Renal and urinary tract Flashcards
What is the single most important factor to address to avoid future cardiovascular disease?
Blood pressure
Cholesterol, smoking, weight loss and diabetes are important, but not as statistically significant as BP
How do ACE-I and ARBs reduce proteinuria and albuminuria?
The reason that these proteins are getting through the glomerular threshold is because the glomerular pressure is too high.
ACE-I prevent the conversion of angiotensin 1 to angiotensin 2
ARBs prevent binding of angiotensin 2 to the angiotensin receptor
The angiotensin receptor acts on the efferent arteriole to constrict it, therefore ACE-I and ARBs prevent the increased glomerular hydrostatic pressure. This relieves the damage being done to the nephrons in CKD, slowing the progression.
How many people suffer from dry cough in ACE-I use?
Approximately 10%
Why must ACE-I and ARBs be stopped if AKI is suspected?
AKI is often due to pre-renal causes e.g. dehydration.
The kidney will be underperfused and so will use RAAS to increase perfusion, ACE-I/ARBs block this system and thereby block homeostasis.
This will exacerbate damage to the kidney.
Funny really: use ACE-I/ARBs in chronic but never acute kidney disease
WhY should serum creatinine be checked if a patient is put on ACE-I or ARBs?
Simply: These drugs have a potentially narrow therapeutic window if the patient has underlying cormorbidities
- Immediately after initiation - to check for rises of creatinine above 30% (increase of 25-30% is normal initially)
- Whenever the dose is changed
A small rise in serum creatinine is expected since we reduce glomerular perfusion pressure and therefore reduce creatinine excreted.
If serum creatinine significantly rises there may be renovascular disease or renal artery stenosis, since the drugs are reducing glomerular perfusion pressure too low - indicating further damage to the kidney
What warnings should you give a patient who is female and of child-bearing age when initiating ACE-I/ARBs?
In short: ACE-I/ARBs are contraindicated in the all trimesters of pregnancy.
Stop all ACE-I/ARBs within two days of positive pregnancy test.
They increase risk of congenital malformations: fetopathy, via inhibition of foetal renal function, and resultant anuria causing kidney malformations. (Not teratogenic)
Also cause: malformation of the cardiovascular system and the CNS.
What should be monitored in patients taking ACE-I/ARBs?
Serum Potassium - risk of hyperkalemia since angiotensin causes NaCl reabsorption and K secretion
Serum Creatinine - large rise may indicate underlying renovascular disease
States of diarrhoea or vomiting - hypovolaemia combined with ACE-I/ARBs can cause AKI, therefore medication must be temporarily stopped in these situations
Checked:
- Before starting treatment
- One week after start
- Whenever dose is changed
In a patient with resistant hypertension and chronic kidney disease, which medication are we particularly worried about, besides ACE-I/ARBs?
Spironolactone - sometimes given for resisting hypertension.
MOA: Binds aldosterone-dependent sodium potassium exchange sites in the DCT and increases NaCl excretion while decreasing potassium secretion.
This has the potential to cause hyperkalemia, especially in combination with ACE-I, since they stop the production of renin, and reduce the conc of aldosterone too.
Why are NSAIDs considered dangerous to the kidney?
Prostanoids facilitate renin release.
NSAIDs prevent renin release by decreasing prostanoid production.
This means they reduce aldosterone production and can cause hyperkalemia.
Which medications should a pregnant woman be given for hypertension?
Labetolol
Methyldopa
Nifedipine
NOT ACE-I/ARBs or chlorthalidone!
Note: targets are higher for BP in pregnant women with chronic HTN (150/100)
What is the treatment for secondary hyperparathyroidism in CKD?
Calcitriol or alphacalcidol - vitamin D analogues
In secondary hyperparathyroidism there is an excess of PTH released in response to hypocalcaemia, this is caused by the kidney failing to produce enough 1,25-dihydroxyvitamin D, which normally causes GI calcium uptake and bone mineralisation, and osteoclast activity (ups the bone turnover)
This simply replaces the vitamin D
What is the treatment for renal anaemia in CKD?
Erythropoietin and IV iron
Aim for a target ferritin >200
What is the treatment for metabolic acidosis in CKD?
Oral alkali - most often sodium bicarbonate
What is the treatment for hyperkalemia in CKD?
This is caused iatrogenically.
The treatment is dietary potassium restriction and then reduction of ACE-I if still necessary.
What is the treatment for fluid overload in CKD?
Fluid restriction
Salt restriction
Diuretics
What are the nutritional aspects to management of CKD?
Adequate calorie intake (inc adequate protein intake!)
Salt restriction
Fluid management
Nutritional supplements
Weight management - independent risk factor
Lipid control - cardiovascular risk factor
What are the BP targets for patients with CKD?
<130/80 in all stages
<125/75 in proteinuric stages (urinary PCR >1g per day)
Why is gastroenteritis a danger in CKD?
CKD normally means treatment with ACE-I/ARBs, if the patient becomes hypovolaemic from vomiting or diarrhoea, they can develop AKI - this can damage their kidney further!
Must stop ACE-I/ARBs in hypovolaemia.
What are the essential preparations before renal replacement? (stage 4 CKD is when preparations begin)
Immunisation:
Pnueumococcal
Influenza
Hepatitis B
Discuss choice of dialysis: Conservative (If unsuitable or won’t benefit) PD HD Transplant Home CAPD Home APD Home HD
Patient will move between dialysis modes during their lifetime, it’s not a single one forever.
What is the nominal treatment for each stage of CKD?
Stage 1+2 = treat cause and reduce CVS risk:
Smoking, exercise, cholesterol, BP
Medication: ACE-I/ARB
Stage 3 = ensure nutrition, immunise, monitor for acidosis/anaemia, and give supplements:
Medications: EPO, Alphacalcidol, bicarbonate and diuretic
Stage 4 = same as stage 3 but immunise again and prepare for renal replacement therapy
Stage 5 = renal replacement therapy and plan end of life care (-Liverpool care pathway for the dying patient)
Which medications must we change in stage 4 CKD?
Stage 4 CKD = GFR <30:
Ramipril max dose is 5mg p/day
Metformin should be stopped entirely and replaced with something else.
What are the six indications for dialysis aside from low GFR?
In short: ACIDIC, HYPERKALEMIC, FLUID O/L, TOXINS, CREATININE, URAEMIC PERICARDITIS
- pH <7.25
- Potassium >7mmol
- Fluid overload
- Toxins: SLIME - salicylate, lithium, isopropopanolol, magnesium and ethylene glycol
- Creatinine >400
- Uraemic pericarditis
Low GFR isn’t an absolute indication for dialysis, since some people do better with later dialysis.
What is the management of patients with CKD who Rd approaching end stage renal failure?
- Patient has eGFR <15
2. Choose between: Conservative Care Transplant Peritoneal dialysis Haemodialysis NOTE CONTRAINDICATIONS FOR EACH TYPE
- Haemodialysis chosen: must create AV fistula early
- Transplant possible: needs transplant before ESRF occurs
- Peritoneal dialysis chosen: must insert Tenckhoff catheter
- Start dialysis when symptomatic
What are the absolute contraindications for peritoneal dialysis?
Active IBD Ischemic bowel Acute diverticulitis Abdominal abscess Pregnancy in the 3rd trimester
PD require you to learn a new skill and the ability to do this may be impaired by drugs, alcohol, cognitive issues (dementia) - this requires lots of help and education. Your abdomen may be contraindicated for peritoneal dialysis due to previous surgery or abdominal conditions.
