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CHAPTER 30 Chronic Kidney Disease
Prevalence (per million)
2200
Year
Incidence rate (per million/year)
400
Year
334.e1
350
300
250
200
150
100
50
0
80
82 84 86 88 90 92 94 96 98
E-Fig. 30.1 Trends in the crude and standardized incidence rates
of ESRD. (From U.S. Renal Data System: USRDS 2018 annual data
report: atlas of chronic kidney disease and end-stage renal disease in
the United States, Bethesda, Md., 2018, National Institutes of Health,
National Institute of Diabetes and Digestive and Kidney Diseases.)
Standardized incidence rate
Crude incidence rate
00 02 04 06 08 10 12 14 16
2000
1800
1600
1400
1200
1000
800
600
400
200
0
82 84 86 88 90 92 94 96 98
80
E-Fig. 30.2 Trends in the crude and standardized prevalence rates
of ESRD. (From U.S. Renal Data System: USRDS 2018 annual data
report: atlas of chronic kidney disease and end-stage renal disease in
the United States, Bethesda, Md., 2018, National Institutes of Health,
National Institute of Diabetes and Digestive and Kidney Diseases.)
Standardized prevalence
Crude prevalence
00 02 04 06 08 10 12 14 16
CHAPTER 30 Chronic Kidney Disease
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TABLE 30.1 Categories of Glomerular Filtration Rate and Albuminuria in CKD
Category GFR (mL/1.73 m2/min) Terms
a
G1
a
G2
G3a 45-59 Mildly to moderately decreased
G3b 30-44 Moderately to severely decreased
G4 15-29 Severely decreased
G5 <15 Kidney failure
AER ACR
Category (mg/24 hours) (mg/g) (mg/mmol) Terms
A1 <30 <30 <3 Normal to mildly increased
A2 30-300 30-300 3-30 Moderately increased
A3 >300 >300 >30 Severely increased
ACR, Albumin-to-creatine ratio; AER, albumin excretion rate; GFR, glomerular filtration rate.
a
G1 and G2 alone, without other evidence of kidney damage, do not meet the criteria for CKD.
Normal to high ≥90 54.9 4.2
G1
)
2
GFR categories
(ml/min/1.73 m
Mildly decreased 60–89 30.2 2.9
G2
Mildly to moderately
G3a
decreased
Moderately to severely
G3b
decreased
Severely decreased 15–29
G4
Kidney failure <15
G5
Fig. 30.1 Distribution of CKD in the United States by GFR and albuminuria categories.
≥90 Normal or high
60-89 Mildly decreased
Albuminuria categories
A1 A2 A3
Normal to mildly
increased
<30 mg/g <3
mg/mmol
45–59 3.6
30–44
Total
1.0 0.4 0.2
0.13 0.10 0.15
0.01
89.9
Moderately
increased
30-300 mg/g 3-30
mg/mmol
0.8 0.3
0.04
8.5
Severely
increased
>300 mg/g >30
mg/mmol
0.5
0.3
0.09
1.6
Total
59.6
33.5
4.7
1.7
0.37
0.13
100
335
β2-microglobulin accumulation in patients with ESRD has been associ-
ated with neuropathy, carpal tunnel syndrome, and amyloid infiltration
of the joints. Finally, certain protein-bound solutes such as indoxyl sulfate and the conjugates of p-cresol, may confer cardiovascular toxicity by
weight loss, and those with severe uremia may also experience stomatitis and enteritis. There may be gastrointestinal bleeding caused by
gastritis, peptic ulceration, and arterial venous malformations in the
setting of platelet dysfunction.
affecting leukocyte, endothelial, and vascular smooth muscle cell function. Major manifestations of uremia are summarized in Fig. 30.3.
