Renal Flashcards
1
Q
For any pt with renal failure need to:
A
- assess degree of renal impairment
- make changes
- change to safer drug
- avoid nephrotoxics
2
Q
Routine tests are:
A
- Plasma
* Urine
3
Q
Plasma routine tests
A
- Creatinine
- Urea
- eGFR
4
Q
Urine routine tests
A
- ACR/Albumin:creatinine ratio
- Osmolality
- specific gravity
- proteinuria/microalbuminuria
- haematuria
- mid stream urine
5
Q
Creatinine
A
GFR = Cr Cl
• freely filtered by kidney
• product of protein metabolism
• 24hr urine collection
6
Q
Limitations in urine collection/creatinine
A
- accuracy of urine collection
* time delay
7
Q
Cockcroft & Gault equation
A
CrCl = [140-age]*IBW / Plasma Cr [umol/l]
* F
(F = 1.23 males, 1.04 females)
8
Q
Limitations with Cockcroft & Gault equation
A
- assume average population data
- unsuitable for children and pregnancy
- renal fn must be stable
9
Q
normal CrCl
A
120ml/min
10
Q
normal CR
A
55 - 125umol/l
11
Q
Metabolism in kidney impairment
A
- less vitD activated
- less insulit met
- less elimination API metabolites
12
Q
eGFR 4 variables
A
age, sex, serum Cr, ethnic origin
13
Q
Stages of eGFR
A
1 >90 Normal 2 60-89 Mild impairment 3a 45-59 3b 30-44 Mod 4 15-29 Severe 5 <15 End stage
14
Q
eGFR units
A
ml/min/1.73m^2
15
Q
Stage 1 G1
A
> 90 Normal
16
Q
Stage 2 G2
A
60-89 Mild impairement
17
Q
Stage 3A G3a
A
45-59
18
Q
Stage 3B G3b
A
30-44 Mod
19
Q
Stage 4 G4
A
15-29 Severe
20
Q
Severe 5 G5
A
<15 End Stage
21
Q
Urea - what is it
A
Breakdown product of protein metabolism
22
Q
Uraemia
A
Urea in blood. >15mmol/l
23
Q
High urea levels also in:
A
- dehydration
- excess protein intake
- haemorrhage
- severe infection
- muscle injury
24
Q
Proteinuria
A
- ACR Albumin:Creatinin Ratio
- predictor of renal disease development
- predicts risk of AE
25
ACR
Albumin:Creatinine Ratio
26
uraemia in absorption
* vomiting diarrhoea, GI, oedema
* reduce Ca2+ absorption
* phosphate binders
27
uraemia in distribution
* reduce protein binding in drugs eg phenytoin
| * reduce tissue binding in drugs eg digoxin
28
kidney impairment in metabolism
* VitD - less activation
* insulin - less met
* API metabolites - less elimination
29
dose adjustments - kidney impairment
* reduce dose
| * increase dose interval
30
Loading dose adjustment - kidney impairment
none
31
Ideal drug in renal impairment
* wide therapeutic index
* liver eliminate
* not nephrotoxic
* not affected by changes in fluid balance, tissue or protein binding
32
kidney fn
* regulatory
* excretory
* endocrine
33
pre renal failure
less renal perfusion
34
intrinsic renal failure
damage to renal tissue
35
post renal failure
```
obstruction to urinary flow eg
• Stones
• structural eg tumour
• nephrotoxicity
• outside urinary tract eg ovarian tumour
```
36
Eg of urinary flow obstruction
* Stones
* Structural eg tumour
* nephrotoxicity
* outside urinary tract eg ovarian tumour
37
AKI reversible?
