14 Chronic Kidney Disease - ClinicalKey

Chronic Kidney Disease - ClinicalKey 8/06/23, 3:02 p.m.
CLINICAL OVERVIEW
Chronic Kidney Disease

Elsevier Point of Care (ver detalles)
Actualizado December 16, 2022. Copyright Elsevier BV. All rights reserved.
Synopsis
Urgent Action
Hyperkalemia
IV calcium (10 mL of 10% calcium chloride or calcium gluconate over 2-3 minutes) to normalize membrane
excitability and stabilize myocardium
IV glucose and insulin to increase cellular uptake of potassium (eg, 10 units regular insulin and 50 mL of 50%
dextrose in water)
Nebulized albuterol increases cellular uptake of potassium
Key Points
Chronic kidney disease is the decline in function of the kidney characterized by at least 3 months of reduced GFR (less than
60 mL/minute/1.73 m²) or at least 3 months of structural or functional kidney damage 1
Assessment of both GFR and albuminuria is necessary to diagnose chronic kidney disease and monitor disease progression
GFR is most commonly estimated by measuring serum creatinine and using GFR estimating equations, either the
Modification of Diet in Renal Disease equation or the Chronic Kidney Disease Epidemiology Collaboration equation
Albuminuria is measured by urine albumin to creatinine ratio; greater than 30 mg/g indicates albuminuria 1
Chronic kidney disease is commonly associated with hypertension, diabetes, and cardiovascular disease
First line therapy includes ACE inhibitors and/or angiotensin II receptor blockers to reduce albuminuria and hypertension
If left untreated, chronic kidney disease can progress to end-stage renal disease, requiring dialysis or renal transplant 1
Symptoms of end-stage renal disease (eg, pruritus, refractory electrolyte imbalances, metabolic acidosis, severe nausea,
neurologic impairments) typically occur when GFR is 5 to 10 mL/minute/1.73 m²
Carefully monitor electrolyte levels, hemoglobin, parathyroid hormone levels, and sodium bicarbonate levels to detect
complications of chronic kidney disease, including cardiovascular disease, anemia, bone mineral disease, and metabolic
acidosis
Pitfalls
Early stages are often asymptomatic, leaving chronic kidney disease untreated and leading to further progression of kidney
https://www-clinicalkey-es.fucsalud.basesdedatosezproxy.com/#!/content/clinical_overview/67-s2.0-26a91efc-ff97-4e11-b49f-c70331e79cee Página 1 de 34
damage and worse prognosis
Terminology
Clinical Clarification
Chronic kidney disease is structural or functional kidney damage that is present for more than 3 months, with implications
for health, irrespective of cause 1
Criteria for chronic kidney disease 1
Either of the following present for more than 3 months:
Markers of kidney damage (1 or more), which include:
Albuminuria (albumin excretion rate of 30 mg/24 hours or more; albumin to creatinine ratio of 30 mg/g or more)
Presence of RBCs, WBCs, or cellular casts in urine
Electrolyte and other abnormalities due to tubular disorders
Histologic abnormalities
Structural abnormalities detected by imaging
History of kidney transplantation
GFR less than 60 mL/minute/1.73 m²
Classification
By GFR category 3 4
G1: normal or high renal function
GFR: greater than 90 mL/minute/1.73 m²
G2: mildly decreased renal function
GFR: 60 to 89 mL/minute/1.73 m²
G3a: mildly to moderately decreased renal function
G3b: moderately to severely decreased renal function
G4: severely decreased renal function
G5: kidney failure
GFR: less than 15 mL/minute/1.73 m²
Patients receiving dialysis are indicated with a "D" (eg, G5D) 5 6

3
By albuminuria category 3
A1: normal to mildly increased
Albumin to creatinine ratio: less than 30 mg/g
Albumin excretion rate: less than 30 mg/24 hours
A2: moderately increased
Albumin to creatinine ratio: 30 to 300 mg/g
Albumin excretion rate: 30 to 300 mg/24 hours
A3: severely increased
Albumin to creatinine ratio: greater than 300 mg/g
Albumin excretion rate: greater than 300 mg/24 hours
Combined GFR and albuminuria stage more accurately denotes risk of progression of chronic kidney disease 3
Diagnosis
Clinical Presentation
History
Symptoms vary by stage and underlying disease process
Often asymptomatic in category G1 through G3b (GFR greater than 30 mL/minute/1.73 m²)
Patients with tubulointerstitial disease, cystic diseases, or nephrotic syndrome are more likely to develop symptoms at
earlier stages
Symptoms of uremia
Fatigue
Nausea
Anorexia
Vomiting
Pruritus
Restless legs
Altered taste and smell
Sleep disturbances
Neurologic changes
Symptoms of uremic neuropathy
Difficulty concentrating, lethargy, and confusion
Symptoms of peripheral neuropathy typically do not occur until GFR falls below 12 to 20 mL/minute/1.73 m² or uremia has
been present for more than 6 months 7
Present in 65% of patients at the initiation of dialysis 7
History of:
Hypertension (more than 60% of patients) 8
Diabetes (40% of patients) 9
Cardiac ischemia or myocardial infarction (35% of patients by time of first nephrology visit) 10
Nephrolithiasis 11
Chronic kidney disease is more prevalent in patients who have had kidney stones (relative risk, 1.52)
Hematuria 12
Indicates potential defect in the glomerular basement membrane or tubules
Physical examination
Signs of anemia
Pale skin
Pale conjunctiva
Poor capillary refill
90% of patients with GFR less than 25 to 30 mL/minute/1.73 m² develop anemia 13
Hypertension (more than 60% of patients) 8
Generalized edema/cushingoid appearance 14
May develop secondary to advanced chronic kidney disease
Occurs in 58% of patients with category G5 disease
Signs of heart failure
Dyspnea at rest or upon exertion
Peripheral edema
Jugular venous distention
Audible S₃
Pulmonary rales
Signs of peripheral arterial disease
Diminished lower extremity pulses
24% of patients with GFR less than 60 mL/minute/1.73 m² have peripheral artery disease versus 2.4% of those with GFR
above 60 mL/minute/1.73 m² 15
Causes and Risk Factors
Causes
Most common causes
Diabetes mellitus (type 1 or type 2) is the most common cause (approximately 30% of cases) 16
Hypertension (15%-30% of cases) 17
Other causes
Glomerulonephritis (less than 10% of cases) 17
Interstitial nephritis
Polycystic kidney disease (2%-3% of cases) 17
Prolonged obstruction of urinary tract
Chronic vasculitis
Recurrent kidney infection
Renal vascular disease (eg, renal artery stenosis, fibromuscular dysplasia)
Risk factors and/or associations
Age
More prevalent in populations older than 60 years (more than 21% of patients over 60 years meet GFR criteria for chronic
kidney disease; 32% meet broader criteria for chronic kidney disease) 18
Sex
Women have higher rates of chronic kidney disease 18
Men have increased risk for progression to end-stage renal disease (male to female odds ratio, 1.41) 19
Genetics
Autosomal dominant polycystic kidney disease (OMIM *601313 20 , *173910 21 )
Characterized by cyst formation that causes a decline in renal function and leads to end-stage renal disease in half of
patients by age 60 years 22
Caused by mutations in either the PKD1 or PKD2 gene
Alport syndrome
Characterized by improper filtration by the glomerular membrane, resulting in a decline in renal function consistent with
chronic kidney disease 23
Caused by mutations in either the COL4A3 or COL4A4 genes (OMIM # 203780) 24 or the COL4A5 gene (OMIM # 301050)
25
Most cases are X-linked, but inheritance can be autosomal dominant or autosomal recessive
Sensorineural hearing loss is common
Medullary cystic kidney disease
Autosomal dominant tubulointerstitial nephropathy (OMIM #174000) 26
Caused by heterozygous mutations in MUC-1
Characterized by formation of renal cysts at the corticomedullary junction and progressive tubulointerstitial fibrosis
Noted by adult onset of impaired renal function with salt wasting, which progresses to end-stage renal disease by the sixth
decade 27
Ethnicity/race
Non-Hispanic Black populations and Mexican American populations have a higher prevalence of albumin to creatinine ratio
of 30 or less but lower prevalence of estimated GFR less than 60 compared with non-Hispanic White populations 18
Incidence rate ratio of end-stage renal disease, compared with White populations, was 2.9 for Black populations, 1.2 for
American Indian/Alaska Native populations, and 1.1 for Asian populations 18
Other risk factors/associations

Urinary stones or obstruction
Patients with urinary stones have a 0.8% to 17.5% risk of developing chronic kidney disease 28
Kidney neoplasia
Patients with radical nephrectomy or partial nephrectomy have a 20.1% and 11.4% risk, respectively, of developing chronic
kidney disease 29
Systemic lupus erythematosus
Patients with systemic lupus erythematosus have a 45.63% chance of developing chronic kidney disease 30
Multiple myeloma
More than 20% of patients with multiple myeloma will develop kidney disease 31
Antineutrophil cytoplasmic antibody–associated vasculitis (including granulomatosis with polyangiitis and microscopic
polyangiitis) 32
Kidney involvement occurs in 75% to 90% of patients with antineutrophil cytoplasmic antibody–associated vasculitis 33
Recovery from acute kidney failure
Patients recovering from acute kidney injury have a 90% increased risk of developing chronic kidney disease 34
Smoking
Former and current smokers have an increased risk (hazard ratio, 3.32 and 4.01, respectively) for progressing to stage G5
(renal failure) relative to patients who have never smoked 35
Obesity
Adults with a BMI of 25 kg/m² or higher have a 3-fold elevated risk for chronic kidney disease relative to lean patients 36
Western diet (ie, high fat, high carbohydrates, high red meat)
Western diet correlates with a decline in GFR 37
38
Use of nephrotoxic drugs 38
Prolonged exposure of kidneys to simple analgesics, calcineurin inhibitors, or lithium can cause chronic renal damage
Use of large cumulative doses of acetaminophen and NSAIDs increases risk of developing end-stage renal disease
Diagnostic Procedures
Primary diagnostic tools

