Kidney disease 1 Flashcards

1
Q

What are the functions of the kidney?

A
  • regulation of bone metabolism
  • regulation of red blood cell production
  • regulation of blood pressure
  • influence on blood pH and acid-base-metabolism
  • excretion of metabolic waste products and water
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2
Q

Describe the range of renal patients

A

“Normal” renal function
Patients with various stages of impairment
Patients not yet having dialysis (pre-dialysis) but rapidly approaching
Patients requiring Renal Replacement therapy
Haemodialysis
Peritoneal dialysis
Transplantation

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3
Q

CKD: what is it? How common is it?
What is moderate to severe CKD associated with?
Treatment goals?

A
  • Abnormal kidney function and/or structure
  • Common
  • Often unrecognised but often exists with other conditions eg diabetes or cardiovascular disease
  • Moderate to severe CKD associated increased risk of other adverse outcomes
  • Not all CKD progresses to end-stage kidney disease

It is detectable and easily tested
Treatment can prevent or delay progression and reduce complications

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4
Q

State markers of kidney disease

A
Albuminuria (ACR >3mg/mmol)
Urine sediment abnormalities
Electrolyte and other abnormalities due to tubular disorders
Abnormalities in histology
Structural abnormalities (imaging)
History of kidney transplantation
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5
Q

GFR
What is it?
Normal value?
Indicative of?

A
  • Glomerular filtration rate is the best measure of overall kidney function
  • It is the composite function of all the nephrons
  • -Normal ~100mls/min
  • Result roughly indicates % of normal function
  • Exact measurement difficult but can be estimated in the lab from serum creatinine, gender and age using a simple formula.
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6
Q

Creatinine-estimated GFR versus

NICE guidance

A

-Laboratories should report an estimate of GFR using a prediction equation and the serum creatinine
-Laboratories should use the Chronic Kidney Disease Epidemiology collaboration (CKD-EPI) creatinine equation to estimate GFRcreatinine
-Apply a correction factor for patients of African-Caribbean or African family origin ((eGFR x 1.159)
In extreme muscle mass
-decreased muscle mass will lead to overestimation and increased muscle mass under estimate GFR

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7
Q

Cystatin C-based GFR

What is it? When is it used?

A

-Laboratories report an estimate of GFR eGFRcystatinC and the serum cystatin C
-Used when an improved assessment of risk is needed
-Caution in patients with uncontrolled thyroid disease
-Used at initial diagnosis to confirm or rule out CKD in people with:
An eGFRcreatinine of 45-60ml/min/1.73m2 for >90 days and
No proteinuria or other marker of kidney disease

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8
Q

Urine dipstick tests
What are they? What do they detect?
What are they associated with?

A
  • Basic test to shows kidney damage (presence and severity)
  • Haematuria (blood in urine)
  • Associated with more rapid decline in kidney function
  • Proteinuria/ albuminuria (protein in urine)
  • Ratio of protein or albumin to creatinine is measured.
  • ACR recommended for people with diabetes
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9
Q

What is CKD? Prevalence?
What can it result in?
What complications can it cause?

A

Estimated to affects about 10% of the general population

Long term, often progressive loss of normal kidney function

May, (but does not always) result in end-stage kidney failure

Usually asymptomatic until renal function severely reduced

Commonly leads to cardiovascular disease (CVD) and other complications

As kidney function deteriorates, the incidence of complications increases eg anaemia, CVD, disordered bone mineral metabolism and calcification of blood vessels.

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10
Q

Risk factors for CKD (clinical conditions)

A
Diabetes
Systemic Hypertension
Acute kidney injury
Cardiovascular disease
Structural renal tract disease, recurrent renal calculi, prostatic hypertrophy
Multisystem disease with potential kidney involvement, eg SLE
Family history of end stage kidney disease
Detection of haematuria 
Proteinuria
Dyslipidaemia
Smoking
Obesity
Alcohol consumption
Low socio-economic status
Drugs and herbs/analgesic abuse
auto-immune disease/obstructive uropathy/stones
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11
Q

Unmodifiable risk factors for CKD

A
  • old age
  • male sex
  • race/ethnicity
  • genetic predisposition
  • family history
  • low birth weight
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12
Q

