Renal Flashcards
(101 cards)
Is eGFR or CrCl used for staging renal function?
eGFR
What are the stages of renal impairment?
Stage 1 (Normal GFR): >90 ml/min/1.73m2
Stage 2 (Mild impairment): 60-89
Stage 3A ( Mild to moderate): 45-59
Stage 3B (Moderate to severe): 30-44
Stage 4 (Severe): 15-29
Stage 5 (established/end stage): <15
What is ureamia?
A build up of nitrogenous breakdown products of protein metabolism.
urea >15 mmol/L = ureamia
Can cause key symptoms in CKD patients e.g. N+V, pruritus
Why is uraemia never used in isolation for a renal diagnosis?
Because urea can also be raised in:
Dehydration
Muscle injury
infection
haemorrhage
excess protein intake
What is ACR?
Albumin:Creatinine ratio
Albumin is a protein found in blood, that should not be present in urine.
What ACR values should consider use of an ACE inhibitor?
> 70 mg/mmol in non diabetics
2.5 in male diabetics and >3.5 in female diabetics
As this indicates an increased risk of renal disease
What are the qualities of ideal drugs in renal impairment?
Wide therapeutic index
eliminated via the liver
not nephrotoxic- may be required for co-morbidities though
Not affected by changes in fluid balance, tissue or protein binding
What are the 3 types of AKI?
Pre-renal
Intrinsic
Post-renal
What is pre-renal AKI and what are possible causes?
Impairment that happens before the kidney e.g. lack of blood supply to the kidney or decreased renal perfusion.
Causes:
- Hypovalemia (low blood volumes) e.g. in dehydration, haemorrhage, burns
- Decreased cardiac output e.g. HF, MI
- Infection
- Liver disease- decreased blood flow through the liver causes decrease in blood supply to the kidneys
- Medications e.g. ACEi, NSAIDs, Ciclosporin, Tacrolimus, Diuretics, Laxative abuse
How is pressure in the glomerular capillaries maintained?
Blood comes from the afferent arteriole into the glomerular capillaries and then leaves via the efferent arteriole.
- Prostaglandins dilate the afferent arteriole = increased blood supply to glomerular caps
- Angiotensin II - constricts the efferent arteriole = Decreased blood out
= Together this increases hydrostatic pressure and increases filtration rate and GFR
What is the effect of taking NSAIDs or ACE/ARBs on the glomerular capillaries and filtration rate/GFR?
- NSAIDs: Inhibit prostaglandins - constriction of afferent arteriole. This causes decreased renal perfusion as less blood reaches the kidney
- ARBS/ACE: Inhibit the renin-angiotensin system = decreases angiotensin II so causes dilation of the efferent arteriole. This decreases the hydrostatic pressure as blood finds it easier to get out of the capillaries.
= decrease HP and GFR
Are ACE inhibitors preferable in AKI and DM?
They are preferable in DM as they have a long-term benefit
However, in an AKI don’t want as they decrease the filtration rate and so worsen the condition short-term
What is intrinsic renal failure and its causes?
This is damage to renal tissue itself.
E.g.
- Glomerular damage- DM, glomerulonephritis
- Tubular- interstitial nephritis, tubular necrosis
- Renovascular e.g. HT
- infection
- nephrotoxicity- NSAIDs (can cause pre-renal and intrinsic failure)- cause vasoconstriction of afferent arteriole = decreased hydrostatic pressure = decreased filtration rate
Which drugs can cause directly toxic reactions (nephrotoxicity) and hypersensitivity reactions?
Directly toxic (more predictable):
Aminoglycosides- vancomycin, gentamicin
Amphoterecin
Ciclosporin
Hypersensitivity ( unpredictable)
phenytoin
penicillins
Cephalosporins
Allopurinol
Azathioprine
What is post-renal failure and some causes?
Problems that occur after the kidney- obstruction to urinary flow causing back pressure into the kidney leading to damage.
e.g.
- Kidney stones- block ureter
- Structural problems e.g. tumours strictures
- Nephrotoxicity by drugs e.g. Cytotoxic drugs, sulphonamides- cause depolarisation or rate crystals in urinary tract= block
- Pressure on urinary tract e.g. enlarged prostate, BPH, ovarian tumour
What types of renal failure can NSAIDs or infection cause?
Pre-renal OR intrinsic RF
(most commonly pre)
Can AKIs be reversed?
Yes
What is an AKI?
Rapid deterioration in renal function that if not treated and lead to organ failure and death.
What are the diagnosis criteria for AKI?
CREATININE:
- increased by >26.5 micromol/L within 48 hours OR
- Increased by > 1.5 fold from their baseline value
- urine output is <0.5ml/kg/hr for 6 hours
What are the stages of AKI?
Based on deviation from baseline creatinine:
STAGE 1: 1.5-1.9 x baseline creatinine
STAGE 2: 2-2.9 x baseline creatinine
STAGE 3: 3.0 + x baseline creatinine
What are the risk factors for AKI?
Diabetes
CKD
Previous AKI
Hepatic disease- decreased blood flow to kidney
Congestive cardiac failure (CCF) or Peripheral vascular disease (PVD)
>65 years old
What are the possible causes of AKI?
Most commonly pre-renal (decreases perfusion due to decreased blood volume or hypovalemic state).
e.g.
Hypotension
infection
dehydration
sepsis
medications- NSAIDs, ACEis/ARBs, Diuretics
Signs and symptoms of AKI?
Volume depletion:
Thirst
Loss of fluid
Clinically dry- dry mucosae
decreased skin elasticity
tachycardia
hypotension
decreased jugular venous pressure
IF untreated, volume depletion can tip into overload- kidney has failed so can’t remove fluid
Volume overload:
Orthopnoea- SOB on lying down
Oedema (swelling of ankles)
pulmonary oedema- crackles in lungs
What is the process of treating AKI?
- Identity cause
- Medical history:
Review and hold meds that can exacerbate AKIs e.g. ACEi, diuretics, NSAIDs
Adjust doses to prevent harm- if renal excreted and so can accumulate e.g. DOACs, Metformin
Remember to restart once AKI has resolved
IF DEHYDRATED: Early and aggressive fluid resuscitation to mimic fluid loss:
- if haemorrhage, give blood
- if fluid loss, give NaCl
- Monitor fluid input and ouput
- 1/3 of patients have dialysis to maintain renal function while treating underlying cause
IF FLUID OVERLOADED:
- Give loop diuretics e.g. Furosemide 1-2g IV over 24 hours. MAX RATE of 4mg/minute due to risk of ototoxicity.
Diuresis (use of diuretics)- increases renal blood flow to remove build of fluid
- Dopamine ( not commonly used, mainly in ITU)- causes renal vasodilation via DA1 receptor to increase renal perfusion and urine output. This only occurs at low doses e.g. 2mcg/kg/min, in high doses >5mcg/kg/min it has the opposite effect = vasoconstriction
OTHER TREATMENTS:
- Antibiotics if caused by an infection
- Electrolyte correction e.g. Hyperkalemia:
>6.5 mmol/L potassium= muscle weakness, ventricular fibrillation, cardiac arrest
if >6, want to treat urgently:
- Calcium glutinate IV- 30mL 10%- Ants
Antagonises K+ at cardiomyocyte membranes- protects heart from arrythmias
- Rapid-acting insulin (with glucose to prevent hypoglycaemia) over 15 mins to stimulate sodium potassium transporters to drive k+ uptake into cells.
- Nebulised salbutamol (rarely used)