L2: CKD Flashcards

1
Q

Start

A

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2
Q

Introduction to CKD

A
  • Chronic kidney disease (CKD) is a significant health threat that can progress to End-Stage Kidney Disease (ESKD)
  • Leading to early death, diminished quality of life, and placing a heavy burden on healthcare systems.
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3
Q

Def of ESKD

A

Irreversible kidney dysfunction with…

▪ eGFR < 15 mL/min/1.73 m2

▪ Manifestations of uremia requiring chronic renal replacement therapy

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4
Q

Def of CKD

A
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5
Q

Criteria of CKD

A
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6
Q

Criteria of CKD

  • General
A
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7
Q

Criteria of CKD

  • Markers for Kidney Damage
A
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8
Q

Markers for Kidney Damage

  • Lab Abnormalities
A
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9
Q

Criteria of CKD

  • Markers of Decresed Function
A

Decreased GFR: < 60 mL/min per 1.73 m2

(i.e.GFR categories G3a–G5)

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10
Q

Criteria of CKD

  • Duration
A
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11
Q

Staging of CKD

A
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12
Q

Staging of CKD

  • Acc to Cause
A
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13
Q

Staging of CKD

  • Acc to GFR
A
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14
Q

GFR in Staging of CKD

  • G1
A
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15
Q

GFR in Staging of CKD

  • G2
A
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16
Q

GFR in Staging of CKD

  • G3
A
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17
Q

GFR in Staging of CKD

  • G4
A
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18
Q

GFR in Staging of CKD

  • G5
A
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19
Q

In the absence of evidence of kidney damage, neither GFR category ….. fulfill the criteria for CKD

A

G1 nor G2

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20
Q

Staging of CKD by Albuminuria

A
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21
Q

Staging of CKD by Albuminuria

  • A1
A
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22
Q

Staging of CKD by Albuminuria

  • A2
A
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23
Q

Staging of CKD by Albuminuria

  • A3
A
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24
Q

CP & Complicaions of CKD

A
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25
Q

Etiology of CKD

A

① Diabetic nephropathy

② Hypertensive nephropathy

③ Glomerulonephritis

④ Other causes (e.g., polycystic kidney disease – analgesic misuse – amyloidosis)

⑤ Unknown causes.

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26
Q

Def of Uremia

A

Accumulation of uremic toxins due to decreased Renal excretion

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27
Q

Naming of Uremia

A

Historically, the first solute recognized to be retained in persons with kidney failure was urea, hence the terms; uremia.

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28
Q

Examples of Potential Uremic Toxins

A

Over 100 substances identified as potential uremic toxins, e.g.,
① Urea.
② Creatinine.
③ β2 microglobulin.

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29
Q

Significance of Uremia

A
  • Most of CKD manifestations are due to uremic toxins.
  • Examples for uremic symptoms: nausea, vomiting, hiccough, pruritis.. etc.
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30
Q

Uremia Symptoms Timeframe

A
  • Patients are often asymptomatic until later stages due to the exceptional compensatory mechanisms of the kidneys.
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31
Q

Volume Status in CKD

A

Hypervolemia resulting from impairments of sodium and water handling

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31
Q

Def of CKD-MBD

A

A systemic disorder manifested by either one or a combination of the following three components:

① Abnormalities in the metabolism

② Abnormalities in bone turnover, mineralization, volume linear growth, or strength

③ Extra-skeletal calcification

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32
Q

CKD-MBD

  • Abnormalities in the Metabolism
A
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33
Q

Po4 in CKD

A
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34
Q

Vit D in CKD

A
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34
Q

FGF23 in CKD

A
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35
Q

Ca in CKD

A
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36
Q

PTH in CKD

A
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37
Q

CKD-MBD

  • Abnormalities in Bone Turnover, Mineralization, Volume Linear Growth, Strength
A
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38
Q

Renal Osteodystrophy Classified acc to Bx into:

A
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39
Q

Renal Osteodystrophy

  • Low Bone Turnover
A
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39
Q

Renal Osteodystrophy

  • High Bone turnover (Osteitis fibrosa cystica)
A
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40
Q

Renal Osteodystrophy

  • Mixed Uremic Osteodystrophy
A

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41
Q

Gold Standard in Dx of Renal Osteodystrophy & Its Classification

A

Bone biopsy

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42
Q
  • The term “renal osteodystrophy” should be used exclusively to define alterations in bone morphology associated with CKD based upon bone biopsy, and it is only one component of the bone abnormalities of CKD-MBD
A

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43
Q

Extra-Skeletal Manifestations of CKD MBD

A
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44
Q

Extra-Skeletal Manifestations of CKD MBD

  • Vascular Calcification
A

For example:

  1. Coronary artery calcification → Increased cardiovascular risk.
  2. Arterioles & capillaries in the dermis & subcutaneous adipose tissue → Calciphylaxis
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45
Q

CVS Abnormalities in CKD

A
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45
Q

Extra-Skeletal Manifestations of CKD MBD

  • Other Calcifications
A

Soft tissue, valvular, etc..

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46
Q

CVS Abnormalities in CKD

  • HTN
A

▪ Salt & water retention.

▪ Note that: Hypertension is a cause and precipitating factor of CKD.

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47
Q

CVS Abnormalities in CKD

  • LVH
A

① Volume overload

② Systolic hypertension

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48
Q

CVS Abnormalities in CKD

  • IVD
A
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49
Q

CVS Abnormalities in CKD

  • HF
A

① Myocardial ischemia
② Left ventricular hypertrophy
③ Frank cardiomyopathy
④ Salt and water retention

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50
Q

CVS Abnormalities in CKD

  • Arrhythmia
A

① Electrolyte disturbances.
② Volume overload.
③ Sympathetic overactivity.
④ Acidosis.

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51
Q

CVS Abnormalities in CKD

  • Pericardial Diseases
A

Uremic pericarditis & Pericardial effusion

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52
Q

What is the Leading Cause of Morbidity & Mortality in patients at every stage of CKD?

A
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53
Q

Hematological Disorders in CKD

A
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54
Q

Hematological Disorders in CKD

  • Hb in Anemia
A
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55
Q

Hematological Disorders in CKD

  • type of Anemia
A
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56
Q

Hematological Disorders in CKD

  • Etiology of Anemia
A
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57
Q

Hematological Disorders in CKD

  • WBCs
A
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58
Q

Hematological Disorders in CKD

  • Platlets
A
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59
Q

Dermatologic Abnormalitis in CKD

A
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60
Q

Dermatologic Abnormalitis in CKD

  • Pigmentations
A
  • d2 failure of kidneys to excrete beta-melanocyte stimulating hormone.
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61
Q

Dermatologic Abnormalitis in CKD

  • Pallor
A

d2 anemia

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62
Q

Dermatologic Abnormalitis in CKD

  • Uremic Pruritis
A

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63
Q

Dermatologic Abnormalitis in CKD

  • Bullous Dermatosis
A

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64
Q

Dermatologic Abnormalitis in CKD

  • Calcific uremic arteriolopathy
A

calciphylaxis

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65
Q

Dermatologic Abnormalitis in CKD

  • Nephrogenic systemic fibrosis
A
  • formerly known as nephrogenic fibrosing dermopathy)
  • The condition is seen in patients with CKD who have been exposed to the magnetic resonance contrast agent gadolinium
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66
Q

Respiratory Problems in CKD

A
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67
Q

Respiratory Problems in CKD

  • Pleurisy
A

Due to uremia.

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68
Q

Respiratory Problems in CKD

  • Pulmonary Edema
A

Multifactorial due to Hypoalbuminemia, Hypervolemia, Heart failure (LVF)

69
Q

Respiratory Problems in CKD

  • Pneumonia & TB
A

Due to impaired immunity.