Clinical disease causes of CKD

A

Diabetes
Chronic (untreated) high blood pressure.
glomerulonephritis (inflammation of the kidney)
pyelonephritis (infection in the kidney)
polycystic kidney disease (an inherited condition where both kidneys are larger than normal due to the gradual growth of masses of cysts)
failure of normal kidney development in an unborn baby while developing in the womb
systemic lupus erythematosus (a condition of the immune system where the body attacks the kidney as if it were foreign tissue)
long-term, regular use of medicines, such as (non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin and ibuprofen
blockages, for example due to kidney stones or prostate disease

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13
Q

Discuss the importance of early detection of CKD

A

Early detection of CKD and its complications can delay or prevent progression to ESRD

Early intervention
Blood pressure control
Glycaemic control for diabetes
Reduce proteinuria

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14
Q

Control of rate of kidney disease progression via:
Blood pressure
Drugs

A
  • Ideally, blood pressure reading should be systolic below 140mmHg Target range 120-139mmHg) and diastolic below 90mmHg
  • kidney disease, diabetes or a condition that affects heart and circulation, target blood pressure should be below 130/80mmHg.
  • 3 or more anti-hypertensives usual
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15
Q

Choice of anti-hypertensive in CKD
Combinations not recommended

Monitoring requirements

A

Choice of agent:
Low cost renin angiotensin antagonist
Do not use combination of ACE and ARB

ACE inhibition/ A2RB/aldosterone blockade
Lower Bp, reduce proteinuria, preserve renal function

Measure serum potassium and estimate GFR before starting
Repeat after 1-2 weeks
Do not give if potassium >5mmol/l pre treatment
Stop if potassium on treatment is >6mmol/l

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16
Q

Diabetes control in CKD

A

Diabetes control

ADVANCE trial showed good glycaemic control can slow down progression of renal disease

17
Q

Drugs to avoid

A

Avoid nephrotoxic drugs eg NSAIDs or at least annual check of renal function

18
Q

Other meds to offer in CKD

A

Statins
Lipid recommendations in NICE CG181

Oral antiplatelets and anticoagulants
offer antiplatelet drugs to people with CKD for the secondary prevention of cardiovascular disease but note increased risk of bleeding

19
Q

Link of CKD and CVD

A

Both may be consequences of same diseases eg diabetes, hypertension ,atherosclerosis
CKD may cause or exacerbate CVD eg anaemia,, oxidative stress, vascular calcification
CVD may cause or exacerbate CKD

20
Q

Management and aims of CKD treatment

A

Definitive Diagnosis
Treatment/prognosis

Depending on the stage of CKD
Prevent or treat complications
Reduce the risk of cardiovascular events and death
Reduce the risk of progressing to end stage renal disease

21
Q

Describe the 5/6 stages of drug treatment for CKD

A
Everyone - Screening for CKD, CKD risk reduction
↓
Stage 1&2: Normal/↓GFR, proteinuria
Slow progression diagnosis and treatment
ACE/ARB 
Strict BP control
CVD risk reduction 
↓
Stage 3
Moderate ↓GFR
Slow progression, treat complications
Stage 1&2 treatment
PLUS
Anaemia 
Acidosis
Bone disease 
CVD risk 
↓
Stage 4 
Severe ↓GFR
Treat complications
Preparation for renal replacement therapy
Stage 3 treatment
PLUS
Choice 
Vascular access
Transplant workup
Living donor 
↓
Stage 5
ESRD
Dialysis 
Transplant
Conservative care
22
Q

Compications of CKD

A

Renal anaemia
Mineral bone disease
Acidosis
Cardiovascular disease

23
Q

Treatment of anaemia in CKD

A

Iron and Erythropoietin replacement
Serum ferritin 200-500micrograms/L
Iron - oral or iv
For people who are not receiving haemodialysis, consider a trial of oral iron before offering intravenous iron therapy. If they are intolerant of oral iron or target Hb levels are not reached within 3months offer intravenous iron therapy.
For people who are receiving haemodialysis, offer intravenous iron therapy. Offer oral iron therapy to people who are receiving haemodialysis only if:
intravenous iron therapy is contraindicatedor
the person chooses not to have intravenous iron therapy after discussing the relative efficacy and side effects of oral and intravenous iron therapy.

