S12) Chronic Kidney Disease Flashcards
What is adult polycystic kidney disease?
- APCKD is an autosomal dominant disease due to a mutation in either PKD1 gene (~85%) or PKD 2 gene
- Cysts grow with age, it generally presents in adulthood and is diagnosed with ultrasound and genetic testing
What are the secondary complications of APCKD?
- Pain
- Bleeding into cyst
- Infection
- Renal stones (stasis)
Identify three other co-morbidities of APCKD
- Hypertension very common (before renal function changes)
- Increased incidence of intra-cranial aneurysms
- Increased incidence of heart valve abnormalities
What is Chronic Kidney Disease?
- CKD is the irreversible and sometimes progressive loss of renal function over a period of months to years
- Renal injury causes renal tissue to be replaced by extracellular matrix in response to tissue damage
Describe the aetiology of chronic kidney disease
- Diabetes
- Hypertension
- Immunological e.g. glomerulonephritis
- Infection e.g. pyelonephritis
- Genetic e.g. APCKD, Alport’s
Which groups of patients have an increased incidence of CKD?
- Elderly
- Multi-morbid
- Ethnic minorities
- Socially disadvantaged
Classify the different stages of CKD in terms of GFR
- G1 – normal/high GFR ( ≥ 90)
- G2 – midly decreased (60-90)
- G3a – midly/moderately decreased (45-59)
- G3b – moderately/severely decreased (30-44)
- G4 – severely decreased (15-29)
- G5 – kidney failure (< 15)
Classify the different stages of CKD according to proteinuria
- A1 – normal/mildly increased (< 30 mg/g)
- A2 – moderately increased (30 - 300 mg/g)
- A3 – severely increased (>300 mg/g)
What investigations should one request for a patient with suspected CKD?
- Blood pressure
- Urine dipstick
Describe the usage of eGF (estimated glomerular filtration rate)
- Only accurate in adults
- Correction needed for black patients (not Asians)
- Defines CKD but not useful in AKI
In 5 steps, outline the clinical approach for CKD
⇒ Define degree of renal impairment
⇒ Define cause of renal impairment
⇒ Provide patient with diagnosis and prognosis
⇒ Identify complications of CKD
⇒ Plan long term treatment (delay progression, plan for dialysis/transplantation)
Identify the 5 general blood tests performed for a patient with suspected CKD
- Urea & Electrolytes
- Bone biochemistry
- Liver function tests (albumin)
- Full blood count
- C reactive protein
- ± PTH / iron levels (ferritin, iron, reticulocyte haemoglobin)
Which other blood tests are performed for a patient with suspected CKD and when should they be performed?
Clincial suspicion of…
- Auto-immune disease – auto-antibody screen, complement levels
- Vasculitis – anti-neutrophil cytoplasmic antibody
- Myeloma – serum immunoglobulin screen, protein electrophoresis
Which imaging techniques are used for a patient with suspected CKD, and why are they performed?
- Ultrasound scan – kidney size, evidence of obstruction (hydronephrosis)
- Kidney biopsy – cause unknown, haematuria, proteinuria (USS first)
- Other investigations:
I. CT scan (stones / mass)
II. MRI scan (mass)
III. MR angiogram (renal artery stenosis)
Identify four modifiable risk factors for CKD
- Lifestyle
- Smoking
- Obesity
- Lack of exercise
Identify two non-modifiable risk factors for CKD
- Uncontrolled diabetes
- Hypertension
Identify three drugs which act as risk factors for CKD
- Proton pump inhibitors
- ACE-Inhibitors / Angiotensin Receptor Blockers (proteinuria - )
Explain the effect of CKD on water/salt handling by the kidney
⇒ Reduced GFR
⇒ Lose ability to maximally dilute and concentrate urine
⇒ Small glomerular filtrate but same solute load → osmotic diuresis (nocturia)
⇒ Low volume of filtrate reduces maximum ability to excrete urine → maximum urine volume is much smaller
Which structures / processes are affected by acidosis?
- Muscle
- Bone
- Renal function progression
How does one treat acidosis?
Oral NaHCO3 tablets
Why does hyperkalaemia occur in CKD?
- Can occur once eGFR < 20 mls / min
- Less likely when good urine output maintained
How can hyperkalaemia be treated in CKD?
- Stop ACEi / ARB
- Avoidance of other drugs that can increase K+ (amiloride, spironolactone, trimethoprim)
- Altering diet to avoid foods with high potassium
What are the four possible consequences of the accumulation of waste products in CKD?
- Contributes to uraemic symptoms
- Reduced appetite
- Nausea and vomiting
- Pruritus
Lots of drugs require dosage alteration in CKD / ESRD.
Why is drug metabolism altered in CKD?
- Due to reduced metabolism and /or elimination
- Drug sensitivity can be increased even if elimination unimpaired (side effects more likely e.g. statins)
Provide five reasons as to why anaemia occurs in CKD
- Decreased EPO production
- CKD mineral and bone disorder
- Bone marrow suppresion by uraemia
- Medication e.g. ACE inhibitors
- Co-morbidities
Why is it important to treat anaemia in CKD?
