Chronic kidney disease Flashcards
Stags of CKD based on eGFR
With added proteinuria/abluminurea = worse outcome
None/mild/Heavy (A1-A3)
Definition of chronic kidney disease
Must have kidney damage or eGFR <60 for greater than three months
Causes of CKD
Glad shop
Chronic glomerulonpehritis - 20%, Chronic refluxnephropathy -15%
Lupus
Analgesiacs
DM - 20% Most common recognised cause
Systemic vascular disease
Hypertesion
Obstruction
Polycystic kidney disease
Renovascular (including hypertension - 15%
Screening
Intervening early in CKD can reduce the progression to ESRF and so screening is recommended for at risk patients with:
- DM
- hypertension
- CV disease
- structural renal disease
- recurrent UTS or childhood history of Vesicoureteric reflux
- family history of ESRF
History in known/suspected CKD
-
Possible cause -
- Ask about previous UTI, LUTS
- PMH of increased BP, DM, IHD
- check drug history and family history
- systemic review: malignancy>
-
Current state:
- Uraemic symptoms such as anorexia, vomitting, restless legs, fatigue, weakness, pruritis, bone pain
- in women ask about ammeonorhoea and impotence in men
Examination in patient with suspected or known CKD
Look for
- cause of ESRF/CKD e.g polycystic kineys, signs of IHD, DM
- current mode of renal replacement therapy and any complications
- previous types of RRT and any compliations
Periphery- hypertension, ateriovenous fistula, signs of previous transplant- bruising from steroids, skin malignancy
Face- pallor of anaemia, yellow tinge of uraemia, gum hypertrophy from cicilosporin, cushingoid appearance
neck- current or previous tunnelled line inserstion , scar from parathyroidectomy
Abdomen: PD catheter or previous catheter (small midline scar just below umbilicus and small rund scar to sife of midline from exit site), signs of previous transplant (hockey-tick scar, palpable mass), ballotable polycystic kidneys
Elsewhere: signs of diabetic nephropahty, retinopathy, cardiovascular or periphieral vascular disease
Symptoms
Rare in the early stages of disease
usually only occur once stage 4 is reached
Late stage disease
- fatigue
- metallic tase
- restless legs
- low urine output
- anorexia - loss of apetite
- shortness of breath pulmonary odema
- ankle swelling - fluid overload
- confusion - severe uraemia
Signs
- increased BP- fluid overload + release of vasoactive hormones
- oedema- peripheral and pulmonary
- pallor/yellow skin pigmentaiton - increased blood urea
- exoriations- pruritis
- pericardial rub- pericarditis
- tachypnea- metabolic acidois
- tetany- hyperphosphataemia
- coma- severe uraemia
What worses with each stage of CKD
Cardiovascular risk factors and should be adressed even in teh early stages
Management of chronic renal failure
Blood pressure control (aim for <130/80mmhg)
- ACE i
- other hypertensives
- diuretics
Reduction in proteinuria- ACE i
Treatment of anaemia
- IV iron
- erythropoetin
Diet
- low salt intake
- low potassium intake
- high calorie intake
Treatment of hyperphosphataemia and hypocalcaemia (renal bone disease)
- phosphate binders
- alpha caclidol
glucose control in diabetes
Hyperlipidaemia control
Volume status monitoring
Avoid nephrotoxic drugs
Clinical presentation of chronic renal failure
RESIN and 8 Ps
Retinopathy
E exoriations (scatch marks)
S skin is yellow
i increased blood pressure
N nails are brown
Pallor,
purpura and brusing
pericarditis
pleural effusions
pulmonary oedema
peripheral oedema
proximal myopathy
peripheral neuropathy
Salt Losing vs Salt retaining
Investigations
Bloods
- ↓Hb – normochromic & normocytic – ↓Epo
- ↑Urea & ↑Creatinine
- ↓ Calcium & ↑Phosphate
- ↑Parathyroid Hormone– due to low Calcium
- increased alk phos (renal osteodystrophy)
Urine
- Microscopy, Culture & Sensitivity
- Dipstick – proteinurea, haematuria
- 24 Hour Urinary Protein
Imaging
- Renal ultrasound – exclude obstruction, assess kidney size (small in CRF)
- CXR – Cardiomegaly, Pleural or Pericardial effusions, Pulmonary Oedema
- Renal biopsy – if cause is unclear & kidneys are normal size