Folic acid (if low folate)
Vitamin B12 (if low B12)
Blood transfusions if symptomatic
ESA – erythropoesis stimulating agents eg aranesp®, eprex ®, mircera ®, neo-recormon ®

24
Q

Causes of Anaemia in CKD

A
Causes: 
-uraemia increases the risk of GI bleeding,
nausea and vomiting decrease appetite
-Shortened life span of red blood cells
-Chronic inflammation
-Secondary hyperparathyroid disease
amount of iron absorbed is decreased
leading to low iron stores
-Decreased erythropoietin (epo) production + impaired bone marrow response
25
Q

Treatment of CKD-MBD

A

Disordered bone metabolism and osteoporosis
CKD-MBD – chronic kidney disease – mineral bone disorder
Systemic disorder – abnormalities in bone and mineral metabolism and extra- skeletal calcification
Patients with CKD may have deranged calcium, raised phosphate and increased levels of parathyroid hormone (secondary hyperparathyroid disease).
Vitamin D
treat deficiency

26
Q

High phosphate can cause what?

A
Mineral- bone disease
Premature death
Calcification of major vessels 
High phosphate symptoms for patients
Severe Itching
Painful, gritty eyes
27
Q

What are phosphate binders? Name the different types

What must be taken into consideration when using these drugs?

A

Calcium based
Calcichew (calcium carbonate) ,
renacet (calcium acetate)

Non-ionic/ non catonic / other binders
Renagel/ renvela (sevelamer)
Fosrenol (Lanthanum carbonate) Metal based
Velphoro (iron) , Magnesium

Metal based
Aluminium hydroxide * rarely used, Magnesium containing

Timing is everything!
Must be taken immediately before or with meals to ensure efficacy
Remember if binds phosphate, what about other drugs?

28
Q

Pruritis
Cause in CKD patients
Treatment
Symptom control

A

Itch
Caused by high phosphate levels and/or uraemia

treatment:
low phosphate diet & phosphate binders. Efficient dialysis.

symptom control:
antihistamines & topical preparations

29
Q

Hyperkalaemia

treatment

A

Treat by reducing potassium in diet

Correct any metabolic acidosis

30
Q

Acidosis
GFR levels
Correct with

A

GFR <30mls/min/1.73m2 (GFR g4 or G5 and serum bicarbonate

Correct with oral sodium bicarbonate

31
Q

Hypertension treatment in CKD

A

May require a number of agents to decrease blood pressure:
diuretics
beta blockers
Centrally acting agents
ACE inhibitors & Angiotensin II inhibitors
MHRA warning about using together so need to monitor patients very closely
Vasodilating drugs eg. calcium channel blockers

32
Q

Ace inhibitors and A2R blockers use: What blood levels to expect?
Incidence of hyperkalaemia in different patients
When do we see this combination?

A

Expect a serum creatinine rise of up to 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 expect a rise of 0.5mmol/l
CKD 4 or 5 more prominent hyperkalaemia
See combination in
Difficult hypertension, proteinuria, diabetes

33
Q

Diuretics in CKD
Examples and doses, RoA
Avoid which ones? Cautions?

A

frusemide , bumetanide
may require high doses eg 500mg frusemide
may be given by prolonged iv infusion
avoid thiazides if moderate to severe renal impairment (eGFR<20mls/min) as ineffective
Caution with potassium sparing diuretics eg spironolactone, amiloride unless careful monitoring of potassium, or patient has severe heart failure

34
Q

Calcium channel blockers in CKD

Side effects

A

Often require maximum doses

Side effect of ankle swelling should not be confused with fluid overload especially with amlodipine

35
Q

Difficult to control hypertensive patients may also require:

A
Centrally acting antihypertensives
Moxonidine
Methyldopa
Minoxidil
Nitrates
Alfa and betablockers eg labetalol
High dose diuretics
36
Q

Nausea in CKD is often caused by what?

Treatment?

A

Caused by a build up of toxins

Treatment: anti-emetics 
metoclopramide
cyclizine
haloperidol (low dose)
ondansetron