Neurologic
Central nervous system (CNS) manifestations are frequent in advanced
Cardiovascular
In addition to hypertension, cardiovascular disorders are common in
patients with CKD. More than 60% of patients with ESRD who start dialysis have echocardiographic manifestations of left ventricular hypertrophy,
dilation, and systolic or diastolic dysfunction. Metabolic consequences of
CKD, including accelerated atherogenesis, contribute to metastatic calcification in the myocardium, cardiac valves, and arteries. Arrhythmias,
including those resulting in sudden death, may be caused by electrolyte
abnormalities, cardiac structural changes or ischemic cardiovascular disease. Pericarditis can occur in patients with uremia before they start dial-
CKD and characterized predominantly by changes in cognitive func-
tion and sleep disturbances. Lethargy, irritability, asterixis, seizures,
and frank encephalopathy with coma are late manifestations of ure-
mia and are usually avoided by timely initiation of kidney replacement
therapy. Peripheral neurologic manifestations appear as a progressive
symmetrical sensory neuropathy in a glove-and-stocking distribution.
Patients have decreased distal tendon reflexes and loss of vibratory per-
ception. Peripheral motor impairment can result in restless legs, foot-
drop, or wristdrop. The majority of these neurologic manifestations
reverse with maintenance dialysis or kidney transplantation.
ysis, as well as in ESRD patients receiving inadequate dialysis.
Musculoskeletal
Gastrointestinal
Gastrointestinal disturbances are among the earliest and most common signs of the uremic syndrome. Patients describe a metallic taste
and loss of appetite. Later, they experience nausea, vomiting, and
Alterations in calcium and phosphate homeostasis, with hyperparathy-
roidism and disturbance of vitamin D metabolism, are also common.
Hypocalcemia and secondary hyperparathyroidism are the result of
phosphate retention and the lack of α1-hydroxylase activity in the failing
Deficiencies
• Urea
Excesses
• β2-microglobulin
• Calcium
• 1,25 Vit. D
• Testosterone
• Estrogen
• Erythropoietin
E-Fig. 30.3 Etiologic factors of uremia. PTH, Parathyroid hormone; 1,25
Vit. D, 1,25-dihydroxyvitamin D.
Uremia
• Trace elements
• Guanidine compounds
• Polyamines
• PTH
• Prolactin
• Phosphorus
• Potassium
CHAPTER 30 Chronic Kidney Disease
335.e1
336 SECTION V Renal Disease
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Cardiovascular
disease
↑ Blood
pressure
↓ Nephron
endowment
↓ Nephron
number
Acquired nephron loss
Primary renal disease
Hereditary nephropathies
Aging Nephrotoxins
Fig. 30.2 A simplified depiction of risk factors interacting with pathophysiologic mechanisms to acceler-
ate chronic kidney disease progression. DM, Diabetes mellitus; FSGS, focal segmental glomerulosclerosis;
TIF, tubulointerstitial fibrosis. (Adapted from Taal MW, Brenner BM: Predicting initiation and progression of
chronic kidney disease: Developing renal risk scores. Kidney Int 70:1694-1705, 2006.)
Skin
• Pruritus
• Yellow
pigmentation
Endocrine/metabolic
• Hyperparathyroidism
• Increased insulin resistance
• Amenorrhea
• Impotence
• Hyperlipidemia
Acid-base/electrolytes
• Anion gap acidosis
• Hyperkalemia
• Fluid overload
• Hypocalcemia
• Hyperphosphatemia
• Hypermagnesemia
Pulmonary
• Noncardiogenic
pulmonary edema
• Pneumonitis
• Pleuritis
Hyperfiltration states;
DM, obesity, high-protein
diet, anemia
Progression
of kidney
disease
↑ Ang II
FSGS
TIF
ACUTE KIDNEY
INJURY
Nervous System
(Central)
• Irritability
• Insomnia
• Lethargy
• Anorexia
• Seizures
• Coma
Uremic Syndrome
(Peripheral)
• Glove-and-stocking
sensory loss
• Restless leg
• Footdrop or wrist
drop
Cardiovascular
• Cardiomyopathy
• Arrhythmias
• Pericarditis
• Accelerated
atherosclerosis
Proteinuria
Dyslipidemia
Glomerular
cell injury
Inflammatory
response
Musculoskeletal
• Muscle weakness
• Gout and pseudogout
• Renal osteodystrophy
Hematologic
• Anemia
• Bleeding disorders
• Leukocyte dysfunction
Gastrointestinal
• Anorexia
• Nausea
• Vomiting
• Disturbance of taste
• Gastritis
• Peptic ulcer
• GI bleeding
Fig. 30.3 Diagrammatic summary of the major manifestations of the uremic syndrome. GI, Gastrointestinal.
