renal disease Flashcards

1
Q

prevalence of kidney disease

A

Up to 10% pop have some aspect of kidney disease

it is part of other conditions - HTN, dm

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2
Q

UTI

A
o	Really common 
o	Kidney tract problem 
o	Usually just infection in bladder 
o	E coli bacteria line bladder wall 
Lifetime risk for females 10-30%
• Lead to 3 million GP visits per year in UK
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3
Q

ways renal disease can present

A
• Haematuria
• Proteinuria
• Nephrotic syndrome
• Nephritic syndrome
• Hypertension
• Acute kidney injury
• Chronic kidney disease
Urinary tract infection
• Abdominal pain
• Complications of
hypertension (esp malignant
hypertension)
• Oliguria or anuria
• Polyuria, nocturia - often a metabolic problem – nothing wrong with kidneys
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4
Q

how long are the kidneys

A

about 3 vertebral bodies

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5
Q

dark white in kidney in CT

A

excreting contrast in collecting system

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6
Q

summarise anatomy of the kidney and tubule

A

• Glomerulus fed by arteriole – comprises of capillary tuft
o Blood leaving glomerulus is blood supplies around tubules
o Filtrate goes through the tubules
o Cortex contains glomerula
o Medulla – loop of henle and collecting duct

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7
Q

what is the renal parenchyma made of

A

cortex and medulla

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8
Q

summarise the anatomy and the function of the glomerulus

A

it is the filtering unit of the kidney
blood enters cap tuft through afferent arteriole
under high pressure the fluid is pushed out of the blood vessel - ceels and proteins are retained in the capillary lumen
specialised filtration to allow this:
Endothelial cell layer of capillaries has pores
–Glomerular basement membrane
–Epithelial cells (podocytes) with slit membranes
blood leaves glomerulus by efferent arteriole
filtrate passes into Bowman’s capsule and into tubule,
becoming urine

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9
Q

role of podocytes

A

allow you to filtrate the blood but maintain blood cells and protein in blood

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10
Q

functions of the kidney

A

Filtration and excretion of waste products
Electrolyte homeostasis
Blood pressure control via renin/angiotensin/aldosterone axis
prostagladins and bradykinin
Acid Base homeostasis

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11
Q

what hormones does the kidney produce

A

Erythropoietin (epo) – red blood cell production
1,25 Calcitriol (active vitamin D) – calcium, phosphate and
bone metabolism

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12
Q

what are the manifestations in patients when kidney function goes wrong

A
anaemia - because not making epo, cause fatigue
acidosis 
bone fractures
poor clearance of waste = fatigue 
reduced excretion of many drugs 
electrolyte abnormalities eg high potassium, low calcium, low
or high sodium…
impaired fluid balance 
high blood pressure
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13
Q

treatability of manifestations of when kidney func goes wrong

A

anaemia - treatable with epo replacement
acidosis - treatable with bicarbonate
bone fractures- treatable by lowering serum phosphate,
replace active vitamin D, suppress PTH
poor clearance of waste - when v poor only
replaceable by dialysis or a transplant
reduced excretion of many drugs - avoid nephrotoxic
drugs and amend drug doses
electrolyte abnormalities - need correcting
impaired fluid balance - oedema usually (excess fluid)
high blood pressure - needs treatment

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14
Q

why not just use creatinine to assess kidney ‘cleaning’ func

A

a product of metabolism of muscle creatine and
phosphocreatine – so muscle mass make big diff to blood creatinine levels
sex difference
so having same blood creatinine doesnt mean have same kidney function
Freely filtered and not reabsorped but there is tubular
secretion

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15
Q

what is glomerular filtration

A

Most common test of kidney function
• Determines the clearance of a substance from the plasma
• Does not determine the cause for kidney disease

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16
Q

what is GFR

A

• Sum of the filtration rates of all functioning nephrons
• Normal 120-130ml/min/1.73m2
• Depends on age, sex, body size, muscle mass
• Reduced GFR means loss of filtering capacity and
accumulation of waste products

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17
Q

how do you measure GFR

A

No direct measurement
• Estimated from urinary clearance of an ideal filtration marker
from the plasma per unit time

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18
Q

what is an ideal marker for measuring GFR

A

freely filtered solute, not secreted or
reabsorbed by the kidney, not metabolised by the kidney
ie it is only removed from the body by the kidney - see how fast this happens