- Improves exercise capacity
- Improves cognitive function
- Regulates LVH
- Slows progression of renal disease
- Reduces mortality
In four steps, outline the clinical approach for treating anaemia in CKD
⇒ Check iron stores first
⇒ If iron low, replace iron first (oral/IV)
⇒ Once iron normalises, re-check haemoglobin
⇒ If haemoglobin low, start EPO stimulating agent (ESA)
Outline the mechanism pathway through which mineral bone disease arises from CKD
How can one treat bone mineral disease arising from CKD?
- Reduce phosphate intake
- Phosphate binders (many contain calcium)
- 1-α-calcidol
- Vitamin D)
When does renal replacement therapy usually need to occur?
- Required when native renal function declines to a level no longer adequate to support health
- Usually when eGFR 8-10 ml/min (normal ~ 100 ml/min)
Define established (end stage) renal failure
Established renal failure is when death is likely without renal replacement therapy (eGFR <15 mls/min)
Identify some symptoms of ESRD / dialysis
- Overwhelming fatigue
- Difficulty sleeping
- Difficulty concentrating
- Nausea & vomiting / reduced appetite
- Restless legs / cramps
- Symptoms of volume overload (SOB, oedema)
What are the four options to treat kidney failure?
- Haemodialysis
- Peritoneal dialysis
- Conservative care
- Transplant
What is the duration of dialysis? (same as haemodialysis)
4 hours, 3 times per week (night time, designated slot)
What are the advantages and disadvantages of dialysis?
- Advantages: less responsibility, days off
- Disadvantages: travel time / waiting, ‘tied’ to dialysis times, restriction on fluid/food intake
What are the contra-indications of haemodialysis?
- Failed vascular access
- Heart failure
- Coagulopathy
What are the complications of haemodialysis?
- Lines: infection, thrombosis, venous stenosis
- AVF: thrombosis, bleeding
- Feel chronically unwell
- Accumulate morbidity (CVS, bone)
What are the benefits of home HD/ nocturnal HD?
- Allows more dialysis hours
- Better large molecule clearance
- Patients often feel better
- Patients often need fewer medications
What are the two types of peritoneal dialysis?
- CAPD – 4-5 bags throughout day (30 min exchange)
- APD – overnight dialysis
What are the advantages and disadvantages if peritoneal dialysis?
- Advantages: independence, less fluid/food restrictions, easy to travel with CAPD, renal function better preserved initially
- Disadvantages: frequent daily exchanges or overnight, responsibility
What are the contra-indications of peritoneal dialysis?
- Failure of peritoneal membrane
- Adhesions, previous abdo surgery, hernia, stoma
- Patient (/carer) unable to connect / disconnect
- Obese/ large muscle mass
What are the complications of peritoneal dialysis?
- Peritonitis (exit or tunnel site)
- Ultrafiltration failure
- Leaks (scrotal, diaphragmatic)
- Development of herniae
What are the advantages and disadvantages of kidney transplant?
- Advantages: reduced mortality and morbidity, better QoL
- Disadvantages: peri-operative risk, malignancy risk, infection risk, diabetes and hypertension risk from meds
how do you stage a CKD
stage proteinuria
- Treat: Stop forcing proteins out blood so can give ACEinhibitor which can lower the glomerular filtrate pressure and
how can diabetes type 2 be a risk factor for chronic kidney disease
- damage to blood vessels and efferent arteriole gets thicker so increases pressure
- If diabetes is poorly controlled:
- hyperfiltration
- glucose reabsorption and sodium follows
- macula densa detects the drop in Na and reduction In Blood pressure
- RAAS activated
- vasoconstriction and Bp increases
- causes damage to glomerular capillaries
what are some primary causes of CKD
- polycystic kidney disease
- ATN
- Recurrent pyelonephritis
- glomerulo - nephritis
what are some secondary causes of CKD
- Diabetes Mellitus
- HTN (hyper tension)
- reno-vascular disease
- Auto-immune
what layer of the kidney goes through atrophy during CKD
- layers of the cortex disappear
why is HbA1c not a good marker during CKD
- kidney is not healthy so isn’t producing healthy Haemoglobin
- It is not producing EPO
- so not a good
= so should use a fasting plasma glucose
how to monitor diabetes in CKD
- HbA1C (Glycosylated Haemoglobin)
- usually its a good test (RBC lifespan is 120)
- it wont be a good test if you have anemia
calcium homeostasis
- impaired renal function
- low Phosphate excretion
- so higher phosphate in plasma
- parathyroid stimulated
- hyperplasia (enlargement of a tissue or organ)
- increased PTH
- Increased bone reabsorption
what is non bone calcification
- deposits of calcium phosphate = painful
- Treat phosphate binders to limit phosphate
what is dialysis
- its a procedure to remove toxins from the body
