pathophysiology of Acute Kidney Disease Flashcards
Why do patients get AKI
- Sepsis
- Hypotension
What are the parameters used in NEWS readings?
- Respiration rate
- O2 saturation
- Systolic BP
- Pulse rate
- Level of consciousness
- Temperature
How can AKI be prevented?
- Recognise those at risk for AKI
- Review medication and stop any ‘bad’ drugs
- ensure adequate hydration
How is renal function measured?
- Urine volume per given time
- Serum Creatinine
- Glomerular filtration rate
What sample would be taken to look at GFR and serum creatinine?
U&E blood sample
GFR derived from serum creatinine
What is the relationship between serum creatinine and GFR?
- Very low levels of Serum creatine will have low GFR
- However GFR needs to very low to see significant changes in serum creatinine (non-linear relationship)
What factors are used to estimate eGFR?
- Age
- Gender
- Ethnicity
- Serum Creatinine
What are the normal GFR fro young/older adults?
younger normal = 100 mL/min
Older normal = Below 100 mL/min
What are the markers used to measure GFR?
- Creatinine
- Cystatin C
Special circumstances: - Inulin or lohexol clearance
- Radio-isotope clearance
What is AKI?
decrease in GFR which occurs within hours to weeks and is potentially reversible
How is AKI recognised?
- Deteriorating NEWS score
- Rising serum creatinine
- Falling urine output
How are AKIs managed/prevented?
Address medication Boost BP Calculate fluid balance Dip urine Exclude obstruction Fast-track to senior
What does normal kidney function depend on?
- Perfusion of kidney with adequate pressure and O2
- Intact nephrons
- Free urinary drainage
What is pre-renal AKI?
disordered perfusion of a kidney which is structurally normal
What is renal AKI?
Damage to nephrons often after prolonged pre-renal insults
What is post-renal AKI?
urinary drainage obstruction
What is the cause of pre-renal AKI?
Shock which is caused by:
- Distributive (generalised vasodilation and decrease in peripheral resistance often caused by sepsis)
- Hypovolaemic (loss circulating BV caused by internal or external losses)
- Cariogenic (pump failure caused by MI, arrhythmias, valvular HF or cardiomyopathy
- Obstructive (mechanical interference with BF caused by pulmonary embolism, cardiac tamponade or tension pneumothorax)
How does a low GFR lead to increase in Ang II?
- less glomerular filtrate entering tubules
- less solute going through tubular lumen is sensed by macula densa cells
- macula densa tell JGA to release renin
- Renin increase Ang II release
What is the benefit of increase in Ang II when a low GFR is sensed?
- Ang II potent vasoconstrictor of efferent arteriole
afferent arteriole will - vasodilator as a result of prostaglandins
- These in combination will increase glomeruli capillary pressure toward normal
What other hormone will be released as a result of renin and angiotensin II?
- Aldosterone
which acts on collecting duct to increase reabsorption of sodium and chloride and water to restore BV
What would the urine of a patient with pre-renal AKI show?
- Increased tubular Na/H2O
- Increased osmolarity
- Increased urine specific gravity
- Decreased urine
- Reduced fractional excretion
How is pre-renal kidney injury treated?
- kidney function can be restored if respond rapidly as kidney still functionally intact
- will respond well to fluids to improve BP
- if not treated can then get renal AKI
What is the pathology of renal AKI?
- ischaemic/hypoxic renal injury impairs tubular sodium reabsorption
- kidney structure very sensitive to hypoxia
- function of kidney therefore compromised
- sodium and water will not be reabsorbed and so get high levels in urine
What will histology of renal AKI show?
- lumen can’t be distinguished
- filled with cellular debris
What are major causes of acute tubular necrosis?
- Renal ischaemia followed by reperfusion (usually caused by pre-renal AKI)
- Exposure to nephrotoxins e.g. Drugs, radio contrast dyes or heme pigments released in muscle injury
What are the features of renal AKI?
- Reduced tubular Na/H20 reabsorption
- Reduced urine osmolarity
- reduced S.G
- Increased urine sodium concentration
- Increased fractional excretion sodium
- reduced tubular potassium and increased serum potassium
- reduced H+ secretion and reduced HCO3- production causing metabolic acidosis
Why should you not give fluids to patients with renal AKI?
- don’t overload with infused fluid as will cause pulmonary oedema and hypoxia
- kidneys won’t respond to fluid challenge
Causes of Post-Renal AKI?
Obstruction:
- within lumen e.g. renal calculi
- within wall e.g. benign prostatic hyperplasia
- outside wall e.g. tumour invading ureters
How should post-renal AKIs be treated?
- exclude/relieve obstruction (rule out urinary retention and if catheter present check functioning)
- Obstruction may still be present above the level of bladder output
- treat underlying cause of obstruction
- prevent or treat any infections
What scan can be used to check for a post-renal AKI?
ultrasound
What other form of AKI is possible (not post, renal or pre)
- AKI in patients with CKD
What can kill patients with AKI?
- Pulmonary oedema and respiratory failure
- Hyperkalaemia causing arrhythmias due to loss of capacity of kidneys to excrete potassium (seen on ECG)
- Acidosis caused by no H+ excretion
What should be done if kidney do fail?
- balance fluid carefully, monitor intake and urine output
- avoid unnecessary drugs
- treat hyperkalemia
- seek senior help
What AKI type is dialysis used for?
Put onto dialysis until renal function improves
What investigations should be done for someone with AKI?
- urine dipstick
- U&E
- ABG
- ECG
- CXR
- Ultrasound
What should be asked in the history of AKI?
- prior CKD
- Fluid losses
- Thirst
- Nephrotoxins
What should be examined in patients with AKI?
- Pulse
- BP
- O2 sats
- urine output
