CKD Flashcards

1
Q

What is the definition of CKD?

A

Sustained and irreversible disease in GFR

can be any of:

  1. <60mL /min/1.73m2 for at least 3 months
  2. persistent haematuria,
  3. proteinuria
  4. or structural abnormalities of the kidney

NB: there are multiple equations used to calculate CKD (MDRD, CKD-EPI, Cockcroft-Gault)

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2
Q

What GFR levels is end stage renal disease?

A

GFR <15

aka need for RRT

most common causes include DM, glomerulonephritis, HTN

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3
Q

What conditions are associated with chronic kidney disease?

A
  1. HTN
  2. CVS complications (RAAS)
  3. anaemia (EPO)
  4. mineral and bone disorders (activation of vitamin D)
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4
Q

what patient groups experience stable vs progressive loss of kidney function?

A
  • Elderly: CKD more prevalent in this population, ~30% patients >65yrs have stable disease
  • Young: CKD less common, but patients typically experience progressive loss of kidney function
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5
Q

How does the presence of CKD stage 1-3 differ from stages 4&5?

A
  • Stages 1-3 (GFR > 30mL/min)
    • frequently asymptomatic e.g. via screening of at-risk patients
  • Stages 4-5 (GFR < 30mL/min)
    • endocrine / metabolic / water / electrolyte disturbances clinically manifest

NB: CKD Can co-exist with other things e.g. nephrotic syndrome

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6
Q

Which stage is GFR between 60-89?

A

Stage 2

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7
Q

What is normal GFR?

A

~120

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8
Q

What stage is GFR ~90?

A

Stage 1 CKD

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9
Q

What symptoms / clinical findings may you expect if GFR ~90 e.g. stage 1 disease?

A

Normal kidney function

but urine findings or structural abnormalities or genetic trait point to kidney disease

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10
Q

What are the complications of CKD stage 1?

A

none

(90+ GFR - Normal kidney function but urine findings or structural abnormalities or genetic trait point to kidney disease)

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11
Q

What is the Rx of GFR ~90+?

A

Stage 1 kidney disease, Rx:

  1. –> observation,
  2. –> control of blood pressure
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12
Q

What symptoms clinical findings may you have with GFR 60-89?

A
  • GFR 60-89 = stage 2 kidney diseaase
  • –> mildly reduced kidney function
    • other findings like for stage 1, that point to kidney disease AKA - normal kidney function but urine findings or structural abnormalities or genetic trait poinnt to kidney disease
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13
Q

What complications may arise if GFR is 60-89 (stage 2 CKD)?

A

Increased CVD

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14
Q

What is the Rx of GFR is 60-89 (stage 2 CKD)?

A
  1. Observation
  2. control of BP
  3. control of RF’s (as increased CVD risk @ stage 2)
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15
Q

What stage is GFR 45-59?

A

3A

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16
Q

What stage is GFR 30-44?

A

3B

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17
Q

What symptoms / clinical findings do you get with stage 3A (GFR 45-59) and 3B (GFR 30-44)?

A

stage 3A (GFR 45-59) and 3B (GFR 30-44) => moderately reduced kidney function

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18
Q

What complications do you get with stage 3A (GFR 45-59) and 3B (GFR 30-44)?

A
  1. increased CVD;
  2. bone disease - high PTH (from kidneys not converting to ative vit D to absorb Ca2+)
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19
Q

How do you Rx stage 3A (GFR 45-59) and 3B (GFR 30-44)?

A
  • Observation,
  • & control of blood pressure
  • & risk factors
    • –> (Increased CVD; bone disease - high PTH)
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20
Q

A patient has GFR 15-29 what stage kidney disease is this?

A

Stage 4

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21
Q

What complication may happen with a gfr of 15-29?

A

e.g. Stage 4

  • Increased CVD;
  • bone disease - low Ca (no vit d) high phosphate
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22
Q

With a GFR of 15-29 what treatment stage planning is needed?