First, calculate GFR and measure albuminuria 3
Obtain serum creatinine measurement to evaluate GFR
Estimate GFR from serum creatinine level using 1 of 2 equations 39
Chronic Kidney Disease Epidemiology Collaboration equation is preferred for reporting estimated GFR; more
accurately represents true GFR, especially at GFR above 60 mL/minute/1.73 m²
Modification of Diet in Renal Disease equation underestimates true GFR in patients with GFR above 60
mL/minute/1.73 m²
Less accurate than Chronic Kidney Disease Epidemiology Collaboration equation but still widely used by many
laboratories
A GFR calculator (using the Chronic Kidney Disease Epidemiology Collaboration equation) is available from the
National Kidney Foundation 40 and the National Institute of Diabetes and Digestive and Kidney Diseases 41
Gold standard is to measure clearance of continuously infused insulin over 24 hours; however, this is neither
practical nor cost effective 42
If GFR is suspected to be inaccurate (eg, severe malnutrition, paraplegia, amputated extremity), testing involves a 24-
hour urine collection 43
Obtain urine for albuminuria measurement
Spot urine test (plus serum creatinine result) for albumin to creatinine ratio or albumin excretion rate
Measure serum electrolyte levels in patients with symptoms, physical examination results, or laboratory findings that
indicate chronic kidney disease 3
All patients are additionally tested with CBC, lipid profile, and plasma glucose measurement 43
Perform ultrasonography to diagnose based on structural abnormalities when routine evaluation and urinalysis are
inconclusive or to distinguish between acute and chronic kidney disease 44
Apply criteria for chronic kidney disease (ie, markers of kidney damage or GFR less than 60 mL/minute/1.73 m²) 1
Verify chronicity of kidney disease
If GFR is less than 60 mL/minute/1.73 m² (GFR categories G3a through G5) or markers of kidney damage are present,
review history and previous measurements to determine duration of kidney disease 16
If duration is greater than 3 months, chronic kidney disease is confirmed 16
If duration is less than 3 months or unclear, chronic kidney disease is not confirmed; patients may have chronic
kidney disease, acute kidney diseases (including acute kidney injury), or both, and tests are repeated accordingly 16
Evaluate for underlying cause
Evaluate clinical context, including personal and family history, social and environmental factors, medications,
physical examination findings, laboratory results, imaging findings, and pathologic diagnosis to determine causes of
kidney disease
Perform laboratory assessment for diabetes
Assign cause of chronic kidney disease based on presence or absence of systemic disease and location of observed or
presumed pathologic-anatomic findings within the kidney
Nephrologist involvement is recommended when cause of chronic kidney disease is not clear
Renal biopsy may be performed to determine cause as well as to predict disease progression and response to therapy
45
Laboratory
Imaging
Procedures
Other diagnostic tools
Differential Diagnosis
Most common
Based on similar presentation
Renal artery stenosis
Narrowing of renal arteries resulting in loss of kidney function and blood pressure alteration
Both renal artery stenosis and chronic kidney disease present with hypertension and reduced GFR
Although also a cause of chronic kidney disease, renal artery stenosis (usually from atherosclerosis) is present before
development of kidney disease
Renal bruit is indicative of renal artery stenosis
Duplex ultrasonography can identify blockage in renal artery and high-velocity flow rate, indicative of renal artery
stenosis
Neoplasm (Related: Renal Cell Carcinoma)
Neoplasm of the kidney is a tumor growth in the renal cells
Both diseases present with RBCs in urine
Neoplasia can be differentiated by detecting tumor mass on kidney
Contrast-enhanced CT or ultrasonography can identify renal neoplasia, which can then be further evaluated with MRI
Chronic/recurrent urinary tract infection (Related: Urinary Tract Infection in Adults)
Defined as 3 or more urinary tract infections per year, 52 or persistent infection lasting longer than 2 weeks, presenting
with WBCs, bacteria, and RBCs in urine
Both diseases present with RBCs in urine
Unlike chronic kidney disease, urinary tract infections present with bacteria in urine
Critical number of uropathogens to define urinary tract infection: 52
Men: 10⁴ CFU/mL or more
Women: at least 10³ CFU/mL for uncomplicated cystitis to at least 10⁵ CFU/mL or more for complicated urinary tract
infections
Treatment
Goals
Recognize chronic kidney disease early in course
Prevent or slow further decline in renal function
Manage associated and underlying conditions and complications
Disposition
Admission criteria
Admit patients requiring urgent dialysis to inpatient care
Evaluate stable patients for dialysis or transplant on an outpatient basis
Criteria for ICU admission

Admit unstable patients presenting with sepsis, myocardial infarction, electrolyte imbalance, or severe acidosis
Recommendations for specialist referral

Refer to nephrologist for co-management of treatment plan in cases of: 1
Unclear cause of kidney disease
Rapid progression of disease (GFR decline greater than 5 mL/minute/1.73 m² per year) 3
Acute kidney injury or abrupt sustained fall in GFR 1
GFR less than 30 mL/minute/1.73 m² (GFR categories G4 and G5) to prepare for renal replacement therapy 1
Consistent finding of significant albuminuria (albumin to creatinine ratio of 300 mg/g or more) 1
Hypertension resistant to treatment with 4 or more antihypertensive agents 1
Difficulty in decreasing level of albuminuria despite implementing ACE inhibitor or angiotensin II receptor blocker
therapy
Persistent electrolyte abnormalities, including hyperkalemia or high serum phosphate level 1
Recurrent or extensive nephrolithiasis
Hereditary kidney disease
Refer to urologist if underlying urinary outflow obstruction is suspected cause 53
Treatment Options
Multifactorial approach to treatment focuses on interventions that are proven to slow the progression of kidney disease as well
as prevent the associated complications
Main components include renin-angiotensin-aldosterone system blockade, blood pressure control, and glycemic control
Additional components include lifestyle modifications, treatment of comorbidities, and renal replacement therapy (when
needed)
Progression of chronic kidney disease can be delayed by optimizing treatment of underlying causes (eg, diabetes, hypertension,
urinary obstruction)
Treatment of diabetes
Intensive measures to optimize glycemic control are indicated in most patients to limit albuminuria and slow progression
of diabetic nephropathy
Glycemic goal for most patients with diabetes is hemoglobin A1C level less than 7% (range is 6.5%-8% based on individual
patient factors) 54 55
Intensive diabetes management delays the onset and progression of nephropathy in both type 1 diabetes and type 2
diabetes; however, the effects on end-stage renal disease and mortality are not clear 56 57 58
Metformin is generally the drug of choice for patients with type 2 diabetes and early-stage kidney disease 59
In addition to metformin, strongly consider utilization of sodium-glucose cotransporter 2 inhibitors or glucagon-like

