17 Terapias de Reemplazo Renal - ClinicalKey

Renal Replacement Therapy, Chronic Kidney Disease - ClinicalKey 9/07/23, 4:11 p.m.
CLINICAL OVERVIEW
Renal Replacement Therapy, Chronic Kidney Disease

Manish K. Saha MD
Actualizado November 16, 2022. Copyright Elsevier BV. All rights reserved.
Summary
Key Points
Decision to start renal replacement therapy is complex and usually based on the complete clinical picture rather than a
stringent set of specific criteria used to guide therapy
Decision to initiate renal replacement therapy depends on many factors including overall clinical picture, trajectory of
metabolic derangements, urine output, volume status, and hemodynamic stability, among others
Initiation of maintenance hemodialysis for a patient with chronic kidney failure is an individualized and patient-centered
process
Consensus agreement is lacking regarding preferred timing (ie, early or late) initiation of renal replacement therapy in
patients with kidney failure
Absolute indications for initiating renal replacement therapy include complications arising secondary to uremia (eg, uremic
pericarditis, uremic encephalopathy, decline in mental status secondary to uremia), given lack of effective medical therapies
for uremia
Other common indications for initiating renal replacement therapy include diuretic-resistant volume overload, severe
metabolic acidosis, severe recalcitrant hypermagnesemia and hypercalcemia, and hyperkalemia-related indications
Additional relative indications for renal replacement therapy in patients with chronic kidney disease may include
malnutrition, recalcitrant pruritis, bleeding diathesis, and extreme fatigue and malaise
Selection of renal replacement therapy modality (continuous renal replacement therapy, intermittent hemodialysis,
peritoneal dialysis) primarily is based on hemodynamic stability, in-center experience and preference, comorbidities, and
other factors in consultation with a nephrologist
Alarm Signs and Symptoms

Altered mental status and cognitive dysfunction may indicate development of uremic encephalopathy; prepare for urgent
dialysis in consultation with nephrologist and consider alternate causes for altered mental status
Shortness of breath and markedly decreased urine output may indicate volume overload and need for urgent renal
replacement therapy
Rash, gross hematuria, hemoptysis, and joint pain or swelling may indicate underlying autoimmune cause of kidney injury
necessitating expedient diagnosis and treatment
https://www-clinicalkey-es.fucsalud.basesdedatosezproxy.com/#!/content/clinical_overview/67-s2.0-V2181 Página 1 de 18
Basic Information
Terminology
Renal replacement therapy
Broad term encompassing procedures most often used for patients with inadequate renal function secondary to significant
kidney injury. Renal replacement therapy is performed to do any of the following:
Remove nitrogenous waste products
Correct electrolyte disorders
Correct disorders of acid-base balance
Alleviate volume overload
Remove toxins
Different modalities of renal replacement therapy include the following:
Intermittent hemodialysis
Blood purification method suitable for hemodynamically stable patients accomplished over a period of several hours a
day and several days a week
Can be performed in an outpatient and inpatient setting
Continuous renal replacement therapy
Blood purification method performed continuously over 24 hours a day; may be used for hemodynamically unstable or
stable patients
Performed only in the ICU
Hybrid therapies
Include combination modalities of intermittent hemodialysis and continuous renal replacement therapy (eg, extended
duration dialysis, sustained low-efficiency dialysis)
Usually performed in an inpatient setting
Peritoneal dialysis
Blood purification method using peritoneal membrane as dialyzer
Can be performed in an outpatient or inpatient setting
Diagnostic criteria and general information
Chronic kidney disease is defined by KDIGO (Kidney Disease Improving Global Outcome) as abnormalities of kidney
structure or function present for more than 3 months with implications for health 1
Diagnosis requires presence of 1 of the following for more than 3 months 2 , 3 :
Reduced GFR: less than 60 mL/minute/1.73 m2
Kidney damage, as indicated by any of the following 4 :
Albuminuria greater than 30 mg/g or 30 mg per 24 hours
Active urinary sediment (eg, RBC casts, WBC casts, oval fat bodies, granular casts, dysmorphic RBCs)
Renal tubular damage (eg, renal tubular acidosis, Fanconi syndrome, channelopathies)
Pathologic abnormalities (eg, glomerulonephritis, interstitial nephritis, interstitial fibrosis)
Structural abnormalities detected by imaging (eg, polycystic kidney disease, kidney atrophy, cortical thinning)
History of kidney transplant
Most common conditions and medications encountered clinically that result in chronic kidney disease include diabetes,
hypertension, glomerulonephritis, interstitial nephritis, and nephrotoxin use
End stage kidney disease
Definitions vary and often are modified from a clinical standpoint 5
Currently, preferred terminology is chronic kidney disease stage 5 or 5D (indicating dialysis dependent) or kidney failure
rather than end-stage kidney disease 5
Staging and Classification

