Acute and Chronic renal Failure 1 Flashcards
What is an AKI?
A potentially reversible abrupt decline in GFR with treatment targeted at diagnosis and reversal of disease.
What is CKD?
An irreversible longstanding decline in GFR with treatment aimed at prevention of complications and progression. (>3 months)
What is acute failure of kidneys?
A rapid reduction in kidney function, leading to an inability to maintain electrolyte, acid-base and fluid homeostasis.
Is an AKI an emergency?
Yes- immediate referral for management in nephrology
What are the stages of an AKI?
AKI Stage 1: Increase in sCr by ≥26 µmol/L, or by 1.5 to 1.9x the reference sCr
AKI Stage 2: Increase in sCr by 2.0 to 2.9x the reference sCr
AKI Stage 3: Increase in sCr by ≥3x the reference sCr, or increase by ≥354 µmol/L
What are the types of AKI?
Pre renal
Renal
Post Renal
What is a pre renal AKI?
Reduced tissue perfusion/ local ischaemia
NO structural abnormality
What is a normal response to reduced circulating volume?
Activation of central baroceptors activates RAS and there is a release of vasopressin and sympathetic system which causes vasoconstriction, increased cardiac output and renal sodium retention.
What are the causes of pre renal AKI?
True volume depletion Hypotension Oedematous states Selective renal ischaemia Drugs affecting glomerular blood flow
Renal artery stenosis
Which class of drugs may commonly predispose patients to developing pre-renal AKI?
ACEi
How do these drugs cuase pre renal AKI: NSAIDS ACEi/ARBs Calcineurin inhibitors Diuretics
NSAIDs - decrease afferent arteriolar dilatation
Calcineurin inhibitors - decrease afferent arteriolar dilatation
ACEi or ARBs - decrease efferent arteriolar constriction
Diuretics – affect tubular function, decrease preload
How can AKI lead to ATN?
Pre-Renal AKI is not associated with structural renal damage and responds immediately to restoration of circulating volume
Prolonged insult leads to ischaemic injury
Acute Tubular Necrosis does not respond to restoration of circulating volume
What is the hallmark of post renal AKI?
Physical obstruction to urine flow.
What may cause post renal AKI?
(Intra-renal obstruction) Ureteric obstruction (bilateral) Prostatic / Urethral obstruction Blocked urinary catheter
What is the pathophysiology of obstructive uropathy?
GFR is dependent on hydraulic pressure gradient
Obstruction results in increased tubular pressure
Immediate decline in GFR
How do you recover from obstructive uropathy?
Immediate relief of obstruction restores GFR fully, with no structural damage
What can prolonged obstruction cause?
Glomerular ischaemia
Tubular damage
Long term interstitial scarring
What is are the types of intrinsic AKI?
Vascular Disease e.g. vasculitis
Glomerular Disease e.g. glomerulonephritis
Tubular Disease e.g. ATN
Interstitial Disease e.g. analgesic nephropathy
How does direct tubular injury occur?
Ischaemia Endogenous toxins (Myoglobin, Igs) Exogenous toxins (Aminoglycosides, amphotericin, acyclovir)
Patient has new onset AKI, haematuria and massive bruising. What is the likely diagnosis?
Rhabdomyolysis (Myoglobin is toxic)
A 40 year old female presents with a papular coalescing rash and AKI is diagnosed. What is the most likely cause of her renal failure from the following list?
Systemic Vasculitis
What are common mechanisms of renal injury?
- Immune dysfunction (Renal inflammation):
a. Glomerulonephritis
b. Vasculitis - Infiltration/ abnormal protein deposition:
a. Amyloidosis
b. Lymphoma
c. Myeloma-related renal disease
What are the important causes?
Pre-renal
ATN
What are the non fatal outcomes of AKI?
Complete or partial recovery of renal function
Discharged with increasing creatinine
Discharged with a requirement for dialysis
How do acute wounds heal?
Haemostasis
Inflammation
Proliferation
Remodeling
What pathology stops renal resolution after an AKI?
Imbalance of scarring and remodelling
Replacement of renal tissue by scar tissue in chronic disease
What is the process of getting CKD?
