Kidney Disease 2 Flashcards
What is chronic kidney disease
Long term, often progressive loss of normal kidney function
–Commonly leads to cardiovascular disease and other complications and may result in end-stage kidney failure
–Affects about 10% of the population and is asymptomatic until renal function severely reduced
–As kidney function deteriorates, the incidence of complications eg anaemia, CVD, disordered bone mineral metabolism and calcification of blood vessels, increases.
–It may, (but does not always) result in end-stage kidney failure
What is the relationship between age and GFR
There is a well recognised decline in gfr from the age of approximately 30yo
End stage renal disease has not improved in recent years. What is the prognosies for the different age categories
5 year survival: Age 18-34 >90% Age 45-54 70% Age 65-74 30% Age >75 <20%
Dialysis patients are 20x more likely to die a CV death than the general population
A cardiac cause is implicated in >40% of all deaths at ESRD
What is the most common cause of death for early ckd patients
Cardiovascular related death (not kidney failure)
Howdo we define CKD
Kidney damage for >3/12 (3 months) as evidenced by structural or functional abnormalities with normal or decreased GFR (GFR>60ml/min/1.73m2).
–Diagnosed using blood/Urine tests or Imaging
- GFR <60ml/min/1.73m2 with or without kidney damage for more than 3/12 .
- higher levels of albinaurea and a severly reduced function, thr risk for adverse outcomes in increased
How common is ckd
Exact prevalence is unknown – many cases of eary ckd are unrecognised
CKD prevalence rises with age from 78 per million <40yrs to 5900 pmp >80
More common in many ethnic minority groups eg in association with diabetes in south east asians and hypertension in black patients
Which stage of ckd is most common
stage 3 - stages beyond that have poorer outcomes (more patients have died)
What are ther risk factors for CKD
-Diabetes
–Hypertension
–Acute kidney injury
–Cardiovascular disease
–Structural renal tract disease, recurrent renal calculi, prostatic hypertrophy
–Multisystem disease with potential kidney involvement, eg SLE, lupus
–Family history of end stage kidney disease
–Detection of haematuria
What are the non-modifiable factors for ckd
Old age Male sex# Race/ ethnicity Genetic predisposition Family history Low birth weight
What are the modifiable factors for ckd
Systemic hypertension Diabetes melilitus Proteinuria Dyslipidaemia Smoking Obesity Alcohol consumption Low socio-economic status Drugs and herbs/analgesic abuse Auto-immune disease/obstructive uropathy/ stones
Which patient types do we refer to secondary care based on nice guidelines
CKD 4/5
Heavy proteinuria (ACR≥70mg/mmol or proteinuria 1g/d) unless on diabetes treatment
Haematuria and proteinuria (ACR≥30mg/mmol or proteinuria 0.5g/d)
Rapidly declining GFR (>5ml/min in 1 yr or >10ml/min over 5yrs)
Poorly controlled BP on 4 agents
Possible genetic/multi-system cause of CKD
Suspected renal artery stenosis
How do we identify progressors
Exclude causes of acute deterioration of GFR eg patients of ace inhibitors
Define as >5ml/min in 1 yr or >10ml/min in 5 yrs
Minimum of 3 GFR estimations required
Focus on those whom continuing decline at observed rate would lead to end stage renal failure within lifetime
What are the most common causes for ckd
Diabetes, unknown (as patients may present at end stage), adpkd (inherited condition), glomelular nephritis
How do we manage ckd
Fist need a definitive Diagnosis
Treatment/prognosis depends on
Stage of CKD
Complications
Risk of cardiovascular events and death
Risk of end stage renal disease
How do we manage each stage of CKD
Increased risk - screen for ckd and introduced ckd risk reduction plans
Stage 1&2 - monitoring of renal function, slow the progression, obtain a diagnosis, control bp, RAAS bikade
Stage 3 - treat complications (anaemia, acidosis, bone disease)
Stage 4 - prepare patient for renal replacement therapuy (give them a choice), consider transplant
Stage 5 - conservative management
What is the link between cardiovascular disease and patients on dialysis
Patients who are on dialysis have a similar annual mortality of patients over 85 in the general population
In which stage of ckd is cvd most common
Stage 4 as many die of cvd before progressing to renal replacement therapy (NB all stages of ckd see an increased risk of cvd in compariston to the general population)
What’s the link between CKD & CVD
Both may be consequences of same diseases eg diabetes, HTN, atherosclerosis
CKD may cause or exacerbate CVD eg anaemia, RAAS activation, oxidative stress, hyperhomocystinaemia, vascular calcification
CVD may cause or exacerbate CKD
Patients with CKD are likely to receive less aggressive therapy for their CVD
What are the traditional CV risk factors more common in CKD
hypertension (almost always present) Diabetes Dyslipidaemia Obesity Reduced physical activity
What are the risk factors more common or unique to advanced CKD
Arteriosclerosis Diastolic dysfunction Vascular calcification Albuminuria Volume overload Anaemia Oxidant stress Inflammation Malnutrition Vitamin D deficiency Accumulation of advance glycation end products LVH Hyperparathyroidism RAS activation + more
How do we manage the raised bp typical of ckd using ace/arbs
Glomerular filtration pressure and increased proteinuria = increased renal injury
ACE/ARB–Decrease arteriolar tone, decrease intraglomerular pressure and decrease proteinuria
–Decrease A2 activity – A2 induced inflammation = decreased fibrosis and scarring
–ACEi affect both angiotensin type 1 and type 2 receptors but may not completely inhibit A2
–ARBs block A1 but not A2
Which diuretics do we use to treat ckd
Frusemide , bumetanide –may require high doses eg 500mg frusemide–may be given by prolonged iv infusion
avoid thiazides if moderate to severe renal impairment as they are ineffective
avoid potassium sparing diuretics eg spironolactone, amiloride as to not excacerbate hyperkalaemia
How do we use calcium channel blockers in the treatment of ckd
Often requires maximum doses
Eg: nifedipine LA 90mg daily, amlodipine 10mg daily
side effect of ankle swelling should not be confused with fluid overload
How do we use Ace inhibitors & A2R blockers blockers in the treatment of ckd
Expect a creatinine rise of 20% or decline in GFR of 15% on initiation
Potassium–Overall incidence of hyperkalaemia (K+>5.1mmol/l) is ~10%–Pts with no kidney disease or CKD 1-3 should expect a rise of 0.5mmol/l–CKD 4 or 5 more prominent
hyperkalaemia
See ace and arb combination in–Difficult hypertension, gross proteinuria, Diabetics
What is the role of SGLT2 inhibitors in CKD
SGLT2 inhibitors offer both cardiovascular and kidney protection in both diabetic and non-diabetic CKD and, additionally, improve glycaemic control in T2DM, making them first-line therapy for CKD independent from diabetic status.