5 stages of chronic kidney disease based on GFR are described by KDIGO (Table 1 (https://www-clinicalkey-
es.fucsalud.basesdedatosezproxy.com/#!/content/clinical_overview/67-s2.0-V2181#t001)) as follows 3 :
G1: GFR 90 mL or more/min/1.73 m2
G2: GFR 60 to 89 mL/min/1.73 m2
G3a: GFR 45 to 59 mL/min/1.73 m2
G3b: GFR 30 to 44 mL/min/1.73 m2
G4: GFR 15 to 29 mL/min/1.73 m2
G5: GFR less than 15 mL/min/1.73 m2
Albuminuria stages are defined by KDIGO as follows 3 :
A1: 10 to 29 mg/g (high normal)
A2: 30 to 300 mg/g (high)
A3: greater than 300 mg/g (very high)
Table 1. Chronic kidney disease staging by GFR.
Chronic kidney disease stage GFR (mL/min/1.73 m 2) Presence of kidney damage
1 >90 Required
2 60-90 Required
3A 45-59 Not required
3B 30-44 Not required
4 15-29 Not required
5 <15 Not required

Título: KDIGO defines chronic kidney disease in the context of abnormalities lasting more than 3 months. Stage 1 chronic kidney disease includes patients with GFR within
reference range but with evidence of persistent kidney damage. Stage 2 chronic kidney disease includes patients with minimally decreased GFR but with evidence of
persistent kidney damage. Patients with diminished GFR less than 60 mL/min/1.73 m2 are classified as having stage 3 to 5 chronic kidney disease regardless of evidence of
persistent kidney damage (eg, albuminuria greater than 30 mg/24 hours, active urine sediment, renal tubular damage, pathologic or structural abnormalities, prior renal
transplant).
Risk Models and Risk Scores

Kidney failure risk equation
Uses demographic and laboratory data to predict progression of chronic kidney disease
(stages 3-5) to kidney failure within 2 and 5 years 6
Figure 1. GFR and albuminuria grid
Variables used in the equation are age, sex, urine albumin-to-creatinine ratio, and reflects the risk of progression by
estimated GFR intensity of coloring. Green, low risk
(if no other markers of kidney
Kidney failure risk equation calculator is available online 7 disease, no chronic kidney disease);
yellow, moderately increased risk;
Chronic kidney disease heatmap, illustrating risk of disease progression according to GFR orange, high risk; red, very high
risk.
and albuminuria categories, is shown in Figure 1 (https://www-clinicalkey-
es.fucsalud.basesdedatosezproxy.com/#!/content/clinical_overview/67-s2.0-V2181#f001)
Treatment
Approach to Treatment
General medical management principles for patients with chronic kidney disease
Optimize management of underlying medical comorbidities (eg, hypertension, diabetes mellitus)
Correct electrolyte derangements and acidosis, and optimize fluid balance
Recommend dietary changes 2 :
Reduce acid-rich foods (eg, animal protein)
Incorporate foods rich in alkali
For patients with high blood pressure and edema: consume low salt diet
For patients with stage G4 to G5 chronic kidney disease: restrict protein to 0.8 g/kg/day. Protein restriction may not be
appropriate for patients at risk for malnutrition or protein wasting syndrome 2
Address underlying anemia and maintain plasma hemoglobin level within an acceptable range of approximately 10 to 11.5
g/dL
Value of greater than 13 g/dL is associated with increased risks without incremental improvement in quality of life 8
Address secondary hyperparathyroidism
Use with care any substances that risk worsening hyperkalemia (eg, antibiotics including sulfamethoxazole)
Avoid nephrotoxins (eg, iodinated contrast, phosphate and magnesium-based enemas)
Adjust medication dosing (eg, antibiotics, oral hypoglycemic agents, heparin) based on kidney function
Monitor urine output, serum creatinine levels, and electrolyte levels
Manage advanced chronic kidney disease (eg, stage G4, stage A3) in consultation with a nephrologist. Multidisciplinary
approach to treatment is optimal for patients with progressive chronic kidney disease
Essential treatment team consultants include dietitian, dialysis nurse educator, and social worker
Shared decision-making approach with patient, family, and treatment team is imperative
Discussions include education regarding in-center versus at-home dialysis modalities, vascular access planning,
expectations, and prognosis
Multidisciplinary approach allows for fluidity and transparency when discussing kidney disease and its short-term and
long-term ramifications
Initiate appropriate referrals in a timely manner
Most experts recommend beginning discussion of longer term management strategies during late stage 4 or stage 5
chronic kidney disease
Refer to appropriate specialist in your region (eg, surgeon, interventional radiologist) for long-term vascular access
placement (ie, arteriovenous fistula or graft) and kidney transplantation
Refer to palliative care specialist when prognosis is guarded
Initiate renal replacement therapy when clinically indicated in consultation with a nephrologist
No sole criterion or estimated GFR value exists that dictates initiation of dialysis
Decision to start dialysis in patients with chronic kidney disease is not always straightforward and requires collaborative
decision-making that includes the patient and nephrologist
Initiation of renal replacement therapy is individualized and patient-centered
Therapy is often long term or lifelong
Usually, a constellation of potential indications (eg, uremia) coupled with presence of signs and symptoms related to
potential indications factor into the decision to initiate renal replacement therapy. There is no absolute threshold value
below which GFR falls that prompts start of renal replacement therapy
Additional considerations that factor into decision to initiate treatment include life expectancy, mobility, and
hemodynamic stability, among others
Precise timing of initiation of dialysis varies once a patient has progressed to stage 5 chronic kidney disease
Timing of initiation
Evidence suggesting lack of benefit from early versus late initiation of dialysis stems from the IDEAL (Initiating Dialysis
Early and Late) study 9
Patients with progressive stage 5 kidney disease were randomized into an early group (estimated GFR 10-14 mL/minute)
or late group (5-7 mL/minute) for planned initiation of dialysis
Data suggest that early initiation of dialysis does not improve survival or clinical outcomes
Study results reveal that most patients develop symptoms of uremia when estimated GFR falls below 10 mL/minute/1.73
m2
General guidance for timing of initiation based on patient and disease characteristics (based on expert opinion and clinical
observation)
Asymptomatic patients with stage 5 chronic kidney disease
Dialysis may be delayed—allowing for safe placement of permanent vascular access or transplant evaluation—
provided patient has stable electrolytes, acid-base levels, and volume status and can be safely observed with medical
management
Symptomatic patients with advanced chronic kidney disease and severe manifestations
Consider maintenance hemodialysis or peritoneal dialysis for patients with refractory hyperkalemia, hyperkalemia
with ECG changes, volume overload, or severe metabolic acidosis irrespective of estimated GFR
Symptomatic patients with manifestations concerning for uremia
Consider dialysis for patients who have signs and symptoms attributable to uremia after excluding other underlying
causes for manifestations
Because overlap exists within the symptomology of uremia and other chronic comorbidities (eg, liver disease), obtain
a detailed history of symptom duration and use clinical judgement before initiating renal replacement therapy 10 , 11
Inpatient versus outpatient initiation
Patients with chronic kidney disease who progress to kidney failure usually start intermittent hemodialysis or peritoneal
dialysis in an outpatient (in-center dialysis) or home (home dialysis) setting
Patients with chronic kidney disease may start renal replacement therapy in an inpatient setting if there is an acute
indication (eg, significant refractory volume overload, electrolyte abnormalities, uremic symptoms) requiring prompt
initiation of renal replacement therapy and close observation
Decision regarding type of renal replacement therapy modality to initiate (eg, intermittent hemodialysis versus
continuous renal replacement therapy) in inpatient setting is primarily based on hemodynamic stability, in-center
experience and preference, and comorbidities, along with several other factors. Make this choice in consultation with a
nephrologist 12
First Line Treatment