70
Q

Neuromuscular Abnormalities in CKD

71
Q

Neuromuscular Abnormalities in CKD

  • CNS
72
Q

Neuromuscular Abnormalities in CKD

  • PNS
73
Q

Neuromuscular Abnormalities in CKD

  • Muscles
A

Uremic Myopathy

74
Q

Infections in CKD

75
Q

2nd Leading Cause of Death in CKD

A

Infections

76
Q

Infections in CKD

  • Etiology
A

Partially due to immune dysfunction, although multiple other factors are involved.

77
Q

Infections in CKD

  • Types
A

Bacterial or viral infection

78
Q

Infections in CKD

  • Which type is more susceptible?
A

There is an increased susceptibility to bacterial infection (particularly staphylococcal)

79
Q

Infections in CKD

  • TB
A

There is an increased risk of reactivation of tuberculosis (with a negative tuberculin skin test response)

80
Q

Infections in CKD

  • HBV & HCV
A

Failure to eliminate HBV and HCV after infection may occur.

81
Q

GIT Abnormalities in CKD

82
Q

GIT Abnormalities in CKD

  • Mouth Odour
83
Q

GIT Abnormalities in CKD

  • Tongue
84
Q

GIT Abnormalities in CKD

  • Esophagus
A

A. Gerd: d2 delayed gastric emptying.
B. Esophagitis.

85
Q

GIT Abnormalities in CKD

  • Stomach
A

A. Gastritis.
B. Delayed gastric emptying.
C. Peptic ulcer.

86
Q

GIT Abnormalities in CKD

  • Intestinal
A

Constipation

87
Q

Nutritional Abnormalities in CKD

88
Q

Nutritional Abnormalities in CKD

  • Incidence
A

Very common problem among patients with advanced CKD and those undergoing maintenance dialysis (MD) therapy.

89
Q

Nutritional Abnormalities in CKD

  • Morbidity & Mortality
A

Associated with high morbidity & mortality.

90
Q

Nutritional Abnormalities in CKD

  • Contributing Factors
91
Q

Glucose Metabolism in CKD

92
Q

ACKD

A

Refers to an acute, often reversible decline in kidney function that occurs in a patient with pre-existing chronic kidney disease (CKD).

93
Q

Done

94
Q

Screening & detection of CKD

  • Rationale
A

The rationale for screening at-risk individuals for CKD is to:

① Permit earlier detection of CKD, and allowing interventions aimed at slowing CKD progression.

② Identify people who are at risk of CKD associated cardiovascular disease (CVD), morbidity and mortality.

95
Q

Screening & detection of CKD

  • Candidates
96
Q

Screening & detection of CKD

  • Methods
A

Screening should consist of:

① Urinalysis.

② Urine albumin or protein estimation (such as PER or ACR).

③ Measurement of serum creatinine and estimation of GFR.

97
Q

Predictors of Progression of CKD

  • Non-Modifiable RF
98
Q

Predictors of Progression of CKD

  • Modifiable RF
99
Q

The most significant predictors of CKD progression are

A

① The degree of impaired kidney function at presentation.

② Hypertension and its control.

③ The severity of proteinuria and albuminuria

100
Q

No single biomarker can identify those at risk of progression with high sensitivity and specificity.

101
Q

Investigation for CKD

A
  • Investigations to detect functional decline
  • Investigations to detect structural renal damage
  • Investigations to identify underlying causes
  • Other Investigations
102
Q

Serum Markers Used in CKD

103
Q

Creatinine & Bun in CKD

A
  • Increased Creatinine & BUN

▪ Patients with BUN > 140 mg/dl, serum creatinine > 13.5 mg/dl, or blood urea > 300 mg/dl who appear relatively well & are still passing normal volumes of urine are much more likely to have chronic than acute kidney disease.

