Chronic kidney disease (CKD) is defined as an abnormality of kidney structure or function that persists for > 3 months and affects health. The most common causes of CKD in the United States are diabetes mellitus, hypertension, and glomerulonephritis. Most patients remain asymptomatic until their kidney function is severely impaired due to the organ's efficient compensatory mechanisms and significant renal reserve. Patients are most commonly diagnosed via routine screening (e.g., screening of high-risk populations, routine blood tests that include serum creatinine to estimate glomerular filtration rate). At advanced disease stages, patients may present with symptoms of fluid overload (e.g., peripheral edema) and/or uremia (e.g., fatigue, pruritus). Patients with CKD have a significantly increased risk of developing atherosclerotic cardiovascular disease (ASCVD). Laboratory studies may show metabolic complications, such as hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis. Management is aimed at slowing CKD progression and preventing and/or managing complications. This includes treating the underlying disease, avoiding nephrotoxic substances, maintaining adequate hydration and nutrition, pharmacotherapy (e.g., RAAS inhibitors, SGLT2 inhibitors, and statins), and addressing complications such as anemia of CKD and CKD-mineral and bone disorder (CKD-MBD). Renal replacement therapy (i.e., dialysis or renal transplantation) is required if CKD progresses to end-stage renal disease (ESRD).

1. Chronic kidney disease Last edited: Sep 13, 2024
Content policy
Learned
Summary
Chronic kidney disease (CKD) is defined as an abnormality of kidney structure or function that persists for > 3 months. The most common
in the United States are diabetes mellitus, hypertension, and glomerulonephritis. The kidney's efficient compensatory mechanisms and
significant renal reserve mean that most patients remain asymptomatic until their kidney function is severely impaired. While patients are most
commonly initially identified because of gradual asymptomatic elevation in serum creatinine, at advanced disease stages, patients may present with
symptoms of fluid overload (e.g., peripheral edema) and/or (e.g., fatigue, pruritus). Patients with CKD also have a significantly increased risk of
developing atherosclerotic cardiovascular disease (ASCVD). Laboratory studies may show metabolic complications, such as hyperkalemia,
hyperphosphatemia, hypocalcemia, and metabolic acidosis. The goal of management is to slow and prevent and manage
complications. This includes treatment of the underlying disease, avoiding nephrotoxic substances, maintaining adequate hydration and nutrition,
management of ASCVD (e.g., using statin therapy and adequate treatment of diabetes mellitus), and addressing complications such as
and . Renal replacement therapy (i.e., dialysis or kidney transplantation) is required if CKD
progresses to ( ).
See also “Acute kidney injury” (AKI) and “Diabetic kidney disease.”
COLLAPSE NOTES FEEDBACK
Epidemiology
Prevalence
An estimated 37 million individuals (15%) in the US have CKD.
726,000 individuals have .
Incidence: > 350 cases of per million individuals annually
Risk factors for CKD
Diabetes
Hypertension
Obesity
Advanced age (> 60 years of age)
Substance use (smoking, alcohol, recreational drugs)
Acute kidney injury
Family history of CKD
African American or Hispanic descent
Epidemiological data refers to the US, unless otherwise specified.
QBANK SESSION
causes of
CKD
uremia
CKD progression
anemia of
chronic kidney disease CKD-mineral and bone disorder
end-stage renal disease ESRD
[1]
ESRD
ESRD [1]
[1]
[2]
[3]
OPTIONS
High-yield Standard Clinician Key exam info on EN
T
STUDENT chronic renal failure
In 2016, approx. 125,000 individuals started initial treatment for ESRD
This is partially due to APOL1, an autosomal recessive mutation, which is found exclusively in people with recent Sub-Saharan African ancestry.
7
⑰
#
#
*
D
#
*