Indications for renal replacement therapy (Table 2 (https://www-clinicalkey-es.fucsalud.basesdedatosezproxy.com/#!/content/clinical_overview/67-
s2.0-V2181#t002))
Decision to initiate renal replacement therapy depends on many factors, including overall clinical picture, trajectory of
metabolic derangements, urine output, volume status, and hemodynamic stability, among others
Do not initiate renal replacement therapy before patient develops a discrete indication for treatment
Complications arising as a result of uremia (eg, uremic pericarditis, uremic encephalopathy) are definitive indications for
renal replacement therapy as there are no effective medical therapies for uremia 10 , 13 , 18 , 19 , 20
Table 2. Indications for renal replacement therapy.
Absolute indications 13 , 14 , 15
Uremic pericarditis, encephalopathy, or neuropathy or myopathy
Decline in mental status related to uremia
Diuretic-resistant volume overload
Hyperkalemia with potassium level higher than 6 mEq/L, hyperkalemia with ECG changes that are not responsive to medical management, or
rapidly rising potassium level
Severe metabolic acidosis with pH less than 7.15 or worsening acidosis on oral bicarbonate replacement therapy
Hypermagnesemia or hypercalcemia not amenable to medical management
Dialyzable toxins or ingestions
Relative indications 10 , 16 , 17
Relative indications may include the following manifestations attributable to advanced chronic kidney disease in patients with GFR range from 5 to
10 mL/min/1.73 m2 when other causes have been excluded:
Progressive deterioration in nutritional status
Cognitive impairment
Recalcitrant pruritis
Uremia in patient with clinical manifestations consistent with uremia
Bleeding diathesis attributed to uremic bleeding
Extreme fatigue and malaise
Drug Therapy
Anticoagulation may be required for both intermittent hemodialysis and continuous renal replacement therapy
Blood contact with extracorporeal circuit may cause activation of coagulation pathway leading to clotting in dialyzer or
filter
Heparin or citrate may be used for anticoagulation if there are no contraindications 21
Heparin is the most common anticoagulant used
Heparin and citrate are most used anticoagulants
Peritoneal dialysis
Routine anticoagulation is not necessary
Nondrug and Supportive Care

