pathophysiology of kidney diseases

Gwangly

Acute kidney injury VS chronic kidney disease จริง ๆ ควรทำและลงสรุปฟิสิโอก่อน แต่ไฟมอดมาก555 หมดไฟงือ

2026.04.09 公開

#pathology #pathophysiology #renal #kidney

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ページ1:

ACUTE KIDNEY
INJURY (AKI)
ACUTE KIDNEY INJURY (AKI)
TOP ZONE
PRERENAL
ZONE
AKI
Mechanism: Reduced Blood
Flow to the Kidneys
Dehydration
(e.g., Vomiting, Diarrhea)
Hemorrhage
Sepsis (e.g., from
severe infection)
Mechanisms and Key Agents of AKI
ADDITIONAL CLINICAL MECHANISMS
Hemodynamic & Vascular Factors.
Reduced GFR Mechanisms
NSAIDS/COX-2
Inhibitors
Reduced
Prostaglandins
Vasoconstriction of
Afferent Arteriole
Vasodilation of
Efferent Arteriole
ACEIS / ARBs
Reduced
Angiotensin II
Vascular Blockage
Other Causes
M.D.
AMI (Acute Myocardial Infarction)
Renal Artery Thrombosis ⚫ others
MIDDLE ZONE
INTRINSIC
RENAL
AKI
Core: Direct Damage to Kidney
Tissue (e.g., Nephrons, Tubules)
ZONE
Acute Tubular Necrosis
(ATN) from prolonged
ischemia or toxins
Acute Interstitial
Nephritis (AIN)
(allergic reaction)
Glomerulonephritis
BOTTOM ZONE
POSTRENAL
AKI
Obstructive Uropathy
(e.g.. Stones)
Benign Prostatic
Hyperplasia (SPH) (m men)
Tumors
Mechanism: Obstruction of Urine
Outflow, causing backpressure
Differentiation based on Location of Injury Source
Pathophysiology of Intrinsic Damage.
ISCHEMIA-MAIN CAUSE OF AKI
Ischemia Vasoconstriction
Toxins and Specific Agents.
Endothelial Inflammatory
Damage
Process
Apoptosis/_
Necrosis
Renal
Dysfunction
Drug-Induced AKI
Specific Toxins
-sulphonamide, uric acid
-high dose acyclovir
-high dose Vit. C
NH
Other Key Drugs
- propranolol
-a-adrenergic blockers
Comprehensive Overview of AKI Differentiation and Specific Pathologies

ページ2:

Clinical Presentation
(Main Title)
•
AK1 Clinical presentation
GClinical presentation
Edema
Pitting edema
Pitting edema
• Change in urinary character (eg, decreased urine output or urine color)
• Edema (swelling)
Dyspnea (shortness of breath)
Reduced
appetite
.
Metabolic &
Fluid Balance
Symptoms
• Loss of appetite
Fatigue (tiredness)
Nausea,
Shortness of breath vomiting
.
• Nausea, vomiting
(Na+) (K+
Sudden weight gain
.
Electrolyte disturbances
• Sudden weight gain
• Severe abdominal or flank pain
☆
Rapid weight change
Severe abdominal or flank
Pain in abdomen or side
Comprehensive English-Only Overview of AK1 Clinical Presentation

ページ3:

ACUTE KIDNEY INJURY (AKI):
LABORATORY TESTS & MANAGEMENT
PART 1: LABORATORY TESTS IN AKI
Immediately Reduce
cla
PRERENAL/
BUN / SCr Ratio (Serum Creatinine)
Urine Output
A
Indicator of AKI:
Rapid reduction in
urine output
> 20:1 →
BUN / SCr
Ratio
Calculation
POSTRENAL AKI
Suggests volume depletion
or obstruction
INTRINSIC AKI
< 20:1
(~ 10:1)
Suggests direct kidney
tissue damage
PART 2: AKI MANAGEMENT
- Key Concept
No specific
treatment can
reverse AKI
pH
Na
K+
Na
CI
Supportive Measures
- Fluid Balance
Core Strategy:
Maintaining optimal
-Acid-Base Balance
K - Electrolyte
Homeostasis
physiologic
conditions while
kidney repair
Differentiating AKI types is crucial for determining supportive care strategies

ページ4:

Onl
CHRONIC KIDNEY DISEASE (CKD)
& ACUTE KIDNEY INJURY (AKI)
AKI vs CKD
กา
Persistent (>3 months).
Acute Kidney Injury (AKI)
Chronic Kidney Disease (CKD)
Timeframe:
Abrupt onset
(within 48 hours).
Reversibility: Potentially reversible.
Main Markers
(Diagnosis):
↑ Serum Creatinine (SCr).
Progression is non-reversible. X
GFR<60 mL/min/1.73 m²
(>3 months)
STAGING OF CKD (KDIGO GUIDELINES)
GFR Categories (G) GFR (ml/min/1.73 m²)
Albuminuria Categories (A) Terms
G1
≥ 90
A1
< 30
<30
Normal or high
G2
60-89
A2
Mildly increased
GFR-
G3a
45-59
A2
30-300
3-30
Moderately increased
G3b
30-44
A4
> 300
>300
Severely increased
G4
15-29
A3
> 300
>300
Severely failure
End-hage renal+G5
<15
disease
Initial pathogenic injury
Diabetes mellitus
Reduced filtration area
Formation of advanced
glycation end products
Adaptive hemodynamic
changes
Arteriosclerosis
Hyperlipidemia
Increased glomerular
blood flow
Increased glomerular
capillary pressure
Mesangial injury
Systemic hypertension
Glomerular hypertrophy
Epithelial injury
Focal detachment of
epithelial foot processes
Glomerular
hyaline deposition
Endethellal injury
Proteineria
Microthromin occluding
glomerular capillaries
Glomerulosclerosis
Progression of
kidney disease
Mesangial expansion
Micronaeurysm formation
PATHOPHYSIOLOGY (Simplified for CKD)
KDIGO

ページ5:

CHRONIC KIDNEY DISEASE (CKD)
DEFINITION & MARKERS
KEY DURATION CRITERIA: >3 MONTHS
MARKERS: MARKERS OF KIDNEY DAMAGE
(One or More)
Albuminuria
Urine Sediment
RBC
Abnormalities
Epithelial cells
Electrolytes Imbalance
Histological Abnormalities
Structural Abnormalities via Imaging
(X-Ray, MRI, CT Scan)
History of Kidney Transplantation
RIGHT PANEL:
DECREASED KIDNEY
FUNCTION
GFR
< 60 mL/min/1.73 m²
(Normal GFR≈ 90-100)
(Follow-up needed after
3 months)
STAGING OF CKD (KDIGO GUIDELINES)
GFR CATEGORIES (G)
GFR Category GFR (ml/min/1.73 m²) Terms
G1
G2
GFR G3a
G3b
G4
End-stage renal
diteate
G5
≥90
Normal or high
60-89
Mildly decreased*
45-59
Mildly to moderately decreased
30-44
Moderately to severely decreased
15-29
Severely decreased
<15
Kidney failure
Abbreviations: CKD, chronic kidney disease; GFR, glomerular filtration rate.
*Relative to young adult level
ALBUMINURIA CATEGORIES (A)
ACR (approximate
equivalent)
Albuminuria
Category
AER
(mg/24 hours)
Terms
(mg/mmol) (mg/g)
A1
<30
<3
<30
Normal to mildly
increased
A2
30-300
3-30
30-300
A3
> 300
>30
> 300
Moderately increased*
Severely increased**
Abbreviations: AER, albumin excretion rate; ACR, albumin-to-creatinine ratio;
CKD, chronic kidney disease.
*Relative to young adult level.
**Including nephrotic syndrome (albumin excretion usually > 2200 mg/24 hours
(ACR>2220 mg/g: > 220 mg/mmoll).

ページ6:

CHRONIC KIDNEY DISEASE (CKD): CLINICAL PRESENTATION & MANAGEMENT
Note: CKD is typically asymptomatic until CKD stages 4 or 5.
1. CLINICAL PRESENTATION
(SYMPTOMS & SIGNS)
Symptoms: Uremia
Fatigue, weakness
(related to anemia)
Shortness of breath
Confusion, nausea &
vomiting (uremia)
Loss of appetite, itching
Cold intolerance,
peripheral neuropathies
Signs
Edema, weight gain
Foaming of urine
(proteinuria)
3. MANAGEMENT & CARE
.
.
.
COMPLICATIONS OF CKD
Hypervolemia
Hypertension
Hyperkalemia
Hypokalemia ⇓
(specific hypokalemia)
.
2. LABORATORY & DIAGNOSTIC TESTS
eGFR
Decreased
Bicarbonate → metabolic acidosis
Hb/Hct (anemia)
Vit D, Albumin, Calcium (in early stages)
Increased
↑ Serum Creatinine, BUN (uremia)
K, P, PTH, BP, LDL, TGS
Other Diagnostic Tests
• Urine Sediment → Hematuria
.
Ultrasound, CT Scan
→ Polycystic Kidneys
→ Renal a. Stenosis
STRATEGIES TO SLOW PROGRESSSION OF CKD
Non-pharmacologic
treatment
High protein diet
restriction
Sodium restriction
Weight control
.
.
0
Metabolic Acidosis
.
0 Anemia
.
Smoking cessation
.
Pharmacologic treatment
• Glycemic control in
DM patients
•⚫ BP control in HTN
patients
Lipid management