2. Etiology
Diabetic nephropathy (38%)
Hypertensive nephropathy (26%)
Glomerulonephritis (16%)
Other causes (15%, e.g., polycystic kidney disease, analgesic misuse, amyloidosis)
Idiopathic (5%)
COLLAPSE NOTES FEEDBACK
Pathophysiology
Pathophysiology depends on the underlying condition, any of which will eventually lead to progressive nephron loss, structural damage, and impaired
kidney function.
Underlying conditions
Diabetic nephropathy
Hyperglycemia → nonenzymatic glycation of proteins → varying degrees of damage to all types of kidney cell.
Pathological changes include:
Hypertrophy and proliferation of mesangial cells, GBM thickening, and ECM protein accumulation → eosinophilic nodular glomerulosclerosis
Thickening and diffuse hyalinization of afferent and efferent arterioles/interlobular arteries
Interstitial fibrosis, TBM thickening, and tubular hypertrophy
Hypertensive nephropathy
Caused by protective autoregulatory vasoconstriction of preglomerular vessels, increases in systemic blood pressure do not normally affect renal
microvessels.
Increased systemic blood pressure (e.g., due to chronic hypertension) below the protective autoregulatory threshold → benign nephrosclerosis
(sclerosis of afferent arterioles and small arteries) → ↓ perfusion → ischemic damage
In case BP exceeds threshold → acute injury → malignant nephrosclerosis (petechial subcapsular hemorrhages, visible infarction with necrosis of
mesangial and endothelial cells, thrombosis of glomeruli capillaries, luminal thrombosis of arterioles, and red blood cell extravasation and
fragmentation) → failure of autoregulatory mechanisms → ↑ damage
Glomerulonephritis (GN)
Noninflammatory GN (e.g., minimal change GN, membranous nephropathy, focal segmental glomerulosclerosis)
Inflammatory GN (e.g., lupus nephritis, poststreptococcal GN, rapid progressive GN, hemolytic uremic syndrome)
[1][4][5]
[6]
[7]
*
*
*
*
PCKD

3. Consequences
Reduced GFR
↓ Production of urine → ↑ extracellular fluid volume → total-body volume overload
↓ Excretion of waste products (e.g., urea, drugs)
↓ Excretion of phosphate → hyperphosphatemia
During the early , plasma phosphate levels will typically be normal due to the increased secretion of fibroblast growth factor 23
( ).
is produced by osteoblasts in response to initial hyperphosphatemia and increased calcitriol.
Increased secretion of leads to increased phosphate secretion and suppressed conversion of 25-hydroxyvitamin D to
1,25-dihydroxyvitamin D.
In advanced CKD, the effects of FGF 23 subside (most likely due to development of resistance in target tissues).
↓ Maintenance of acid-base balance → metabolic acidosis
↓ Maintenance of electrolyte concentrations → electrolyte imbalances (e.g., Na retention)
Reduced endocrine activity
↓ Hydroxylation of calcifediol → ↓ production of calcitriol → (in combination with ↓ excretion of phosphate) → ↓ serum Ca → ↑ PTH
↓ Erythropoietin → ↓ stimulation of erythropoiesis
Reduced gluconeogenesis
↑ Risk of hypoglycemia
COLLAPSE NOTES FEEDBACK
Clinical features
Patients are oFen asymptomatic until later stages due to the exceptional compensatory mechanisms of the kidneys.
Manifestations of Na /H O retention
Hypertension and heart failure
Pulmonary and peripheral edema
Manifestations of uremia
Definition: is defined as the accumulation of toxic substances due to decreased renal excretion. These toxic substances are mostly
metabolites of proteins such as urea, creatinine, β microglobulin, and parathyroid hormone.
Constitutional symptoms
Fatigue
Weakness
Headaches
stages of CKD
FGF23 [8]
FGF23
FGF23
[8]
+
2+
+
2
Uremia
2
As CKD progresses, the kidneys lose their ability to clear organic acids from the body, leading to accumulation in the blood.
Usually interstitial pulmonary edema
↑ Na + fluid-HTN+ He a Edema
ca
+
2
M Fluid
RBC
-
I
Ereph-
I Enthropoitin
Nat Glucos-
- PT ↓
↑
Hyper
Natr- -
*
~

4. Gastrointestinal symptoms
Nausea and vomiting
Loss of appetite
Uremic fetor: characteristic ammonia- or urine-like breath odor
Dermatological manifestations
Pruritus
Skin color changes (e.g., hyperpigmentation, pallor due to anemia)
Uremic frost: leads to high levels of urea secreted in the sweat, the evaporation of which may result in tiny crystallized yellow-white urea
deposits on the skin.
Serositis
Uremic pericarditis: a complication of chronic kidney disease that causes fibrinous pericarditis
Clinical features: chest pain worsened by inhalation
Physical examination findings
Friction rub on auscultation
ECG changes normally seen in nonuremic pericarditis (e.g., diffuse ST-segment elevation) are not usually seen.
Pleuritis
Neurological symptoms
Asterixis
Signs of uremic encephalopathy
Seizures
Somnolence
Coma
Peripheral neuropathy → paresthesias
Hematologic symptoms
Anemia
Leukocyte dysfunction → ↑ risk of infection
↑ Bleeding tendency caused by abnormal platelet adhesion and aggregation
uremia
[9]
Kidney OUTAGES: hyperKalemia, renal Osteodystrophy, Uremia, Triglyceridemia, Acidosis (metabolic), Growth delay, Erythropoietin
deficiency (anemia), Sodium/water retention (consequences of chronic kidney disease)
Uremic frost Fibrinous pericarditis in
uremia
Chronic kidney disease
fact sheet
The exact cause is unknown. Hypotheses include accumulation of histamine, deposition of urate crystals, increased levels of parathyroid hormone, neuronal changes, and minor inflammatory reactions.
Scalp and forehead of a patient with a markedly elevated blood urea nitrogen level
(approx. 100 mg/dL)
The widely disseminated tiny white spots are crystallized urea resulting from the
evaporation of sweat that contains high amounts of urea.
This finding is a sign of severe azotemia, which is rare in settings where renal
replacement therapy is available.
Although the risk of pericarditis correlates with the degree of azotemia, it
does not correlate specifically with increased BUN or creatinine levels.
Since uremic pericarditis does not cause
inflammatory cells to invade the myocardium,
there are generally no ECG findings.
Studies have shown that administration of desmopressin leads to increased plasma concentrations of vWF and
factor VIII. After administration, a shortened bleeding timecould be observed in uremic individuals.
*
in urmic
2
"Flapping tremor"
RV frost
X
ear
↑
Fibr.
Peri-