peptide 1 receptor agonists 4 60 61 62
Use a sodium-glucose cotransporter 2 inhibitor in patients with type 2 diabetes and chronic kidney disease with an
estimated glomerular filtration rate ≥20 mL/minute/1.73 m² and urinary albumin ≥300 mg/g creatinine 4 63
The sodium-glucose cotransporter 2 inhibitors that have been shown to slow chronic kidney disease progression for
patients with type 2 diabetes and diabetic kidney disease are empagliflozin, canagliflozin, and dapagliflozin 64
These three agents also demonstrate reduction in cardiovascular events and reduce risk of heart failure exacerbations
64
GLP-1 receptor agonists are suggested for cardiovascular risk reduction if burden of atherosclerotic cardiovascular
disease is predominant 4 62
The glucagon-like peptide 1 receptor agonists that have been shown to reduce cardiovascular events are liraglutide,
dulaglutide, and semaglutide; they may also slow chronic kidney disease progression, but definitive data on renal
outcomes are pending results from ongoing trials 65 66 67 68
Renin-angiotensin-aldosterone system blockade and treatment of hypertension
Renin-angiotensin-aldosterone system blockade is the primary treatment for patients with chronic kidney disease and
proteinuria; it reduces proteinuria, lowers blood pressure, and slows progression of kidney disease 53
Both ACE inhibitors and angiotensin receptor blockers have the dual effect of controlling blood pressure and slowing
progression of kidney damage 4
Blood pressure target goals vary
2021 guidelines by Kidney Disease: Improving Global Outcomes recommend a target systolic blood pressure below 120
mm Hg for patients with chronic kidney disease 69
An ACE inhibitor or angiotensin receptor blocker is recommended for patients with high blood pressure, chronic
kidney disease, or moderate or severely increased albuminuria, with or without diabetes
2021 Association of British Clinical Diabetologists and the Renal Association UK guideline proposes a target blood
pressure of 120/80 mm Hg for younger adults with diabetes and chronic kidney disease with no significant proteinuria
and for those with significant proteinuria 130/80 mm Hg or lower 70
Target blood pressure of 140/90mm Hg is recommended for those aged over 65
2017 American College of Cardiology/American Heart Association hypertension guidelines set a blood pressure goal less
than 130/80 mm Hg for all patients with chronic kidney disease (and others at elevated cardiovascular risk) 71
Several trials suggest this goal will result in reduced mortality for patients with chronic kidney disease 72
In patients with proteinuric chronic kidney disease, a lower blood pressure goal appears to reduce progression of
chronic kidney disease 72
Data are more limited for patients with concomitant diabetes and later stages (stages G4-G5) of chronic kidney disease
72
2018 European Society of Cardiology/European Society of Hypertension guidelines recommend systolic blood pressure
target of 130 to 139 mm Hg and diastolic blood pressure target of 70 to 79 mm Hg for patients with chronic kidney
disease 73
2018 Japanese Society of Nephrology guidelines recommend a target blood pressure of 130/80 mm Hg or lower for
patients with chronic kidney disease and diabetes or moderate to severe proteinuria (level A2 or A3); target of less than
140/90 mm Hg is recommended for nondiabetic patients with mild proteinuria (A1) and higher target of up to 150/90
mm Hg is recommended for elderly patients 74
Treatment recommended for children with blood pressure consistently above the 90th percentile for age, sex, and height
3
Treat until systolic and diastolic readings are at the 50th percentile or below for age, sex, and height
Often, multiple hypertensive agents are necessary to achieve optimal blood pressure; use in the following order:
ACE inhibitors or angiotensin receptor blockers are used as first line therapy to treat hypertension in adults and
children with chronic kidney disease 4
Preferred first line agent for blood pressure treatment in patients with diabetes 4
No clear indication whether to use ACE inhibitors or angiotensin receptor blockers 75
Diuretics are indicated for patients with refractory hypertension if disease is nonresponsive to ACE inhibitors or
angiotensin receptor blockers 76
Diuretics are also indicated to correct fluid imbalance in patients with edema
Calcium channel blockers are indicated in addition to ACE inhibitors or angiotensin receptor blockers, with or without
diuretics 77
β-blockers are indicated in patients with refractory hypertension in addition to ACE inhibitors or angiotensin receptor
blockers, diuretics, and calcium channel blockers 78
Aldosterone receptor antagonists are considered in patients with severe albuminuria, with input from a nephrologist 79
Treatment of urinary outflow obstruction
May include medication, catheterization, or nephrostomy, depending on location of obstruction 53
Bladder outflow obstruction is common in elderly males and may be a cause of acute deterioration in renal function
Mineralocorticoid receptor antagonism
Consider addition of finerenone, a nonsteroidal selective mineralocorticoid receptor antagonist, in patients with type 2
diabetes and chronic kidney disease who are treated with maximum tolerated doses of ACE inhibitors or angiotensin receptor
blockers 80
Finerenone has been shown to improve cardiorenal outcomes, slow chronic kidney disease progression, and reduce all-
cause mortality in patients with type 2 diabetes and diabetic kidney disease 81 82 83
Finerenone does not lower blood pressure substantially but may slightly increase potassium levels
Serum potassium must be monitored at regular intervals 84
Manage electrolyte disturbances 85
Hyperkalemia and hypokalemia
High (greater than 5.5 mEq/L) 86 or low (less than 4 mEq/L) 87 potassium levels are associated with increased mortality for
patients with chronic kidney disease
Patients with chronic kidney disease have a high risk of developing hyperkalemia, which can cause cardiac arrhythmias and
sudden death 47
8% to 73% of patients with chronic kidney disease develop hyperkalemia compared with 2.6% to 3.2% in the general
population 47
Patients with hypokalemia have an 82% increased risk of reaching end-stage renal disease 87
Hyperphosphatemia
Target serum phosphorus level is 2.7 to 4.6 mg/dL for categories G3 and G4, and 3.5 to 5.5 mg/dL for category G5 88
Reduce phosphorus intake and consult nephrologist for treatment with phosphate binders
Consider renal replacement therapy when chronic kidney disease progresses to end-stage renal failure (category G5) 89
Dialysis or renal transplant is indicated when 1 or more of the following are present:
Severe uremic symptoms including pruritus, nausea, vomiting, and neurologic changes
Progressive deterioration in nutritional status refractory to dietary intervention
Inability to control volume status or blood pressure
Patient has reached category G4 chronic kidney disease (GFR less than 30 mL/minute/1.73 m²)
Preemptive renal transplant with a living kidney donor is the preferred treatment for eligible patients 90
Renal transplant generally offers superior survival and quality of life compared with dialysis
Refer all potential candidates for transplant assessment at least 6 to 12 months before anticipated need for renal
replacement therapy to determine eligibility and plan for transplant
Kidney Disease: Improving Global Outcomes has published guidance on the evaluation and management of potential
renal transplant candidates 90
Initiating maintenance dialysis is a decision based on assessment of signs and symptoms of uremia, evidence of protein-
energy wasting, and ability to safely manage volume overload and/or metabolic derangements medically; it is no longer based
on specific levels of kidney function in the absence of signs and symptoms
Drug therapy
Select drug dosages based on GFR, and carefully monitor kidney function when prescribing nephrotoxic medications because
change in renal function alters drug metabolism 91
Consult the Kidney Disease: Improving Global Outcomes conference report for detailed dosing considerations and strategies
for acute and chronic kidney disease 92
Considerations for drugs commonly used by patients with chronic kidney disease
ACE inhibitors
Used to reduce blood pressure in kidneys and reduce albuminuria 3
Dual therapy with angiotensin receptor blockers is not recommended 85
Use lower dose in patients with GFR less than 45 mL/minute/1.73 m²; do not routinely discontinue when GFR is less
than 30 mL/minute/1.73 m² (remains nephroprotective) 91
Follow serum potassium level
Angiotensin receptor blockers
Used to reduce blood pressure in kidneys and reduce albuminuria 85
Dual therapy with ACE inhibitor is not recommended 85
Use lower dose in patients with GFR less than 45 mL/minute/1.73 m²; do not routinely discontinue when GFR is less
than 30 mL/minute/1.73 m² (remains nephroprotective) 91
Follow serum potassium level 85
Calcium channel blockers
Used in combination with ACE inhibitor or angiotensin receptor blocker to control hypertension 93
Avoid prescribing calcium channel blockers without ACE inhibitor or angiotensin II receptor blocker because sole use
can lead to increased hyperfiltration and increased albuminuria 94
3 main classes 93
Benzothiazepines (diltiazem)
Preferred over dihydropyridines owing to an antiproteinuric effect
Phenylalkylamines (verapamil)
Preferred over dihydropyridines because it has an antiproteinuric effect (no clear indication to discriminate
between use of benzothiazepines and phenylalkylamines)
Dihydropyridines (eg, nifedipine, amlodipine) 93
Aldosterone receptor antagonists
Spironolactone (nonselective) 79
Carefully monitor for hyperkalemia
Eplerenone (selective) 79
Finerenone 84
Antidiabetic agents
Choice of therapy depends on type of diabetes, degree of glycemic control needed, and level of current kidney function
First line treatment for patients with type 2 diabetes is metformin and a sodium-glucose cotransporter-2 inhibitor 55
Biguanides
Metformin
Contraindicated when GFR is less than 30 mL/minute/1.73 m² 91
Use with caution when GFR is between 30 and 45 mL/minute/1.73 m² 95
Sodium-glucose cotransporter 2 inhibitors
These drugs have nephroprotective and cardioprotective properties 60 96 97 98
Empagliflozin and canagliflozin are contraindicated if estimated GFR falls below 45 mL/minute/1.73 m² (category G3b
and higher chronic kidney disease)
Dapagliflozin is contraindicated if estimated GFR falls below 60 mL/minute/1.73 m² (category G3a and higher chronic
kidney disease)
Glucagon-like peptide 1 receptor agonists
These drugs have cardioprotective and nephroprotective properties; however, the renal benefits are less well-
established than those of sodium-glucose cotransporter 2 inhibitors 99 100
Liraglutide, albiglutide, and dulaglutide can be used without dose alterations in category G2, G3a, or G3b chronic
kidney disease
All glucagon-like peptide 1 receptor agonists are contraindicated in categories G4 and G5 chronic kidney disease
(estimated GFR less than 30 mL/minute/1.73 m²)
Sulfonylureas
First-generation sulfonylureas are contraindicated as they are affected by kidney function and increase risks of
hypoglycemia 91
Second-generation sulfonylurea; preferred in patients with chronic kidney disease as it is metabolized primarily in
the liver
If this class is used, carefully monitor blood glucose level and give conservative dosing
Most sulfonylureas are contraindicated in patients with category G4 or G5 chronic kidney disease (estimated GFR less
than 30 mL/minute/1.73 m²)
Insulin
May need dose reduction when GFR is less than 30 mL/minute/1.73 m² to avoid hypoglycemia because insulin is
partly renally excreted 101
No evidence-based guidelines or recommendations exist specifying which types of insulin to use or avoid depending
on severity of chronic kidney disease
Diuretics
Current guidelines and protocols support use of loop diuretics when GFR is less than 30 mL/minute/1.73 m² (categories
G4 and G5), preferring the use of a thiazide during earlier stages of chronic kidney disease 102
Monitor for hyperkalemia and hypotension because diuretics can cause fluid imbalance, resulting in electrolyte level
disparities 103
Thiazide
Once-daily use is recommended in patients with GFR of 30 mL/minute/1.73 m² or higher (categories G1 through G3)
102
Loop diuretics
Once- or twice-daily use is recommended in patients with GFR less than 30 mL/minute/1.73 m² (categories G4 and G5)
102
Analgesics
Acetaminophen is the analgesic recommended for short-term treatment of mild to moderate pain in patients with
stages 3 to 5 chronic kidney disease; considered analgesic of choice for all patients with chronic kidney disease 43
NSAIDs may be used for short-term therapy in patients up to stage 3 chronic kidney disease, with regular monitoring of
renal function 43
Potassium-binding resins
Adjunctive therapy to lower serum potassium level after emergency management of acute hyperkalemia and as
treatment for chronic hyperkalemia 104
Kayexalate (sodium polystyrene sulfonate) 2
Oral or rectal administration
Patiromer 2
Oral administration
Nondrug and supportive care