Yes
38
AKi secondary to?
decreased circulation (pre-renal failure)
39
AKI is
regulatory & excretory failure
40
AKI defined in terms of Cr
increased Cr ≥ 26 µmol/l
41
AKI defined in terms of urine output
decreased urine output to <0.5ml/kg/hr for >6hrs
42
Risk factors AKI
* Past AKI
* pre-existing CRF
* age >65yrs
* CCF
* PVD
* DM
* hepatic disease
43
AKI trigger factors
* sepsis/infection
* hypovolaemia (dehydration, bleeding)
* Hypotension
* drugs eg NSAIDs, ACEIs, ARBs, Diuretics
44
Drugs that could trigger AKI
* NSAIDS
* ACEIs
* ARBs
* Diuretics
45
AKI prevention
* avoid nephrotoxic drugs
* Monitor renal function for drugs known to cause renal impairment
* Review meds known to exacerbate AKI
46
Meds that exacerbate AKI
ACEI,
CRB,
diuretics
47
Signs of AKI
* Volume depletion
| * Volume overload
48
Volume depletion signs of AKI
* Thirst
* Fluid loss ++
* Oliguria
* Dry mucosae
* low skin elasticity
* tachycardia
* hypotension
* low JVP
49
Volume overload (if left untreated)
* increased orthopnoea/fluid in lungs
* increased PND/ nocturnal dyspnoea
* SOA
* Oedema
* pulmonary oedema
* pulmonary crackles
50
PND
paroxysmal noctural dyspnoea
51
Treatment of AKI - Underlying causes
* Restoration of renal perfusion - IV fluids, blood
* Dialysis
* Review drug therapy - stop/withhold nephrotoxic drugs
52
AKI restoration of renal perfusion
* IV fluids eg NaCl 0.9%
| * Blood
53
AKI Loop diuretics - what,
Furosemide IV
| • doses 1-2g IV over 24hrs
54
AKI Loop diuretics - why
* produces diuresis, which decreases tubular cell metabolic demands & renal blood flow.
* increases renal prostaglandins/PG
* caution for dehydration
55
AKI Furosemide max rate IV
4mg/min (higher causes ototoxicity)
56
Ototoxicity
damage hear, hearing loss, balance disorders, ringing/tinnitus
57
Dopamine in AKI why
* renal vasodilation mediated through D1 receptors.
| * increases renal perfusion
58
Dopamine in AKI dose
* low dose (2mcg/min)
| * high dose >5mcg/kg/min can cause vasoconstriction
59
Antibiotics in AKI
if cause is infection
60
CKD
Chronic Kidney Disease
61
CKD what is it
* Regulatory, excretory & endocrine failure
* secondary to renal tissue damage
* subtle & slow onset
* irreversible by the time pt presents with symptoms
62
CKI reversible?
irreversible by the time pt presents with symptoms
63
ESRF
End Stage Renal Failure
64
ESRF treatment
* renal replacement therapy needed eg.
| * dialysis or transplantation
65
Acute on Chronic Renal Failure
• sudden fast decline due to underlying cause eg dehydration. infection, drugs
66
Clinical manifestations of CKD
* Urinary symptoms
* Proteinuria
* Fluid retention
* Uraemia
* Anaemia
* electrolyte disturbance
* HYP
* muscle dysfn
67
Urinary symptoms CKD
* v. early stages only polyuria
* polyuria
* medullary damage
* osmotic effect of urea (>40mmol/l)
* loss of ability to [urine]
* nocturia
68
Proteinuria CKD
* degree of proteinuria in all CKD
* proteinuria >2g in 24hr leads to glomerular disease
* >5g in 24hr leads to severe disease = Nephrotic syndrome
69
Nephronic syndrome
>5g in 24hr proteinuria
70
proteinuria
protein in urine
71
Glomerular disease
>2g in 24hr
72
Fluid retention CKD
* CKD progress = GFR lowers
* kidneys can't excrete Na+ & water leads to peripheral and pulmonary oedema & ascites
* 80% of CKD pt have volume dependent HT
73
Uraemia CKD
* measurement of toxin level in blood
* often used to decide when to start dialysis
* Symptoms eg anorexia, N&V
74
Uraemia symptoms
```
anorexia
N&V
constipation
foul taste
skin discoloration
• pruritis
```
75
Anaemia CKD
* failure of kidney to produce erythropoetin hormone
* regulates RBC proliferation in bone marrow
* symptoms eg fatigue
76
Anaemia symptoms
* fatigue and lethargy
* breathlessness
* angina
77
Electrolyte disturbance CKD
* hyperkalaemia
| * Acidosis
78
Hyperkalaemia
* kidneys unable to remove K+
| * >7mmol/l = medical emergency & risk of cardiac arrest
79
Acidosis
* kidneys cant remove H+
| * reduce plasma bicarbonate
80
Hypertension
* majority CKD pt have it
* mainly due to circulatory volume expansion due to Na+ retention
* increases rate of decline of renal fn
81
Muscle dysfunction
* cramps & restless legs
* especially at night
* general nutritional deficiencies & electrolyte disturbances
82
Renal bone disease/ osteodystrophy from what?
