Hello people! π€
This thread is about
Intrarenal Acute kidney INJURY π§
.
This thread is about
Intrarenal Acute kidney INJURY π§
.
Quick Recapπ
As you know the kidney functions by removing waste, regulating electrolytes and water levels as well as producing hormones like Erythropoietinπ§
Blood starts from the renal arteryππΌto the glomeruli where its filtered either reabsorbed or secretedππΌfinally to urine
As you know the kidney functions by removing waste, regulating electrolytes and water levels as well as producing hormones like Erythropoietinπ§
Blood starts from the renal arteryππΌto the glomeruli where its filtered either reabsorbed or secretedππΌfinally to urine
Intrarenal or sometimes called intrinsic acute kidney injury happens when damage to the kidneys tubules like glomerulus, interstitium, causes a sudden loss in kidney function.
The most common cause of Intrarenal Acute Kidney injury is
Acute Tubular Necrosis (ATN)
Which is a condition in where the small filtering tubes in the kidney are injured (epithelial cells die due to ischemia)
Pictureβs from: researchgate.net
Acute Tubular Necrosis (ATN)
Which is a condition in where the small filtering tubes in the kidney are injured (epithelial cells die due to ischemia)
Pictureβs from: researchgate.net
Since it causes ischemia then itβs a result of decreased blood flow
Decreased blood flow can be a result of:
- severe hypotension (as in hypovolemic patientβs)
- Thromboembolism or cholesterol embolism, etc
Decreased blood flow can be a result of:
- severe hypotension (as in hypovolemic patientβs)
- Thromboembolism or cholesterol embolism, etc
Another cause can be
Nephrotoxins
ππΌ substances that directly damage the epithelial cells, like:
- Infection ( Sepsis
- Medications (e.g aminoglycosides, amphotericin B)
- Myoglobin from damaged muscles
- Heavy medials
Nephrotoxins
ππΌ substances that directly damage the epithelial cells, like:
- Infection ( Sepsis
- Medications (e.g aminoglycosides, amphotericin B)
- Myoglobin from damaged muscles
- Heavy medials
What happens?
proximal tubular cells fall into the tubular lumenβdebris build up & obstruct tubulesβleads to High pressure tubules β blood moves from high p blood vessels to high pressure tublesβ decrease blood filteredβ decreased GFR
Picture from: researchgate.net
proximal tubular cells fall into the tubular lumenβdebris build up & obstruct tubulesβleads to High pressure tubules β blood moves from high p blood vessels to high pressure tublesβ decrease blood filteredβ decreased GFR
Picture from: researchgate.net
This this will lead to decreased urine outputππΌOliguria
Urea and creatinine will not be filtered properlyππΌincrease retention of them in bloodππΌ azotemia
Since the cells are ischemic canβt filter blood, eventually itβll lead to Hyperkalemia, metabolic acidosis and uraemia βΉοΈ
Urea and creatinine will not be filtered properlyππΌincrease retention of them in bloodππΌ azotemia
Since the cells are ischemic canβt filter blood, eventually itβll lead to Hyperkalemia, metabolic acidosis and uraemia βΉοΈ
Later on, dead cells that have built in the tubules will form a brown granular caste
This brown cast will be excreted which will cause the diagnostic features of Muddy brown granular cast in urineππΌ
Picture is from: renalfellow.org
This brown cast will be excreted which will cause the diagnostic features of Muddy brown granular cast in urineππΌ
Picture is from: renalfellow.org
Upon the cause, the patient is managed
Some patients will experience tubular re-epithelialisation and gain full-recovery when treated adequately πππΌ
Some patients will experience tubular re-epithelialisation and gain full-recovery when treated adequately πππΌ
Another cause of Intrarenal AKI is
Glomerulonephritis β¨
Which is a condition where the tiny blood vessels in the kidneys become inflamed and damaged
Glomerulonephritis β¨
Which is a condition where the tiny blood vessels in the kidneys become inflamed and damaged
Itβs usually caused by antigen-antibody complexes deposition in the glomerular tissueππΌactivate complement system ππΌ lead to inflammation π³
Quick recap!π
The endothelium of the fenestrated capillaries are covered with negatively charged proteoglycans & glycosaminoglycans.
Quick recap!π
The endothelium of the fenestrated capillaries are covered with negatively charged proteoglycans & glycosaminoglycans.
The glomerular basement membrane connects the capillaries and the surrounding Bowmanβs capsule thus it is also covered with proteoglycansππΌ negatively charged
Picture is from: cjasn.asnjournals.org
Picture is from: cjasn.asnjournals.org
The cells of the visceral layer of Bowmanβs capsule are called podocytes, whose processes also form a kind of meshwork
This meshwork prevents filtration of large molecules and anions
πͺπΌπ€
This meshwork prevents filtration of large molecules and anions
πͺπΌπ€
When damaged the membrane permeability β¬οΈ and large molecules like protein and blood are filtered βΉοΈ
It can cause the diagnostic features of proteinuria and hematuria
Picture is from: healthychildren.org
It can cause the diagnostic features of proteinuria and hematuria
Picture is from: healthychildren.org
Since the door is open & large molecules enterππΌfluid leakage will β¬οΈpressure difference ππΌ will eventually decrease the GFR due to ongoing damage in the glomeruli
Low GFRππΌLow urine output
Possible increased fluid retention
ππΌ Oedema
Pictureβs from: armandoh.org
Low GFRππΌLow urine output
Possible increased fluid retention
ππΌ Oedema
Pictureβs from: armandoh.org
The classification of glomerulopathies and the difference between nephrotic and nephritic syndrome ππΌπ
Image is from: google.com
Image is from: google.com
I hope you enjoyed this summarised thread
Thank you for reading it ππΌβΊοΈ
Thank you for reading it ππΌβΊοΈ
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