Address practical requirements before initiating intermittent hemodialysis:
Patent dialysis access
Dialysis machine and nursing availability
Adequate plumbing system
Hemodynamic stability
Treatment Procedures
Diffusion and convection are the primary mechanisms by which solute and water move through membrane in renal
replacement therapy 12
Fluid transport across semipermeable membrane is driven by ultrafiltration 22
Diffusion
Movement of a solute across a semipermeable membrane occurs based on concentration gradient in 2 compartments:
blood and dialysate
Transfer of solute can occur from blood to dialysate or vice versa based on concentration gradient
Smaller solutes are effectively removed by diffusion
Convection 22
Process by which solutes pass through membrane pores; solute is dragged by fluid movement (ie, ultrafiltration)
caused by a hydrostatic or osmotic transmembrane pressure gradient
Larger solutes are better removed by convection compared with diffusion
Ultrafiltration refers to movement of only plasma water (only solvent, no cells or colloids) across a semipermeable
membrane, driven by a pressure gradient 22
Depending on type of membrane used for different techniques, ultrafiltration may be used in the following ways:
Isolated: used to remove only fluids for volume control
Part of hemofiltration: ultrafiltrate is partially or completely replaced with a sterile substitution fluid to achieve
volume and solute control
Combined with diffusion methods such as hemodialysis or hemodiafiltration, which are types of continuous renal
replacement therapy
Movement of water also results in a process known as solvent drag (movement of solutes along with water across the
membrane), resulting in a convective form of solute clearance
Description and comparison of commonly used renal replacement therapy treatment modalities (Table 3 (https://www-clinicalkey-
es.fucsalud.basesdedatosezproxy.com/#!/content/clinical_overview/67-s2.0-V2181#t003))
Blood-based purification method in which solute and fluid control are achieved by diffusion, convection, or both
Performed continuously 24 hours a day
Requires presence of a vascular access (large bore double lumen catheter), preferable in right internal jugular vein
Is performed using pump-driven venovenous extracorporeal circuits 23
May be used for hemodynamically unstable or stable patients in an intensive care setting
Selection of specific extracorporeal modality is largely based on institutional preference and experience 24
Common types include 4 , 12 :
Continuous venovenous hemofiltration: removal of solute by convection
Continuous venovenous hemodialysis: removal of solute by diffusion
Continuous venovenous hemodiafiltration: removal of solute by both convection and diffusion
Appropriate antibiotic and medication dosing according to renal clearance is important, and consultation with clinical
pharmacist is helpful
May result in loss of amino acids and water-soluble vitamins; nutritional management is very important 23
Contraindications primarily involve terminal conditions because, in patients with terminal conditions, focus of care is
comfort and hospice
Preferred over intermittent hemodialysis for certain scenarios, including:
Hemodynamic instability
Brain injury or cerebral edema
Acute liver failure
Preferred by some experts for those with indication for renal replacement therapy and concomitant severe chronic
hyponatremia 23
Blood-based purification method in which solute and fluid control are mainly achieved by diffusion and ultrafiltration
Performed using an extracorporeal blood circuit consisting of dialysis catheter and needles, blood tubing, peristaltic
blood pump, and dialyzer membrane
Dialysis is accomplished over several hours per day multiple days a week
Suitable for hemodynamically stable patients
May be performed in an inpatient or outpatient setting
Primary contraindication is hemodynamic instability
May be preferred over continuous renal replacement therapy in certain patients, including:
Those who are hemodynamically stable
Those who need rapid electrolyte correction or toxin removal
Peritoneal dialysis 25
Uses vascular inner lining of peritoneal cavity as dialysis membrane
Intraperitoneal instillation of hypertonic glucose concentration creates an osmotic and diffusive gradient for removal of
water and uremic solutes
Can be performed both as an inpatient and at home
Chronic treatment requires a period of healing after peritoneal catheter placement (usually several weeks)
Usually performed 7 days a week
Relative contraindications include presence of ventriculoperitoneal shunts, morbid obesity, inflammatory bowel disease,
previous multiple abdominal surgeries, peritoneal adhesions, and physical limitation or cognitive dysfunction
May be preferred over other modalities in certain scenarios, including:
Chronic cardiorenal syndrome in patients unable to tolerate hemodialysis owing to hemodynamic status
Patients who lack of adequate vascular access
Table 3. Advantages and disadvantages for intermittent hemodialysis, prolonged, and continuous renal
replacement therapy.
Treatments Advantages Disadvantages
Rapid removal of toxins circulating

solutes
Rapid fluid removal and frequent hypotension
Reduced downtime for diagnostic and
IHD therapeutic procedures Dialysis disequilibrium and risk of cerebral edema
Reduced exposure to anticoagulation Technically complex
Lower cost than CRRT
Slower volume and solute removal than

IHD
Faster volume and solute removal than CRRT (at risk for
Faster solutes clearance than CRRT
Prolonged (eg, sustained low- hypotension and disequilibrium syndrome in at-risk patients)
efficiency daily dialysis)
Reduced downtime than CRRT
Technically complex
Reduced exposure to anticoagulation
than CRRT
Continuous removal of toxin and

Slower solutes clearance than IHD
solutes (avoid concentration rebound)
Need for prolonged anticoagulation
Hemodynamic tolerability
CRRT Reduced possibility of patients’ mobilization
Easy control of fluid balance
Hypothermia
Lower risk of disequilibrium syndrome
Increased costs than IHD
User-friendly machines
Título: IHD, intermittent hemodialysis; CRRT, continuous renal replacement therapy.

From Villa G et al. Renal replacement therapy. Crit Care Clin. 2015;31(4):839-848, Table 3.
Special Considerations
Hyperkalemia
Begin urgent medical management (eg, calcium, insulin and dextrose, albuterol, resin binders) while preparations for urgent
renal replacement therapy are arranged
Hepatorenal Syndrome With Cirrhosis

Renal replacement therapy may be indicated and serve as a bridge to liver transplantation in listed candidates who have
worsening renal function despite medical management 26
For patients who are not candidates for liver transplantation, multidisciplinary discussion with hepatologist, nephrologist,
and palliative care team is essential to determine dialysis candidacy
Potential Contrast Agent Requirement
Iodinated Contrast Agent
Avoid iodinated contrast agents in patients with chronic kidney disease owing to potential for worsening of kidney function
If contrast administration is essential:
Consult with a nephrologist to discuss potential risks of worsening kidney function (recommended)
Not recommended to provide prophylactic renal replacement therapy during or after administering contrast agent to
prevent contrast-induced nephropathy
Immediate dialysis after exposure to contrast agent is not indicated in a hemodialysis patient with kidney failure, unless
volume overload is of concern
Gadolinium-Based Contrast Agent