* Cholecalciferol (inactive precursor of vitD) absorbed from GIT & produced in dkin from sunlight
* To produce active vitD calcitriol, cholecalciferol needs hydroxylation in 25 position in liver and 1𝒶 position in kidney.
* leads to VitD deficiency
* defective bone mineralisation
* osteomalacia/ bone softening
83
osteomalacia
bone softening
84
How VitD deficiency?
* cholecalciferol needs hydroxylation in 25 position in liver. 1𝒶 position in kidney.
* ESFR cannot do this.
* active vitD decrease
* vitD deficiency
* defective bone mineralisation
* osteomalacia/ bone softening
85
vitD leads to?
| Why low Ca2+?
* vitD cannot absorb Ca2+ from gut
* less vitD = less Ca2+
* low bone mineralisation/ osteomalacia
86
hypocalcaemia leads to?
* release of PTH/parathyroid hormone
* 2º/leads to hyperparathyroidism/hyperplasia of parathyroid gland
* disrupt bone structure
* bone hardening/osteosclerosis
87
hypocalcaemia can be exacerbated by
* hyperphosphataemia as kidney cannot excrete phosphate
| * Phosphate ions can sequester Ca2+ into calcium phosphate in bones.
88
Why hyperphosphataemia?
* kidney cant excrete phosphate
| * leads to hypocalcaemia as Phosphate ions sequester Ca2+ as calcium phosphate in bones.
89
Hyperphosphataemia can lead to?
* lead to pruritis
* leads to hypocalcaemia
* disturb bone architecture
* osteosclerosis/ bone hardening
* bone pain
90
PTH
parathyroid hormone
91
PTH in osteodystrophy
* Ca2+ and Phosphate met controlled by PTH
* kidney cant respond to PTH to increase renal Ca2+ reabsorption
* persistent hyperparathyroidism.
* persistent hyperplasia of thyroid glands - may have to remove.
* hyperparathyroidism
92
Treat CKD two areas?
* conservative eg diet and drugs, treat symptoms
| * renal replacement therapy
93
Renal replacement therapy CKD
* dialysis
| * transplantation
94
Drug treatment with HYP & CKD
* diuretics
* BB
* alpha blockers
95
Diuretic CKD & HYP
* only LOOP eg Furosemide
* occasionally used for HYP mainly for oedema.
* thiazides ineffective at CrCl<25ml/min
* K sparing increases risk of hyperkalaemia
96
Diuretic thiazide
except metolozone, ineffective at CrCl<25ml/min
97
BB CKD & HYP
* cardioselective eg metoprolol, atenolol, bisoprolol
* Metoprolol cleared through liver
* start low dose, titrate up
98
Why metaprolol for HYP & CKD
* cardioselective
| * cleared via liver
99
CCB HYP & CKD
• can produce oedema
especially Nifedipine
• confusion with symptoms of fluid overload
100
ACEis/ARB
* can decline renal fn
* fine is ESFR but increases risk of SE
* C/I: renal artery stenosis
101
Renal artery stenosis
blood flow to kidney relied upon Angiotensin 2 vasoconstriction
102
alpha-blokers
eg. doxazosin
| • cleared through liver
103
vasodilators CKD & HYP
* eg hydralazine, minoxidil
* reserved when HYP not controlled by others
* SE: fluid retention so use w diuretic, reflex tachycardia
104
BP targets
<140/90
| & DM: <130/80
105
Oedema CKD
* pulmonary
* diuretic
* LOOP in pre-dialysis stage
* Furosemide up to 2g OD (500mg tablet)
* Fluid and Na2+ restriction
* stop when dialysis starts
106
Hyperkalaemia CKD
* >7mmol/l imperative due to risk of cardiac arrest.
