Renal Flashcards
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)
What are the benefits/disadvantages of ACE inhibitors/ARBs long and short term in AKI?
ACE/ARBs: Prevent angiotensin-II mediated vasoconstriction of the efferent arteriole = vasodilation = decreased hydrostatic pressure and glomerular filtration rate.
Long-term this is protective- prevents sustained vasoconstriciton and stenosis of the efferent arteriole and loss of nephron function = good
BUT, in AKI states, reduction of hydrostatic pressure worsens AKI as we want to preserve filtration rate = HOLD ACE/ARB IN AKI and restart when treated to preserve ongoing function long-term
What is the max rate of furosemide delivery in AKI?
4mg/min due to risk of ototoxicity (hearing or balance problems)
How do you treat hyperkaleima in AKI?
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)
What is CKD?
Chronic kidney disease- worsening, progressive, irreversible loss of kidney function
What are the diagnosis criteria for CKD?
Patients with abnormalities for more than 3 months:
- eGFR less than 60mL/minute/1.73m2 on at least 2 occasions 90 days apart
- or with markers of kidney damage e.g. albuminuria, haematuria, kidney transplant
What are possible causes of CKD?
- AKI- if irreversible intrinsic damage
- Hypertension- vessel thickening and narrowing leads to decreased blood flow
- Diabetic nephropathy- fibrosis, membrane thickening
- Glomerulopathies
- vasculitis
- polycystic kidney disease
ALL lead to kidney sclerosis (hardening of tissue) = Blood flow is diverted to nephrons that still work causing hyperfiltration in these nephrons. this is good short term but increased pressure ling-term will lead to sclerosis in these nephrons too and loss of the nephron.
What are the possible complication of CKD?
- Water and electrolyte imbalance- hyperkalemia, acidosis
- uraemia
- renal bone disease
- renal anemia
How do you regulate water imbalance as a complication of CKD?
Fluid restriction “Turn off tap”:
- Restrict fluid intake per day to prevent water build up:
If not on dialysis and still passing urine + minimum of 1 L per day
- on dialysis will decrease to around 500mL per day
- Also sodium restriction via dietary measures
- Patients must measure their weight and BP daily at home- have a target dry weight
IF this is insufficient:
“Take plug out”- prescribe diuretics:
- first line is loop diuretics e.g. Furosemide up to 2g/day
- can use bumetanide- better absorbed patient has a lot of fluid accumulated in the abdomen
- Can use Metolazone (Thiazide-like diuretic)- very potent so needs close monitoring
Usually, diuretics are stopped when patient starts dialysis
How do you regulate Potassium electrolytes to manage this complication of CKD?
Target potassium = 4-6mmol/L pre-dialysis:
- Prescribe potassium binder- Calcium resonium- binds to K+ in GI tract and removed it from the body. But, does release calcium ions in exchange which can cause constipation so co-prescribe lactulose
- Sodium Zirconium cyclosilicate- now approved by NICE for high K+ in some circumstances to allow patients o remain on ACE/ARBs for longer and at a higher dose (K+ In blood is increased as a s/e of ACE/ARB) and to increase adherence.
How do you regulate bicarbonate electrolytes to manage this complication of CKD?
Acidosis = decreased bicarbonate ions in blood
- Sodium bicarbonate PO 500mg TDS
What us uraemia?
Decrease in waste product excretion and so they build up in the blood.
This can cause pruritus, Anorexia, n+v, foul metallic taste
What drug can be used to manage pruritus as a result of harm-dialysis?
Difelikefalin- 0.5mcg/kg 3-4 times a week
What are the muscle dysfunction symptoms that can be caused by CKD and their treatments?
Cramps, restlessness especially at night or when on dialysis
Treatment:
- lifestyle measures- no caffeine or alcohol before bed, better sleep hygiene
- check iron levels
- Quinine (cramps)- 300mg ON
- Ropinorole (restlessness)- 250mcg ON
What causes hypertension in CKD?
Increased sodium and water retention causes an increase in circulatory volume, leading to artery stenosis and HTN and increased rate of renal function decline.
What is the target BP of a patient with low proteinuria (ACR<70 or PCR <100)?
<140/90 mm/Hg
What ACR values are indicative in imitation of an ARB/ACEi?
If patient has CKD with HTN and ACR >30mg/mmol
OR
is diabetic and ACR >3 mg/mmol
START ACE OR ARB
ALSO, of patient doesn’t have diabetes or HTN but has an ACR 70mg/mmol+