kidney, with consequent deficiency of the most active form of vitamin D. Over time, maladaptive parathyroid hypertrophy (i.e., tertiary
hyperparathyroidism) leads to bone disease and tissue calcification.
progresses. EPO and iron deficiency are common causes of anemia in
CKD. Administration of synthetic EPO results in correction of anemia,
improved quality of life and anemia-related symptoms, and decreased
dependence on blood transfusions. Caution must be exercised because
Hematologic and Immunologic
Erythropoietin (EPO), a hormone produced by the kidney that regulates erythrocyte production, becomes progressively deficient as CKD
higher doses of EPO resulting in elevations of the serum hemoglobin
to more than 13 g/dL may be associated with a higher risk for adverse
cardiovascular events. Bleeding disorders, primarily from defects in
CHAPTER 30 Chronic Kidney Disease
337
platelet adherence and aggregation, are common in patients with uremia. Uremic bleeding can be generally controlled with cryoprecipitate,
desmopressin, conjugated estrogens, treatment of anemia, and dialysis.
Defects occur in both the humoral and cellular immune systems
in patients with CKD. Although the leukocyte count is normal and
appropriately responsive in advanced CKD, patients are generally
immunosuppressed and susceptible to infections. This may be due to
functional abnormalities of polymorphonuclear leukocytes, lymphocytes, and other cellular host defenses. Additionally, patients with CKD
may have a variable immune response to vaccination.
Endocrine and Metabolic
Thyroid function testing may be less reliable in uremia. Common laboratory findings include an increased triiodothyronine resin uptake,
a low triiodothyronine level resulting from the impaired conversion
of thyroxine to triiodothyronine peripherally, and normal thyroxine
levels. Thyroid-stimulating hormone levels are usually normal.
A deranged pituitary-gonadal axis can result in sexual dysfunction
exhibited by impotence, decreased libido, amenorrhea, sterility, and
uterine bleeding. Patients have decreased plasma levels of testosterone, estrogen, and progesterone, with normal or increased levels of
follicle-stimulating hormone, luteinizing hormones, and prolactin.
Pregnancy is uncommon in female patients who have a GFR of less
than 30 mL per minute.
Lipid abnormalities are also common in CKD. They are most consistent with type IV hyperlipoproteinemia, with a marked increase in
plasma triglycerides and less of an increase in total cholesterol. The
activity of lipoprotein lipase is decreased in uremia, with a reduction
in the conversion of very-low-density lipoprotein to low-density lipoprotein and thus hypertriglyceridemia. The treatment of choice is the
hydroxymethylglutaryl–coenzyme A reductase (HMG-CoA) inhibitor
class of drugs, especially in CKD patients not yet on maintenance dialysis,
because of their pluripotent effects on inflammation and atherosclerosis.
Electrolytes
Hyperkalemia occurs in patients with CKD as a result of decreased
renal clearance of potassium, intracellular to extracellular shifts of
potassium in the setting of metabolic acidosis related to kidney failure,
and the concomitant use of medications such as RAAS blockers. The
primary method of treatment is dietary reduction of potassium but
may also include use of loop diuretics or potassium-binding medications. Hypokalemia is much less common in CKD but may occur in
the setting of very poor nutritional intake or use of high-dose potassium-wasting diuretic medications.
Skin
Uremic hue, a yellowish skin color, is likely the result of retained liposoluble pigments, such as lipochromes and carotenoids. Uremic hue usually responds to dialysis, control of hyperparathyroidism, improved
calcium and phosphate balance, and, occasionally, ultraviolet rays. Nail
findings of uremia include the half-and-half nail, characterized by red,
pink, or brownish discoloration of the distal nail bed, pale nails, and
splinter hemorrhages. Other common signs and symptoms include
pruritus, and ecchymoses due to disorders of bleeding. Calciphylaxis,
or calcific uremic arteriolopathy, results in painful skin calcification and
is often seen in patients with uncontrolled hyperparathyroidism. Use of
warfarin is suggested to be a risk factor for this condition.