Why is anaemia a common side effect of ckd
Causes:
uraemia increases the risk of GI bleeding (more significant cause),
nausea and vomiting decreased appetite
amount of iron absorbed is decreased
leading to low iron stores
Decreased erythropoietin production
Impaired bone marrow response to epo. and the lifespan of rbcs is also reduced
Anaemia is also present in those with diabetes. When does it become common in terms of eGFR ratios
Anaemia with an hb <10 becomes common in patients with a GFR of <30
Anaemia due to reduced renal function is usually an isolated normacytic anaemia. How do we treat this
Iron - oral or iv
blood transfusions
ESA – erythropoesis stimulating agents (takes 2-3 months to reach steady states)
Is the administration of iv iron beneficial for ckd patients on dialysis
Higher dose iv iron given to dialysis patients decreased the risk of death, hospitalisation for heart failure and other major cardiovascular events, decreased dose of epo required and of blood transfusions
What is the next steps for the treatment of anaemic ckd patients
Roxadustat, an oral medicine, is the first in a new class of medicines called HIF-PH inhibitors that promotes erythropoiesis, (red blood cell production) , through increased endogenous production of erythropoietin, improved iron absorption and mobilisation, and downregulation of hepcidin. Roxadustat is also in clinical development for anaemia associated with MDS and for chemotherapy-induced anaemia.
Not currently licenced in europe
What is another recognised complication of ckd
Mineral bone disorder
What is ckd-mbd
Disturbances of calcium and phosphate metabolism are usually seen in patients with CKD stage G4 and G5.
•CKD –MBD is a systemic disorder strongly linked to cardiovascular disease and mortality
What are the primary drivers of ckd mbd
The primary drivers are –phosphate retention due to reduced renal clearance,
–disordered vitamin D metabolism –hyperparathyroidism
Howdo we treat ckd-mbd
Treatment of CKD-MBD in all stages of CKD should be based on serial measurements of phosphate, calcium and PTH and individualised.
General -keep serum Ca and Phosphate within the normal range, keep bone turnover and strength as near normal as possible, keep serum PTH appropriate to these and prevent the development of parathyroid hyperplasia
Why is high phosphate problematic
Calcification of major vessels •Also called renal bone disease •High phosphate symptoms for patients –Severe Itching –Painful, gritty eyes
Describe the feedback loop seen in patients with secondary hyperparathyroidism and
In renal failure there is a decrease in 1-25 dihydroxycholecalciferol (vitamin d precursor) and and increase in phosphate due to reduced renal clearance. This corresponds with low serum calcium, detected in the hyperparathyroid gland, which is stimulated to produce more pth which has an impact on bones and systemic toxicity
What 2 types of arterial narrowing do patients with ckd demonstrate
uraemic arteriopathy and atherosclerosis
How does vitamin D play a role in kidney disease
Active vitamin D is essential to maintain normal calcium levels
- Vitamin D is activated by the kidney then liver
- In kidney disease, vitamin D supplements such as alfacalcidol may be prescribed.
- Doses of alfacalcidol/ calcitriol may be daily, alternate days or twice a week.
What does a lack of vitamin d result in and how do we treat and monitor it
- Osteomalacia
- Secondary hyperparathyroidism
- Low serum calcium
•Alfacalcidol - treatment •Measure parathyroid hormone levels (PTH) - monitoring
Why do patients with ckd experience pruritis and how do we treat it
Caused by high phosphate levels and/or uraemia
- treatment:–dialysis, phosphate binders
- symptom control:–antihistamines & topical preparation
Why do patients with ckd experience nausea and how do we treat it
Caused by a build up of toxins
•Treatment: anti-emetics –metoclopramide –cyclizine –haloperidol (low dose) –Ondansetron –levomepromazine