Engage in regular exercise 105
Combination of aerobic and muscle strengthening exercise is recommended
Encourage at least 150 minutes of moderate-intensity aerobic activity per week
Recommend activities aimed at improving or maintaining muscle strength, balance and flexibility on at least 2 days a week
Infection prevention
The following immunizations are recommended, in addition to other age-appropriate immunizations, providing there are no
contraindications: 74 106
Pneumococcal vaccine
Hepatitis B vaccine
Annual influenza vaccination
Weight control 3 105
107
Recommend weight loss in those with BMI greater than 25 kg/m² 107
Dietary modification 1
Protein intake of 0.8 to 1.0 g/kg/day in adults with or without diabetes and GFR less than 30 mL/minute/1.73 m² 4
Higher protein intake of 1.1 to 1.2 g/day is recommended for patients on peritoneal dialysis (up to 1.4 g/day for
hemodialysis patients) 107
Reducing the amount of dietary protein below the recommended daily allowance of 0.8 g/kg/day is not recommended
because it does not alter glycemic measures, cardiovascular risk measures, or the course of GFR decline 4
Adults at risk for chronic kidney disease progression should avoid high protein intake (greater than 1.3 g/kg/day)
Adults should limit salt intake to less than 2300 mg/day 4
Sodium intake should be less than 2 g/day (equivalent to 5 g of sodium chloride) for adults with hypertension and chronic
kidney disease 69
Smoking cessation 3 74 105
Procedures
Dialysis
General explanation
A process to filter waste products and excess fluid from the blood
Indication
Indicated in patients who develop symptoms or signs attributable to kidney failure (any of the following):
Often (but not invariably) occurs when GFR is 5 to 10 mL/minute/1.73 m² 108
Acid/base or electrolyte abnormalities or pruritus
Inability to control volume status or blood pressure
Deterioration in nutritional status unresponsive to dietary intervention
Timing of dialysis initiation is controversial, as later initiation is associated with decreased mortality
Do not base initiation on GFR alone 108
Complications
Hypotension
Hypertension
Arrhythmia
Infection
Muscle cramping
Nausea/vomiting
Headache
Confusion
Air embolism
Renal transplant
General explanation
Surgical implantation of a healthy donor kidney
Indication
Patients with GFR category G4 or G5 who are declining rapidly 1
Evidence of progressive and irreversible chronic kidney disease over the preceding 6 to 12 months, including pruritus,
refractory electrolyte imbalances, metabolic acidosis, severe nausea, or neurologic impairments 1
There is no defined GFR for initiating renal replacement, but these symptoms typically occur when GFR is 5 to 10
mL/minute/1.73 m² 108
Contraindications
Disseminated or untreated cancer
Severe psychiatric disease
Persistent substance misuse
Inoperable coronary artery disease or refractory congestive heart failure
Pregnancy
Complications
Thrombosis
Anastomotic leakage
Rejection
Failure of donated kidney
Infection
Bleeding
Comorbidities
Dyslipidemia 109
Common among patients with chronic kidney disease
Patients with chronic kidney disease are at increased risk of cardiovascular disease
Consider statin therapy for patients with chronic kidney disease who are:
Older than 50 years
Aged 18 to 50 years and at high risk for atherosclerotic cardiovascular disease (eg, history of cardiovascular disease,
stroke, or diabetes; 10-year atherosclerotic cardiovascular disease risk of greater than 10%)
Statin-ezetimibe combination is an option for patients with G3a through G5 chronic kidney disease
Statins or statin plus ezetimibe are not recommended for patients on dialysis
Congestive heart failure
Congestive heart failure often coexists with chronic kidney disease, and there is a complex relationship between the
conditions 110
Cardiorenal syndrome refers to acute or chronic dysfunction in heart or kidneys that is induced by acute or chronic
dysfunction in the other organ
Management of heart failure exacerbations may be challenging and concerns about renal function may lead to suboptimal
management of heart failure 111 112
Diuretic therapy may improve deterioration in renal function owing to reduced renal perfusion in the setting of fluid
overload 53
Diabetes mellitus
Manage patients with diabetes and chronic kidney disease as with patients who have diabetic nephropathy (Related:
Diabetic Kidney Disease)
Intensive measures to optimize glycemic control are indicated in most patients to limit albuminuria and slow progression
of nephropathy
Glycemic goal for most patients with diabetes is hemoglobin A1C level less than 7%; goal may range from 6.5% to 8%
depending on individual patient factors 54 55
Choice of antihyperglycemic drug is influenced by several factors:
Type of diabetes
Insulin is always required in type 1 diabetes
Oral or injectable drugs can be used in early stages of type 2 diabetes
Metformin is typical first line agent in patients with type 2 diabetes and early chronic kidney disease 59
Intended intensity of diabetes treatment
More potent diabetes drugs (eg, insulin, sulfonylureas, glucagon-like peptide 1 receptor agonists) are more effective in
achieving lower hemoglobin A1C levels
Stage of kidney disease
Greater degree of renal dysfunction can increase the toxicity of some medications owing to impaired drug clearance
113
At higher levels of albuminuria or higher serum creatinine level, there is greater risk of severe hypoglycemia;
therefore, for patients most at risk for adverse outcomes with hypoglycemia (ie, elderly patients, those with several
comorbidities), agents that promote hypoglycemia are less desirable 113
Generally avoid sulfonylureas owing to risk of hypoglycemia; most are contraindicated in patients with stage G4
chronic kidney disease
Metformin is contraindicated when estimated GFR is less than 30 mL/minute/1.73 m² 4 or in any situation in which
there is an elevated risk of lactic acidosis
Effect on progression of kidney disease
Metformin is the first line treatment for type 2 diabetes and chronic kidney disease 55
Consider selected sodium-glucose cotransporter 2 inhibitors (ie, empagliflozin and canagliflozin) and/or glucagon-
like peptide 1 receptor agonists (liraglutide, dulaglutide and semaglutide) for patients who require a drug added to
metformin to attain glycemic goals 4 55 62
Sodium-glucose cotransporter 2 inhibitors have nephroprotective and cardioprotective properties 96
Empagliflozin was shown to reduce incidence of nephropathy, slow its progression, and lower the rate of renal
replacement therapy in patients with type 2 diabetes whose GFR was at least 30 mL/minute/1.73 m² 98
Canagliflozin was shown to improve renal outcomes in patients with type 2 diabetes whose GFR was at least 30
mL/minute/1.73 m² 60
Empagliflozin and canagliflozin are contraindicated if estimated GFR falls below 45 mL/minute/1.73 m² (category
G3b and higher chronic kidney disease)
Glucagon-like peptide 1 receptor agonists have cardioprotective and nephroprotective properties; however, the
renal benefits are less well-established than those of sodium-glucose cotransporter 2 inhibitors 99 100
Contraindicated in stages G4 and G5 chronic kidney disease (GFR less than 30 mL/minute/1.73 m²)
Both liraglutide and semaglutide reduce the risk of new or worsening nephropathy
Prescribe an angiotensin receptor blocker or ACE inhibitor in diabetic adults with chronic kidney disease and urine
albumin excretion of 30 to 300 mg/24 hours 1
Consider addition of finerenone to improve cardiovascular outcomes and reduce the risk of chronic kidney disease
progression in patients with type 2 diabetes and chronic kidney disease who are treated with maximum tolerated doses of
ACE inhibitors or angiotensin receptor blockers 80
Hepatitis C
High level of transmission within dialysis units reflecting insufficient attention to body fluid precautions 114
Most patients infected with hepatitis C have an absence of biochemical liver dysfunction, which contributes to the lack of
recognition of its presence
If hepatitis C infection is identified during routine screening:
Perform noninvasive evaluation of liver fibrosis (eg, transient elastography) and consider liver biopsy if results are
discordant or uncertain 114
Evaluate patient for antiviral therapy; an interferon-free regimen is recommended 114
All treatment candidates should undergo testing for hepatitis B virus infection before therapy; if HBsAg is present,
assess patient for hepatitis B virus therapy
Treat patients with GFR of 30 mL/minute/1.73 m² or higher (categories G1-G3b) with any licensed direct-acting
antiviral-based regimen
Treat patients with GFR less than 30 mL/minute/1.73 m² (categories G4-G5D) with a ribavirin-free direct-acting
antiviral-based regimen; specific recommendations are available from the Kidney Disease: Improving Global
Outcomes 2018 Clinical Practice Guidelines for the Prevention, Diagnosis, Evaluation, and Treatment of Hepatitis C
in Chronic Kidney Disease 114
Special populations
Children 1
Start antihypertensives when blood pressure is consistently above the 90th percentile for age, sex, and height
Target blood pressure goals: systolic and diastolic measurements less than or equal to the 50th percentile for age, sex, and
height, unless achieving these targets is limited by signs or symptoms of hypotension
Prescribe an angiotensin receptor blocker or ACE inhibitor in children with chronic kidney disease in whom treatment
with blood pressure–lowering drugs is indicated, irrespective of proteinuria level
Restrict salt intake for children with chronic kidney disease and hypertension (systolic and/or diastolic blood pressure
above 95th percentile) or prehypertension (systolic and/or diastolic blood pressure above 90th percentile but below 95th
percentile), following the age-based recommended daily intake
Patients requiring contrast-enhanced MRI or CT scans
Gadolinium-based contrast media 115
Gadolinium-enhanced MRI examinations are first line imaging investigation for many indications; however, there are
concerns about risk of nephrogenic systemic fibrosis and nephrotoxicity in patients with impaired kidney function
Risk of nephrogenic systemic fibrosis varies between different types of gadolinium-based contrast media; can be
stratified into 3 groups:
Group I: highest risk
Group II: very low risk
Group III: likely very low risk but limited evidence
Patients with stage 4 or 5 chronic kidney disease who are exposed to a group I gadolinium-based contrast media,
especially repeated, higher off-label doses, are at the greatest risk for developing nephrogenic systemic fibrosis
Risk of nephrogenic systemic fibrosis from administration of group II gadolinium-based contrast media is reported to
be very low even in patients with eGFR less than 30 mL/minute per 1.73 m²
Group II gadolinium-based contrast media should not be delayed or withheld if harm would result from not proceeding
with an indicated contrast-enhanced MRI
Iodinated contrast media 116
True risk of contrast induced-acute kidney injury is unclear; however, necessary contrast-enhanced CT imaging should
not be avoided solely based on this risk in the absence of a suitable imaging alternative
Prophylaxis with IV normal saline is indicated for patients who have an estimated glomerular filtration rate less than 30
mL/minute/1.73 m² who are not undergoing maintenance dialysis
In high-risk circumstances, prophylaxis may be considered in patients with an eGFR of 30 to 44 mL/minute/1.73 m²
Monitoring
Monitor progression of disease 1
Assess GFR and albuminuria at least annually in patients with chronic kidney disease
Assess GFR and albuminuria more often in patients at higher risk of progression (eg, categories G4 or G5, diabetes) or
where measurement will impact therapeutic decisions
Recommended frequency of monitoring (times per year) by GFR and albuminuria categories: 3
G1
A1: 1 time
https://www-clinicalkey-es.fucsalud.basesdedatosezproxy.com/#!/con…nt/clinical_overview/67-s2.0-26a91efc-ff97-4e11-b49f-c70331e79cee Página 20 de 34
A2: 1 time
A3: 1 time
G2
A1: 1 time
A2: 1 time
A3: 2 times
G3a
A1: 1 time
A2: 2 times
A3: 3 times
G3b
A1: 2 times
A2: 3 times
A3: 3 times
G4
A1: 3 times
A2: 3 times
A3: 4 or more times
G5
A1: 4 or more times
A2: 4 or more times
A3: 4 or more times
Determine chronic kidney disease progression based on 1 or more of the following: 1
Decline in GFR category; drop in GFR category accompanied by a 25% or greater drop in GFR from baseline
Rapid progression is defined as a sustained decline in GFR of more than 5 mL/minute/1.73 m² per year
If rapid progression occurs, review current management, examine for reversible causes of progression, and refer to a
specialist
Monitor clinical status of patients with chronic kidney disease 43
Anemia (in all chronic kidney disease stages)
CBC with differential, reticulocyte count, serum iron level, ferritin level, and transferrin level annually; more frequently
if abnormal
Electrolyte and acid/base disturbance (in all chronic kidney disease stages)
Serum electrolytes, calcium, phosphorus, and bicarbonate levels at least annually; more frequently as renal function
85
declines 85
Renal function (in all chronic kidney disease stages)
Blood pressure, GFR determination, and albumin level at least annually; more frequently as renal function declines 85
Malnutrition (categories G3-G5)
Weight, serum albumin level, and dietary history every 6 to 12 months for category G3 and every 1 to 3 months for
categories G4 and G5
Metabolic bone disease (categories G3-G5)
Alkaline phosphatase level once in category G3 and annually in categories G4 and G5
Calcium and phosphorus levels every 6 to 12 months in category G3, every 3 to 6 months in category G4, and every 1 to 3
months in category G5
Measure serum phosphorus every month if phosphorus restriction is required (serum phosphorus greater than 4.6
mg/dL in categories G4 and G5 and greater than 5.5 mg/dL in category G5) 88
25-hydroxyvitamin D level once, then as indicated
Parathyroid hormone level once, then as indicated in category G3; every 6 to 12 months in category G4; and every 3 to 6
months in category G5
Neuropathy (categories G3-G5)
Evaluate routinely for paresthesias, mental status changes, and sleep disturbances (eg, restless legs) as indicated; consider
sleep and nerve conduction studies
Hepatitis C status
Screening for hepatitis C infection is recommended at initial evaluation for chronic kidney disease, at initiation of
peritoneal dialysis or hemodialysis, and every 6 months for patients receiving in-center hemodialysis (with additional
testing if a new case is identified within a hemodialysis center) 114
Initial evaluation includes an immunoassay followed by nucleic acid testing if immunoassay result is positive 114
Ongoing monitoring of patients receiving in-center hemodialysis
Either nucleic acid testing alone or an immunoassay followed by nucleic acid testing if immunoassay result is
positive
Monitor ALT monthly
Monitor patients with chronic kidney disease after starting on ACE inhibitor or angiotensin receptor blocker
Measure blood pressure, GFR, and serum potassium levels within 4 weeks of initial dose or dosage adjustment if any of the
following are present: 85
Systolic blood pressure below 120 mm Hg or above 140 mm Hg
GFR less than 60 mL/minute/1.73 m²
Decline in GFR greater than 15% in the last 2 months
Potassium level greater than 4.5 mEq/L
Monitor transplant patients 3
Monitor for allograft dysfunction (eg, hypertension, increased creatinine, decreased GFR, increased albuminuria) because
patients who receive kidney transplants have increased risk for mortality and kidney failure
Allograft biopsy is recommended if increased serum creatinine or unexplained albuminuria persists 117
Assess medications for interactions with immunosuppressive drugs
Complications and Prognosis
Complications
Hypertension
Both a cause and a result of chronic kidney disease
Development of hypertension increases in patients as GFR decreases
Chronic kidney disease can worsen hypertension owing to increased systemic vascular resistance and volume expansion
Hyperkalemia 118
Most common electrolyte disorder in patients with kidney disease, particularly in those with diabetes and heart failure or
those treated with renin-angiotensin-aldosterone system inhibitors
Carries risk of life-threatening cardiac arrhythmia
Requires urgent medical treatment with IV calcium, IV glucose, IV insulin, and nebulized albuterol when serum level is
above 5.5 mEq/L 2
Adjunct (subacute) therapy may include dialysis, loop diuretics, sodium bicarbonate, kayexalate, or patiromer 2
Anemia
Declining renal function decreases renal output of erythropoietin, leading to anemia
Other factors may also contribute, such as: 119
Shortened RBC survival
Blood loss (especially in dialysis patients)
Impaired absorption of dietary iron
90% of patients with GFR less than 25 to 30 mL/minute/1.73 m² will develop anemia 13
Treat iron deficiency first, if present 120
Treat with erythropoiesis-stimulating agent if hemoglobin is lower than 10 g/dL; recommended hemoglobin targets range
from up to 11.5 g/dL to 11 to 13 g/dL 74 121
Bone mineral disease
Typically apparent in categories G3 through G5 5 6
Declining renal function results in increased phosphate output and decreased parathyroid hormone, which leads to
abnormal calcium and vitamin D metabolism and consequent bone turnover abnormalities 5 6
Lower phosphate levels toward reference range; limit dietary phosphate intake
Avoid hypercalcemia
Routine use of vitamin D analogues and calcitriol in patients not receiving dialysis is not recommended; reserved for
patients with progressive, severe hyperparathyroidism
Fracture risk increases and healing is prolonged
Metabolic acidosis
30% to 50% of those with GFR below 30 mL/minute/1.73 m² have metabolic acidosis due to defects in renal acid output 122
Lower serum bicarbonate is associated with an increased risk of kidney disease progression 123
Treat metabolic acidosis with bicarbonate or sodium citrate when serum bicarbonate concentration is under 22 mmol/L 1
Cardiovascular disease
GFR of 30 mL/minute/1.73 m² is associated with a cardiovascular disease risk of 40%, compared with 15% risk for those
with GFR within the reference range (130 mL/minute/1.73 m²) 124
Most patients with chronic kidney disease die from cardiovascular disease before reaching end-stage renal disease 125
Cardiovascular mortality is 2 times higher in patients with category G3 and 3 times higher in patients with category G4
than in patients with normal kidney function 126
Uremia
Common at low GFR, though some features (eg, lethargy, anorexia) may present at all stages of chronic kidney disease 127
Peripheral arterial disease
Neuropathy
Typically manifests as peripheral neuropathies in sensory-motor function 128
Present in 65% of patients at the initiation of dialysis 1
Patients with chronic kidney disease are at greater risk of developing acute kidney injury, more likely to require renal
replacement therapy for treatment, and less likely to recover to baseline renal function 53
Acute kidney injury
Causes are same as those in general population
Important to promptly identify and address any reversible causes of acute deterioration in renal function
Prognosis
Overall mortality rate for Medicare patients aged 66 and older is 122 per 1000 patient-years 18
Decline in estimated GFR associated with subsequent increased risk of end-stage renal disease and mortality 18
Only 1% of patients with chronic kidney disease require dialysis and/or kidney transplant 17
Patients who refuse dialysis have a median life expectancy of 6.3 to 23.4 months 129 130
Sepsis mortality is 100 to 300 times higher for patients on chronic dialysis compared with the general public 124
Increased albuminuria and decreased GFR are associated with infection-related mortality (hazard ratio, 2.11 for patients
with albumin to creatinine ratio above 30 mg/g; hazard ratio, 1.94 for patients with GFR below 60 mL/minute/1.73 m²) 131
Screening and Prevention
Screening
At-risk populations
As defined by the National Kidney Foundation, the following groups are at risk for chronic kidney disease and should be
screened: 7
Patients with a family history of chronic kidney disease
Patients with sickle cell trait
Patients aged 60 years and older
Patients with diabetes, hypertension, cardiovascular disease, recurrent urinary tract infections, urinary obstruction, or
systemic disease that affects the kidneys (eg, HIV, hepatitis C, malignancy)
Specific racial groups: African Americans, Asian people/Pacific Islanders, Hispanic people, Native Americans
Screening tests
National Kidney Foundation recommends screening at-risk populations annually by urinalysis and measuring both GFR and
urine albumin to creatinine ratio 17
Begin screening for chronic kidney disease in patients with type 1 diabetes starting 5 years after diabetes diagnosis
Begin screening for chronic kidney disease in patients with type 2 diabetes starting at the time of diabetes diagnosis
Prevention
Treatment of conditions that underlie the development of chronic kidney disease (eg, diabetes, hypertension) can slow its
progression 3
Additionally, lifestyle interventions (eg, reducing sodium to less than 2 g/day, quitting smoking, exercising for 30 minutes 5
times weekly, maintaining a healthy BMI) are known to reduce proteinuria and slow progression of the disease
Referencias
1 International Society of Nephrology (ISN): Kidney Disease: Improving Global Outcomes: KDIGO: 2012 clinical practice guideline for the
evaluation and management of chronic kidney disease. Kidney Int Suppl. 3(1):1-150, 2013
Ver en el Artículo | Referencia cruzada (https://kdigo.org/wp-content/uploads/2017/02/KDIGO_2012_CKD_GL.pdf )
2 Rafique Z et al: Expert panel recommendations for the identification and management of hyperkalemia and role of patiromer in patients
with chronic kidney disease and heart failure. J Manag Care Spec Pharm. 23(4-a Suppl):S10-9, 2017
Ver en el Artículo | Referencia cruzada (https://pubmed-ncbi-nlm-nih-gov.fucsalud.basesdedatosezproxy.com/28485203)
3 Stevens PE et al: Evaluation and management of chronic kidney disease: synopsis of the Kidney Disease: Improving Global Outcomes 2012
clinical practice guideline. Ann Intern Med. 158(11):825-30, 2013
4 American Diabetes Association Professional Practice Committee et al: 11. Chronic kidney disease and risk management: Standards of
Medical Care in Diabetes-2022. Diabetes Care. 45(Suppl 1):S175-84, 2022
5 Ketteler M et al: Diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder: synopsis of the
Kidney Disease: Improving Global Outcomes 2017 clinical practice guideline update. Ann Intern Med. 168(6):422-30, 2018
6 Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work Group: KDIGO 2017 clinical practice guideline update for
the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD). Kidney Int Suppl
(2011). 7(1):1-59, 2017
7 National Kidney Foundation: K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification.
Am J Kidney Dis. 39(2 Suppl 1):S1-266, 2002
8 Muntner P et al: Hypertension awareness, treatment, and control in adults with CKD: results from the Chronic Renal Insufficiency Cohort
(CRIC) Study. Am J Kidney Dis. 55(3):441-51, 2010
9 Levey AS et al: Chronic kidney disease. Lancet. 379(9811):165-80, 2012

