Mind map
Renal Conditions

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Renal Conditions
Chronic Kidney Disease
- Epidemiology
- 1/10 adults have indication of CKD
- Risk Factors
- Diabetiics
- Indigenous Australians at inc. risk
- Aetiology
- Glomerulonephritis
- Diabetes
- Pathophys
- The underlying aetiology (cause dependent) causes a progressive destruction of nephrons
- Proteins in blood (albumin) are lost in filtrate
- Leads to oedema due to loss of oncotic pressure
- Other nephrons attempt to compensate - leads to increased pressure in remaining nephrons - causing further damage
- Stages of CKD
- Stage 1: GFR > 90 - no symptoms
- Stage 2: GFR 60 - 89 - still very little symptomology. Treat any cardiac related symptoms
- Stage 3 a: GFR 45 - 59: mod. d/c in functn. May start to display some symptoms
- Stage 3b: GFR 30 - 44: marked d/c in functn: Check for anaemia. Target BP is <135/85
- Stage 4: GFR 15 - 29: Severely impaired functn
- Stage 5: GFR > 15. End stage CKD: Consider dialysis or transplant if appropriate
- End-stage Treatment
- Haemodialysis
- Uses the principles of ultra filtration and diffusion to remove excess electrolytes, waste products and H2O from circulation
- Usually 3 x a week. 3 - 8 hrs each time
- Also peritoneal dialysis
- Dialysate is infused into the peritoneum which is used as the sem-permeable membrane for diffusion - dialysate is then removed
- Kidney Transplant
- Waiting list
- Immunosuppressant (anti-rejection) drugs
- Haemodialysis
- Epidemiology
Acute Kidney Injury
- Pre-renal AKI
- Aetiology
- Caused by loss in circulating vol. or obstruction in perfusion to kidneys
- 40 - 55 % of AKI
- Pathophysiology
- Manifestations
- Oliguria/anuria
- Increased BP due to RAAS activation
- Aetiology
- Intra-renal AKI
- Acute Glomerulonephritis
- Aetiology
- Infections
- Nephrotoxic drugs
- Autoimmune disease e.g lupus
- Manifestations
- Inc. BP
- Dark haematuria
- Oedema - facial
- Fatigue
- N + V
- Testing
- Urinalysis
- Protein, blood and WBC in blood, inc. spec grav
- Bloods
- Pt may be uraemic (> 8.3 mmol/L)
- Anaemia due to v in erythropoetin prod.
- Urinalysis
- Treatment
- Cause of inflammation must be treated
- Cause of inflammation must be treated
- Pathophys
- Inflammation leads to inc. gaps in endothelial cells
- Leads to loss of proteins + other blood components in urine
- Can also lead to build up of Urea & Creatinine in the blood
- Leads to loss of proteins + other blood components in urine
- Inflammation leads to inc. gaps in endothelial cells
- Inflammation of the glomerulus which can lead to d/c blood flow
- Aetiology
- Acute Tubular Necrosis
- Aetiology
- Prolonged ischaemia i.e untreated pre-renal AKI or nephrotoxins
- Pathophys
- Nephrotoxic injury
- Tubular cells are damaged directly or indirectly (i.e vasoconstriction)
- Ischaemia
- Prolonged ischaemia leads to ATP depletion & accummulation of Ca - free radicals damage cells which become necrotic & rupture
- Injured cells release debris - combine with proteins to form CASTS
- These + necrotic cells can occlude the lumen & inc. pressure leading to v GFR
- Inc. pressure sees filtrate pushed back into interstium
- These + necrotic cells can occlude the lumen & inc. pressure leading to v GFR
- Nephrotoxic injury
- Testing
- Urinalysis typically indicative of renal tubule cells & casts
- Treatment
- Aetiology
- Acute Glomerulonephritis
- Post-renal AKI
- Aetiology
- Blockage or compression leads to filtrate build up and backflow
- Can occur b/w renal pelvis and urethral meatus
- i.e cervical Ca or prostatomegaly
- Blockage or compression leads to filtrate build up and backflow