Increased Risk
Early Damage
Reduced GFR
Renal Failure
Death
What are the stages of CKD?
1, Kidney damage with normal GFR, >90, 3.3 %
2, Mild GFR, 60-89, 3 %
3, Moderate GFR, 30-59, 4.3 %
4, Severe GFR, 15-29, 0.2 %
5, End-stage kidney failure, GFR <15 or dialysis, 0.2 %
What are the causes of CKD?
Diabetes Atherosclerotic renal disease Hypertension Chronic Glomerulonephritis Infective or obstructive uropathy Polycystic kidney disease
What are the functions of the kidney?
Excretion of water-soluble waste
Water balance
Electrolyte balance
Acid-base homeostasis
Endocrine functions (EPO, RAS, Vit D)
What are the consequences of CKD?
Progressive loss of homeostatic function (acidosis and hyperkalaemia)
Progressive failure of hormonal function (Anaemia, renal bone disease)
Cardiovascular disease (vascular calcification, uraemic cardiomyopathy)
Uraemia and death
What does renal acidosis cause?
Muscle and protein degradation
Osteopenia due to mobilization of bone calcium
Cardiac dysfunction
What is the treatment of renal acidosis?
NaHCO3, PO
What is potassium used for?
Major intracellular cation
Membrane depolarisation
Cardiac function
Muscle function
What medications can cause hyperkalaemia?
ACEi
Spirinolactone
Potassium sparing diuretics
What is anaemia of chronic renal disease?
Normochromic, normocytic anaemia
Usually noted when GFR<30mL/min
(Loss of EPO cells)
What are the ESAs (Erythropoiesis- stimulating agents)?
Erythropoietin alfa (Eprex) Erythropoietin beta (NeoRecormon) Darbopoietin (Aranesp)
Your patient with CKD has been started on an ESA but does not respond. What could be the cause?
TB Malignancy (Chronic Disease) B12/ Folate/ IDA Hyper-parathyroidism
What are the renal bone diseases?
Osteitis fibrosa
Osteomalacia
Adynamic bone disease
Mixed osteodystrophy
What is osteitis fibrosa?
Osteoclastic resorption of calcified bone and replacement by fibrous tissue
Comes with hyperparathyroidism
What is osteomalacia?
Insufficient mineralisation of bone osteoid
What is adynamic bone disease?
Excessive suppression of PTH results in low turnover and reduced osteoid
What is the treatment of renal bone disease?
Phosphate control: dietary, phosphate binders
Vit D receptor activators: 1-alpha calcidol, paricalcitol
Direct PTH suppression: Cinacalcet
What is associated with atherosclerosis?
Cholesterol
Hypertension
What are the 3 phases of uraemic cardiomyopathy?
Left ventricle (LV) hypertrophy
LV dilatation
LV dysfunction
What are relative contraindications to renal transplant?
Conditions: Untreated coronary artery disease, HIV, Chronic Hep B/C
Age >65 years
Previous Malignancy
Obesity/ Co morbidity
What are absolute contraindications to renal transplant?
Untreated malignancy
Active infection
Untreated HIV infection or AIDS
any condition where life expectancy is under two years.
What two measures do we use to define acute kidney injury?
Creatinine and Urine output
How is AKI defined using creatinine and urine output?
Stage 1:
1.5–1.9 times baseline OR ⩾0.3 mg/dl (⩾26.5 μmol/l) increase
UO = <0.5 ml/kg/h for 6–12 hours
Stage 2:
2.0–2.9 times baseline
UO = <0.5 ml/kg/h for ⩾12 hours
Stage 3:
3.0 times baseline OR Increase in serum creatinine to ⩾4.0 mg/dl (⩾353.6 μmol/l)*
UO = <0.3 ml/kg/h for ⩾24 hours OR Anuria for ⩾12 hours
*OR Initiation of renal replacement therapy OR, In patients <18 years, decrease in eGFR to <35 ml/min per 1.73 m2
What measures aid prognosis in CKD?
eGFR
ACR (Albumin-Creatinine Ration) in the urine
What foods can cause hyperkalaemia in CKD?
Tomatoes
Chocolate
Dried fruits
DIET RESTRICTION IS IMPORTANT