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19
Q

markers used for measuring GFR

A
• Inulin – best molecule, but too complex to use in practice - not used 
Radioactive markers (eg EDTA, iothalamate, iohexol) –
expensive, low dose radioactivity, takes 2-4h and iv injection, need blood test, or radioactive body count? - cant do it regularly 
Creatinine – good endogenous substance
• Cystatin c – probably best marker but not widely available - not affected by muscle mass
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20
Q

summarise eGFR

A

GFR determined from serum Creatinine or Cystatin C is an

ESTIMATED GFR

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21
Q

how is creatinine used to determine eGFR

A

Used to be common to collect 24 hour urine samples to
measure Creatinine clearance as measure of GFR (from urine
creatinine, serum, urine volume)- not now (– difficult to do – people forget some samples)
based on mathematical eqn
Cockcroft Gault: includes body weight and creatinine
eGFR from MDRD or CKD-EPI or other Equations: uses serum
creatinine and age only

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22
Q

problems with eGFR

A

still uses creatinine
Only relevant in stable patients, not for AKI, dependant on
muscle mass
USEFUL if have serial measurements

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23
Q

urine dip

A
helps tell where the
problem is and guides
investigations
Especially if protein or blood 
bedside investigation
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24
Q

causes of red/brown urine

A

– myoglobinuria (from rabdomyolysis - muscle crushing trauma) or haemoglobinuria
– food dyes or beetroot ingestion
– porphyria
– rifampicin

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25
Q

causes of white urine

A

pyuria, phosphate crystals, chyluria

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26
Q

causes of black urine

A

haemoglobinuria , alkaptonuria

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27
Q

what does proteinuria indicate

A

glomerular problem/damage (usually)

Can be a benign variant (Orthostatic proteinuria)

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28
Q

how do you assess proteinuria

A

urine dipstick tells you that it is present
need to quantitate
spot urine Protein:creatinine ratio (PCR) or
albumin:creatinine ration (ACR)
?? normal up to 30 - low level protein excretion

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29
Q

what is AKI

A

A rapid decline in renal function over hours or days
with:
Accumulation of (nitrogenous) waste products
Potentially life threatening metabolic consequences
With or without reduction in urine output.

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30
Q

definition of AKI

A

Serum creatinine rise by greater than 26 umol/L within 48 hrs
OR
Serum creatinine rise 1.5 x from the reference value which is
known or presumed to have occurred within one week
OR
Urine output is less than 0.5ml/kg/hr for 6 consecutive hours

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31
Q

what reference serum creatinine should be used

A

lowest creatinine

value recorded within 3 months of the event

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32
Q

different stages of AKI

A

1 - Serum creatinine rise by greater than 26 umol/L within 48 hrs, Urine output is less than 0.5ml/kg/hr for 6 consecutive hours
2 - SCr increase >=2-2.9 fold from baseline, <0.5mL/Kg/h for 12hr
3 - SCr increase >=3 fold from baseline, or >=354umol/L or initiated on RRT, Urine output is less than 0.5ml/kg/hr for 24 consecutive hours or anuria for 12hr

33
Q

is minor AKI fine

A

no - can be critical
associated with significant
increase in mortality from other conditions

34
Q

seeing AKI as a spectrum of disease

A

normal - increased risk - damage - reduced GFR - kidney failure - death
o Want to recognise people at increased risk – flag to minimise risk they progress down route
o Route reversible in most pts but not always

35
Q

why is it important to recognise RF for AKI

A

occurs most commonly in patients who are at risk, who
either are acutely ill or have had major surgery
allows simple preventative
measures, eg ensuring adequate hydration, consideration of drugs, regular blood tests

36
Q

RF for AKI

A

Age >75 years
• Pre-existing CKD (eGFR <60 mL/kg/1.73 m2)
• Previous episode of AKI
• Debility and dementia
• Heart failure
• Liver disease
• Diabetes mellitus
• Hypotension (Mean arterial pressure <65mmHg, systolic BP <90mmHg)
• Sepsis
• Hypovolaemia
• Nephrotoxins, eg gentamicin, NSAIDs, iodinated contrast
• Continued antihypertensives in setting of hypotension, eg ACE
inhibitors, loop diuretics

37
Q

3 categories of causes of AKI

A

pre-renal - blood flow into the kidney, all about volume - check BP, JVP and vol
intrinsic renal
post-renal - obstruction to outflow, need US

38
Q

epidemiology

A

o 20% pre-renal – low bp, vol depletion
o 13% obstruction
o 45% intrinsic – acute tubular necrosis – multiple insult- sepsis, low bp, drugs = damage to kidney – tubules fallen apart, but reversible just need to get everything else right – vol and stop nephrotoxic agents

