Chronic Kidney Disease Flashcards
Role of Kidney
A WETBED
A WETBED
Acid base balance maintaining Water balance maintaining Electrolyte balance Toxin removal BP control Erythropoietin synthesis Vit D metabolism
CKD
Presence of: Kidney damage (albuminuria) OR Decreased kidney function (GFR<60 ml/minute per 1.73m2) for 3 months or more
CKD causes
Diabetes (40%) Hypertension (30%) Glomerulonephridites (7%) Polycystic kidney disease (3%) Chronic obstruction
CKD Stage 1
Normal eGFR (>90) With other evidence of kidney damage (persistent microalbuminuria or proteinuria, haematuria, structural abnormalities, biopsy proven glomerulonephritis)
CKD Stage 2
eGFR 60-90
With other evidence of kidney damage
CKD Stage 3a
eGFR 45-59
CKD Stage 3b
30-44
CKD Stage 4
eGFR 15-29
CKD Stage 5
eGFR < 15
CKD presentation
Commonly asymptomatic, picked up at screening
Non specific symptoms
CKD non specific symptoms
Fatigue Weakness Nausea Anorexia Dyspnoea Peripheral oedema Sore mouth Vomiting + diarrhoea Bad breath Increased thirst and urine production
CKD screening
Screen by checking GFR and urine albumin-creatinine ratio (ACR)
Patients at risk of CKD
AKI Diabetes Cardiovascular disease Structural kidney disease Uropathy (BPH, recurrent renal calculi) Multisystem disease with potential renal involvement (SLE etc)
CKD vs AKI
Important in patients presenting with renal dysfunction, but unknown baseline level
Can be difficult
CKD vs AKI distinguishing features
Clues include:
Non-specific symptoms of CKD (fatigue, weight loss, anorexia, nocturia, pruritic)
Presence of anaemia
Renal ultrasound- small kidneys? structural abnormalities?
CKD annual monitoring
eGFR
Urine albumin:creatinine ration (ACR)
- correlates with rate of progression of disease
- most reliable prognostic factor in CKD
CKD specialist referral when:
GFR<30 ACR>70mg/mmol ACR>30mg/mmol in presence of haematuria Hypertension despite 4 antihypertensives Accelerated progression of CKD- reduction of GFR by 25% with change in GFR category within 12 months, reduction in GFR of >-15 or more within 12 months
CKD management
Underlying cause
Slow progression
Manage complications
Renal replacement therapy
CKD- reducing albuminuria
ACE-inhibitors to patient with CKD and: - diabetes with albuminuria >30mg/mmol -hypertension and albuminuria >30mg/mmol -albuminuria >70mg/mmol Check GFR 1-2wks after starting ACE-Inh
CKD complications
Mineral bone disease CV disease Electrolyte disturbance Fluid disturbance Hypertension
CKD- Anaemia due to number of factors:
Reduced erythropoietin levels (normochromic normocytic anaemia)
Toxic effect of uraemia on bone marrow
Anorexia/nausea due to uraemia causing Vit deficiency
Reduced red cell survival (patients on haemodialysis)
–> may lead to LVH and 3x mortality rates
CKD anaemia- management
Ensure not iron deficient (and B12 + folate)
Give erythropoietin
CKD complication- Mineral bone disease
Reduced renal function leads to reduced filtration and excretion of phosphate
Raised serum phosphate binds to serum calcium, leading to reduced free calcium
–> stimulates parathyroid gland to release PTH
PTH stimulates osteoclasts
Mobilises calcium and phosphate from skeleton
Further elevates serum phosphate
CKD- vit D
Less Vit D activation
–> less calcium absorbed from GI tract
Mineral bone disease tends to occur only when GCF<30ml/minute/1.73m2
CKD- Hyperphosphataemia management
Low phosphate diet
Phosphate binder- calcium acetate
When does mineral bone disease tend to occur
GCF<30ml/min
CKD- low Vit D management
offer supplements only if Vit D deficient
if Vit D deplete + CKD bone disorders persist, offer alfacalcidiol or calcitriol
Alfacalcidol
1 alpha hydroxycolecalciferol
Calcitriol
1,25-dihydroxycolecalciferol
Leading cause of death in patients with CKD
Cardiovascular disease- 50%
CKD- CV disease, multi-factorial
Hypertension Underlying diabetes Vascular calcium deposits Anaemia Fluid overload Endothelial dysfunction and inflammation
CKD management- CVD prevention