5. Diagnostic criteria and classification
Diagnostic criteria
Criteria for chronic kidney disease (CKD) include the persistence of eGFR < 60 mL/min/1.73 m (≥ G3a) and/or of any of the following markers of
kidney damage for > 3 months:
Albuminuria: e.g., urine albumin-to-creatinine ratio (UACR) > 30 mg/g (≥ A2)
Urine sediment abnormalities: e.g., hematuria
Abnormalities due to tubulointerstitial dysfunction, e.g.:
Electrolyte and acid-base imbalances
Retention of nitrogenous wastes
Reduced production of erythropoietin, 1,25-dihydroxyvitamin D, and/or renin
Histological abnormalities on biopsy
Imaging showing structural abnormalities: e.g., polycystic kidney disease
History of renal transplant
CKD progression is the presence of either of the following:
A decline in renal function, leading to a change in
A sustained decline in eGFR of > 5 mL/min/1.73 m per year
End-stage renal disease ( )
Irreversible kidney dysfunction with eGFR < 15 mL/min/1.73 m
AND manifestations of requiring chronic renal replacement therapy with either dialysis (hemofiltration or hemodiafiltration) or renal
transplantation
Prognosis: approx. 50% of individuals with die of cardiovascular disease.
CGA classification of chronic kidney disease
CKD is classified according to the cause, , and ; this is referred to as the .
Clinical uses
Standardized documentation of
Identification of
Determination of the frequency of patient monitoring
Interpretation: Higher stages correlate with a poorer prognosis.
Increased and mortality (e.g., all-cause mortality, cardiovascular mortality)
Increased risk of developing complications (e.g., AKI, )
Cause
1. Systemic vs. primary cause: Determine if kidney disease is associated with a systemic disease (e.g., diabetes) or if it is primary kidney disease (e.g.,
polycystic kidney disease).
2. Location: Determine the location (presumed or confirmed) of the damage within the kidney.
Glomerular
[5]
2
eGFR category
2
ESRD [10]
2
uremia
ESRD
[4][5]
eGFR category albuminuria category CGA classification
CKD stages
CKD progression
[11]
risk of CKD progression
CKD-mineral and bone disorder
[5]
A definite decline is defined as a change to a worse eGFR category AND a ≥ 25% drop in eGFR from baseline.
This is known as rapid progression.
There is currently no consensus on the definition of ESRD. It is sometimes applied to anyone with CKD category G5 (i.e., eGFR< 15 mL/min/1.73 m2), however,
many patients with this degree of renal dysfunction may not develop manifestations of uremia or require renal replacement therapy for several years.
Most likely due to associated complications (e.g., anemia of chronic kidney
disease) and increased cardiovascular risk factors (e.g., hypertension)
E.g., “Diabetic kidney disease G3A2”
KDIGO guidelines recommend that low to moderate risk patients should be monitored once a
year, high-risk patients twice per year, and very high-risk patients three to four times per year.
it
, Not,
cat , Phos
Urea