39
Q

pre-renal causes of AKI

A

Hypovolaemia
low cardiac output
Hypotension
Renal artery thrombosis

40
Q

renal

A
Acute tubular necrosis
Glomerulonephritis
Vasculitis
Nephrotoxins, contrast, rhabdomyolysis
Interstitial nephritis
HUS/TTP
Malignant hypertension
Myeloma
41
Q

post-renal

A
Ureteric obstruction
Urethral obstruction
Blocked urinary
catheter
Bladder tumour
42
Q

difference between AKI and CKD

A

AKI - potentially reversible
CKD - impaired kidney function, usually
progressive, and potentially resulting in end
stage kidney disease (ESKD) over months to
years, often multifactorial. Not reversible

43
Q

thought process when see high serum creatinine/reduced eGFR

A

is it acute/chronic
if acute - what is the cause? Is it treatable?
if chronic - can you identify cause, can progression be slowed, control and treat complications, plan for ESKD (dialysis, transplant, conservative care)

44
Q

AKI presentation

A

Commonly non-specific symptoms
• Symptoms of uraemia (nausea, vomiting, anorexia)
• Features of the underlying disease
• Decreased urine output
• Systemic features (rash, myalgia, arthralgia, headaches)
• Abnormal biochemistry (rise in serum urea and creat)
• Acidosis, hyperkalaemia, salt and water retention

45
Q

what are you looking for in AKI history

A

Duration
• Systemic features
• Past history, especially vascular, childhood renal disease,
UTI’s, diabetes, hypertension
• Family history, inc early death & strokes
• Drugs, inc herbals, over-the-counter medications (not
“drugs” esp analgesics), recreational drugs - – ketamine causes kidney problem

46
Q

what are you looking for in AKI examination

A
For any features indicating cause
• For features of systemic disease
• Bladder? Palpable kidneys?
• For complications
• Volume status of patient
• URINE analysis, microscopy
47
Q

urine analysis in AKI

A

glomerular disease -Red cells, red cell casts,
proteinuria (often heavy)
tubular disease - minimal blood, small protein, granular or white cell casts - – nothing going down the tubule so no blood leaking from glomerulus – no blood in urine
pre-renal causes - no blood or protein. no casts

48
Q

common causes of AKI

A
ATN
⧫ Functional - low BP and low flow 
⧫ Myeloma
⧫ ATIN - inflammation in kidney caused by drugs 
⧫ Athero-embolic
⧫ Rhabdomyolysis
49
Q

exotic causes of AKI

A
⧫ Systemic vasculitis
⧫ Acute GN
⧫ Lupus Nephritis
⧫ Anti-GBM disease
(Goodpasture’s disease)
50
Q

what do you want to know when someone comes in with high creatinine

A
previous renal func 
ABG for hypoxia and acidosis 
Ca, phos 
US - see obstruction and size of kidneys
CXR - for fluid overload, chest infection 
assessment of volume status 
urinalysis
51
Q

investigations for AKI

A
volume status (for ATN)
• Urine microscopy and dipstick
• Imaging (U/S) *** Obstruction ***
• ANCA, Anti-GBM, SLE immunology (ANA, dsDNA, complements) - if worried about glomerular disease
• Creatinine kinase
• FBC, clotting
• Inflammatory markers
• Myeloma screen (protein electrophoresis, urine BJP) - in older pts 
• May need biopsy
52
Q

steps in AKI management

A
What is the cause?
• What needs treating NOW?
• Reverse underlying factors
• Treat the cause if possible
• Prevent and manage complications
53
Q

complications in AKI that need managing

A
Potassium (kills) 
• Pulmonary oedema (kills)
• Acidosis
• Hypertension
• Uraemia (brain, nerves, heart)
54
Q

management of hyperkalaemia

A
Intravenous calcium
• Insulin and dextrose
• Nebulised salbutamol
• Calcium resonium or newer binding agents eg SZC or patiromer
• Dialysis
55
Q

what are you thinking AKI wise if see purpuric rash o/e

A

need to consider immunology

56
Q

if see small scarred kidneys on US what does this suggest

A

CKD
if in young person: either congenital o Or childhood reflux nephropathy and UTIs - asymptomatic mostly
means dont have to start dialysis straight away

57
Q

what is CKD

A

• A “syndrome” for which there is a cause, although
often not identified
Often first presentation is at end stage
• Kidneys may be normal size, but often small

58
Q

what is the aim of management for CKD

A

identify cause if possible,
treat and prevent complications, slow progression,
plan for future ESKD

59
Q

how is CKD defined

A

by GFR:
GFR 60-90 and no other evidence- not CKD, if do have other evidence- could be chronic eg on US
as albuminuria gets worse = worse outcomes overall = higher death rate and risks of CVS complications