10 Levin A: Clinical epidemiology of cardiovascular disease in chronic kidney disease prior to dialysis. Semin Dial. 16(2):101-5, 2003
11 Zhe M et al: Nephrolithiasis as a risk factor of chronic kidney disease: a meta-analysis of cohort studies with 4,770,691 participants.
Urolithiasis. 45(5):441-8, 2017
12 Moreno JA et al: Haematuria: the forgotten CKD factor? Nephrol Dial Transplant. 27(1):28-34, 2012
13 Kazmi WH et al: Anemia: an early complication of chronic renal insufficiency. Am J Kidney Dis. 38(4):803-12, 2001
14 Murtagh FE et al: Symptoms in advanced renal disease: a cross-sectional survey of symptom prevalence in stage 5 chronic kidney disease
managed without dialysis. J Palliat Med. 10(6):1266-76, 2007
15 O'Hare AM et al: High prevalence of peripheral arterial disease in persons with renal insufficiency: results from the National Health and
Nutrition Examination Survey 1999-2000. Circulation. 109(3):320-3, 2004
16 Kiefer MM et al: Primary care of the patient with chronic kidney disease. Med Clin North Am. 99(5):935-52, 2015
17 Snyder S et al: Detection and evaluation of chronic kidney disease. Am Fam Physician. 72(9):1723-32, 2005
18 US Renal Data System (USRDS): 2018 USRDS Annual Data Report: Volume 1: CKD in the United States. USRDS website. Published 2018.
Accessed October 11, 2022. https://www.usrds.org/media/2282/2018_volume_1_ckd_in_the_us.pdf
Ver en el Artículo | Referencia cruzada (https://www.usrds.org/media/2282/2018_volume_1_ckd_in_the_us.pdf )
19 Iseki K et al: Risk of developing end-stage renal disease in a cohort of mass screening. Kidney Int. 49(3):800-5, 1996
20 Online Mendelian Inheritance in Man, OMIM. OMIM website. Johns Hopkins University, MIM 601313: Polycystin 1; PKD1. Updated
November 20, 2018. Edited June 22, 2022. Accessed December 5, 2022. https://www.omim.org/entry/601313
Ver en el Artículo | Referencia cruzada (https://www.omim.org/entry/601313)
21 Online Mendelian Inheritance in Man, OMIM. OMIM website. Johns Hopkins University, MIM 173910: Polycystin 2; PKD2. Updated
November 20, 2018. Accessed December 5, 2022. https://www.omim.org/entry/173910
22 Silverman J et al: Autosomal dominant polycystic kidney disease. Dis Mon. 61(10):442-7, 2015
23 Savige J: Alport syndrome: its effects on the glomerular filtration barrier and implications for future treatment. J Physiol. 592(Pt 18):4013-
23, 2014
24 Online Mendelian Inheritance in Man. OMIM website. Johns Hopkins University, MIM 203780: Alport Syndrome 2, Autosomal Recessive;
ATS2. Updated July 10, 2015. Edited January 31, 2019. Accessed December 5, 2022. https://www.omim.org/entry/203780
25 Online Mendelian Inheritance in Man, OMIM. OMIM website. Johns Hopkins University, MIM 301050: Alport Syndrome 1, X-Linked;
ATS1. Updated July 10, 2015. Edited August 2, 2019. Accessed December 5, 2022. https://www.omim.org/entry/301050
26 Online Mendelian Inheritance in Man, OMIM. OMIM website. Johns Hopkins University, MIM 174000: Medullary Cystic Kidney Disease
1; MCKD1. Updated January 26, 2021. Edited February 8, 2021. Accessed December 5, 2022. https://www.omim.org/entry/174000
27 Eckardt KU et al: Autosomal dominant tubulointerstitial kidney disease: diagnosis, classification, and management--a KDIGO consensus
report. Kidney Int. 88(4):676-83, 2015
28 Kartha G et al: Impact of stone disease: chronic kidney disease and quality of life. Urol Clin North Am. 40(1):135-47, 2013
29 Choi SK et al: Risk of chronic kidney disease after nephrectomy for renal cell carcinoma. Korean J Urol. 55(10):636-42, 2014
30 Sui M et al: Epidemiology and risk factors for chronic kidney disease in Chinese patients with biopsy-proven lupus nephritis. Intern Med J.
45(11):1167-72, 2015
31 Eleutherakis-Papaiakovou V et al: Renal failure in multiple myeloma: incidence, correlations, and prognostic significance. Leuk
Lymphoma. 48(2):337-41, 2007
32 Kamesh L et al: ANCA-positive vasculitis. J Am Soc Nephrol. 13(7):1953-60, 2002