6. Tubulointerstitial
Vascular
Cystic and congenital
eGFR and albuminuria
MAXIMIZE TABLE TABLE QUIZ
Risk of progression and complications of CKD based on eGFR and
eGFR category (mL/min/1.73 m )
Albuminuria category (UACR)
A1: < 30 mg/g or < 3 mg/mmol
(normal to mildly increased)
A2: 30–300 mg/g or 3–30 mg/mmol
(microalbuminuria)
A3: > 300 mg/g or > 30 mg/mmol
(macroalbuminuria)
Stage G1 CKD: ≥ 90 (normal or high)
Low risk* Moderate risk High risk
Stage G2 CKD: 60–89 (mildly low)
Stage G3 CKD
G3a: 45–59 (mildly to moderately low) Moderate risk High risk
Very high risk
G3b: 30–44 (moderately to severely low) High risk
Very high risk
Stage G4 CKD: 15–29 (severely low)
Very high risk
Stage G5 CKD: < 15 ( )
*Stages G1A1 and G2A1 do not indicate CKD in the absence of other .
COLLAPSE NOTES FEEDBACK
Diagnosis
The goals of the diagnostic evaluation include confirming the chronicity of kidney dysfunction and identifying the cause of kidney disease.
Initial laboratory studies
Parameters of renal function
Serum markers: ↑ creatinine and BUN (alternatively, ↑ cystatin C)
Glomerular filtration rate: ↓ eGFR
Serum creatine-based eGFR (preferred): e.g., CKD-EPI equation, MDRD equation
Serum cystatin C-based eGFR
[5]
albuminuria category [5]
2
kidney failure
markers of kidney damage
The CKD-EPI equation is usually preferred, as it has been found to be more accurate than the MDRD
equation, especially in patients with a mildly decreased or normal GFR (i.e., GFR ≥ 60 mL/min/1.73 m2).
S.
cre.,
S.
one
,
CS . C
T
=
eGFR
-
> urine proteinuria + waxy cast
+ Heaturia
= U/S
*
#
e - race
crea-

7. Urine studies
↑ Spot UACR: used to determine the for .
↑ Spot urine protein-to-creatinine ratio (UPCR): Nephrotic-range proteinuria may be seen.
Urine dipstick: may show hematuria or proteinuria
Urine microscopy: may show abnormal urine sediment, e.g., the presence of waxy casts
Other
Hemostasis: ↑ bleeding time, normal PT, PTT and platelet count (see “Diagnostic workup of bleeding disorders”)
Ultrasound of the kidneys and urinary tract
First-line imaging technique for the assessment of kidney structure
Consider obtaining for all patients to further support the diagnosis and help determine the etiology.
Findings that suggest chronic kidney damage include:
↓ Kidney length (< 10 cm)
↓ Parenchymal and/or cortical thickness
↑ Cortical echogenicity
Cysts
Calcifications
Findings that suggest specific etiologies
Ureteral or renal pelvic dilation suggests obstructive nephropathy.
Bilaterally enlarged kidneys with multiple cysts suggest polycystic kidney disease.
Additional investigations to identify underlying causes
Additional investigations should be considered based on clinical suspicion or if an underlying cause of CKD is not apparent following an initial
assessment.
albuminuria category CKD staging
[12]
Ultrasound in chronic
renal disease
Consider obtaining an ultrasound of the kidneys and urinary tract as part of the routine evaluation of all patients with CKD.
Integration of information from the patient's clinical presentation, laboratory tests, imaging, and in some cases, pathology, is needed to
determine the underlying cause.
While increased echogenicity in itself is a nonspecific finding, the combined presence of
decreased kidney length and increased cortical echogenicity suggests irreversible kidney disease.
*
*
#
pleen
Peri
It
14 -
Normal

8. Noninvasive testing
MAXIMIZE TABLE TABLE QUIZ
Investigations for specific underlying
Examples Suggestive features Common additional studies
Diabetes
Symptoms of diabetes mellitus
Age > 35 years and/or the presence of other risk factors for type 2 diabetes mellitus
Nephrotic syndrome or nephrotic-range proteinuria
Fasting plasma glucose
HbA1c
See also “Diabetic kidney disease.”
Glomerulonephritis
Evidence of extrarenal disease (e.g., clinical features of SLE, anti-GBM disease, pauci-immune
glomerulonephritis)
History of IV drug use
Nephritic syndrome or nephrotic syndrome
Urinalysis abnormalities (any of the following):
Nephritic sediment
Nephrotic sediment
Nephrotic-range proteinuria
Serology, e.g.:
ANA
ANCA
anti-GBM antibody
Viral serology (e.g., HIV, HBV, HCV)
Complement levels
Multiple myeloma CRAB criteria
Serum protein electrophoresis
Urine Bence Jones protein
Serum and urine free light chains
Renal artery
stenosis
Treatment-resistant hypertension
Abdominal bruit heard over the flank or epigastrium
Evidence of other atherosclerotic diseases (e.g., CAD, PAD)
Duplex ultrasonography of the renal
arteries
Amyloidosis
History of a chronic inflammatory condition (e.g., IBD, RA) or chronic infectious disease (e.g., tuberculosis,
osteomyelitis)
History of plasma cell dyscrasia
Evidence of other organ involvement (e.g., macroglossia, restrictive cardiomyopathy, hepatosplenomegaly,
malabsorption)
Serum protein electrophoresis
Urine Bence Jones protein
Serum and urine free light chains
Renal biopsy
Not routinely indicated
Consider in either of the following situations:
Rapid and unexplained decline in eGFR
Need for diagnostic confirmation of the underlying etiology (e.g., glomerulonephritis) prior to initiating disease-specific therapy
COLLAPSE NOTES FEEDBACK
causes of CKD
[5][14]
Renal biopsy is only indicated in patients in whom the underlying cause of CKD is still unclear a^er noninvasive testing, the results are
likely to influence management, and the potential benefits are thought to outweigh the risks.
May be seen with diabetic nephropathy
In most patients, the cause of CKD can be inferred from the initial assessment and noninvasive studies; pathological confirmation is usually not required.