DIAGNOSIS
Comprehensive care of kidney disease includes screening, diagnosing, and treating CKD and complications of CKD to prevent CKD
development and progression (E-Fig. 30.4). Screening for CKD is
recommended in patients with high-risk comorbid disease, including
diabetes mellitus and hypertension and those with a family history
of kidney disease. The diagnosis of chronic kidney disease requires
demonstrating evidence of kidney damage that has been persistent
for at least 3 months. Imaging abnormalities may be consistent with
kidney damage, but more commonly this is shown by detection of
albuminuria or by reductions in the clearance of toxins by the kidney.
Albuminuria may be detected in a spot collection of urine and is best
when reported as an albumin-to-creatinine ratio (ACR). In general, an
ACR of 30 mg/g or greater confirmed on repeat sample and without
evidence of urinary infection raises concern for a diagnosis of CKD and
warrants additional investigation.
Measurement of clearance of toxins by the kidney is most often
estimated as the glomerular filtration rate (eGFR). Initial assessment
should be performed using a serum creatinine-based estimating equation. These include the Modification of Diet in Renal Disease (MDRD)
Study Equation and the Chronic Kidney Disease Epidemiology
Collaboration (CKD-EPI) equation. Each of these has limitations and
cautions regarding application of its results, and a detailed overview
can be found in the KDIGO 2012 Clinical Practice Guidelines. Another
serum biomarker, cystatin C, may be considered and integrated into
another estimating equation for patients who have an eGFR 45-59 mL/
min/1.73 m2 and who may not have albuminuria or kidney imaging
abnormalities to confirm evidence of CKD.
Once a diagnosis of CKD is established, management goals include
(1) prevention of progression of CKD, (2) identifying and treating
symptoms and complications of CKD, and (3) preparing patients for
renal replacement therapy (RRT) where appropriate.
TREATMENT
Prevention of Progression
In addition to treatment of the specific underlying cause of kidney
disease, methods used to slow progression of CKD include optimal
control of hypertension, diabetes, and other cardiovascular disease
risk factors (i.e., tobacco cessation), use of medications that block the
RAAS pathway, diet modifications, avoidance of nephrotoxins, and
addressing potentially reversible causes of acute kidney injury in the
setting of CKD.
Management of Hypertension and Diabetes
Several controlled trials have conclusively confirmed that treatment
of hypertension attenuates the rate of progression of kidney disease.
The present recommendation is to target blood pressure to lower than
130/80 mm Hg in patients with diabetes or kidney disease. However, the
evidence supporting this recommendation in CKD is limited and there
is debate suggesting a higher target may be acceptable. Medications
that block the production or effect of angiotensin II prevent the progression of CKD above and beyond control of hypertension in patients
with proteinuria. Dihydropyridine calcium-channel blockers have not
been shown to be as beneficial as ACE inhibitors or ARBs in slowing
CKD progression.
For patients with diabetes mellitus, adequate glycemic control has
been shown to prevent progression of CKD. Recommended goal glycosylated hemoglobin (A1c) measures are less than 7% irrespective of
a concurrent diagnosis of CKD, although this level of glycemic control warrants caution due to hypoglycemic risk (see Chapter 68). ACE
inhibitors and ARBs may be considered in patients with diabetes and
proteinuria, but without hypertension, to slow CKD progression. More
recently, use of sodium-glucose cotransporter-2 (SGLT2) inhibitors
have shown beneficial effects on kidney outcomes mainly in patients
CHAPTER 30 Chronic Kidney Disease
Screening f
Slow progression
replacement
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Complications
337.e1
Normal
or CKD
risk factors
E-Fig. 30.4 Approach to care for patients with chronic kidney disease (CKD) and its complications: screening,
diagnosis, and treatment. GFR, Glomerular filtration rate. (From National Kidney Foundation: K/DOQI clinical
practice guidelines for chronic kidney disease: evaluation, classification, and stratification, Am J Kidney Dis
39[2 Suppl 1]:S1-S266, 2002.)