- Rarest form - 5% of cases
- Manifestations
- Oliguria/anuria - Difficulty passing - pt may strain
- Bladder distension
- Oedema
- HTN
- Lower back pain
- Severe haematuria
- Aetiology
- General Progression of AKI
- 1) Initiation phase
- Cause of AKI (e.g haemorrhage)
- Lasts hours - days
- Can by unsymptomatic
- If untreated
- 2) Maintenance Phase
- Sig. v in GFR
- Uraemia
- Fluid retention - oedema
- electrolyte imbalance
- Impaired K levels
- If not treated quickly at this stage
- 3) Diuretic Phase
- Recovery pt. 1
- 1-2 weeks
- Inc. diuresis due to impaired tubule wall patency during healing
- Urea & Na are not retained
- 4) Recovery Phase
- GFR slowly returns to 'normal''
- Can take up to 1 yr
- *Not all pts follow this course*
- 1) Initiation phase
- Kidney Trauma
- Signs & Manifestations
- Oliguria
- Haematuria
- Flank/abdo pain
- Localised swelling/bruising/subcut bleeding
- Marked GFR decrease
- PT may exhibit signs of shock
- Due to external blunt force trauma (beating/stabbing/fall etc)
- Signs & Manifestations
- Pre-renal AKI
Kidney Function
- Regulatory
- Removes metabolic waste
- Excretory
- Reabsorption
- Substances prev. filtered are partially reabsorbed back into circulation
- Substances prev. filtered are partially reabsorbed back into circulation
- Secretion
- Substances are secreted from circulation into filtrate
- Substances are secreted from circulation into filtrate
- Reabsorption
- Hormonal
- R-A-A-S
- Decrease in BP detected by baroreceptors in Juxtoglomerular apparatus
- Renin is released
- Renin meets Angiotensinogen (created by the liver) in the blood
- This creates Angiotensin I
- Angiotensin I floats around until it reaches the lungs and meets Angiotensin Converting Enzyme (ACE)
- ACE turns it into Angiotensin II
- Angiotensin II travels back to the kidney
- Causes a release in Aldosterone from the adrenals
- Aldosterone causes:
- Reabsorption of Na+ and H2O into circulation
- Reabsorption of Na+ and H2O into circulation
- Aldosterone causes:
- Angiotensin II causes:
- Vasoconstriction: ^ BP
- Pituitary releases ADH in response, inc. circ. vol
- Vasoconstriction: ^ BP
- Causes a release in Aldosterone from the adrenals
- Angiotensin II travels back to the kidney
- ACE turns it into Angiotensin II
- Angiotensin I floats around until it reaches the lungs and meets Angiotensin Converting Enzyme (ACE)
- This creates Angiotensin I
- Renin meets Angiotensinogen (created by the liver) in the blood
- Renin is released
- Collectively leads to ^ BP
- Decrease in BP detected by baroreceptors in Juxtoglomerular apparatus
- Erythropoetin
- Activation of Vit D
- R-A-A-S
- GFR - the amount of blood filtered through the glomerulus in 1 min.
- Normal Lab Vals.
- pH of urine
- 4.5 - 8
- Serum Urea
- 3 - 8.3 mmol/L
- Serum creatinine
- 44- 133 micromol/L
- Serum K
- 3.3 - 5 mmol/L
- Serum Na
- 135 - 145 mmol/L
- pH of urine
- Regulatory
Renal Tumours
- Primary
- Mostly from renal cells
- Secondary
- Mets from lung, breast melanoma, lymphoma
- Prolonged haemodialysis is risk factor
- Primary
Medications
- Diuretics
- Loop
- Frusemide, ethacrynic acid
- Thiazides
- Hydrochlorothiazide
- Potassium Sparing
- Spironolactone
- Osmotic
- Mannitol (IV)
- Carbonic Anhydrase Inhibitor
- Acetazalomide
- Inhibits reabsorption of bicarbonates from renal tubules
- Loop
- Electrolytes
- K
- Ca
- Na
- Anti-diuretics
- Diuretics
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- Mind Map on Renal Conditions, created by Em J on 13/11/2018.
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- Em J
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