L4: CKD Flashcards

(179 cards)

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

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5
Q

Criteria of CKD

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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
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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

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25
Etiology of **CKD**
① Diabetic nephropathy ② Hypertensive nephropathy ③ Glomerulonephritis ④ Other causes (e.g., polycystic kidney disease – analgesic misuse – amyloidosis) ⑤ Unknown causes.
26
Def of **Uremia**
Accumulation of uremic toxins due to decreased Renal excretion
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Naming of **Uremia**
Historically, the first solute recognized to be retained in persons with kidney failure was urea, hence the terms; uremia.
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Examples of Potential Uremic Toxins
Over 100 substances identified as potential uremic toxins, e.g., ① Urea. ② Creatinine. ③ β2 microglobulin.
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Significance of **Uremia**
- Most of CKD manifestations are due to uremic toxins. - Examples for uremic symptoms: nausea, vomiting, hiccough, pruritis.. etc.
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Uremia Symptoms Timeframe
- Patients are often asymptomatic until later stages due to the exceptional compensatory mechanisms of the kidneys.
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Volume Status in **CKD**
Hypervolemia resulting from impairments of sodium and water handling
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Def of **CKD-MBD**
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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**CKD-MBD** - Abnormalities in the Metabolism
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Po4 in CKD
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Vit D in CKD
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FGF23 in CKD
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Ca in CKD
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PTH in CKD
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**CKD-MBD** - Abnormalities in Bone Turnover, Mineralization, Volume Linear Growth, Strength
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Renal Osteodystrophy Classified acc to Bx into:
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Renal Osteodystrophy - Low Bone Turnover
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Renal Osteodystrophy - High Bone turnover (Osteitis fibrosa cystica)
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Renal Osteodystrophy - Mixed Uremic Osteodystrophy
...
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Gold Standard in Dx of Renal Osteodystrophy & Its Classification
Bone biopsy
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- 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
...
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Extra-Skeletal Manifestations of **CKD MBD**
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Extra-Skeletal Manifestations of **CKD MBD** - Vascular Calcification
For example: 1. Coronary artery calcification → Increased cardiovascular risk. 2. Arterioles & capillaries in the dermis & subcutaneous adipose tissue → Calciphylaxis
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CVS Abnormalities in **CKD**
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Extra-Skeletal Manifestations of **CKD MBD** - Other Calcifications
Soft tissue, valvular, etc..
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CVS Abnormalities in **CKD** - HTN
▪ Salt & water retention. ▪ Note that: Hypertension is a cause and precipitating factor of CKD.
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CVS Abnormalities in **CKD** - LVH
① Volume overload ② Systolic hypertension
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CVS Abnormalities in **CKD** - IVD
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CVS Abnormalities in **CKD** - HF
① Myocardial ischemia ② Left ventricular hypertrophy ③ Frank cardiomyopathy ④ Salt and water retention
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CVS Abnormalities in **CKD** - Arrhythmia
① Electrolyte disturbances. ② Volume overload. ③ Sympathetic overactivity. ④ Acidosis.
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CVS Abnormalities in **CKD** - Pericardial Diseases
Uremic pericarditis & Pericardial effusion
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What is the Leading Cause of Morbidity & Mortality in patients at every stage of CKD?
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Hematological Disorders in CKD
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Hematological Disorders in CKD - Hb in Anemia
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Hematological Disorders in CKD - type of Anemia
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Hematological Disorders in CKD - Etiology of Anemia
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Hematological Disorders in CKD - WBCs
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Hematological Disorders in CKD - Platlets
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Dermatologic Abnormalitis in CKD
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Dermatologic Abnormalitis in CKD - Pigmentations
- d2 failure of kidneys to excrete beta-melanocyte stimulating hormone.
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Dermatologic Abnormalitis in CKD - Pallor
d2 anemia
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Dermatologic Abnormalitis in CKD - Uremic Pruritis
...
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Dermatologic Abnormalitis in CKD - Bullous Dermatosis
...
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Dermatologic Abnormalitis in CKD - Calcific uremic arteriolopathy
calciphylaxis
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Dermatologic Abnormalitis in CKD - Nephrogenic systemic fibrosis
- 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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Respiratory Problems in CKD
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Respiratory Problems in CKD - Pleurisy
Due to uremia.
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Respiratory Problems in CKD - Pulmonary Edema
Multifactorial due to Hypoalbuminemia, Hypervolemia, Heart failure (LVF)
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Respiratory Problems in CKD - Pneumonia & TB
Due to impaired immunity.
