may progress to irreversible chronic
renal failure. For a discussion of acute renal failure, see
Chapter 32.
A new classification has been made to delineate chronic
kidney disease (CKD) by varying degrees of reduced GFR
(or creatinine clearance). This is presented in Table 34–1.
This has been useful in studies of the progression of CKD,
especially in varying drug regimens to reduce the rate of
worsening of GFRs.
The incidence of end-stage renal disease (ESRD) is 330
cases per million population. These patients with ESRD
require chronic dialysis or renal transplantation for life
support. All age groups are affected. The severity and the
rapidity of development of uremia are hard to predict. The
use of dialysis and transplantation is expanding rapidly
worldwide. A large increase in CKD in the past 20 years
has been due to type 2 diabetes. Over 330,000 ESRD
patients in the United States are currently treated with
dialysis. Besides diabetes, increasingly older patients are
being treated for other renal diseases. At the present time,
128,000 patients have functioning kidney transplants.
Historical Background
There are various causes of progressive renal dysfunction
leading to end-stage or terminal renal failure. In the
1800s, Bright described several dying patients who pre-
535
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34
sented with edema, hematuria, and proteinuria. Chemi-
cal analyses of sera drew attention to retained nitroge-
nous compounds and an association was made between
this and the clinical findings of uremia. Although the
pathologic state of uremia was well described, long-term
survival was not achieved until chronic renal dialysis and
renal transplantation became available after 1960–1970.
Significant improvements in patient survival have been
made in the past 50 years.
Etiology
A variety of disorders are associated with CKD. Either a
primary renal process (eg, glomerulonephritis, pyelone-
phritis, congenital hypoplasia) or a secondary one (owing
to a systemic process such as diabetes mellitus or lupus
erythematosus) may be responsible. Once there is kidney
injury, it is now felt that hyperfiltration to undamaged
nephron units produces further stress and injury to rem-
nant kidney tissue. The patient will show progression from
one stage of CKD severity to the next. Superimposed
physiologic alterations secondary to dehydration, infec-
tion, obstructive uropathy, or hypertension may put a bor-
derline patient into uncompensated chronic uremia.
Clinical Findings
A. SYMPTOMS AND SIGNS
With milder CKD, there may be no clinical symptoms.
Symptoms such as pruritus, generalized malaise, lassitude,
forgetfulness, loss of libido, nausea, and easy fatigability are
frequent and nonfocal complaints in moderate to severe
CKD. Growth failure is a primary complaint in preadoles-
cent patients. Symptoms of a multisystem disorder (eg,
systemic lupus erythematosus) may be present coinciden-
tally. Most patients with CKD have elevated blood pres-
sure secondary to volume overload or from hyperrenine-
mia. However, the blood pressure may be normal or low if
patients have marked renal salt-losing tendencies (eg, med-
ullary cystic disease). The pulse and respiratory rates are
rapid as manifestations of anemia and metabolic acidosis.
Clinical findings of uremic fetor, pericarditis, neurologic
findings of asterixis, altered mentation, and peripheral neu-
ropathy are present only with severe, stage V CKD. Palpa-
ble kidneys suggest polycystic disease. Ophthalmoscopic
536 / CHAPTER 34
Table 34–1. Chronic Kidney Disease (CKD) Stages.
GFR (cc/min)
Stage I >90 with microalbuminuria
Stage II 60–89 with microalbuminuria
Stage III 30–59
Stage IV 15–29
Stage V <15 or dialysis
Ref. K/DOQI Guidelines for Chronic Liver Disease: Evaluation, classifi-
cation, and stratification (excerpts). Am J Kidney Dis 2002;39(Suppl
1):1.
examination may show hypertensive or diabetic retinop-
athy. Alterations involving the cornea have been associated
with metabolic disease (eg, Fabry disease, cystinosis, and
Alport hereditary nephritis).
B. HISTORY
In 20% of cases, there is a family history of CKD. A report
of antecedent nephritis episodes or a history of previous
proteinuria may be elicited. It is important to review drug
usage and possible toxic exposures (eg, lead).
C. LABORATORY FINDINGS
1. Urine composition—The urine volume varies depend-
ing on the type of renal disease. Quantitatively normal
amounts of water and salt losses in urine can be associated
with polycystic and interstitial forms of disease. Usually,
however, urine volumes are quite low when the GFR falls
below 5% of normal. The urinary concentrating and acidi-
fication mechanisms are impaired. Daily salt losses become
more fixed, and, if they are low, a state of positive sodium
balance occurs with resulting edema. Proteinuria can be
variable. Urinalysis examinations may reveal mononuclear
white blood cells (leukocytes) and occasionally broad waxy
casts, but usually the urinalysis is nonspecific and inactive.