Lifestyle changes
Statins- offer to all CKD patients
Antiplatelet- offer to all patients with CKD, but is increased risk of bleeding
CKD- Hypertension
Can be vicious cycle of hypertension + worsening renal function
CKD causes hypertension by
Reduced GFR causes production of renin
Reduced GFR leads to reduced sodium and water excretion
CKD- BP control
Target <140/90
For patients with diabetes, target 130/80
ACE inhibitors are good choice
CKD- water and electrolyte imbalance
Can result from end-stage renal failure
If patient oliguric/anuric, fluid restrict to 500ml/day
Can cause fluid overload + Hyperkalaemia
Fluid overload + hyperkalaemia are indications for
Dialysis
CKD- CV disease management
Lifestyle
Statin
Antiplatelet
CKD- bone mineral disease management
Low phosphate diet
Phosphate binders
Vit D supplementation
CKD- hypertension management
Tight BP control
ACE Inh also reduce albuminuria
CKD- anaemia management
Correct other deficiencies
EPO
CKD- water and electrolyte management
Fluid restrict if oliguric/anuria
Dialyse if overloaded + hyperkalaemic
End stage renal failure
Patients with stage 4-5 CKD
Or those with rapidly progressing stage 3 CKD
Should be referred to nephrologist
Discuss management ESRF
End stage renal disease management options
Conservative management and symptom control
Dialysis
Renal transplant
End stage renal failure- Conservative care
Dialysis may not improve QOL in patients with extensive comorbidities
Very elderly or unwell patients may not have their lives prolonged by dialysis
Many patients opt for symptom control- EPO, bone mineral disease management, antipruritics, antiemetics
End Stage RF- Dialysis
Usually starts when GFR <10, or <15 in diabetics
2 options- haemodialysis or peritoneal dialysis
Peritoneal dialysis
Usually preferred in patients who:
Have residual renal function
Do not have significant other comorbidities
Haemodialysis
Pump blood through artificial kidney
Blood surrounded by a solution of electrolytes (the dialysate)
Solutes in the serum (urea, potassium, creatinine) diffuse into the dialysate and are removed
Ultrafiltration used to regulate distribution of water
Vol of water can be controlled by altering pressure on either side of membrane
Haemodialysis access
Vascular- arterio-venous fistula
Large bore central catheter
Usually performed 3x week for 4 hours
Peritoneal dialysis MOA
Dialysate infused into peritoneal cavity
Blood flowing through peritoneal capillaries acts as blood source
Ultrafiltration controlled by altering the osmolality of the dialysate + drawing water out of the intravascular compartment
Peritoneal dialysis times
Continuous ambulatory peritoneal dialysis (CAPD)- 4 exchanges of 20 mins spaced throughout the day
OR automated peritoneal dialysis which can be used to do number of exchanges overnight
Can be performed at home, aiding independence
Renal transplant
Best long term outcome Cadaveric 85-90% Receiving patient native kidneys not generally removed Transplanted kidney iliac fossa Long term immunosuppression needed
Renal transplant complications- Hyperacute
Within minutes
Due to donor-recipient mismatch
Renal transplant complications- Accelerated
Within few days
Aggressive- mainly T cell mediated
Fever, swollen transplanted kidney, rapidly increasing serum creatinine
Can be salvaged with high dose steroids + antilymphatic antibodies but long term survival affected
Renal transplant complications- acute cellular
Usually in 1-3 weeks but can occur up to 12 weeks
25% patients
Fluid retention, rising BP, rapid creatinine increase
IV steroids after diagnosis by biopsy
Renal transplant complications- chronic
Gradual rise serum creatinine + proteinuria, resistant hypertension
Graft biopsy shows vascular changes, fibrosis + tubular atrophy
Not responsive to increasing immunosuppression therapy
Renal transplant opportunistic infections
Viral (particularly herpes simplex in first 4 weeks, then CMV later)
Fungal
Bacterial
Renal transplant malignancies
Lymphomas
Skin cancers