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Neuromuscular Abnormalities in CKD
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Neuromuscular Abnormalities in CKD - CNS
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Neuromuscular Abnormalities in CKD - PNS
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Neuromuscular Abnormalities in CKD - Muscles
Uremic Myopathy
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Infections in CKD
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2nd Leading Cause of Death in CKD
Infections
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Infections in CKD - Etiology
Partially due to immune dysfunction, although multiple other factors are involved.
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Infections in CKD - Types
Bacterial or viral infection
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Infections in CKD - Which type is more susceptible?
There is an increased susceptibility to bacterial infection (particularly staphylococcal)
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Infections in CKD - TB
There is an increased risk of reactivation of tuberculosis (with a negative tuberculin skin test response)
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Infections in CKD - HBV & HCV
Failure to eliminate HBV and HCV after infection may occur.
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GIT Abnormalities in CKD
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GIT Abnormalities in CKD - Mouth Odour
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GIT Abnormalities in CKD - Tongue
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GIT Abnormalities in CKD - Esophagus
A. Gerd: d2 delayed gastric emptying. B. Esophagitis.
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GIT Abnormalities in CKD - Stomach
A. Gastritis. B. Delayed gastric emptying. C. Peptic ulcer.
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GIT Abnormalities in CKD - Intestinal
Constipation
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Nutritional Abnormalities in CKD
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Nutritional Abnormalities in CKD - Incidence
Very common problem among patients with advanced CKD and those undergoing maintenance dialysis (MD) therapy.
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Nutritional Abnormalities in CKD - Morbidity & Mortality
Associated with high morbidity & mortality.
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Nutritional Abnormalities in CKD - Contributing Factors
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Glucose Metabolism in CKD
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ACKD
Refers to an acute, often reversible decline in kidney function that occurs in a patient with pre-existing chronic kidney disease (CKD).
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Done
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Screening & detection of **CKD** - Rationale
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.
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Screening & detection of **CKD** - Candidates
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Screening & detection of **CKD** - Methods
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.
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Predictors of Progression of **CKD** - Non-Modifiable RF
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Predictors of Progression of **CKD** - Modifiable RF
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The most significant predictors of CKD progression are
① The degree of impaired kidney function at presentation. ② Hypertension and its control. ③ The severity of proteinuria and albuminuria
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No single biomarker can identify those at risk of progression with high sensitivity and specificity.
...
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Investigation for **CKD**
- Investigations to detect functional decline - Investigations to detect structural renal damage - Investigations to identify underlying causes - Other Investigations
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Serum Markers Used in **CKD**
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Creatinine & Bun in **CKD**
- 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.**
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Cystatin C in **CKD**
Increased
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GFR in **CKD**
Decreased
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Methods of Estimation of GFR in **CKD**
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Na in **CKD**
Na+ retention: Occurs once GFR is severely reduced, and sodium intake is unchanged.
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K in **CKD**
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Ca in **CKD**
Decreased
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PO4 in **CKD**
Increased
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ABG in **CKD**
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Urinary Albumin in **CKD**
▪ AER ≥ 30 mg/24h ▪ ACR ≥ 30 mg/g
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Urine Dipsticks in **CKD**
May show hematuria or proteinuria
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Urine MIcroscopy in **CKD**
May show abnormal urine sediments (e.g., waxy casts)
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Imaging in **CKD**
Renal US: (1st line imaging technique for the assessment of kidney structure)
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Imaging in **CKD** - Findings Suggestive of CKD
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Imaging in **CKD** - Findings Suggestive of Other Etiologies
① Ureteral or renal pelvic dilation suggests obstructive nephropathy. ② Bilaterally enlarged kidneys with multiple cysts suggest polycystic kidney disease.
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In CKD, Kidneys are bilaterally shrunken EXCEPT IN ......
(DM – Polycystic kidney disease – Amyloidosis – Hydronephrosis)
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Bx in **CKD**
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.
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Investigations for Underlying Causes of **CKD** - DM
▪ Fasting plasma glucose ▪ HbA1c
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Investigations for Underlying Causes of **CKD** - GN
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Investigations for Underlying Causes of **CKD** - PCKD
APKD ( genetic testing)
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Other Investigations for CKD