2. Blood studies—Anemia is the rule with normal plate-
let counts. Platelet dysfunction or thrombasthenia is char-
acterized by abnormal bleeding times. Several abnormali-
ties in serum electrolytes and mineral metabolism become
manifest when the GFR drops below 30 mL/min. Progres-
sive reduction of body buffer stores and an inability to
excrete titrable acids result in progressive acidosis charac-
terized by reduced serum bicarbonate and compensatory
respiratory hyperventilation. The metabolic acidosis of
uremia is associated with a normal anion gap, hyperchlore-
mia, and normokalemia. Hyperkalemia is not usually seen
unless the GFR is below 5 mL/min. In patients with inter-
stitial renal diseases, gouty nephropathy, or diabetic neph-
ropathy, hyperchloremic metabolic acidosis with hyper-
kalemia (renal tubular acidosis, type IV) may develop. In
these cases the acidosis and hyperkalemia are out of pro-
portion to the degree of renal failure and are related to a
decrease in renin and aldosterone secretion. In moderate to
severe CKD, multiple factors lead to an increase in serum
phosphate and a decrease in serum calcium. The hyper-
phosphatemia develops as a consequence of reduced phos-
phate clearance by the kidney. In addition, vitamin D
activity is diminished because of reduced conversion of
vitamin D2 to the active form of vitamin D3 in the kidney.
These alterations lead to secondary hyperparathyroidism
with skeletal changes of both osteomalacia and osteitis fib-
rosa cystica. Uric acid levels are frequently elevated but
rarely lead to calculi or gout during chronic uremia.
D. X-RAY FINDINGS
Patients with reduced renal function should not be rou-
tinely subjected to contrast studies. Renal sonograms are
helpful in determining renal size (usually small) and corti-
cal thickness (usually thin) and in localizing tissue for per-
cutaneous renal biopsy. Bone x-rays may show retarded
growth, osteomalacia (renal rickets), or osteitis fibrosa.
Soft-tissue or vascular calcification may be noted on plain
films. Patients with polycystic kidney disease will have vari-
ably large kidneys with evident cysts (on sonograms or
plain abdominal CT scans).
E. RENAL BIOPSY
Renal biopsies may not reveal much except nonspecific
interstitial fibrosis and glomerulosclerosis. There may be
pronounced vascular changes consisting of thickening of
the media, fragmentation of elastic fibers, and intimal pro-
liferation, which may be secondary to uremic hypertension
or due to primary arteriolar nephrosclerosis. Percutaneous
or open biopsies of end-stage shrunken kidneys are associ-
ated with a high morbidity rate, particularly bleeding.
Treatment
Recent studies indicate some benefit of drugs to reduce
progression of CKD. These approaches include the use
of angiotensin-converting enzyme inhibitors, angiotensin
receptor blockers, lipid-lowering agents, and aldosterone
antagonists. Patients need to be followed closely for poten-
tial hyperkalemia.
Overall, management should be conservative until it
becomes impossible for patients to continue their custom-
ary lifestyles. Restriction of dietary protein (0.5 g/kg/day),
potassium, and phosphorus is recommended. As well,
maintenance of close sodium balance in the diet is neces-
sary so that patients become neither sodium-expanded nor
-depleted. This is best done by the accurate and frequent
monitoring of the patient’s weight. Use of oral bicarbonate
can be helpful when moderate acidemia occurs. Anemia
can be treated with recombinant erythropoietin given sub-
cutaneously. Prevention of possible uremic osteodystrophy
and secondary hyperparathyroidism requires close atten-

tion to calcium and phosphorus balance. Phosphate-
retaining antacids and calcium or vitamin D supplements
may be needed to maintain the balance. Cinacalet can
directly reduce parathyroid hormone secretion. If severe
secondary hyperparathyroidism occurs, subtotal parathy-
roidectomy may be needed.
A. CHRONIC PERITONEAL DIALYSIS
Chronic peritoneal dialysis is used electively or when cir-
cumstances (ie, no available vascular access) prohibit
chronic hemodialysis. Ten percent of dialysis is done with
this treatment. Improved soft catheters can be used for
repetitive peritoneal lavages. In comparison to hemodialy-
sis, small molecules (such as creatinine and urea) are
cleared less effectively than larger molecules, but excellent
treatment can be accomplished. Intermittent thrice-weekly
treatment (IPPD), continuous cycler-assisted peritoneal
dialysis (CCPD), or chronic ambulatory peritoneal dialysis
(CAPD) is possible. With the latter, the patient performs
3–5 daily exchanges using 1–2 L of dialysate at each
exchange. The dialysate contains a high glucose concentra-
tion and the peritoneal surface serves as the semipermeable
membrane. Bacterial contamination and peritonitis are
becoming less common with improvements in technology.
B. CHRONIC HEMODIALYSIS
Chronic hemodialysis using semipermeable dialysis
membranes is now widely performed. Access to the vas-
cular system is provided by an arteriovenous fistula, vas-
cular grafts (with autologous saphenous vein or synthetic
material), or by a percutaneous permcatheter (placed
either surgically or with interventional radiology). The
actual dialyzers are of various geometries. Body solutes
and excessive body fluids can be easily cleared by using
dialysate fluids of known chemical composition. Newer,
high-efficiency membranes (high/flux) are serving to
reduce dialysis treatment time.