33 Quintana LF et al: ANCA serotype and histopathological classification for the prediction of renal outcome in ANCA-associated
glomerulonephritis. Nephrol Dial Transplant. 29(9):1764-9, 2014
34 Bucaloiu ID et al: Increased risk of death and de novo chronic kidney disease following reversible acute kidney injury. Kidney Int.
81(5):477-85, 2012
35 Hallan SI et al: Smoking is a risk factor in the progression to kidney failure. Kidney Int. 80(5):516-23, 2011
36 Ejerblad E et al: Obesity and risk for chronic renal failure. J Am Soc Nephrol. 17(6):1695-702, 2006
37 Odermatt A: The Western-style diet: a major risk factor for impaired kidney function and chronic kidney disease. Am J Physiol Renal
Physiol. 301(5):F919-31, 2011
38 Choudhury D et al: Drug-associated renal dysfunction and injury. Nat Clin Pract Nephrol. 2(2):80-91, 2006
39 Earley A et al: Estimating equations for glomerular filtration rate in the era of creatinine standardization: a systematic review. Ann Intern
Med. 156(11):785-95, W-270-8, 2012
40 National Kidney Foundation (NKF): eGFR Calculator. NKF website. Accessed December 5, 2022.
https://www.kidney.org/professionals/KDOQI/gfr_calculator
Ver en el Artículo | Referencia cruzada (https://www.kidney.org/professionals/KDOQI/gfr_calculator)
41 National Institute of Diabetes and Digestive and Kidney Diseases: GFR Calculators. NIDDK website. Accessed December 5, 2022.
https://www-niddk-nih-gov.fucsalud.basesdedatosezproxy.com/health-information/professionals/clinical-tools-patient-
management/kidney-disease/laboratory-evaluation/glomerular-filtration-rate-calculators?dkrd=hispt1299
Ver en el Artículo | Referencia cruzada (https://www-niddk-nih-gov.fucsalud.basesdedatosezproxy.com/health-
information/professionals/clinical-tools-patient-management/kidney-disease/laboratory-evaluation/glomerular-filtration-rate-calculators?dkrd=hispt1299)
42 Sandilands EA et al: Measurement of renal function in patients with chronic kidney disease. Br J Clin Pharmacol. 76(4):504-15, 2013
43 Baumgarten M et al: Chronic kidney disease: detection and evaluation. Am Fam Physician. 84(10):1138-48, 2011
44 Ozmen CA et al: Ultrasound as a diagnostic tool to differentiate acute from chronic renal failure. Clin Nephrol. 74(1):46-52, 2010
45 Dhaun N et al: Utility of renal biopsy in the clinical management of renal disease. Kidney Int. 85(5):1039-48, 2014
46 Simerville JA et al: Urinalysis: a comprehensive review. Am Fam Physician. 71(6):1153-62, 2005

