Renal injury and disease Flashcards
Where are glomeruli located?
Cortex
Where do you take a biopsy from?
Cortex only
Why is the proximal tubule much pinker?
Full of mitochondria - 90% of solute reabsorbed here
Kidney function
- Formation of urine
- Control of water balance
- Control of electrolytes
- Drug metabolism
- Drug excretion
- Hormone synthesis
- Calcium/phosphate regulation
- Acid-base regulation
- BP control
Which membrane surrounds arteriole?
Glomerular
Function of Bowman’s space
Collects urine before concentration in tubules
Function of JGA
Recognises drop in perfusion/BP to release renin
Function of angiotensin ii
Vasoconstriction of efferent arteriole
GFR
- Filtration happens in glomerulus
- Driven by hydrostatic pressure of blood
- RBCs and large molecules don’t pass through filter
- To assess, look at urine output and serum creatinine - state creatinine is inversely proportional to GFR
CKD
- Chronic kidney disease: long time, irreversible, often due to injury etc or due to diabetes/hypertension
- CKD: damage over 3 months with decreased GFR, pathological abnormalities or markers of kidney damage, 2 blood tests
Acute kidney disease
Deterioration of kidney function over long period
Acute on chronic kidney disease
Acute injury with background of CKD
Stage 1 GFR
90+, normal kidney function but urine abnormalities - annual observation of BP
Stage 2 GFR
60-89, mildly reduced kidney function, BP, monitoring, find out why
Stage 3 GFR
30-59, moderately reduced function, probable diagnosis made
Stage 4 GFR
15-29, severely reduced kidney function, management of complications, plan for renal failure
Stage 5 GFR
<15, very severe/end stage, renal replacement therapy needed
Acute kidney disease
- Acute decline of function with risk of clinically significant toxicity which is potentially reversible and potentially requires RRT
- Very common in hospitals
- RIFLE: risk, injury, failure, loss, ESRD
- Impacts: inflammatory response - activated leukocytes and ischemic kidney
Causes of acute kidney disease
Pre-renal (diabetes, hypertension etc), intra-renal (ATN, glomerular, vascular, nephritis), post-renal
Class I AKI
Increase of serum creatinine by 1.5-2x baseline
Low urine output (<0.5ml/hr)
Class II AKI
Increase serum creatinine by 2-3x baseline
Class III AKI
Increase of serum creating by 3x baseline
AKI consequences on heart
- Potassium increase because of no excretion
- Look at heart
- Hyperkalaemia: high t-waves, wide QRS complexes, bradycardia
- Hypokalaemia: tachyarrythmias
Hyperkalaemia
- Assess: is pt passing urine (yes = medical therapy, no = dialysis)
- How high is potassium? 5.5-6.5 (no risk of cardiac arrest), 6.5-7.5 (moderate risk, treatment needed), >7.5 (high risk, impending cardiac arrest
- Antagonise K+ effect (IV calcium)
- Shift K+ into cells (beta-antagonist e.g. salbutamol, insulin, acidosis with sodium bicarbonate)
- Remove potassium from body - diet, drugs, dialysis