104
Q

Cystatin C in CKD

105
Q

GFR in CKD

106
Q

Methods of Estimation of GFR in CKD

107
Q

Na in CKD

A

Na+ retention: Occurs once GFR is severely reduced, and sodium intake is unchanged.

108
Q

K in CKD

109
Q

Ca in CKD

110
Q

PO4 in CKD

111
Q

ABG in CKD

112
Q

Urinary Albumin in CKD

A

▪ AER ≥ 30 mg/24h
▪ ACR ≥ 30 mg/g

113
Q

Urine Dipsticks in CKD

A

May show hematuria or proteinuria

114
Q

Urine MIcroscopy in CKD

A

May show abnormal urine sediments (e.g., waxy casts)

115
Q

Imaging in CKD

A

Renal US: (1st line imaging technique for the assessment of kidney structure)

116
Q

Imaging in CKD

  • Findings Suggestive of CKD
117
Q

Imaging in CKD

  • Findings Suggestive of Other Etiologies
A

① Ureteral or renal pelvic dilation suggests obstructive nephropathy.

② Bilaterally enlarged kidneys with multiple cysts suggest polycystic kidney disease.

118
Q

In CKD, Kidneys are bilaterally shrunken EXCEPT IN ……

A

(DM – Polycystic kidney disease – Amyloidosis – Hydronephrosis)

119
Q

Bx in CKD

A

Not routinely indicated - consider in either of the following:

① Rapid & unexplained decline in eGFR.

② Need for diagnostic confirmation of the underlying etiology (e.g., glomerulonephritis) prior to initiating disease-specific therapy.

120
Q

Investigations for Underlying Causes of CKD

  • DM
A

▪ Fasting plasma glucose
▪ HbA1c

121
Q

Investigations for Underlying Causes of CKD

  • GN
122
Q

Investigations for Underlying Causes of CKD

  • PCKD
A

APKD ( genetic testing)

123
Q

Other Investigations for CKD

124
Q

Managment of CKD

125
Q

Managment of CKD

  • TTT of Cause
A

E.g., Diabetes Mellites & Hypertension.

126
Q

Managment of CKD

  • Supportive Care
127
Q

How to Manage Medications in CKD?

128
Q

Managment of Volume Status in CKD

A

① Dietary salt restriction.

② Use of diuretics (loop diuretics, occasionally in combination with metolazone)

129
Q

Managment of Electrolyte Status in CKD

130
Q

Managmnet of Na in CKD

A

Na restriction.

131
Q

Managmnet of K in CKD

A
  • Dietary restriction of potassium.
  • Use of kaliuretic diuretics. + Refer to “Potassium disorders” Lecture
132
Q
  • Some patients with renal dysfunction develop renal wasting of Na+ (Salt wasting nephropathy) and they are usually hypotensive and may benefit from liberalization of salt in their diet.
133
Q

Managment of Acid-Base Disturbance in CKD

134
Q

Managment of Acid-Base Disturbance in CKD

  • Alkali Suppmentation
135
Q

Managment of Acid-Base Disturbance in CKD

  • Diet
A
  • A low-protein diet can decreased acid production.
  • Base-inducing fruits & vegetables ⇢ Increase Serum [HCO3−]

Fruits & Vegetables increase risk of Hyperkalemia

136
Q

Managment of MBD in CKD

137
Q

Managment of MBD in CKD

  • Goal
A

goal is to normalize phosphate, calcium, and PTH levels

138
Q

Managment of MBD in CKD

  • Hyperphosphatemia
139
Q

Managment of MBD in CKD

  • Vit D
140
Q

Managment of MBD in CKD

  • Avoid Hypocalcemia
A

① Correcting hyperphosphatemia & treating vitamin D deficiency.

② Dietary calcium should be increased to 1500 mg of elemental calcium daily.

