CKD Flashcards

1
Q

CKD - pathophysiology, causes / rf

A

chronic reduction in kidney function- permanent and progressive. subtle decrease in OVER 3 months (AKI <3months)

causes:
1. Diabetes= excess gluose sticks to protein (nonenzymatic glycaration) effecting the efferent arteriole to be stiff and narrow. diffiuclt for blood to leave so gets forced through hyperfiltration.

  1. Hypertension- walls of the artery thicken to withstand high pressure= narrow= less blood to o2- ischaemic damage to glomerulus. foam cells and macrophage.
  2. Age-related decline
    lupus,
  3. RA
  4. Glomerulonephritis
  5. Polycystic kidney disease
  6. Medications such as NSAIDS, proton pump inhibitors and lithium
  7. infection (HIV)
risk factors:
Older age
Hypertension
Diabetes
Smoking
Use of medications that affect the kidneys
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2
Q

CKD presentation / clinical features

A

asymptomatic (routine testing)

pruritus (uraemia)
loss of appetite
nausea
oedema
muscle cramps
peripheral neuropathy
pallor
hypertension
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3
Q

CKD investigations

A

bedisde:
haematuria
urine dipstick
1+ bood. (rule out malignancy)

bloods:
eGFR
U+E’s
*two testes are required 3 months apart to confirm CKD
creatinine level
**estimates how quickly kidneys are filtering blood and producing urine

proteinuria
urine albumin: creatinine ratio >3mg/mmol is significant
(normally expect for kidneys to filter creatinine but its not normal for albumin to end up in the urine because this is a bigger protein)

imaging:
renal ultrasound- investigate accelerated chronic kidney disease

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4
Q

stages of CKD

A

G score (eGFR) (glomerular filtration rate)

G1 = eGFR >90
G2 = eGFR 60-89
G3a = eGFR 45-59
G3b = eGFR 30-44
G4 = eGFR 15-29
G5 = eGFR <15 (known as “end-stage renal failure”)

A score (albumin:creatine ratio) (measure of proteinuria)

A1 = < 3mg/mmol
A2 = 3 – 30mg/mmol
A3 = > 30mg/mmol

eFR <60 or proteinuria for a diagnosis of CKD

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5
Q

referral CKD

A

NICE suggest referral to a specialist when there is:

eGFR < 30
ACR ≥ 70 mg/mmol
Accelerated progression defined as a decrease in eGFR of 15 or 25% or 15 ml/min in 1 year
Uncontrolled hypertension despite ≥ 4 antihypertensives

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6
Q

complications of CKD

A
Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
End stage kidney disease
Dialysis related problems

*urea not filitered out so more in blood. azotemia, nausea, loss of appetitie. if effects CNS- ecenphalopathy, esterixis.

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7
Q

management of CKD

A
  1. slow progression of the disease
    - optimise diabetic control
    - optimise HTN control
    - treat glomerulonephritis
  2. reduce the risk of complication
    exercise, healthy weight, stop smoking, dietary advice K+, PO, Na+, H2o
    atorvostatin20mg for primary CVD
  3. managing complications:

oral sodium bicarbonate (to treat metabolic acidosis)

iron (erythropoietin to treat anaemia)

vitamin D renal bone disease

dialysis end-stage renal failure

renal transplant in end-stage renal failure

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8
Q

anaemia of CKD

A

healthy cells produce erythropoietin which stimulates the production of RBC. if kidney cells are damaged in CKD- drop in erythropoietin- drop in RBC = (normocytic) anaemia

if microcytic then this could be due to iron deficiency

exogenous erythropoietin
blood transfusion- sensitise the immune system (allosensitsation) (give externally produced EPO to stimulate production of RBC)

limit blood transfusion incase having kidney transplant as more likely to be rejected in future

if iron deficiency IV iron then treat this before EPO

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9
Q

renal bone idsease

A

CKD- mineral and bone disorder
osteomalacia
osteoporosis (brittle)
osteosclerosis (hardening of bones)

xray: spine xray shows sclerosis (dense and white at both ends of vertebrae)

osteomalacia (centre of vertebra - less white)
rugger jursey spine

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10
Q

pathophysiology of mineral and bone disorder in CKD

A

High serum phosphate occurs due to reduced phosphate excretion.

Low active vitamin D because the kidney is essential in metabolising vitamin D to its active form. (Active vitamin D is essential in calcium absorption from the intestines and kidneys. Vitamin D also regulates bone turnover.)

Secondary hyperparathyroidism occurs because the parathyroid glands react to the low serum calcium and high serum phosphate by excreting more parathyroid hormone. (to increase the amount of ca2+ in the blood via GI/kidney/bones) This leads to increased osteoclast activity. Osteoclast activity lead to the absorption of calcium from bone.

Osteomalacia occurs due to increased turnover of bones without adequate calcium supply.

Osteosclerosis occurs when the osteoblasts respond by increasing their activity to match the osteoclasts by creating new tissue in the bone, however, due to the low calcium level, this new tissue is not properly mineralised.

Osteoporosis can exist alongside renal bone disease due to other risk factors such as age and use of steroids.

manage:

with active forms of vitamin D (alfacalcidol and calcitriol)
Low phosphate diet
Bisphosphonates can be used to treat osteoporosis

*drop in GFR so kidneys sense this as low BP so secrete more renin= vicious cycle.

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11
Q

renal transplant

A

A renal transplant is placed in the right or left iliac fossa with vascular anastomoses on the iliac vessels. The transplant ureter is anastomosed to the bladder, and often a ureteric stent is placed at operation. The operation usually lasts 90 minutes. Postoperative care is focused on accurate blood pressure and fluid balance management, pain relief, and early mobilisation. Immunosuppression is titrated, and patients are monitored for early signs of rejection. The donor kidney can be injured by the events leading to donor death, the retrieval operation, ischaemia, and reperfusion in the recipient.

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12
Q

signs of renal failure:

A
Uraemia
Acidosis
Fluid overload
Hypertension
Hyperkalaemia
Hypocalcaemia, hyperphosphataemia
Drug toxicity
Anaemia
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13
Q

normal physiological response to decreased blood volume

A
Afferent vasodilation
prostaglandins, NO
Efferent vasoconstriction
Angio II, Noradrenaline, local myenteric response
Increased salt and water retention 
Renin Aldosterone System
ADH
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14
Q

rhabdomyolysis

A
CK > 20,000
Often > 100,000
Ensure hydrated
Consider alkalinization of urine
Consider diuretics + fluids!
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15
Q

assessing fluid balance

A
Pulse
Blood pressure
JVP
Skin turgor
Capillary refill
Thirst
Oedema
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16
Q

renal anatomy/physiology

A

electrolytes from the filtrate to blood = reabsorption

blood to filtrate = secretion

waste like urea and creatinine is filtered
healthy blood urea nitrogen (BUN) ratio: 5-20 molecules or urea for every 1 molecule of creatinine

17
Q

kidney function

A

remove waste, electrolyte levels, regulate water levels, produce hormones (vitamin d)

18
Q

examples of nephrotoxic drugs

A

analgesics NSAIDs
antimicrobials aminoglycosides
anticonvulsants lamtrigine
PPI’s, furosemide, ACEi

19
Q

HTN in CKD

A

ACEi are the 1st line treatment (lisinopril) offered

Diabetes and A:C >3mg/mmol,

HTN + A:C >30mg/mmol,

all even if not HTN or diabetic with A:C >70mg/mmol

*measure serum K+ as CKD and ACEi can cause hyperkalaemia