Increased
risk
CKD risk
reduction,
Screening
for CKD
Damage
Diagnosis
and treatment,
Treat comorbid
conditions,
↓ GFR
Estimate
progression,
Treat complications,
Prepare for
Kidney
failure
Replacement
by dialysis and
transplantation
CKD
death
338 SECTION V Renal Disease
TABLE 30.2 Drug Dosages in Chronic Kidney Disease
Major Dosage Reduction Minor or No Reduction Avoid Usage
Antibiotics
Aminoglycosides Erythromycin
Penicillin Nafcillin Nitrofurantoin
Cephalosporins Clindamycin Nalidixic acid
Sulfonamides Chloramphenicol Tetracycline
Vancomycin Isoniazid, rifampin
Quinolones Amphotericin B
Fluconazole Aztreonam, tazobactam
Acyclovir, ganciclovir Doxycycline
Foscarnet
Imipenem
Others
Digoxin Antihypertensives Aspirin
Procainamide Benzodiazepines Sulfonylureas
H2 antagonists Quinidine Lithium carbonate
Meperidine Lidocaine Acetazolamide
Codeine Spironolactone NSAIDs
Propoxyphene Triamterene Phosphate-containing bowel-preparation agents
NSAIDs, Nonsteroidal anti-inflammatory drugs.
with type 2 diabetes and established atherosclerotic cardiovascular disease. Several other studies suggested that treatment with glucagon-like
peptide-1 (GLP-1) receptor agonists could also have beneficial effects
on kidney outcomes in patients with type 2 diabetes.
Diet
Dietary protein restriction is advocated to slow progression of CKD.
Several meta-analyses indicate that reduced protein diets may be
modestly beneficial to slow CKD progression, but the largest clinical
trial, the MDRD study, did not show a significant benefit. The recommended dietary protein intake in advanced CKD is 0.60 g/kg per
day with at least 50% of the protein being of high biologic value. The
present consensus is that aggressive dietary management in patients
with CKD, with proper restriction of sodium, potassium, phosphorus,
and protein intake under the supervision of a dietician, may reduce
progression of CKD, albeit to a small extent.
Avoidance of Toxic Drug Effects
Many drugs that are excreted by the kidney should be avoided, or
their doses should be reduced, as shown in Table 30.2. Drugs may
injure the kidney in many ways, including direct toxicity leading to
acute tubular necrosis, induction of interstitial nephritis, or development of urinary crystals that obstruct the kidney. Common classes
of medications that injure the kidney include antibiotics, specifically
aminoglycosides; nonsteroidal anti-inflammatory drugs, including
cyclo-oxygenase-2 (COX-2) inhibitors; and antiretroviral medications. Over-the-counter herbal medications, including aristolochic
acids, may cause CKD. Others, such as St. John’s Wort, may interact
with kidney transplant medications and should be avoided. Iodinated
radiocontrast agents can cause acute worsening of kidney function,
especially in patients with CKD. Iso-osmolar contrast agents are less
toxic than high-osmolar agents. Patients at high risk for contrastinduced kidney injury should receive adequate hydration, and the
volume of the contrast should be minimized. The magnetic resonance
imaging (MRI) contrast agent gadolinium, has been associated with
the severe fibrotic skin condition of nephrogenic systemic fibrosis in
patients with advanced CKD.
Reversible Causes of Acute Deterioration in Kidney Function
The rate of decline in GFR for individual patients is generally log linear. Accordingly, plotting 1/serum creatinine against time usually predicts the rate at which a specific patient will reach ESRD (E-Fig. 30.5).
When such a patient suddenly shows acute worsening of kidney function, the differential diagnosis should be considered and investigated,
as described in Chapter 29.
Care for the Patient With End-Stage Renal Disease
As CKD progresses to kidney failure, preparation is needed for RRT.
Patients with moderate CKD should be referred to a nephrologist for
co-management, including evaluation of risk for CKD progression,
estimation of timing until initiation of RRT, and education related
to RRT. Late referral (<3 months before ESRD) is associated with a
higher risk for death after initiation of RRT.