A

stage 4 GFR need planning/educaate for end stage (whereas stage 3 was observation, control of blood pressure & RFs)

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23
Q

What happens to a patient who has a GFR < 15?

A

GFR <15 or on diaysis = stage 5 renal disease = very severe or endstage kidney failure

(sometimes called established renal failure)

this is the treatment stage where you need renal replacement therapy

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24
Q

What are the complciations of having a GFR <15?

A
  • increased CVD
  • bone diseaes
  • pruritus
  • bleeding
  • malnutrition
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25
Q

What findings are needed to confirm stage 1 or 2 CKD because gfr alone is insufficient?

A

the definition of CKD = sustained and irreversible decrease in GFR (<60) e.g. stage 2 when you start to get complicatons. or persistent haematuria, proteinuria or structural abnormalities of the kidney so they need to include those in dx:

  • Albuminuria
    • (albumin excretion >30 mg/24 hr
    • or albumin:creatinine ratio >30 mg/g [>3 mg/mmol]) [raised creatinine 1.5x baseline = AKI]
  • Urine sediment abnormalities
  • Electrolyte and other abnormalities due to tubular disorders
  • Histologic abnormalities
  • Structural abnormalities detected by imaging
  • History of kidney transplantation in such cases
26
Q

What pathological manifestation of CKD is salt & fluid restriction, loop diuretic the management for?

A

the abnormal excretory funciton of the kidney causing fluid retention –> HTN

27
Q

What pathological manifestation of CKD is managed by low K+ diet and correcting acidosis?

A

due to the abnormal excretory function of the kidney and potassium retention –> hyperkalaemia (muscle fatigue, weakness, arrhythmias)

[normally aldosterone is na retain and K and H loss)

28
Q

What pathological manifestation of CKD’s management is a low phosphate diet, phosphate binders?

A

(phosphate binders = tablets taken just before eating, they bind phosphate in the gut and stop it being absorbed)

due to the abnormal excretory funciton of the kidney you get phosphate retention

–> hyper-phosphataemia

29
Q

What pathological manifestation of CKD is managed by sodium bicarbonate therapy?

A

abnormal excretory function –> retention of acid –> metabolic acidosis –> sodium bicarb therapy

30
Q

What are the pathological manifestations of CKD due to abnormal excretory function and their rx?

A
  1. Fluid retention –> HTN –> salt and fluid restriction, loop diuretic
  2. potasisum retnention –> hyperkalaemia (muscle fatigue, weakness, arrhythmias)
  3. phosphate retention –> hyperphosphataemia (low phos diet, phos binders)
  4. retention of acid –> metabolic acidosis –> Na bicarb therapy

NB: renal diet = limit K, phos, salt and dc water too if needed

31
Q

For what pathological manifestation of CKD do you get rx’d with epotin, iron and ferritin?

A

due to lack of EPO production –> anaemia –> tiredness and LVH that needs Rx with epotin, iron & ferritin

(EPO is made in the interstitial fibroblast cells around the PCT)

32
Q

What pathological manifestation of CKD is Rx’d by vit D/calcium supplementation?

A

the lack of 1,15 vit D production –> hypocalcaemia –> bone pain

rx: vit D/calcium supplementation

33
Q

What pathological manifestation of CKD is Rx’ed by

Phosphate-binders, vit D/analogues, calcimimetics

1-alpha-calcidiol (1- hydroxylation done by kidney, note 25- hydroxylation first & is in liver)

A

hypocalcaemia from lack of 1,25 vit D production –> hypocalcaemia –> raised PTH –> #, osteomalacia, osteitis fibrosa

34
Q

In the pathological manifestations of CKD is the mangagement of ACEi and ARB used for?

A

the effefct of kidney abnormality on CVS heathl

e.g. RAAS activation –> LVH

needs ACEi or ARB

35
Q

What kidney abnormality needs BP control <130/80?