Treatment is intermittent—usually 3–5 hours three
times weekly. Computer modeling, using measurements of
urea kinetics, has provided more precise hemodialysis pre-
scriptions. Treatments may be given in a kidney center, a
satellite unit, or the home. Home dialysis is optimal
because it provides greater scheduling flexibility and is gen-
erally more comfortable and convenient for the patient,
but only 20% of dialysis patients meet the requirements
for this type of therapy.
More widespread use of dialytic techniques has permit-
ted greater patient mobility. Treatment on vacations and
business trips can be provided by prior arrangement.
Common problems with either type of chronic dialysis
include infection, bone symptoms, technical accidents, per-
sistent anemia, and psychological disorders. The excessive
morbidity and mortality associated with atherosclerosis
often occurs with long-term treatment. It is now recognized
that occasionally uremic patients, despite dialysis, can
CHRONIC RENAL FAILURE & DIALYSIS / 537
develop wasting syndrome, cardiomyopathy, polyneuropa-
thy, and secondary dialysis-amyloidosis so that kidney
transplant must be urgently done. Routine bilateral nephre-
ctomy should be avoided because it increases the transfu-
sion requirements of dialysis patients. Nephrectomy in dial-
ysis patients should be performed in cases of refractory
hypertension, reflux with infection, and cystic disease with
recurrent bleeding and pain. The dialysis patient can occa-
sionally have acquired renal-cystic disease. Such patients
need close monitoring for the development of in situ renal
cell carcinoma.
Yearly costs range from an average of $50,000 for
patients who receive dialysis at home to as much as
$50,000–$75,000 for patients treated at dialysis centers,
but much of this is absorbed under HR-1 (Medicare) leg-
islation. If the patient has no other systemic problems
(eg, diabetes), the mortality rates are 8–10%/year once
maintenance dialysis therapy is instituted. Despite these
medical, psychological, social, and financial difficulties,
most patients lead productive lives while receiving dialy-
sis treatment.
C. RENAL TRANSPLANTATION
After immunosuppression techniques and genetic match-
ing were developed, renal homotransplantation became an
acceptable alternative to maintenance hemodialysis.
Improved transplantation results are now noted owing to
the development of newer immunosuppressant drugs.
Currently employed posttransplant drugs include predni-
sone, azathioprine, mycophenolate mofetil, cyclosporine,
tacrolimus, sirolimus, and a variety of injectable bioagents.
The great advantage of transplantation is reestablishment
of nearly normal and constant body physiology and chem-
istry. Diet can be less restrictive. The disadvantages include
bone marrow suppression, susceptibility to infection,
oncogenesis risks, and the psychological uncertainty of the
homograft’s future. Most of the disadvantages of trans-
plantation are related to the medicines given to counteract
the rejection. Later problems with transplantation include
recurrent disease in the transplanted kidney and an
increased incidence of cancer. Genitourinary infection
appears to be of minor importance if structural urologic
complications (eg, leaks) do not occur.
Nephrology centers, with close cooperation between
medical and surgical staff, attempt to use these treatment
alternatives of dialysis and transplantation in an integrated
fashion.
For a more detailed review, see Chapter 35.
REFERENCES
Atkins RC et al: Proteinuria reduction and progression to renal failure
in patients with type 2 diabetes mellitus and overt nephropathy.
Am J Kidney Disease 2005;45:281.
Astor BC et al: Type of vascular access and survival among incident he-
modialysis patients. J Amer Soc Neph 2005;16:1449.
538 / CHAPTER 34
Clinical Practice Guidelines and Clinical Practice Recommendations
2006: K/DOQI Advisory Panel (Excerpts). Am J Kidney Dis
2006;48(Suppl 1):1.
Coresh J et al: Chronic kidney disease awareness, prevalence and trends
among U.S. adults. J Am Soc Neph 2005;16:180.
Daugas E et al: HAART-related nephropathies in HIV-infected pa-
tients. Kidney Int 2005;67:393.
El Nahas M: The global challenge of chronic kidney disease. Kidney
Int 2005;68:2918.
Go AS et al: Chronic kidney disease and the risks of death, cardiovas-
cular events, and hospitalization. N Engl J Med 2004;351:1296.
Hsu CY et al: Elevated blood pressure and risk of end-stage renal
disease in subjects without baseline kidney disease. Arch Int
Med 2005;165:923.
K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease:
Evaluation, classification, and stratification (excerpts). Am J Kid-
ney Dis 2002;39(Suppl 1):1.
Remuzzi G et al: Chronic renal disease: Renoprotection benefits of
renin-angiotensin system inhibition. Ann Intern Med 2002;136:
304.
Stewart JH et al: Cancers of the kidney and urinary tract in patients on
dialysis for end-stage renal disease. J Amer Soc Neph 2003;14:197.
U.S. Renal Data System 2005: Annual Data Report (Excerpts). Am J
Kidney Dis 2006;47(Suppl 1):1.