9. Management
Nutritional management
Fluid intake: Ensure appropriate fluid intake and avoid dehydration.
Protein and energy consumption
Mediterranean diet, ↑ fruit and vegetable intake
Protein restriction (e.g., 0.55–0.60 g/kg/day) in patients with G3–G5
Electrolytes
Sodium restriction (< 2.3 g/day)
Potassium intake adjustment
Phosphorus intake adjustment
Micronutrients: Consider multivitamin supplementation for patients with inadequate dietary vitamin (e.g., vitamin D) intake.
Medication management
Renally cleared medications: Adjust dosing based on the patient's eGFR.
Potentially nephrotoxic substances
Avoid use (except when the benefits outweigh the risks).
Contrast imaging
The risk of contrast-induced nephropathy is highest in patients with eGFR < 30 mL/min/1.73 m .
For information on prevention, see “Contrast-induced nephropathy.”
Renal replacement therapy
Nonoperative (hemodialysis or peritoneal dialysis)
Indications include:
Hemodynamic or metabolic complications that are refractory to medical therapy, e.g.:
Volume overload or hypertension
Metabolic acidosis
Hyperkalemia
Serositis: e.g.,
Other : e.g., signs of encephalopathy
Refractory deterioration in nutritional status
Operative: kidney transplantation
[15]
CKD category
[15]
[5][14]
2
Weigh the risks and benefits of potentially nephrotoxic substances on a case-by-case basis.
[5]
uremic pericarditis
symptoms of uremia
If there are indications for acute dialysis,
urgently initiate renal replacement therapy
Indications for urgent RRT: “A.E.I.O.U.”
• Acidosis
• Electrolyte abnormalities (hyperkalemia)
• Ingestion (of poisons)
• Overload (fluid)
• Uremic symptoms
Can significantly improve the lipid profile and weight and blood pressure control
This reduces blood pressure and helps achieve better
volume control; it may also help reduce proteinuria.
Patients with CKD are at risk of
vitamin B1 deficiency, vitamin B2 deficiency,
vitamin B6 deficiency, vitamin C deficiency,
vitamin K deficiency,
and/or vitamin D deficiency.
Medications with active forms or metabolites that are eliminated primarily by the kidneys through excretion and/or metabolism (e.g.,
metformin, digoxin). May accumulate in patients with acute or chronic kidney dysfunction and therefore often require renal dose
adjustment.
For creatinine-based GFR estimation, the CKD-EPI equation is thought to provide a better correlation with renal drug
clearancecompared to the Cockcroft-Gault equation. For drugs with a narrow therapeutic indexthat require dosing precision, consider
using cystatin C to estimate GFR.
Given the increased risk of AKI in acutely ill patients with CKD, consider temporarily holding renally cleared
medications and medications that can detrimentally affect glomerular perfusion (e.g., NSAIDs, ACEIs, ARBs).
X
*
A
B