A

the effect of kidney abnormality on CVS health

Microinflammation and HTN (from fluid retention/RAAS)

–> CAD, CHF, arrythmias

36
Q

What are these SSx of?

  • CNS: encephalopathy, fits, twitch or tremor, tiredness
  • Peripheral neuropathy, restless leg syndrome
  • GI: anorexia (loss of appetite & weight), N&V, colitis, metallic taste, halitosis
  • Lungs: pleuritis, pleural effusion
  • Heart: pericarditis
  • Endocrine: growth retardation, sexual dysfunction, amenorrhoea
  • Skin: pruritus, dry skin, ecchymosis, “half-and-half” nails
  • PRO-HAEMORRHAGIC - impaired platelet function
A

Uraemia SSx

  • CNS: encephalopathy, fits, twitch or tremor, tiredness
  • Peripheral neuropathy, restless leg syndrome
  • GI: anorexia (loss of appetite & weight), N&V, colitis, metallic taste, halitosis
  • Lungs: pleuritis, pleural effusion
  • Heart: pericarditis
  • Endocrine: growth retardation, sexual dysfunction, amenorrhoea
  • Skin: pruritus, dry skin, ecchymosis, “half-and-half” nails
  • PRO-HAEMORRHAGIC - impaired platelet function
37
Q

What is the pathophysiology of CKD?

A

primary kidney injury –> nephron loss –> hyperfiltration (compensating for the loss) –> sclerosis of those nephrons –> nephron loss w/ ensuing GFR decline

38
Q

What problems can cause primary kidney injury in the pathophysiology of CKD?

aka: primary kidney injury –> nephron loss –> hyperfiltration (compensating for the loss) –> sclerosis of those nephrons –> nephron loss w/ ensuing GFR decline

A
  • *Diabetes
  • Glomerulonephritis
      • commonly IgA nephropathy,
    • also rare disorders e.g. mesangiocapillary GN,
    • systemic disorders e.g. SLE, vasculitis
  • Hypertension or reno-vascular disease
  • Pyelonephritis & reflux nephropathy
39
Q

In CKD there is increased glomerular capullary pressure that may damage the capillaries, where does this come from?

A

damage to the capillaries by increased glomerular capillary pressure occurs in hyperfiltration and hypertrophy of residual nephrons*

  1. primary kidney injury –>
  2. nephron loss –>
  3. _*hyperfiltration (residual nephrons compensating for the loss)_ –>
  4. sclerosis of those hyperfiltering nephrons –>
  5. nephron loss w/ ensuing GFR decline
40
Q

What process happens to lose nephrons at a certain point in the pathophysiology of CKD?

A

aka: primary kidney injury –> nephron loss –> hyperfiltration (compensating for the loss) –> sclerosis of those nephrons –> nephron loss w/ ensuing GFR decline
* at a certain point the remaining nephrons begin a process of irreversible sclerosis & progressive decline in GFR ensues

41
Q

What other influencing fators are there on CKD pathopgenesis/physiology?

A

Other influencing factors:

  1. nephrotoxins (e.g. NSAIDs),
  2. decreased perfusion (e.g. dehydration, shock),
  3. proteinuria,
  4. hyperlipidaemia,
  5. hyperphosphatemia with calcium phsophate deposition,
  6. smoking
    7.
42
Q

The aim of Ix in CKD is to determine aetiology and evaluate complications…

What Ix should be done for CKD?

A

Blood:

  • FBC (anaemia), ESR, U&E, glucose,
  • low Ca, high phosphate, high ALP, high PTH

Urine:

  • dip, MC&S, albumin : creatinine ratio
  • significant proteinuria (glomerular disease)
  • dysmorphic RBCs, RBC casts (glomerulonephritis)
  • Bence Jones (myeloma)

Imaging/invasive:

  • US kidney (small in CKD)
  • & USS bladder (obstruction)
  • Biopsy
43
Q

What is the management of CKD?