In general, avoid in patients with acute kidney injury, advanced chronic kidney disease, or kidney failure owing to risk of
nephrogenic systemic fibrosis
Specific recommendations are evolving. If contrast agent administration is essential, consult with radiologist and
nephrologist before the study to discuss and arrange for possible postexposure renal replacement therapy, if needed
Consider new low-dose macrocyclic gadolinium compounds, if available 27
Uremic Pericarditis
Immediately initiate dialysis in hemodynamically stable patients without large pericardial effusion or tamponade;
aggressively intensify renal replacement therapy as clinically indicated 28
Large effusion or tamponade physiology requires drainage via pericardiocentesis
Some experts suggest avoiding heparin during dialysis owing to risk of cardiac tamponade
Treat in consultation with cardiologist
Uremic Encephalopathy
Minimize or treat potential contributors to elevated BUN, including catabolic state, protein intake, upper gastrointestinal
bleeding, and corticosteroid use 29
Additional evaluation (eg, central nervous system imaging, lumbar puncture) may be required to exclude alternate underlying
cause for encephalopathy (eg, delirium-posterior reversible encephalopathy, infections, drug-induced neurotoxicity)
Treatment involves urgent initiation of renal replacement therapy with intensification of therapy gauged by clinical
response 30
Treat in consultation with neurologist
Follow-Up
Monitoring
Pattern of follow-up depends on chronic kidney disease stage and rapidity of disease progression
Most experts recommend follow-up about every 1 to 3 months with nephrologist for patients with stage 5 chronic kidney
disease
Laboratory monitoring recommendations are not rigorously standardized
Individualize monitoring parameters based on underlying severity of disease
Typical monitoring parameters include CBC, renal function testing, urinalysis, and electrolyte levels
Complications
Intermittent Hemodialysis/Continuous Renal Replacement Therapy
Common
Hypotension 31
Occurs in up to 30% of intermittent hemodialysis treatments 32
Infection
May include bacteremia with potential for subsequent seeding of distant anatomic sites with or without infection involving
vascular access device or graft
Vascular access hemorrhage or venous needle dislodgement
Uncommon
Cardiac arrest
Allergic reaction to the dialyzer and its components 33
Hemolysis
Dialysis disequilibrium 33
Development of cerebral edema that may be encountered, typically after the first or second session of dialysis, in patients
with very high serum BUN levels
Uncommon complication thought to occur owing to faster decline in serum BUN levels compared with urea nitrogen
levels in the brain during the dialysis session, leading to an osmotic gradient and subsequent movement of water into
brain resulting in cerebral edema
Risk factors include very high BUN level, hyponatremia, liver disease, extreme age, metabolic acidosis, and existing
neurologic conditions 34
Symptoms include vomiting, headache, confusion, and seizures
Air embolism
Peritoneal Dialysis
Infection
May include peritonitis with or without bacteremia and potential for seeding of distant anatomic sites
Infection may involve peritoneal dialysis catheter
Abdominal pain
Leakage
Metabolic complications
Related to systemic glucose absorption from dialysate and may include weight gain, dyslipidemia, and insulin resistance
Renal Replacement Therapy