10. Monitoring and management of ASCVD risk factors
Specific recommendations for ASCVD risk management in patients with CKD are reviewed below; see also “Hypertension,” “Lipid disorders,”
“Diabetes,” and “ASCVD.”
ASCVD risk assessment
Perform for all patients (untreated CKD is an ASCVD risk-enhancing factor).
Includes:
Diabetes mellitus screening
Screening for hypertension
Screening for lipid disorders
ASCVD risk calculation (e.g., using pooled cohort equation)
Blood pressure control
Systolic blood pressure (SBP) target
SBP < 120 mm Hg is recommended (if tolerated).
Consider higher targets (e.g., < 130–140 mm Hg) for selected patients.
Pharmacological therapy
First-line therapy: RAAS inhibitors (i.e., ACEI or ARB)
Benefits: nephroprotection and reduced proteinuria
Risks: may cause hyperkalemia and/or an initial decline in GFR
Consider combination therapy (e.g., RAAS inhibitor PLUS a calcium channel blocker and/or a thiazide diuretic):
For patients with an initial SBP ≥ 20 mm Hg above target
For patients who do not reach the target while on monotherapy at the optimal dose
Second-line agents include:
Loop diuretics or thiazide diuretics
Calcium channel blockers (CCBs)
Beta-blockers: usually reserved for patients with cardiovascular comorbidities
Aldosterone receptor antagonists: usually reserved for treatment resistant hypertension
See “Antihypertensive therapy” for information on medication dosages and contraindications.
Nonpharmacological management: Recommend for all patients; see “Lifestyle changes for managing hypertension.”
Management of ASCVD not only reduces cardiovascular morbidity and mortality, but also helps prevent .
CKD progression
Cardiovascular disease (e.g., coronary artery disease, stroke) is the leading cause of death in patients with CKD. The risk of
cardiovascular events is higher in patients with more advanced .
stages of CKD [5]
[17]
[17]
Society and expert panel guidelines vary in their specific recommendations
This strict SBP target has been associated with reduced ASCVD risk and all-cause mortality in most patients with CKD.
However, the benefit remains uncertain for patients in eGFR categories G4–G5 and those with concomitant diabetes mellitus.
E.g., patients with limited life expectancy, significant comorbidities, or symptomatic postural hypotension
Depending on the eGFR category, some antihypertensives may require dose adjustments.

11. Lipid management
Goal: reduction of ASCVD risk
Fasting lipid panel
May show dyslipidemia (↑ triglycerides are common)
Statin therapy; indications include:
Prevention of ASCVD in patients with CKD
Start for all patients ≥ 50 years of age.
Consider for patients 18–49 years of age with concomitant diabetes mellitus and/or 10-year ASCVD risk > 10%.
Management of ASCVD
Nonpharmacological management: Recommend as adjunctive therapy for all patients with hypercholesterolemia.
Diabetes management
HbA1c may not accurately reflect glycemic control in patients with CKD and eGFR < 30 mL/min/1.73 m .
Medications may need to be reduced or stopped as eGFR declines.
See “Diabetic kidney disease” for further information on managing DM in patients with renal impairment.
Antiplatelet therapy
Usually indicated for management of ASCVD
May be considered for primary prevention of ASCVD in high-risk individuals (e.g., patients with CKD and diabetes)
Avoid any combination of an ACEI, ARB, and/or direct renin inhibitor because of the increased risk of hyperkalemia and AKI.
Good blood pressure control is essential to prevent ASCVD complications, reduce mortality, and help delay disease progression in
patients with CKD.
[18][19]
[19][20][21]
For patients with eGFR < 60 mL/min/1.73 m ( G3–G5), adjustments to the recommended statin doses are
required to reduce their potential for toxicity.
2
eGFR category
Individuals with CKD ohen have dyslipidemia (e.g., ↑ triglycerides, ↑ LDL, ↓ HDL) due to alterations in lipoprotein metabolism.
[22]
2
SGLT-2 inhibitors and GLP-1 receptor agonists have been shown to slow and reduce urinary albumin excretion
and ASCVD events.
CKD progression
[22][23]
[5][23]
These recommendations are consistent with the 2014 KDIGO clinical practice guideline for lipid management in CKD.
In patients with CKD category G4–G5 who were previously on metformin and/or an SGLT-2 inhibitor, metformin should be discontinued; the SGLT-2 inhibitor may be continued if tolerated.
The risk of bleeding in
patients without
established ASCVD may
outweigh the benefits of
aspirin.