(5x steps)

A
  1. Identify & treat reversible causes
  2. Delaying or halting the progression of CKD
  3. Manage CVD risk
  4. Diagnosing and treating the pathologic manifestations of CKD
  5. Timely planning for long-term renal replacement therapy
44
Q

The management of CKD involves identifying and treating reversible causes, what is the Rx of this?

A

Relieve obstruction

avoid nephrotoxins e.g. radiocontrast, NSAIDS, aminoglycosides

45
Q

The Rx of CKD involved the delaying or halting of the progression of CKD, what is this refering to?

A
  • BP
  • even a small drop may save significant renal function
    • 2 or 3 anti-hypertensives e.g. ACEIs, angiotensin-II receptor antagonists; salt restriction
46
Q

The Rx of CKD involved managning the CVD risk, how is this done?

A

Lifestyle factors

BP, lipid & glycaemic control

47
Q

The Rx of CKD involves diagnosing and treating the pathologic manifestations of CKD.

What does this involve?

A
  • Treat anaemia
      • B12, folic acid, iron (IV can be useful), EPO stimulation
    • If suspect red cell aplasia (anti-EPO antibodies) get haematology help
  • Treat restless legs/cramps
    • –> made worse by/caused by anaemia, low iron or high calcium; uraemia also gives restless leg
    • –> check ferrtin, clonazepam or gabapentin may help, quinine helps with cramps
  • Treat mineral & bone disorders
      • Vit D analogues, phosphate binders, Ca supplements
  • Treat acidosis
      • consider sodium bicarbonate supplements (caution as can raise BP)
  • Treat oedema
      • furosemide 250mg02g/24h +/- metolazone 5-10mg/24hr PO, fluid & sodium restriction
        *
48
Q

one of the last steps in management of CKD is timely planning for long term renal replacement therapy, what does this involve?

A
  • haemodialysis (complications: hypotension, bleeding, vascular access clot, G+ve blood steam infection)
    • Usually begin dialysis when GFR <10mL/min (<15 in diabetics)
    • Or when uremic symptoms [pericarditis, peripheral neuropathy/restless let, pruritis, anorexia, N&V}
  • peritoneal dialysis (complications: infectious peritonitis)
  • renal transplantation (complications: rejection, infection with unusual organisms e.g. CMV, PCP, fungi, delayed graft function (ATN in graft due to ischaemia-reperfusion injury), drug toxicity, malignancy, cardiovascular disease
49
Q

What are the indications for dialysis?

A
  1. refractory metabolic acidosis
  2. refractory hyper-K+ after 3x rounds of treatment [e.g. insulin dex, salbutamol etc]
  3. refractory anuria/uraemia (increased blood urea from ammonia)
  4. BLAST drugs (can be filtered out body as not bound to any proteins):
    • barbiturates,
    • lithium,
    • alcohol,
    • salicylates,
    • theophylline’s
50
Q

Which is more brutal, haemofiltration or haemodialysis?

Why is this used?

A

Haemofiltration = less brutal than haemodialysis

TF haemofiltration is suitable for much more sick ITU patients

51
Q

What is the difference between haemodialysis and peritoneal dialysis?

A

haemodialysis uses an external membrane

peritoneal dialysis uses a peritoneum filter

52
Q

What are the positives of having haemodialysis e.g. an external membrane?

A
  • HCPs can watch for any problems. 
  • Meet other people having dialysis - may give you emotional support. 
  • You don’t have to do it yourself
  • Shorter time & fewer days each week
  • Home haemodialysis: more flexibility in when, where, and how long you have dialysis
53
Q

What are the negatives of haemodialysis (external membrane)?

A
  • Site needed – Arterio-venous fistula (adequate blood flow)
    • Takes weeks to mature; ideally be fashioned 3-6 months before starting
  • Requires regular hospital visits
  • 3-5hrs 3x a week PLUS travel
  • Feel tired on the day of the treatments. 
  • Need to be able to cope with cardiovascular strain of huge changes in blood volume
  • Home hemodialysis expensive, home moderations etc & these candidates are usually good for transplant!
54
Q

What are the positives of peritoneal dialysis e.g. peritoneum filter?