60
Q

prevalence of CKD

A

high - increasing by age

most common in elderly with comorbidities

61
Q

RF for chronic kidney disease

A
Elderly
 Hypertension
 Diabetes
 IHD
 Family History CKD
 African American
 Obesity
62
Q

causes of CKD

A

Diabetes (~30%)
• Chronic glomerulonephritis (~30%)
• Vascular diseases including hypertension, ischaemic heart
disease (~15%)
• Autosomal dominant polycystic kidney disease (~10%)
•Congenital/reflux/childho0d infections
• Genetic risks .. with another insult (eg ApoL1 risk variants
in black patients)

63
Q

investigating CKD

A

Identify cause - important for progression, systemic
features, recurrence after transplant …. This might
be treatable
• Ensure patient understanding
• Ensure regular follow-up
• Investigate for complications (metabolic, CV, BP,
proteinuria)

64
Q

complications of CKD

A

AKI
CVS mortality
kidney failure

65
Q

preventing progression of CK D

A

BP control, ACEi/ARB and reducing proteinuria, SGLTi drugs - slows down eGFR decline (irbesartan reduces incidence of dm nephropathy)
minimise other CV risks - smoking
encouraging exercise, low salt and low protein, measure BP, take med even when asymptomatic

66
Q

effect of SGLT2 inhibitors in CKD

A
slow
progression of renal
disease in CKD, reduce
deaths, reduce CV
morbidity, reduce
hospitalisations
67
Q

management of CKD

A

Encourage/support /activate patients to understand this
BP < 125-130/75-80 (usually 3+ drugs), lower BP target
if proteinuria
ACEi/ARB .. More ACEi/ARB … Maximal doses
• Second and third line agents for BP and proteinuria
• Reduce proteinuria as much as possible
• CV risks (aspirin, statins, ezetimibe ..)
• Stop smoking, encourage exercise, healthy diet, avoid
nephrotoxins eg NSAIDs
avoid dehydration

68
Q

how does CKD affect bv

A

calcification of bv = CVS, atheroma = narrowing of vessels

treat calcification by treating the BP

69
Q

what is nephrotic syndrome

A

(heavy proteinuria, oedema, hypoalbuminaemia)

70
Q

proteinuria

A

Incidental finding to full blown nephrotic syndrome
pt concern is swollen legs, painful, limit walking
Normal protein < 300 mg/day (U PCR < 30 mg/mmol)
• Nephrotic > 3 g/day (Urine PCR > 300 mg/mmol)
• Urine Protein:creatinine ratio < 30 “normal”
100 ~ 1 g/day
300 ~ 3 g/day
o Albumin creatinine ratio in urine – if >3 seen as abnormal – sign of microalbuminae in dm. could still be normal if not dm

71
Q

what is the most useful investigation for proteinuria

A

kidney biopsy
Quantitate proteinuria (urine protein:creatinine
ratio)
• Serum albumin and cholesterol
• Serum creatinine, U+Es
• Glucose, SLE tests, virology - can cause nephrotic syndrome (Hep B,C and HIV),
myeloma screen

72
Q

causes of proteinuria

A
ALWAYS indicated glomerular pathology
• Diabetes
• Minimal change (glomerular) disease (and FSGS)
• Membranous nephropathy
• Amyloid
• SLE
73
Q

management of proteinuria

A

Control oedema – low salt diet, diuretics
• ACEi/ARB (reduce proteinuria)
• Treat the cause ! (if possible)
• Sometimes steroids or immunosuppression
• Uncontrolled proteinuria is a major risk for
progressive CKD and ultimate ESKD

74
Q

do you need to do a cystoscopy for people with haematuria

A

not gor everyone
 Look in bladder if worry had bladder cancer – but only 24yr, unless other RF
 Has a kidney problem
 If he were 50yr – would defo need cystoscopy

75
Q

approach to haematuria

A

With pain – think urological cause ie stones or cancers
(kidneys, ureter, bladder, prostate)
• Age > 40 years, must exclude cancer in urinary tract
• BUT age < 40 or protein also present, most likely
intrinsic microscopic renal (glomerular) cause
may need kidney biopsy

76
Q

glomerular injury causing haematuria

A

Thin glomerular basement membrane disease or
variant eg Alport’s syndrome
IgA nephropathy

77
Q

investigations for haematuria

A

If “surgical” or cancer/stone most likely – start
with imaging (US, CT) and cystoscopy
If cause within kidney glomerulus most likely –
check urine for protein, eGFR, then blood tests for
underlying systemic or immune disease, then
possibly renal biopsy.

78
Q

management of end stage kidney disease

A

No recovery possible
• Need dialysis or a transplant or decide not to do
either and treat symptoms (conservative care)