Renal Replacement Therapies
For patients who are suspected to progress to ESRD, discussions to
inform patients and their family about available options of RRT should
occur early and be paired with an assessment of the expectations and
values of the patient. Options include kidney transplantation, dialysis
or medical management without dialysis, sometimes referred to as conservative care. In suitable candidates, kidney transplantation is encouraged because it allows a better quality of life, increased survival rate, and
greater chance for rehabilitation. In 2016, 87.3% of incident individuals began renal replacement therapy with hemodialysis (HD), 9.7%
started with peritoneal dialysis (PD), and 2.8% received a preemptive
kidney transplant. Kidney transplants may be from either deceased or
living donors. In the United States in 2016, 20,161 kidney transplants
were performed, 28% of which were from living donors. There are
two types of dialysis, hemodialysis and peritoneal dialysis. The distribution of patients receiving various modalities differs in other countries. Maintenance dialysis is initiated when the patient displays signs of
uremia, usually when eGFR is 10 mL per minute or less and there are
no apparent reversible causes of kidney failure. However, maintenance
dialysis may be started at any time when complications of ESRD, such
as volume overload and hyperkalemia, cannot be controlled medically.
CHAPTER 30 Chronic Kidney Disease
1.0
0.8
0.6
0.4
0.2
Years of observation
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338.e1
I/P
cr
Accelerated
loss
0
E-Fig. 30.5 Use of the reciprocal of plasma creatinine concentration (1/
PCr) to follow the progress of glomerular disease in a patient. CCr, Creatinine clearance rate. (Data from Sullivan LP, Grantham JJ: Physiology of
the kidney, ed 2, Philadelphia, 1982, Lea & Febiger.)
Successful treatment
Constant
decrease in
Ccr/yr
CHAPTER 30 Chronic Kidney Disease
detector
Venous
pressure
339
Dialyzer
Heparin pump
Blood
pump
Dialysate
out
Arterial
pressure
monitor
Fig. 30.4 Essential components of a dialysis delivery system that,
together with the dialyzer, make up an artificial kidney. In isolated ultrafiltration, no dialysis fluid is used (bypass mode). Also shown is the
apparatus for using a single needle for inflow and outflow of blood from
the patient. (From Keshaviah PR: Hemodialysis monitors and monitoring. In Maher JF [ed]: Replacement of renal function by dialysis, 3rd ed.
Boston, Kluwer Academic Publishers, 1989. Reprinted by permission of
Kluwer Academic Publishers.)
Automatic clamps
for single needle
Dialysis
fluid in
monitor
Air
Automatic
clamp
Hemodialysis
As illustrated in Fig. 30.4, blood is pumped from a vascular access into
tubing that leads to a large number of capillaries bundled together in
a dialyzer (E-Fig. 30.6). The capillaries are made up of semisynthetic
materials and are semipermeable, capable of allowing exchange of
small molecules. Moving in the opposite direction to blood is a dialysate solution that is passing through outside the capillaries, thus allowing countercurrent exchange. This solution contains sodium chloride,
bicarbonate, and varying concentrations of potassium. Diffusion
through the membrane allows low-molecular-weight substances such
as urea and organic acids to move across according to the concentration gradient. Fluid is removed by ultrafiltration, which is achieved by
applying transmembrane hydrostatic pressure across the dialyzer.
In the setting of ESRD, an average patient undergoing intermittent
maintenance hemodialysis requires 4 hours of dialysis 3 times a week.
Common complications during hemodialysis include hypotension
and muscle cramping. Avoiding excessive fluid weight gain can minimize these complications.
Access for hemodialysis. The recommended access for hemodialysis
is a permanent access such as an arteriovenous fistula (AVF) or
arteriovenous graft (AVG), rather than an indwelling catheter. Although
the goal is for more than 70% of prevalent hemodialysis patients to use
an AVF or AVG for dialysis access (http://www.healthypeople.gov/2020/),
many patients continue to use catheters, especially at the time of initiation
of maintenance hemodialysis. Temporary catheters are placed into the
internal jugular, subclavian, or femoral veins similar to other central
venous lines. Permanent catheters have a cuff around the outer wall of
the tubing and tunnel under the chest wall skin for some distance before
entering the internal jugular vein. Catheters have higher rates of infection
and a higher risk for mortality compared with AVF and AVG.