12. Monitoring for complications
Screening tests for complications are indicated in all patients with CKD at diagnosis to establish a baseline.
Patients with CKD categories G3–G5 require repeat testing at regular intervals.
MAXIMIZE TABLE TABLE QUIZ
Overview of
Screening test Potential findings
CBC Normochromic, normocytic anemia
Potassium Hyperkalemia: usually seen in advanced CKD
Mineral and bone disorder panel
PTH
↑ PTH
Suggests secondary hyperparathyroidism
May be seen with any and worsens as GFR declines
Phosphate and total
calcium
Hyperphosphatemia and hypocalcemia : typically seen in patients with eGFR < 30 mL/min/1.73 m
Vitamin D
↓ Calcidiol
↓ Calcitriol
Coagulation screen
Normal PT, PTT, and platelet count
↑ Bleeding time due to uremic platelet dysfunction
Blood gases May show metabolic acidosis
COLLAPSE NOTES FEEDBACK
In CKD, close surveillance of serum potassium, calcium, and phosphate levels is essential.
screening for CKD complications [5]
[14]
[24]
stage of CKD
2
[24]
[24]
[25]
Screening and periodic monitoring for complications are indicated in all patients with CKD and eGFR < 60 mL/min/1.73 m .
2
The recommended tests and their frequency can vary and should be tailored to each patient.
Especially in patients who become oliguric or have other
risk factors for hyperkalemia (e.g., high potassium diet,
RAAS inhibitor therapy, insulin deficiency)
Hyperphosphatemia is caused by decreased urinary phosphate clearance,
while hypocalcemia is mediated by hyperphosphatemia and decreased vitamin D production.
This is because earlier in the disease course, mild imbalances tend to be normalized
by a reactive rise in PTH levels (i.e., secondary hyperparathyroidism).
Levels reflect total body vitamin D stores.
Due to decreased renal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D;
may be seen with any stage of CKD and worsens as GFR declines
The kidneys are often no longer able to maintain acid-base balance when the GFRdrops
below 30 mL/min/1.73 m2. An accumulation of hydrogen ions leads to acidosis.

13. Complications
Common acute complications
Pulmonary edema
Hyperkalemia
Infection
Bacteremia secondary to UTI or pneumonia
IV catheter-related infection
Hemodialysis catheter-related infection
Peritoneal dialysis-associated peritonitis
Drug toxicity
See also “Complications of hemodialysis” and “Complications of peritoneal dialysis.”
Calciphylaxis
Definition: a rare but potentially life-threatening condition characterized by dermal and subcutaneous arteriolar calcifications that cause painful skin
necrosis
Risk factors
Most commonly seen in patients with who are receiving dialysis
Comorbidities: diabetes mellitus, obesity, , warfarin therapy
Clinical features
Intensely painful skin lesions, e.g.: livedo reticularis, purpura, plaques, nodules
Necrotic skin ulcerations typically covered with black eschar
Areas of firm, painful, subcutaneous tissue
Secondary bacteremia and sepsis
Diagnosis
A skin biopsy is required for definitive diagnosis but may provoke new lesions.
Clinical diagnosis may be made in patients with with a typical presentation.
Differential diagnosis
Warfarin skin necrosis
Nephrogenic systemic fibrosis
Vasculitis
Purpura fulminans
Cholesterol emboli
Treatment
Multidisciplinary care
Supportive measures
Provide wound care and aggressive pain management.
Consider holding potentially offending medications: warfarin, calcium and iron supplements, vitamin D preparations.
[26]
[27]
[28]
[30][31]
ESRD
CKD-mineral and bone disorder
ESRD [31]
[30][31]

14. Treat .
Optimize renal replacement therapy.
Monitor for infection and initiate appropriate sepsis management if indicated.
Pharmacotherapy: Consider a trial of sodium thiosulfate in consultation with a specialist.
Anemia of chronic kidney disease
Pathophysiology: ↓ synthesis of erythropoietin → ↓ stimulation of RBC production → normocytic, normochromic anemia
Laboratory findings
↓ Hemoglobin (Hb)
MCV is usually normal.
Management
Manage correctable causes of anemia.
Obtain diagnostic studies for iron deficiency.
Check for and potentially treat vitamin B deficiency and folate deficiency.
Consider erythropoietin-stimulating agents (ESAs): for patients with Hb < 10.0 g/dL
Treatment target: usually Hb concentration between 11 and 12 g/dL
Measure TSAT and ferritin at least every 3 months to determine if adjunctive iron replacement therapy is needed.
Adverse effects include increased risk of thrombosis, an increase in blood pressure, and headache.
Avoid blood transfusions: particularly in patients eligible for renal transplantation (risk of alloimmunization)
Chronic kidney disease-mineral and bone disorder ( )
Definitions:
refers to abnormalities in mineral and/or bone metabolism in CKD.
Renal osteodystrophy refers specifically to issues with bone metabolism due to CKD.
Pathophysiology
CKD results in hypocalcemia via different mechanisms.
↓ Renal excretion of phosphate → hyperphosphatemia → calcium phosphate precipitation in tissues → ↓ Ca
CKD-mineral and bone disorder
[30][31]
Calciphylaxis
[5][32][33]
12
[33]
Treatment with ESAs is not recommended for patients with Hb levels ≥ 10 g/dL because their use has been associated with increased
mortality, stroke, and venous thromboembolism.
CKD-MBD [34][35]
CKD-MBD
2+
These recommendations are consistent with the 2012 KDIGO clinical practice guideline for anemia in CKD.
Anemia is worsened by uremia because uremia induces
hemolysis and coagulopathies and inhibits erythropoiesis.
In patients > 15 years of age with CKD, anemia is defined as an Hb level of < 13.0 g/dL in male individuals and < 12.0 g/dL in female individuals.
MCV may be low if there is concurrent iron deficiency.
The decision to initiate therapy with ESAs should be made on a case-by-case basis,
considering factors such as the rate of fall of Hb concentration, risk of requiring a transfusion,
the presence of signs of anemia, and the need for renal replacement therapy.
Measure Hb frequently: every month initially and at least every 3 months once Hb levels are stable
Consider for patients with severe anemia, symptomatic
patients who do not respond to ESA therapy, and those in
need of rapid preoperative Hb correction.