Anti-proteinuric action of ACE inhibitors
- Reduction of systemic blood pressure
- Relaxation of efferent arteriole from glomerulus (so additional reduction of intraglomerular pressure)
- Gradual reduction in glomerular permeability to protein ?cause
Response of kidneys to blood pressure
Hypotensive
- kidneys respond by releasing renin (activating RAS), leading to release of angiotensin II which causes contriction of the efferent arteriole
- Also causes release of prostaglandins to dilate the afferent arteriole
- ultimately maintaining pressure
Functions of the kidney, effect of failure and management
Calcium and phosphate metabolism in chronic kidney disease
- When a patient has chronic kidney disease (esp 4 or 5) leads to r
- Reduced production of 1,25(OH)2D3
- Malabsoprtion of calcium
- Hyperphosphataemia (failure of excretion as kidneys not working(
- This triggers the parathyroid to increase PTH (secondary hyperthyroidism)
- Causes increased bone disease (source of calcium) and increased demand on kidney
Softens the bones and hardens the arteries
Clinical features of renal osterodystrophy
- osteoporosis
- osteomalacia
- areas of osteosclerosis
Treatment of renal osteodystrophy
Prevention
- phosphate binders (calcium acetate)
- vitamin D (alpha-calcidol)
Treatment
- parathyroidectomy
- cinacalcet
Uraemia
Urea accumulates, leading to axotaemia and ultimatlely uraemia. Symptoms can be non-sepcific. However, with rising uaemia the patient may develop severe sympoms and complications like:
- pericarditis
- encephalopathy
- pulmonary oedema
- confusion
- coma
- seizures
Key signs to identify in patients suspected of CKD and possible uraemia are:
- uraemic fetor- uraemic fetor is a urine-like odor on the breath of persons with uraemia
- Uraemic frost- crystallized urea deposits that can be fpund on the skin of those affected by chronic kidney disease
Complications of CKD
CKD compromises the physiology of the kidney. The GFR is reduced therefore reabsorption in the tubules are reduced. Also the kidenys loses its ability to produce hormones
- Rise in BP - due to fluid overload and production of vasoactive hormones created by the kidney via RAAS leass to increased risk of hypertension and congestive HF
- Hyperkalaemia - due to reduced clearance
- anaemia - due to reduced production of EPO
- pulmonay oedema or pitting oedema - fluid overload
- hyperphosphataemia - reduced phosphate excretion, follows the decrease in glomerular filtration
- hypocalcaemia - due to 1,25 dihydroxyvitamin D3 deficiency. Later this progresses to secondary hyperparathyroidsimm, renal osteodystrophy and vascular calcification that further impair cardiac function
- metabolic acidosis (due to accumulationof sulfates, phosphates, uric acid etc)
Treatment: Lifestyle advice
lifestyle changes
- smoking cessation
- diet-healthy balance diet (low fat)
- restricting salt intake
- limitng NSAID use
- moderate alcohol intake so i is within recommended limitis
- losing weight if overweight or obese
- regular exercise
Medical therapy
*
Treatment: Medical
- anti-hypertensives (ACEi/ARB)
- medication to reduce cholesterol - statins
- treatment of anaemia - daily ferrous sulphate tablets, injections of erythropoetin
- correction of phosphate balance - reduce food containing phosphate (red meats, eggs), phosphate binders (sevelamer hydrocholride)
- Vitamin D supplements
Supportive therapy
Supportive treatment includes, medical, physciological and practical care for both the eprson with kidney failure and their family, including discussion about how they fell and planning for the end of life
Why might patients choose supportive therapy:
- unlikely to benefit or have the quality of life with treatment
- do not want to go through the inconvenience of treatment with dialysis
- are advised against dilaysis because they have other serious illnesses that will shorten their life, and the negative aspects of reatment ouweigh any likely benefits
- have been on dialysis but have decided to stop