47 Kovesdy CP: Management of hyperkalemia: an update for the internist. Am J Med. 128(12):1281-7, 2015
48 Levin A et al: Prevalence of abnormal serum vitamin D, PTH, calcium, and phosphorus in patients with chronic kidney disease: results of
the study to evaluate early kidney disease. Kidney Int. 71(1):31-8, 2007
49 American Diabetes Association Professional Practice Committee et al: 2. Classification and diagnosis of diabetes: Standards of Medical
Care in Diabetes-2022. Diabetes Care. 45(Suppl 1):S17-38, 2022
50 Topham PS et al: Renal biopsy. In: Feehally J et al, eds: Comprehensive Clinical Nephrology. 6th ed. Elsevier; 2019:72-9.e1
Ver en el Artículo
51 Lamb EJ et al: Estimating and measuring glomerular filtration rate: methods of measurement and markers for estimation. Curr Opin
Nephrol Hypertens. 23(3):258-66, 2014
52 Smelov V et al: Improved classification of urinary tract infection: future considerations. Eur Urol Suppl. 15(4):71-80, 2016
Ver en el Artículo | Referencia cruzada (http://dx.doi.org.fucsalud.basesdedatosezproxy.com/10.1016/j.eursup.2016.04.002)
53 Weir VA et al: A practical guide to diagnosis and assessment of chronic kidney disease for the non-nephrologist. J R Coll Physicians Edinb.
50(1):67-74, 2020
54
54 American Diabetes Association Professional Practice Committee et al: 6. Glycemic targets: Standards of Medical Care in Diabetes-2022.
Diabetes Care. 45(Suppl 1):S83-96, 2022
55
55 de Boer IH et al: Diabetes management in chronic kidney disease: a consensus report by the American Diabetes Association (ADA) and
Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 102(5):974-89, 2022
56
56 Lo C et al: Intensive glucose control in patients with diabetes prevents onset and progression of microalbuminuria, but effects on end-
stage kidney disease are still uncertain. Evid Based Med. 22(6):219-20, 2017
57
57 Effect of intensive therapy on the development and progression of diabetic nephropathy in the Diabetes Control and Complications Trial.
The Diabetes Control and Complications (DCCT) Research Group. Kidney Int. 47(6):1703-20, 1995
58
58 Ruospo M et al: Glucose targets for preventing diabetic kidney disease and its progression. Cochrane Database Syst Rev. 6:CD010137, 2017
59
59 Ioannidis I: Diabetes treatment in patients with renal disease: Is the landscape clear enough? World J Diabetes. 5(5):651-8, 2014
60
60 Perkovic V et al: Canagliflozin and renal outcomes in type 2 diabetes and nephropathy. N Engl J Med. 380(24):2295-306, 2019
61
61 Rangaswami J et al: Cardiorenal protection with the newer antidiabetic agents in patients with diabetes and chronic kidney disease: a
scientific statement from the American Heart Association. Circulation. 142(17):e265-86, 2020
62
62 American Diabetes Association Professional Practice Committee et al: 10. Cardiovascular disease and risk management: Standards of
Medical Care in Diabetes-2022. Diabetes Care. 45(Suppl 1):S144-74, 2022
63
63 American Diabetes Association Professional Practice Committee et al. Addendum. 11. Chronic kidney disease and risk management:
Standards of Medical Care in Diabetes-2022: Diabetes Care 2022;45(Suppl. 1):S175-S184. Diabetes Care. 45(9):2182-4, 2022
64
64 McGuire DK et al: Association of SGLT2 inhibitors with cardiovascular and kidney outcomes in patients with type 2 diabetes: a meta-
analysis. JAMA Cardiol. 6(2):148-58, 2021
65
65 Marso SP et al: Liraglutide and cardiovascular outcomes in type 2 diabetes. N Engl J Med. ePub, 2016
66
66 Gerstein HC et al: Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND): a double-blind, randomised placebo-controlled
trial. Lancet. 394(10193):121-30, 2019
67
67 Zelniker TA et al: Comparison of the effects of glucagon-like peptide receptor agonists and sodium-glucose cotransporter 2 inhibitors for
prevention of major adverse cardiovascular and renal outcomes in type 2 diabetes mellitus. Circulation. 139(17):2022-31, 2019
68
68 Marso SP et al: Semaglutide and cardiovascular outcomes in patients with type 2 diabetes. N Engl J Med. 375(19):1834-44, 2016
69
69 Kidney Disease Improving Global Outcomes: KDIGO 2021 Clinical Practice Guideline on the Management of Blood Pressure in Chronic
Kidney Disease. KDIGO website. Published March 2021. Accessed December 5, 2022. https://kdigo.org/guidelines/blood-pressure-in-ckd/
Ver en el Artículo | Referencia cruzada (https://kdigo.org/guidelines/blood-pressure-in-ckd/)
70
70 Banerjee D et al: Management of hypertension and renin-angiotensin-aldosterone system blockade in adults with diabetic kidney disease:
Association of British Clinical Diabetologists and the Renal Association UK guideline update 2021. BMC Nephrol. 23(1):9, 2022
71
71 Whelton PK et al: 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation,
and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force
on Clinical Practice Guidelines. J Am Coll Cardiol. 71(19):e127-248, 2018
72
72 Chang AR et al: Blood pressure goals in patients with CKD: a review of evidence and guidelines. Clin J Am Soc Nephrol. 14(1):161-9, 2019
73
73 Williams B et al: 2018 ESC/ESH guidelines for the management of arterial hypertension. Eur Heart J. 39(33):3021-104, 2018
74
74 Japanese Society of Nephrology: Essential points from evidence-based clinical practice guidelines for chronic kidney disease 2018. Clin Exp
Nephrol. 23(1):1-15, 2019
75
75 Laverman GD et al: ACE inhibition versus angiotensin receptor blockade: which is better for renal and cardiovascular protection? J Am Soc
Nephrol. 15(1 Suppl):S64-70, 2004
76
76 Tomson C et al: Management of chronic kidney disease. Medicine. 35(8):442-6, 2007
Ver en el Artículo | Referencia cruzada (https://doi-org.fucsalud.basesdedatosezproxy.com/10.1016/j.mpmed.2007.05.010)
77
77 Toto RD: Management of hypertensive chronic kidney disease: role of calcium channel blockers. J Clin Hypertens (Greenwich). 7(4 Suppl
1):15-20, 2005
78
78 Toto RD: Treatment of hypertension in chronic kidney disease. Semin Nephrol. 25(6):435-9, 2005
79
79 Epstein M: Reduction of cardiovascular risk in chronic kidney disease by mineralocorticoid receptor antagonism. Lancet Diabetes
Endocrinol. 3(12):993-1003, 2015
80
80 American Diabetes Association Professional Practice Committee et al. Addendum. 10. Cardiovascular disease and risk management:
Standards of Medical Care in Diabetes-2022. Diabetes Care 2022;45(Suppl. 1):S144-S174. Diabetes Care. 45(9):2178-81
81
81 Filippatos G et al: Finerenone and cardiovascular outcomes in patients with chronic kidney disease and type 2 diabetes. Circulation.
143(6):540-52, 2021
82
82 Pitt B et al: Cardiovascular events with finerenone in kidney disease and type 2 diabetes. N Engl J Med. 385(24):2252-63, 2021
83
83 Bakris GL et al: Effect of finerenone on chronic kidney disease outcomes in type 2 diabetes. N Engl J Med. 383(23):2219-29, 2020
84
84 Epstein M et al: Hyperkalemia with mineralocorticoid receptor antagonist use in people with CKD: understanding and mitigating the
risks. Clin J Am Soc Nephrol. 17(3):455-7, 2022
85
85 Drawz P et al: Chronic kidney disease. Ann Intern Med. 162(11):ITC1-16, 2015
86
86 Kovesdy CP: Management of hyperkalaemia in chronic kidney disease. Nat Rev Nephrol. 10(11):653-62, 2014
87
87 Wang HH et al: Hypokalemia, its contributing factors and renal outcomes in patients with chronic kidney disease. PLoS One. 8(7):e67140,
2013
88
88 National Kidney Foundation: K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney
Dis. 42(4 Suppl 3):S1-201, 2003
89
89 National Kidney Foundation: KDOQI clinical practice guideline for hemodialysis adequacy: 2015 update. Am J Kidney Dis. 66(5):884-930,
2015
90
90 Chadban SJ et al: Summary of the Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline on the evaluation and
management of candidates for kidney transplantation. Transplantation. 104(4):708-14, 2020
91
91 Inker LA et al: KDOQI US commentary on the 2012 KDIGO clinical practice guideline for the evaluation and management of CKD. Am J
Kidney Dis. 63(5):713-35, 2014
92
92 Matzke GR et al: Drug dosing consideration in patients with acute and chronic kidney disease-a clinical update from Kidney Disease:
Improving Global Outcomes (KDIGO). Kidney Int. 80(11):1122-37, 2011
93
93 Segura J et al: Calcium channel blockers and renal protection: insights from the latest clinical trials. J Am Soc Nephrol. 16(3 Suppl 1):S64-6,
2005
94
94 Bakris GL et al: Combined effects of an angiotensin converting enzyme inhibitor and a calcium antagonist on renal injury. J Hypertens.
15(10):1181-5, 1997
95
95 FDA: FDA Drug Safety Communication: FDA Revises Warnings Regarding Use of the Diabetes Medicine Metformin in Certain Patients
With Reduced Kidney Function. FDA website. Updated November 14, 2017. Accessed December 5, 2022. https://www.fda.gov/drugs/drug-
safety-and-availability/fda-drug-safety-communication-fda-revises-warnings-regarding-use-diabetes-medicine-metformin-certain
Ver en el Artículo | Referencia cruzada (https://www.fda.gov/drugs/drug-safety-and-availability/fda-drug-safety-communication-fda-revises-
warnings-regarding-use-diabetes-medicine-metformin-certain)
96
96 Weir MR et al: Renal and cardiovascular effects of sodium glucose co-transporter 2 inhibitors in patients with type 2 diabetes and chronic
kidney disease: perspectives on the Canagliflozin and Renal Events in Diabetes with Established Nephropathy Clinical Evaluation trial
results. Am J Nephrol. 51(4):276-88, 2020
97
97 Heerspink HJL et al: Dapagliflozin in patients with chronic kidney disease. N Engl J Med. ePub, 2020
98
98 Wanner C et al: Empagliflozin and progression of kidney disease in type 2 diabetes. N Engl J Med. 375(4):323-34, 2016
99
99 Kristensen SL et al: Cardiovascular, mortality, and kidney outcomes with GLP-1 receptor agonists in patients with type 2 diabetes: a
systematic review and meta-analysis of cardiovascular outcome trials. Lancet Diabetes Endocrinol. 7(10):776-85, 2019
100
100 Yin WL et al: The effect of glucagon-like peptide-1 receptor agonists on renal outcomes in type 2 diabetes. Diabetes Ther. 11(4):835-44, 2020
101
101 Sampanis Ch: Management of hyperglycemia in patients with diabetes mellitus and chronic renal failure. Hippokratia. 12(1):22-7, 2008
102
102 Elliott WJ et al: Loop diuretics are most appropriate for hypertension treatment in chronic kidney disease. J Am Soc Hypertens. 10(4):285-7,
2016
103
103 Greenberg A: Diuretic complications. Am J Med Sci. 319(1):10-24, 2000
104
104 Palmer BF et al: Diagnosis and treatment of hyperkalemia. Cleve Clin J Med. 84(12):934-42, 2017
105
105 Baker LA et al: Clinical practice guideline exercise and lifestyle in chronic kidney disease. BMC Nephrol. 23(1):75, 2022
106
106 Krueger KM et al: Practical guide to vaccination in all stages of CKD, including patients treated by dialysis or kidney transplantation. Am J
Kidney Dis. 75(3):417-25, 2020
107
107 Wright M et al: Clinical practice guideline on undernutrition in chronic kidney disease. BMC Nephrol. 20(1):370, 2019
108
108 Wright S et al: Timing of dialysis initiation and survival in ESRD. Clin J Am Soc Nephrol. 5(10):1828-35, 2010
109
109 Sarnak MJ et al: KDOQI US commentary on the 2013 KDIGO clinical practice guideline for lipid management in CKD. Am J Kidney Dis.
65(3):354-66, 2015
110
110 Zannad F et al: Cardiorenal syndrome revisited. Circulation. 138(9):929-44, 2018
111
111 Chahal RS et al: Heart failure and acute renal dysfunction in the cardiorenal syndrome. Clin Med (Lond). 20(2):146-50, 2020
112
112 Clark AL et al: Change in renal function associated with drug treatment in heart failure: national guidance. Heart. 105(12):904-10, 2019
113
113 Lovre D et al: Managing diabetes and cardiovascular risk in chronic kidney disease patients. Endocrinol Metab Clin North Am. 47(1):237-
57, 2018
114
114 Kidney Disease: Improving Global Outcomes (KDIGO) Hepatitis C Work Group: KDIGO 2018 clinical practice guideline for the
prevention, diagnosis, evaluation, and treatment of hepatitis C in chronic kidney disease. Kidney Int Suppl (2011). 8(3):91-165, 2018
115
115 Weinreb JC et al: Use of intravenous gadolinium-based contrast media in patients with kidney disease: consensus statements from the
American College of Radiology and the National Kidney Foundation. Kidney Med. 3(1):142-50, 2021
116
116 Davenport MS et al: Use of intravenous iodinated contrast media in patients with kidney disease: consensus statements from the American
College of Radiology and the National Kidney Foundation. Kidney Med. 2(1):85-93, 2020
117
117 Kasiske BL et al: KDIGO clinical practice guideline for the care of kidney transplant recipients: a summary. Kidney Int. 77(4):299-311, 2010
118
118 Bianchi S et al: Management of hyperkalemia in patients with kidney disease: a position paper endorsed by the Italian Society of
Nephrology. J Nephrol. 32(4):499-516, 2019
119
119 Palaka E et al: The impact of CKD anaemia on patients: incidence, risk factors, and clinical outcomes--a systematic literature review. Int J
Nephrol. 2020:7692376, 2020
120
120 Vassalotti JA et al: Practical approach to detection and management of chronic kidney disease for the primary care clinician. Am J Med.
129(2):153-62.e7, 2016
121
121 Kliger AS et al: KDOQI US commentary on the 2012 KDIGO clinical practice guideline for anemia in CKD. Am J Kidney Dis. 62(5):849-59,
2013
122
122 Shah SN et al: Serum bicarbonate levels and the progression of kidney disease: a cohort study. Am J Kidney Dis. 54(2):270-7, 2009
123
123 Chen W et al: Metabolic acidosis and the progression of chronic kidney disease. BMC Nephrol. 15:55, 2014
124
124 Sarnak MJ et al: Mortality caused by sepsis in patients with end-stage renal disease compared with the general population. Kidney Int.
58(4):1758-64, 2000
125
125 Saran AM et al: Cardiovascular disease in chronic kidney disease. Ther Adv Cardiovasc Dis. 2(6):425-34, 2008
126
126 Gansevoort RT et al: Chronic kidney disease and cardiovascular risk: epidemiology, mechanisms, and prevention. Lancet. 382(9889):339-52,
2013
127
127 Meyer TW et al: Uremia. N Engl J Med. 357(13):1316-25, 2007
128
128 Chikotas N et al: Uremic syndrome and end-stage renal disease: physical manifestations and beyond. J Am Acad Nurse Pract. 18(5):195-202,
2006
129
129 Smith C et al: Choosing not to dialyse: evaluation of planned non-dialytic management in a cohort of patients with end-stage renal failure.
Nephron Clin Pract. 95(2):c40-6, 2003
130
130 Wong CF et al: Factors affecting survival in advanced chronic kidney disease patients who choose not to receive dialysis. Ren Fail. 29(6):653-
9, 2007
131
131 Wang HE et al: Chronic kidney disease and risk of death from infection. Am J Nephrol. 34(4):330-6, 2011
(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.
Did you find your answer? ×
Yes No