141
Q

Managment of MBD in CKD

  • Avoid Hyperparathyroidism
A
  • Correction of Ca++, P & Vit D.
  • Parathyroidectomy (last-line therapy if medical ttt is failed)
141
Q

Managment of HTN in CKD

142
Q

Managment of HTN in CKD

  • Target BP
A
  • Target blood pressure in patients with CKD: < 130/80 “Acc. to (ACC/AHA) Recommendation”
143
Q

Managment of HTN in CKD

  • Aspects
A
  • Non-pharmacological Treatment
  • Pharmacological Treatment
144
Q

Managment of HTN in CKD

  • Non-Pharmacological TTT
A

① Maintaining healthy weight

② Lower salt intake (<5 gm of NaCl)

③ Regular exercise if not contraindicated

④ Stop smoking and alcohol.

145
Q

Managment of HTN in CKD

  • Pharmacological TTT
146
Q

U-shaped curve of SBP has been reported in which very low, and very high SBP is associated with faster rates of decline in eGFR.

147
Q

Managment of Anemia in CKD

148
Q

Managment of Anemia in CKD

  • Rationale of TTT
149
Q

Managment of Anemia in CKD

  • Options of TTT
A

① Iron therapy.
② Check for & Treat Vit B12 & Folate deficiency.
③ Erythropoiesis-stimulating agent (The Best)
④ Blood transfusion

150
Q

Managment of Anemia in CKD

  • Best Option of TTT
A

Erythropoiesis-stimulating agent

151
Q

Managment of Anemia in CKD

  • Blood Transfusion
152
Q

Managment of Pruritis in CKD

153
Q

Managment of Glycemic Control in CKD

154
Q

Managment of Glycemic Control in CKD

  • Target
A

▪ For diabetic patient with CKD → is to keep HbA1c not exceed 7 %

▪ If the patient has limited life expectancy comorbidities or risk of hypoglycemia → It may be > 7%

155
Q

Managment of Glycemic Control in CKD

  • TTT Options
156
Q

Managment of Glycemic Control in CKD

  • Use Insulin?
A
  • Insulin treatment should be used with caution in patients with reduced eGFR due to the increased risk of hypoglycemia.
157
Q

Managment of Lifestyle in CKD

  • PTN
A

Low protein diet 0.8 g/kg/day (unless the patients start dialysis)

158
Q

Managment of Lifestyle in CKD

  • Cal
A

High (25 – 35 Kcal/Kg IBW/day)

159
Q

Managment of Lifestyle in CKD

  • Salt
A
  • Restricted (< 5 gm/day) → To correct hypervolemia & Hypertension
160
Q

Managment of Lifestyle in CKD

  • Fluids
A

Fluid balance → To avoid volume overload

161
Q

Managment of Lifestyle in CKD

  • K
A

Restricted → To correct hyperkalemia.

162
Q

Managment of Lifestyle in CKD

  • PO4
A

Restricted → To correct hyperphosphatemia.

163
Q

Managment of Lifestyle in CKD

  • Ca
A

Allowed within the dietary recommendations.

164
Q

Managment of Lifestyle in CKD

  • Smoking
165
Q

Managment of Lifestyle in CKD

  • Obesity
166
Q

Managment of Lifestyle in CKD

  • Dyslipidemia
167
Q

Managment of CKD

  • Retarding CKD Progression
168
Q

Retarding CKD Progression

  • Goals
A

① To reduce proteinuria as much as possible, ideally to less than 500 mg/day.

② Slow GFR decline as much as possible, ideally to about 1 ml/min/yr, which is the rate of GFR decline attributable to the nephropathy of aging.

169
Q

Retarding CKD Progression

  • Methods
A

By managing modifiable risk factors

170
Q

RRT in CKD

171
Q

RRT in CKD

  • Options of Non-Operative TTT
A
  • Hemodialysis
  • Peritoneal dialysis
172
Q

RRT in CKD

  • Indications of Non-Operative TTT
173
Q

RRT in CKD

  • Operative TTT
174
Q

Done

A

Doneeeeeee