Commonly encountered complications of chronic kidney disease include:
Fluid overload
Metabolic abnormalities (eg, hyperkalemia, hypermagnesemia, hypocalcemia)
Metabolic acidosis
General complications related to uremia (eg, nausea, fatigue, pruritis)
Uremia
Uremia is a condition resulting from accumulation of organic waste products normally cleared by kidneys
Uremia is defined by BUN level elevated above reference range; however, uremia is not clinically significant until
symptoms and signs develop that are attributable to uremia after exclusion of alternate causes for clinical manifestations
There is no absolute numerical threshold that defines clinically significant uremia. Clinical manifestations may develop
in different patients at different BUN level elevations
Common clinical manifestations often associated with uremia include the following 24 :
Neural and muscular: fatigue, peripheral neuropathy, nausea, vomiting, anorexia, altered taste, sleep disturbances, altered
mental status, confusion, and seizures
Endocrine and metabolic: insulin resistance, amenorrhea, and bone disease
Others: serositis, itching, hiccups, and bleeding diathesis
Specific uremic syndromes include:
Uremic pericarditis 28 , 35
Pericarditis may present as uremic pericarditis or dialysis pericarditis
Clinical manifestations begin before or within 8 weeks of starting renal replacement therapy
Also can occur in patients on long-term dialysis if they are underdialyzed or not compliant to treatment
Common presentation pattern includes chest pain, shortness of breath, lightheadedness, tachycardia, and pericardial
friction rub
Laboratory data may include elevated erythrocyte sedimentation rate, C-reactive protein, and WBC count
ECG findings include diffuse ST- and T-wave changes
Echocardiogram is diagnostic and determines cardiac function, pericardial effusion, and presence of cardiac tamponade
Uremic encephalopathy
Presents with confusion, lethargy, seizures, coma (in advanced cases), tremors, myoclonus, or asterixis
Although serum BUN level is significantly elevated in patients with uremic encephalopathy, no set value predicts its
onset
Cause of uremic encephalopathy is related to accumulation of many neurotoxins in patients with advanced kidney
disease; BUN level probably is not the sole cause but rather a surrogate marker for the other toxins
Some other potential causes and contributors to elevated BUN level include corticosteroid use, catabolic state, protein
intake, and upper gastrointestinal bleeding 29
Uremic neuropathy or myopathy
Myopathy
Presents with proximal muscle weakness and muscle atrophy
Confirm with EMG
Neuropathy 36
Involves both sensory and motor axons
Presents with tingling, numbness, or paresthesia
Confirm with nerve conduction studies
Pruritis
Common debilitating symptom seen in patients with advanced chronic kidney disease or kidney failure
Usually generalized or may be limited to back, face, or arm with arteriovenous access
Occasionally secondary to underlying conditions other than renal disease; exclude alternate causes
Although initiating dialysis may help alleviate symptoms, some patients continue to have persistent symptoms 37 , 38
Cognitive impairment
Patients with chronic kidney disease are at higher risk of developing cognitive impairment compared with the general
population 39
Underlying cause is multifactorial including cerebrovascular disease and accumulation of uremic metabolites
Strategies aimed at reducing albuminuria and controlling blood pressure may reduce risk
Maintain vigilance to exclude reversible and alternate potential underlying causes
Malnutrition
Progressive deterioration in nutritional status is not uncommon among patients with progressive or longstanding disease
Chronic kidney disease–mineral bone disorder
Broad clinical syndrome of mineral, bone, and calcific cardiovascular abnormalities that develops owing to progressive
chronic kidney disease
Biochemical abnormalities that characterize chronic kidney disease–metabolic bone disease are those consistent with
secondary hyperparathyroidism (eg, hyperphosphatemia, hypocalcemia, elevated pituitary thyroid hormone level); in some
patients, vitamin D deficiency or osteoporosis coexists
Condition is associated with an increased risk of fractures, cardiovascular disease, and mortality
Bleeding diathesis
Increased risk of bleeding is a known consequence of advanced kidney disease
Uremic toxins and other factors result in dysfunctional von Willebrand factor
Patients may present with ecchymoses, epistaxis, or bruises; gastrointestinal and intracranial bleeding may occur
Consider bleeding time and platelet function assays to exclude alternate causes in consultation with hematologist 40
Prognosis
Online risk stratification tools are available to help predict risk of dialysis in patients with chronic kidney disease, including
the kidney failure risk equation 6 , 7
Mortality risk is heavily influenced by numerous factors, including underlying cause of renal disease, severity of disease, rate
of disease progression, and presence of other associated comorbidity
Referral
Manage all patients with chronic kidney disease stage G4 or A3 and with kidney failure in consultation with a nephrologist
Additional indications for referral are available from KDIGO 41
Disposition
Admission criteria
Some common admission criteria for patients with chronic kidney disease requiring renal replacement therapy include the
following (expert opinion)
Potassium level higher than 6 mEq/L or hyperkalemia with ECG changes
Large pericardial effusion or cardiac tamponade
Volume overload resistant to oral diuretics
Severe metabolic acidosis with pH less than 7.1 or rapidly worsening serum HCO3 level on oral bicarbonate replacement
Symptomatic uremia with severe clinical manifestations
Rapidly progressive decline in kidney function
Referencias
1 Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group: KDIGO 2012 clinical practice guideline for the evaluation and
management of chronic kidney disease. Kidney Int Suppl (2011). 2013;3(1):1-150.
Ver en el Artículo
2 Chen TK et al. Chronic kidney disease diagnosis and management: a review. JAMA. 2019;322(13):1294-1304.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1001/jama.2019.14745)
3 Levey AS et al. Chronic kidney disease. Lancet. 2012;379(9811):165-180.

Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1016/S0140-6736(11)60178-5)
4 Neri M et al. Nomenclature for renal replacement therapy in acute kidney injury: basic principles. Crit Care. 2016;20(1):318.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1186/s13054-016-1489-9)
5 Levey AS et al. Nomenclature for kidney function and disease: report of a Kidney Disease: Improving Global Outcomes (KDIGO) consensus
conference. Kidney Int. 2020;97(6):1117-1129.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1016/j.kint.2020.02.010)
6 Tangri N et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1001/jama.2011.451)
7 The Kidney Failure Risk Equation. The Kidney Failure Risk Equation website. Accessed November 30, 2021.
Ver en el Artículo | Referencia cruzada (https://kidneyfailurerisk.com/)
8 Singh AK, etal. Correction of anemia with epoetin alpha in chronic kidney disease. N Engl J Med. 2006;355(20):2085-2098.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1056/NEJMoa065485)
9 Cooper BA et al. The Initiating Dialysis Early and Late (IDEAL) study: study rationale and design. Perit Dial Int. 2004;24(2):176-181.
Ver en el Artículo | Referencia cruzada (https://pubmed-ncbi-nlm-nih-gov.fucsalud.basesdedatosezproxy.com/15119639)
10 Cabrera VJ et al. Symptom management of the patient with CKD: the role of dialysis. Clin J Am Soc Nephrol. 2017;12(4):687-693.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.2215/CJN.01650216)
11 Mehrotra R. Initiation of dialysis should be timely: neither early nor late. Semin Dial. 2013;26(6):644-649.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1111/sdi.12127)
12 Tolwani A. Continuous renal-replacement therapy for acute kidney injury. N Engl J Med. 2012;367(26):2505-2514.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1056/NEJMct1206045)
13 Howard SC et al. The tumor lysis syndrome. N Engl J Med. 2011;364(19):1844-1854.

Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1056/NEJMra0904569)
14 Wilson FP et al. Tumor lysis syndrome: new challenges and recent advances. Adv Chronic Kidney Dis. 2014;21(1):18-26.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1053/j.ackd.2013.07.001)
15 Bosch X et al. Rhabdomyolysis and acute kidney injury. N Engl J Med. 2009;361(1):62-72.
16 Hanna RM et al. A practical approach to nutrition, protein-energy wasting, sarcopenia, and cachexia in patients with chronic kidney disease.
Blood Purif. 2020;49(1-2):202-211.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1159/000504240)
17 Couch P et al. Management of uremic bleeding. Clin Pharm. 1990;9(9):673-681.

Ver en el Artículo | Referencia cruzada (https://pubmed-ncbi-nlm-nih-gov.fucsalud.basesdedatosezproxy.com/2171866)
18 Gaudry S et al. Timing of renal replacement therapy for severe acute kidney injury in critically ill patients. Am J Respir Crit Care Med.
2019;199(9):1066-1075.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1164/rccm.201810-1906CP)
19 Lameire N et al. Acute renal failure. Lancet. 2005;365(9457):417-430.

Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1016/S0140-6736(05)17831-3)
20 Clase CM et al. Potassium homeostasis and management of dyskalemia in kidney diseases: conclusions from a Kidney Disease: Improving
Global Outcomes (KDIGO) controversies conference. Kidney Int. 2020;97(1):42-61.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1016/j.kint.2019.09.018)
21 Morabito S et al. Regional citrate anticoagulation for RRTs in critically ill patients with AKI. Clin J Am Soc Nephrol. 2014;9(12):2173-2188.
22 Misra M. Basic mechanisms governing solute and fluid transport in hemodialysis. Hemodial Int. 2008;12 Suppl 2:S25-S28.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1111/j.1542-4758.2008.00320.x)
23 Tandukar S et al. Continuous renal replacement therapy: who, when, why, and how. Chest. 2019;155(3):626-638.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1016/j.chest.2018.09.004)
24 Meyer TW et al. Uremia. N Engl J Med. 2007;357(13):1316-1325.
25 Perl J et al. Peritoneal dialysis: from bench to bedside and bench to bench. Am J Physiol Renal Physiol. 2016;311(5):F999-F1004.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1152/ajprenal.00012.2016)
26 Francoz C et al. Hepatorenal syndrome. Clin J Am Soc Nephrol. 2019;14(5):774-781.

27 Rudnick MR et al. Risks and options with gadolinium-based contrast agents in patients with CKD: a review. Am J Kidney Dis. 2021;77(4):517-
528.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1053/j.ajkd.2020.07.012)
28 Rehman KA et al. Uremic pericarditis, pericardial effusion, and constrictive pericarditis in end-stage renal disease: insights and
pathophysiology. Clin Cardiol. 2017;40(10):839-846.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1002/clc.22770)
29 Waikar SS et al. Can we rely on blood urea nitrogen as a biomarker to determine when to initiate dialysis? Clin J Am Soc Nephrol.
2006;1(5):903-904.
30 Seifter JL et al. Uremic encephalopathy and other brain disorders associated with renal failure. Semin Neurol. 2011;31(2):139-143.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1055/s-0031-1277984)
31 Saha M et al. Diagnosis, treatment, and prevention of hemodialysis emergencies. Clin J Am Soc Nephrol. 2017;12(2):357-369.
32 Selby NM et al. A systematic review of the clinical effects of reducing dialysate fluid temperature. Nephrol Dial Transplant. 2006;21(7):1883-
1898.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1093/ndt/gfl126)
33 Saha M et al. Diagnosis, treatment, and prevention of hemodialysis emergencies. Clin J Am Soc Nephrol. 2017;12(2):357-369.
34 Greenberg KI et al. Hemodialysis emergencies: core curriculum 2021. Am J Kidney Dis. 2021;77(5):796-809.
35 Rehman KA et al. Uremic pericarditis, pericardial effusion, and constrictive pericarditis in end-stage renal disease: insights and
pathophysiology. Clin Cardiol. 2017;40(10):839-846.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1002/clc.22770)
36 Jabbari B et al. The nature, consequences, and management of neurological disorders in chronic kidney disease. Hemodial Int.
2018;22(2):150-160.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1111/hdi.12587)
37 Simonsen E et al. Treatment of uremic pruritus: a systematic review. Am J Kidney Dis. 2017;70(5):638-655.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/28720208)
38 Mettang T et al. Uremic pruritus. Kidney Int. 2015;87(4):685-691.

Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1038/ki.2013.454)
39 Drew DA et al. Cognitive impairment in CKD: pathophysiology, management, and prevention. Am J Kidney Dis. 2019;74(6):782-790.
40 Hedges SJ et al. Evidence-based treatment recommendations for uremic bleeding. Nat Clin Pract Nephrol. 2007;3(3):138-153.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1038/ncpneph0421)
41 Chapter 5: Referral to specialists and models of care. Kidney Int Suppl (2011). 2013;3(1):112-119.
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1038/kisup.2012.68)
(https://play.google.com/store/apps/details?id=com.elsevier.cs.ck&hl=es) (https://itunes.apple.com/es/app/clinicalkey/id1041998175) (https://www.facebook.com/ClinicalKey)

(https://www.linkedin.com/company/3969981) (https://www.twitter.com/ClinicalKey)
Contáctenos (https://es-service-elsevier-com.fucsalud.basesdedatosezproxy.com/app/contact/supporthub/clinicalkey/)
Centro de Recursos (https://www-elsevier-com.fucsalud.basesdedatosezproxy.com/es-es/solutions/clinicalkey/resource-center?campid=CK_Es_LinkInFooter&dgcid=camp
(http://www.elsevier.com/) Términos y condiciones (https://www-elsevier-com.fucsalud.basesdedatosezproxy.com/legal/elsevier-website-terms-and-conditions)
Política de privacidad (https://www-elsevier-com.fucsalud.basesdedatosezproxy.com/legal/privacy-policy-es-es)
Acuerdo de Usuario Registrado (http://www.elsevier.com.fucsalud.basesdedatosezproxy.com/legal/elsevier-registered-user-agreement)
Ayuda (https://es-service-elsevier-com.fucsalud.basesdedatosezproxy.com/app/home/supporthub/clinicalkey/)
Accesibilidad (https://service-elsevier-com.fucsalud.basesdedatosezproxy.com/app/answers/detail/a_id/19138/c/10546/supporthub/clinicalkey/)
(https://www.elsevier.com/legal/elsevier-website-terms-and-conditions) (http://www.elsevier.com/legal/privacy-policy)
We use cookies to help provide and enhance our service and tailor content. By continuing you agree to the use of cookies (http://www.elsevier.com/legal/us
Copyright © 2023 Elsevier B.V. or its licensors or contributors.

17 Terapias de Reemplazo Renal - ClinicalKey

Uploaded by

Copyright:

Available Formats

You might also like

17 Terapias de Reemplazo Renal - ClinicalKey

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

17 Terapias de Reemplazo Renal - ClinicalKey

Uploaded by

Copyright:

Available Formats

Renal Replacement Therapy, Chronic Kidney Disease - ClinicalKey 9/07/23, 4:11 p.m.

Renal Replacement Therapy, Chronic Kidney Disease

Alarm Signs and Symptoms

Remove nitrogenous waste products

Correct electrolyte disorders

Correct disorders of acid-base balance

Alleviate volume overload

Different modalities of renal replacement therapy include the following:

Can be performed in an outpatient and inpatient setting

Continuous renal replacement therapy

Performed only in the ICU

Usually performed in an inpatient setting

Blood purification method using peritoneal membrane as dialyzer

Can be performed in an outpatient or inpatient setting

Diagnostic criteria and general information

Diagnosis requires presence of 1 of the following for more than 3 months 2 , 3 :

Reduced GFR: less than 60 mL/minute/1.73 m2

Kidney damage, as indicated by any of the following 4 :

Albuminuria greater than 30 mg/g or 30 mg per 24 hours

Pathologic abnormalities (eg, glomerulonephritis, interstitial nephritis, interstitial fibrosis)

History of kidney transplant

End stage kidney disease

Definitions vary and often are modified from a clinical standpoint 5

Staging and Classification

G1: GFR 90 mL or more/min/1.73 m2

G2: GFR 60 to 89 mL/min/1.73 m2

G3a: GFR 45 to 59 mL/min/1.73 m2

G3b: GFR 30 to 44 mL/min/1.73 m2

G4: GFR 15 to 29 mL/min/1.73 m2

G5: GFR less than 15 mL/min/1.73 m2

Albuminuria stages are defined by KDIGO as follows 3 :

A1: 10 to 29 mg/g (high normal)

A2: 30 to 300 mg/g (high)

A3: greater than 300 mg/g (very high)

Table 1. Chronic kidney disease staging by GFR.

Chronic kidney disease stage GFR (mL/min/1.73 m 2) Presence of kidney damage

3A 45-59 Not required

3B 30-44 Not required

4 15-29 Not required

5 <15 Not required

Risk Models and Risk Scores

Optimize management of underlying medical comorbidities (eg, hypertension, diabetes mellitus)

Correct electrolyte derangements and acidosis, and optimize fluid balance

Recommend dietary changes 2 :

Reduce acid-rich foods (eg, animal protein)

Incorporate foods rich in alkali

Address secondary hyperparathyroidism

Avoid nephrotoxins (eg, iodinated contrast, phosphate and magnesium-based enemas)

Monitor urine output, serum creatinine levels, and electrolyte levels

Initiate appropriate referrals in a timely manner

Refer to palliative care specialist when prognosis is guarded

Initiation of renal replacement therapy is individualized and patient-centered

Therapy is often long term or lifelong

Asymptomatic patients with stage 5 chronic kidney disease

Symptomatic patients with manifestations concerning for uremia

Inpatient versus outpatient initiation

First Line Treatment

Table 2. Indications for renal replacement therapy.