| * emergency treatments calcium gluconate, insulin + glucose, calcium resonium
107
Emergency treatment for hyperkalaemia & doses
* Calcium gluconate [10ml 10% IV over 5-10min]
* Insulin (20IU soluble) + Glucose (50ml 50% IV)
* Calcium resonium [15-30g powder oral/enema] with Lactulose 10ml/ 15g dose
108
Why Insulin & Glucose in hyperkalaemia treatment - pharmacology
* Insulin stimulates intracellular K+ uptake
| * Glucose prevent hypoglycaemia
109
Why calcium resonium in hyperkalaemia treatment - pharmacology
* Ion exchange resin binds to K+ in GIT & releases Ca2+ in exchange
* always give with lactulose 10ml for each 15g dose as very constipating
110
Acidosis why & treatment
* kidney cant excrete H+ ions
* sodium bicarbonate 500-600mg TDS tab or powder
* only problem in pre-dialysis
111
Hyperphosphataemia why & treatment
* kidney cant excrete phosphate
| * Phosphate binders eg Aluminium hydroxide, calcium carbonate, calcium acetate, sevelamer
112
Phosphate binder eg
* Aluminium hydroxide
* Calcium carbonate
* Calcium acetate
* Sevelamer
113
Phosphate binder pharamcology
* bind with phosphate in food in gut
* take with or just before meal
* dose by meal size
114
Hypocalcaemia why & treatment
* kidney cant produce active vitD
* Calcitrol 250ng OD- fully active
* Alfacalcidol 500ng-1mcg OD- partial active
115
Anaemia why & treatment
* kidney cant produce EPO, erythropoetin
* Recombinant human erythropoetins injections IV/SC
* Iron therapy
* avoid blood transfusions
116
Iron therapy in anaemia CKD. eg
* Iron sucrose [Venofer]
| * Ferric cerboxymaltose [Ferinject]
117
Iron sucrose brand
Venofer
118
Ferric carboxymaltose brand
Ferinject
119
Venofer
Iron sucrose
120
Ferinject
Ferric carboxymaltose
121
Recombinant human erythropoetin inject SE
HYP
| pure red cell aplasia
122
Cramps & restless legs CKS
* cramps at night/on dialysis
| * restless leg syndrome
123
Cramps treatment CKD
• Quinine sulphate 300mg
124
Restless leg syndrome treatment
• Clonazepam 0.5-1mg nocte
125
Vitamin supplements CKD
* eg Renavit
* dietary advice
* water soluble vit removed by dialysis
126
Hepatitis B vaccine
* CKD pt
* get booster every 5yr
* HD pt monitored annually for antibodies and re-immunised if needed
* 3 doses of 40mcg [double normal dose]
127
which vaccine do CKD pt need
Hepatitis B
• every 5 years, booster
• monitor HD pt yearly
128
Dialysis types
* Haemo
| * peritoneal
129
principal of dialysis
* artificial kidney, mimics normal kidney.
| * mimic ultrafiltration & reabsorption
130
Membranes in dialysis HD and peritoneal
* HD = artificial membrane
| * peritoneal = pt own peritoneal membrane
131
Ultrafiltration in dialysis
* remove waste
| * remove water
132
How waste removed in dialysis
* diffuse down conc grad across membrane
| * waste solutes from blood (high conc) to dialysate fluid (low conc)
133
how water removed in HD
hydrostatically with negative pressure grad from pump in HD machine
134
how water removed in peritoneal dialysis
osmotically using dialysate fluids containing various glucose concentrations
135
How reabsorption in dialysis
dialysate fluid = desired substances at normal conc to prevent diffusion/ no conc gradient.