14 Chronic Kidney Disease - ClinicalKey

Uploaded by

Document Information

Original Description:

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

14 Chronic Kidney Disease - ClinicalKey

Uploaded by

Copyright:

Available Formats

Chronic Kidney Disease - ClinicalKey 8/06/23, 3:02 p.m.

Chronic Kidney Disease

Nebulized albuterol increases cellular uptake of potassium

damage and worse prognosis

Criteria for chronic kidney disease 1

Either of the following present for more than 3 months:

Markers of kidney damage (1 or more), which include:

Presence of RBCs, WBCs, or cellular casts in urine

Electrolyte and other abnormalities due to tubular disorders

Structural abnormalities detected by imaging

History of kidney transplantation

GFR less than 60 mL/minute/1.73 m²

G1: normal or high renal function

GFR: greater than 90 mL/minute/1.73 m²

G2: mildly decreased renal function

G3a: mildly to moderately decreased renal function

G3b: moderately to severely decreased renal function

G4: severely decreased renal function

G5: kidney failure

GFR: less than 15 mL/minute/1.73 m²

Patients receiving dialysis are indicated with a "D" (eg, G5D) 5 6

A1: normal to mildly increased

Albumin to creatinine ratio: less than 30 mg/g

Albumin excretion rate: less than 30 mg/24 hours

A2: moderately increased

Albumin to creatinine ratio: 30 to 300 mg/g

Albumin excretion rate: 30 to 300 mg/24 hours

A3: severely increased

Albumin to creatinine ratio: greater than 300 mg/g

Albumin excretion rate: greater than 300 mg/24 hours

Altered taste and smell

Symptoms of uremic neuropathy

Difficulty concentrating, lethargy, and confusion

Present in 65% of patients at the initiation of dialysis 7

Hypertension (more than 60% of patients) 8

Diabetes (40% of patients) 9

Indicates potential defect in the glomerular basement membrane or tubules

Poor capillary refill

90% of patients with GFR less than 25 to 30 mL/minute/1.73 m² develop anemia 13

Hypertension (more than 60% of patients) 8

Generalized edema/cushingoid appearance 14

May develop secondary to advanced chronic kidney disease

Occurs in 58% of patients with category G5 disease

Signs of heart failure

Dyspnea at rest or upon exertion

Jugular venous distention

Signs of peripheral arterial disease

Diminished lower extremity pulses

Causes and Risk Factors

Hypertension (15%-30% of cases) 17

Glomerulonephritis (less than 10% of cases) 17

Polycystic kidney disease (2%-3% of cases) 17

Prolonged obstruction of urinary tract

Recurrent kidney infection

Renal vascular disease (eg, renal artery stenosis, fibromuscular dysplasia)

Risk factors and/or associations

Caused by mutations in either the PKD1 or PKD2 gene

Sensorineural hearing loss is common

Medullary cystic kidney disease

Autosomal dominant tubulointerstitial nephropathy (OMIM #174000) 26

Caused by heterozygous mutations in MUC-1

Other risk factors/associations

Systemic lupus erythematosus