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Managment of **CKD**
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Managment of **CKD** - TTT of Cause
E.g., Diabetes Mellites & Hypertension.
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Managment of **CKD** - Supportive Care
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How to Manage Medications in **CKD**?
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Managment of **Volume Status** in CKD
① Dietary salt restriction. ② Use of diuretics (loop diuretics, occasionally in combination with metolazone)
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Managment of **Electrolyte Status** in CKD
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Managmnet of Na in CKD
Na restriction.
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Managmnet of K in CKD
- Dietary restriction of potassium. - Use of kaliuretic diuretics. **+ Refer to “Potassium disorders” Lecture**
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- 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.
...
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Managment of **Acid-Base Disturbance** in CKD
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Managment of **Acid-Base Disturbance** in CKD - Alkali Suppmentation
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Managment of **Acid-Base Disturbance** in CKD - Diet
- A low-protein diet can decreased acid production. - Base-inducing fruits & vegetables ⇢ Increase Serum [HCO3−] **Fruits & Vegetables increase risk of Hyperkalemia**
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Managment of **MBD** in CKD
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Managment of **MBD** in CKD - Goal
goal is to normalize phosphate, calcium, and PTH levels
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Managment of **MBD** in CKD - Hyperphosphatemia
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Managment of **MBD** in CKD - Vit D
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Managment of **MBD** in CKD - Avoid Hypocalcemia
① Correcting hyperphosphatemia & treating vitamin D deficiency. ② Dietary calcium should be increased to 1500 mg of elemental calcium daily.
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Managment of **MBD** in CKD - Avoid Hyperparathyroidism
- Correction of Ca++, P & Vit D. - Parathyroidectomy (last-line therapy if medical ttt is failed)
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Managment of **HTN** in CKD
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Managment of **HTN** in CKD - Target BP
- Target blood pressure in patients with CKD: < 130/80 “Acc. to (ACC/AHA) Recommendation”
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Managment of **HTN** in CKD - Aspects
- Non-pharmacological Treatment - Pharmacological Treatment
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Managment of **HTN** in CKD - Non-Pharmacological TTT
① Maintaining healthy weight ② Lower salt intake (<5 gm of NaCl) ③ Regular exercise if not contraindicated ④ Stop smoking and alcohol.
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Managment of **HTN** in CKD - Pharmacological TTT
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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.
...
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Managment of **Anemia** in **CKD**
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Managment of **Anemia** in **CKD** - Rationale of TTT
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Managment of **Anemia** in **CKD** - Options of TTT
① Iron therapy. ② Check for & Treat Vit B12 & Folate deficiency. ③ Erythropoiesis-stimulating agent (The Best) ④ Blood transfusion
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Managment of **Anemia** in **CKD** - Best Option of TTT
Erythropoiesis-stimulating agent
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Managment of **Anemia** in **CKD** - Blood Transfusion
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Managment of **Pruritis** in **CKD**
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Managment of **Glycemic Control** in **CKD**
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Managment of **Glycemic Control** in **CKD** - Target
▪ 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%
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Managment of **Glycemic Control** in **CKD** - TTT Options
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Managment of **Glycemic Control** in **CKD** - Use Insulin?
- Insulin treatment should be used with caution in patients with reduced eGFR due to the increased risk of hypoglycemia.
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Managment of **Lifestyle** in **CKD** - PTN
Low protein diet 0.8 g/kg/day (unless the patients start dialysis)
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Managment of **Lifestyle** in **CKD** - Cal
High (25 – 35 Kcal/Kg IBW/day)
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Managment of **Lifestyle** in **CKD** - Salt
- Restricted (< 5 gm/day) → To correct hypervolemia & Hypertension
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Managment of **Lifestyle** in **CKD** - Fluids
Fluid balance → To avoid volume overload
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Managment of **Lifestyle** in **CKD** - K
Restricted → To correct hyperkalemia.
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Managment of **Lifestyle** in **CKD** - PO4
Restricted → To correct hyperphosphatemia.
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Managment of **Lifestyle** in **CKD** - Ca
Allowed within the dietary recommendations.
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Managment of **Lifestyle** in **CKD** - Smoking
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Managment of **Lifestyle** in **CKD** - Obesity
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Managment of **Lifestyle** in **CKD** - Dyslipidemia
167
Managment of **CKD** - Retarding CKD Progression
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Retarding CKD Progression - Goals
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.
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Retarding CKD Progression - Methods
By managing modifiable risk factors
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RRT in **CKD**
171
RRT in **CKD** - Options of Non-Operative TTT
- Hemodialysis - Peritoneal dialysis
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RRT in **CKD** - Indications of Non-Operative TTT
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RRT in **CKD** - Operative TTT
174
Done
Doneeeeeee