136
Haemodialysis what is done?
* atrial blood taken from body
* anticoagulated (heparin)
* passed through artificial kidney
* countercurrent dialysate fluid bathes fibres & maximises conc grad.
* return to vein & dialysate discarded
137
Artificial kidney in HD made from?
hollow fibres.
| • semi permeable membrane
138
HD where?
• hospital or home
139
HD when?
2-3 times a week, 3-4 hours.
140
HD fluid restriction
should not put on >1.5Kg above dry weight
141
Gain vascular access in HD
* subclavian
| * ateriovenous fistula
142
Ateriovenous fistula in HD
* artery joined to vein
* matures over 6 wks
* 2 enlarged blood vessels to allow needling
* dont cover tightly or injure
143
Sub-clavian
* tunnelled under skin to subclavian vein
| * temporary risk of infection
144
Ateriovenous shunt in HD
• two silastic tubes w Teflon connector inserted into vein and artery
145
Why Peritoneal membrane?
peritoneal membrane lines all internal organs & has rich blood supply
146
Peritoneal dialysis how?
* 1.5/2L sterile dialysis fluid run into peritoneal cavity under gravity
* fluid in abdomen for set time period
* diffusion occurs
* fluid drained out under gravity & discarded
* new fluid drained in
* repeated QDS
147
Access PD
* indwelling silastic catheter
* tunnelled through abdominal wall & distal end sits in peritoneal cavity
* aseptic techniques required when changing bags
* Peritonitis risk
* other risks eg loss of protein.
148
Types of PD
* CAPD - continuous ambulatory PD
* APD - automated peritoneal dialysis
* IPD - intermittent peritoneal dialysis
149
CAPD
continuous ambulatory PD
150
APD
automated PD
151
IPD
intermittent PD
152
Diet in PD
* healthy [low fat, low salt, high fibre]
* low K
* low phosphate
* high protein in CAPD
153
Fluid restriction
HD: urine output + 500ml/day
PD: urine output + 750ml/day
154
HD drugs removal
| PD drugs removal
* low % plasma protein bound
* low Vd
* low m. wt/ molecular weight
* increase water solubility
* increase renal clearance in normal RF
155
increase HD via dialysis
* duration
* blood flow
* type of membrane
* flow rate & composition of fluid
156
Increase PD via dialysis
* composition of dialysate
* pathology of peritoneum
* volume & exchange rate of dialysate in peritoneal cavity • osmotic concentration gradient
157
Pre renal nephrotoxicity
* diuretics
* g.i.losses [D&V, laxative abuse]
* NSAIDs
* ACEIs
158
Classification of nephrotoxicity
* Pre-renal
* Intra-renal
* Post-renal
159
Intra-renal what? eg?
hypersensitivity reactions & unpredictable
• Glomerular lesions
• Interstitial damage
160
Glomerular lesions
* passive trapping of immune complexes in glomerulus causing inflammatory response
* eg gold, penicillamine, phenytoin, penicillins
161
Interstitial damage
* inflammation of cells lying between nephrons
| * eg penicillins, allopurinol, azathioprine
162
Directly toxic and more predictable in dialysis
* can occur with single dose
| * eg aminoglycosides, cyclosporin, amphotericin
163
Post renal what? eg?
* urinary tract obstruction eg methotrexate
* causing crystalluria
* crystals block outflow of urine, leads to back pressure, leads to damage to kidneys
164
Nephrotoxic drugs in renal patients?
sometimes essential
• monitor renal fn and signs of toxicity constantly
• ESFR, fine to use.
165
pruritis
itchy skin due to hyperphosphataemia
