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
causes of white urine
pyuria, phosphate crystals, chyluria
26
causes of black urine
haemoglobinuria , alkaptonuria
27
what does proteinuria indicate
glomerular problem/damage (usually) | Can be a benign variant (Orthostatic proteinuria)
28
how do you assess proteinuria
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
29
what is AKI
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.
30
definition of AKI
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
31
what reference serum creatinine should be used
lowest creatinine | value recorded within 3 months of the event
32
different stages of AKI
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
is minor AKI fine
no - can be critical associated with significant increase in mortality from other conditions
34
seeing AKI as a spectrum of disease
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
why is it important to recognise RF for AKI
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
RF for AKI
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
3 categories of causes of AKI
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
epidemiology
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
pre-renal causes of AKI
Hypovolaemia low cardiac output Hypotension Renal artery thrombosis
40
renal
``` Acute tubular necrosis Glomerulonephritis Vasculitis Nephrotoxins, contrast, rhabdomyolysis Interstitial nephritis HUS/TTP Malignant hypertension Myeloma ```
41
post-renal
``` Ureteric obstruction Urethral obstruction Blocked urinary catheter Bladder tumour ```
42
difference between AKI and CKD
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
thought process when see high serum creatinine/reduced eGFR
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
AKI presentation
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
what are you looking for in AKI history
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
what are you looking for in AKI examination
``` For any features indicating cause • For features of systemic disease • Bladder? Palpable kidneys? • For complications • Volume status of patient • URINE analysis, microscopy ```
47
urine analysis in AKI
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
common causes of AKI
``` ATN ⧫ Functional - low BP and low flow ⧫ Myeloma ⧫ ATIN - inflammation in kidney caused by drugs ⧫ Athero-embolic ⧫ Rhabdomyolysis ```
49
exotic causes of AKI
``` ⧫ Systemic vasculitis ⧫ Acute GN ⧫ Lupus Nephritis ⧫ Anti-GBM disease (Goodpasture’s disease) ```
50
what do you want to know when someone comes in with high creatinine
``` 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
investigations for AKI
``` 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
steps in AKI management
``` What is the cause? • What needs treating NOW? • Reverse underlying factors • Treat the cause if possible • Prevent and manage complications ```
53
complications in AKI that need managing
``` Potassium (kills) • Pulmonary oedema (kills) • Acidosis • Hypertension • Uraemia (brain, nerves, heart) ```
54
management of hyperkalaemia
``` Intravenous calcium • Insulin and dextrose • Nebulised salbutamol • Calcium resonium or newer binding agents eg SZC or patiromer • Dialysis ```
55
what are you thinking AKI wise if see purpuric rash o/e
need to consider immunology
56
if see small scarred kidneys on US what does this suggest
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
what is CKD
• 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
what is the aim of management for CKD
identify cause if possible, treat and prevent complications, slow progression, plan for future ESKD
59
how is CKD defined
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
prevalence of CKD
high - increasing by age | most common in elderly with comorbidities
61
RF for chronic kidney disease
``` Elderly  Hypertension  Diabetes  IHD  Family History CKD  African American  Obesity ```
62
causes of CKD
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
investigating CKD
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
complications of CKD
AKI CVS mortality kidney failure
65
preventing progression of CK D
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
effect of SGLT2 inhibitors in CKD
``` slow progression of renal disease in CKD, reduce deaths, reduce CV morbidity, reduce hospitalisations ```
67
management of CKD
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
how does CKD affect bv
calcification of bv = CVS, atheroma = narrowing of vessels | treat calcification by treating the BP
69
what is nephrotic syndrome
(heavy proteinuria, oedema, hypoalbuminaemia)
70
proteinuria
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
what is the most useful investigation for proteinuria
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
causes of proteinuria
``` ALWAYS indicated glomerular pathology • Diabetes • Minimal change (glomerular) disease (and FSGS) • Membranous nephropathy • Amyloid • SLE ```
73
management of proteinuria
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
do you need to do a cystoscopy for people with haematuria
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
approach to haematuria
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
glomerular injury causing haematuria
Thin glomerular basement membrane disease or variant eg Alport’s syndrome IgA nephropathy
77
investigations for haematuria
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
management of end stage kidney disease
No recovery possible • Need dialysis or a transplant or decide not to do either and treat symptoms (conservative care)