Renal 2 Flashcards
(29 cards)
Compare and contrast AKI and CKD in terms of:
a) GFR
b) Reversibility
c) Targets of treatment
a) AKI abrupt decline, CKD longstanding decline
b) AKI reversible, CKD irreversible
c) AKI treatment targeted to precise cause of AKI, CKD treatment targeted to prevention of complications of CKD
Define AKI
Rapid reduction in kidney function, leading to inability to maintain electrolyte, acid-base and fluid homeostasis
Raised creatinine, decreased urine output
3 types of AKI
Pre-renal
Post-renal
Intrinsic renal
What is the hallmark of pre-renal AKI?
Reduced renal perfusion pressure (w/o structural abnormalities)
5 causes of pre-renal AKI
True volume depletion e.g. haemorrhage
Hypotension
Oedematous state
Selective renal ischaemia e.g. renal artery stenosis
DRUGS e.g. ACEi, ARBs, NSAIDS, diuretics, calcineurin inhibitors
What is a key difference between AKI and acute tubular necrosis?
No structural renal damage in AKI, but prolonged AKI –> ATN –> renal damage
How does the response to restoration of normal circulating volume differ in AKI and ATN?
AKI resolves with restoration of normal circulating volume, ATN doesn’t
What key finding would you see on urine microscopy in ATN?
Epithelial cell casts
Describe the normal renal response to reduced circulating volume
Low pressure detected by baroreceptors RAAS activated Vasopressin release SNS activated Vasoconstriction, increased cardiac output, renal Na retention
Name and explain the two mechanisms by which renal blood flow remains constant despite varying pressure
Myogenic Stretch – if the afferent arteriole gets stretched due to high pressure, it will constrict to reduce the transmission of that high pressure into the Bowman’s capsule, thereby keeping the GFR steady
Tubuloglomerular Feedback – high chloride concentration in the early distal tubule (sign of high GFR) stimulates constriction of the afferent arteriole which lowers GFR and reduced chloride level in the distal tubule
Causes of post-renal AKI
Ureteric obstruction (bilateral)
Prostatic / urethral obstruction
Blocked urinary catheter
Retroperitoneal fibrosis / Ormond’s disease
Pathophysiology of post-renal AKI
GFR is dependent on the hydraulic pressure gradient
Obstruction results in increased tubular pressure
This results in an immediate decline in GFR
3 mechanisms of renal injury that cause intrinsic renal AKI (with examples)
Direct Tubular Injury (Common) – ischaemia or toxins:
- Most commonly ischaemic
- Endogenous toxins –> myoglobin (i.e. rhabdomyolysis from muscle injury), immunoglobulins
- Exogenous toxins –> contrast medium > aminoglycosides, amphotericin, aciclovir
Immune dysfunction causing renal inflammation (Common)
- Glomerulonephritis
- Vasculitis (i.e. 40yo presenting with systemic purpura and AKI diagnosis)
Infiltration/Abnormal Protein Deposition
- Amyloidosis (causes nephrotic syndrome)
- Lymphoma
- Multiple Myeloma
Most common intrinsic renal cause of AKI?
Acute tubular necrosis
Why do some AKIs resolve and others don’t?
Pathological responses are characterised by an imbalance between scarring and remodelling
Replacement of renal tissue by scar tissue results in chronic disease
Causes of CKD
DIABETES HYPERTENSION Chronic Glomerulonephritis Infective or obstructive uropathy Polycystic kidney disease
Give some homeostatic, hormonal and cardiovascular consequences of CKD
Progressive failure of homeostatic function
- Acidosis
- Hyperkalaemia
Progressive failure of hormonal function
- Anaemia
- Renal bone disease
Cardiovascular disease
- Vascular calcification (renal osteodystrophy)
- Uraemic cardiomyopathy
Uraemia and death
Describe the consequences of renal acidosis in CKD
Treatment?
Metabolic acidosis (failure of renal excretion of protons) leads to:
- Muscle and protein degradation
- Osteopaenia due to mobilisation of bone calcium (because protons can be stored in bone)
- Cardiac dysfunction
TREATMENT: oral sodium bicarbonate
Describe the consequences of hyperkalaemia in CKD
Cardiac arrhythmias
Muscle weakness
What sort of anaemia do you get in CKD and how?
Normochromic, normocytic anaemia
Because get loss of EPO-producing cells as GFR declines
How do you treat anaemia of CKD?
Artificial erythropoiesis-stimulating agents (ESAs) e.g.
Erythropoietin alfa (Eprex) Erythropoietin beta (NeoRecormon) Darbopoietin (Aranesp)
4 types of renal bone disease in CKD
Osteitis fibrosa cystica
Osteomalacia
Adynamic bone disease
Renal osteodystrophy
Pathophysiology of renal osteodystrophy
Unable to: excrete phosphate from kidneys / make vitamin D
FGF-23/klotho produced –> lower vitamin D –> 2nd HPT
Excess phosphate –> complexes with Ca2+ –> hypocalcaemia
Phosphate-calcium crystals deposit –> renal osteodystrophy
Pathophysiology of osteitis fibrosa cystica
Caused by osteoclastic resorption of calcified bone and replacement by fibrous tissue
This is a feature of hyperparathyroidism