A
  • Arguably more freedom than hemodialysis
    • At home – no travel to hospital
    • On holiday
    • While asleep
    • You can do it by yourself.
  • Not as many food and fluid restrictions
  • It doesn’t use needles.
55
Q

What are the negatives of peritoneal dialysis (uses a peritoneum filter)?

A
  • The process of doing peritoneal dialysis is called an exchange.
    • You will usually complete 4 to 6 exchanges every day.
  • Requires teaching patient/careers
  • The procedure may be hard for some people to do.
  • ST lifespan - membrane changes after a few years!
56
Q

What are the CI’s for peritoneal dialysis?

A
  • Absolute:
    • Intra-abdominal adhesions and abdominal wall stoma.
  • Relative CI:
    • `Obesity, intestinal disease, respiratory disease and hernias are relative contra-indications.

57
Q

What are the risks of haemodialysis?

A
  • Access-related:
    • local infection, endocarditis, osteomyelitis, creation of stenosis, thrombosis or aneurysm.
    • Fever: infected central lines.
  • Haemodyalysis itself:
    • Hypotension (common), cardiac arrhythmias, air embolism.
    • Nausea and vomiting, headache, cramps.
  • Dialyser reactions:
    • anaphylactic reaction to sterilising agents.
  • Heparin-induced thrombocytopenia, haemolysis.
    • [UFH administered at dialysis time to prevent clotting in blood circuit]
  • Disequilibration syndrome:
    • restlessness, headache, tremors, fits and coma.
  • Depression.

Rememeber for haemodialysis pt needs to be able to come with CVS strain of huge BV changes

58
Q

What are the risks of peritoneal dialysis (peritoneum filter)?

A
  • Peritonitis, sclerosing peritonitis.
  • Catheter problems:
    • infection, blockage, kinking, leaks or slow drainage.
  • Constipation, fluid retention, hyperglycaemia, weight gain.
  • Hernias
    • (incisional, inguinal, umbilical).
  • Back pain.
  • Malnutrition.
  • Depression.

(rememeber peritoneal dialysis has ST lifespan as membrane changes after a few years)

59
Q

What are these complications of?

  • Cardiovascular disease - MI & CVA
  • Malnutrition
  • Renal bone disease
  • Infection
  • Malignancy e.g. urothelium tumours
A

Renal replacement therapy complications

  • Cardiovascular disease - MI & CVA
  • Malnutrition
  • Renal bone disease
  • Infection
  • Malignancy e.g. urothelium tumours
60
Q

Name this drug.

used to prevent & control excessive thirst, urination & dehydration caused by injury, surgery, or medical condition ..

A

= desmopressin!

a chemical that is similar to Antidiuretic Hormone (ADH), a synthetic analogue, which is found naturally in the body - ↑s urine concentration & ↓s urine production.

61
Q

What are the different uses of oral and intranasal/parenteral formulations of desmopressin?

A
  • Oral formulations indications:
    • Primary nocturnal enuresis in adults
    • Vasopressin sensitive diabetes insipidus
    • Control of temporary polyuria and polydipsia following head trauma or surgery in the pituitary region.
  • Intranasal and parenteral formulations:
    • Spontaneous or trauma-induced bleeds (e.g. hemarthrosis, intramuscular hematoma, mucosal bleeding) in patients with hemophilia A or von Willebrand’s disease Type [clotting disorders, e.g. get blood volume back up]
    • Prevent or treat bleeding in patients with uraemia

So overall parenteral/intranasal used for uraemia bleeds or clotting disorder trauma bleeds; oral desmopressin/ synthetic ADH = diabetes insipidus, and enuresis. Also for head/pituitary trauma –> thirst and weeing.