15. ↓ Renal hydroxylation of vitamin D → ↓ 1,25-dihydroxyvitamin D → ↓ intestinal Ca absorption → ↓ Ca
Chronically decreased calcium levels can cause secondary hyperparathyroidism, which can progress to tertiary hyperparathyroidism.
Histological classification
Secondary hyperparathyroidism: high turnover bone disease or osteitis fibrosa cystica (metabolic bone disease)
Osteomalacia: defective bone mineralization
Mixed uremic bone disease: secondary hyperparathyroidism with osteomalacia
Adynamic bone disease: decreased bone formation without osteomalacia
Clinical features (may be asymptomatic initially)
Musculoskeletal
Fractures
Bone and periarticular pain
Muscular weakness and pain
Extraskeletal
Focal vascular calcification (atherosclerotic plaques)
Diffuse vascular calcification (medial calcific sclerosis and )
Diagnostics
Laboratory studies: frequent monitoring with a
Imaging (not routinely indicated)
X-ray may show sclerotic changes (rugger jersey spine), brown tumors, and/or subperiosteal bone thinning.
Consider bone mineral density testing for patients with G3–G5.
Treatment (under specialist guidance): The goal is to normalize phosphate, calcium, and PTH levels.
Treatment of hyperphosphatemia, e.g.:
Dietary phosphate restriction
Phosphate binders (e.g., sevelamer)
Treatment of hyperparathyroidism, e.g.:
Cholecalciferol or ergocalciferol supplementation for vitamin D deficiency or insufficiency
Calcitriol (not routinely recommended)
Calcimimetics (e.g., cinacalcet)
Parathyroidectomy (last-line therapy)
Growth delay and developmental delay in children
Contributing factors include:
Malnutrition (protein and calorie deficit)
Metabolic acidosis
Growth hormone resistance
Anemia
2+ 2+
calcific uremic arteriolopathy
[35]
mineral and bone disorder panel
CKD category
[34][35]
Hyperphosphatemia, hypocalcemia, and insufficient production of vitamin D in patients with CKD may lead to secondary
hyperparathyroidism and consequent .
renal osteodystrophy

16. We list the most important complications. The selection is not exhaustive.
COLLAPSE NOTES FEEDBACK
Special patient groups
Chronic kidney disease in pregnancy
Overview
Prevalence of CKD in women of childbearing age is estimated to be 0.1–4%.
Research suggests that pregnancy negatively affects kidney function in women with CKD (as evidenced by, e.g., doubling of creatinine,
progression to next stage).
CKD negatively influences pregnancy outcomes by increasing the risk of maternal and fetal complications (see below).
Physiological anatomic (e.g., dilation of the renal collecting system, changes in kidney length and volume) and hemodynamic changes (e.g.,
decreased mean arterial pressure) can pose a challenge to monitoring kidney function and diagnosing complications.
Maternal complications
Preeclampsia
Concomitant hypertension and proteinuria
Preterm delivery
Cesarean delivery
Fetal complications
Intrauterine growth restriction
Low birth weight
Fetal/neonatal death
Management
Patients should be cared for by a multidisciplinary team, including nephrologists, neonatologists, and health care personnel specialized in high-risk
obstetrics.
Optimization of blood pressure (i.e., < 140/90 mm Hg) to reduce the risk of preeclampsia and other complications (see “Overview of
antihypertensives to avoid during pregnancy” for details)
Minimization of proteinuria: Treatment depends on the underlying etiology (e.g., pregnancy-safe immunosuppression with prednisone or
calcineurin inhibitors in lupus nephritis).
Consideration of anticoagulation in individuals with severe proteinuria
Prevention of preeclampsia with aspirin before 16 weeks of gestation and calcium and vitamin D supplementation throughout the pregnancy
COLLAPSE NOTES FEEDBACK
Renal osteodystrophy
[36]