Peritoneal Dialysis
In peritoneal dialysis, the peritoneal capillaries act as a semipermeable
membrane like a hemodialysis dialyzer. This technique has several
advantages over hemodialysis because it allows independence from the
long time spent in dialysis units, it does not require as stringent dietary
restrictions, and more patients return to full-time employment. In continuous ambulatory peritoneal dialysis, dialysate of 2- to 3-L volumes
is instilled through a peritoneal catheter (E-Fig. 30.7) into the peritoneal cavity for varying amounts of time and exchanged 4 to 6 times
daily. In continuous cyclic peritoneal dialysis, the patient is connected
to a machine referred to as a cycler that allows inflow of smaller volumes of dialysate with shorter dwell time overnight while the patient
sleeps. Modifications in this regimen can be made to fit a patient’s
lifestyle and still achieve adequate clearance of toxins and removal of
fluid. Ultrafiltration is achieved through increasing dextrose concentration in the dialysate. Two major drawbacks of peritoneal dialysis are
peritonitis and difficulty in achieving adequate clearances in patients
with excess body mass. Peritonitis can be treated with intraperitoneal
antibiotics. Additionally, a slow deterioration occurs in the permeability of the peritoneal membrane, especially after one or more peritonitis
episodes, leading to inadequate dialysis and, ultimately, the need to
change the modality of RRT.
Kidney Transplantation
Kidney transplantation is the preferred modality of RRT. In suitable
candidates, it provides patients with superior survival and a better
quality of life compared to remaining on maintenance dialysis. It is
also a more cost-effective long-term treatment option compared to
maintenance dialysis. The variety of available immunosuppressive
therapies, including calcineurin inhibitors (cyclosporine and tacrolimus), mammalian target of rapamycin (mTOR) inhibitors (sirolimus and everolimus), mycophenolate mofetil/mycophenolic acid,
and novel agents such as belatacept have resulted in excellent shortand long-term graft survival.
Types of kidney transplants. Kidney transplant donors may
be deceased or living and, among those living, may be related or
unrelated. The majority of deceased donation occurs after brain death
but can also occur after cardiac death. Deceased donor 1-year and
5-year graft survival is 93% and 75%, and a living donor is 98% and
85%, respectively.
There is an effort to increase living donation because the deceased
donor supply is inadequate, resulting in prolonged waiting times
for recipient candidates on the deceased donor waiting list. The
advantages and disadvantages of living versus deceased donor transplantation are summarized in Table 30.3. The use of kidney paired
donation and/or desensitization allows for transplantation of recipients with potential donors who are blood group or immunologically
incompatible. Kidney paired donation utilizes exchange algorithms
to bypass incompatibility by matching blood group or human leukocyte antigen (HLA)-incompatible recipient-donor pairs with other
incompatible pairs, resulting in each donor donating a kidney to the
other person’s intended recipient. On the other hand, desensitization
utilizes antibody-directed therapy such as plasmapheresis or intravenous immunoglobulin to reduce donor-specific HLA antibodies
or blood group antibodies in recipients to prevent acute rejection
despite blood group or HLA incompatibility. As a means of expanding the supply of deceased donor kidneys and reducing deceased
donor waiting times, kidneys from marginal donors such as those of
advanced age or with comorbid conditions such as hypertension and
cerebrovascular disease are utilized in selected recipients who would
benefit from earlier transplantation. In addition, increased Public
Health Service risk donors, such as those who have a history of intravenous drug abuse, are increasingly being utilized. In the setting of
negative nucleic acid testing, the absolute risk of transmission of hepatitis C, human immunodeficiency virus, and hepatitis B virus from
these donors is less than 1%.
CHAPTER 30 Chronic Kidney Disease
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339.e1
E-Fig. 30.6 Dialyzers for hemodialysis.
E-Fig. 30.7 Figure demonstrating basic peritoneal dialysis. (Courtesy
David Schlosser.)
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