renal Flashcards
what are the 3 main endocrine functions of the kidneys?
- produce renin (renin-angiotensin system, increases fluid retention)
- produces erythropoetin (epo)
- activates vit D into active form
what are the 5 broad causes of vascular damage (which lead to kidney damage)?
thrombotic microangiopathy
- thrombi in arterioles/capillaries (secondary to endothelial damage - lots of causes)
vasculitis
- acute/chronic vessel wall inflammation -> narrowing of lumen
hypertension
diabetes
atheroma (eg renal artery stenosis)
what are the broad causes of glomerar damage, leading to kidney damage:
- immunological? 3
- non-immunological? 4
immunological:
- circulating immune complexes deposit in glomerulus
- circulating antigens deposit in glomerulus
- autoimmune antibodies to basement membrane/glomerular components
nb all of the immunoligcal causes lead to: - complemetn activation - neutrophil activation - reactive oxygen species - increased clotting factors which all -> glomerular damage
non-immunological:
- vessel damage/endothelial injury
- altered basement membrane
- abnormal basement membrane or podocytes due to inherited disease
- abnormal protein deposition (amyloid) impair function
give two examples of conditions which result in circulating immune complexes which deposit in the glomerulus, leading to kidney damage?
SLE
IgA/membranous nephropathy
give two examples of autoimmune conditions which consist of antibodies being created against basement membrane/glomerular components, leading to kidney damage.
goodpasture’s syndrome
- against BM in lungs + kidneys
post-infective glomerolunephritis
name a non-immunological cause of altered basement membrane
diabetes mellitus hyperglycaemia
name one inherited condition which leads to abnormal basement membrane, leading to kidney damage
alport disease/syndrome
inherited defect in type 4 collagen
leads to problems with kidneys, ears + eyes
name 3 conditions which can have abnormal protein deposition in the glomerulus, impairing function + leading to kidney damage
RA
bronchiectasis
myeloma
what is an amyloid protein?
universally used term that refers to abnormal intracellular or extracellular deposition of proteins as fibrils. Amyloid fibrils may be deposited in a variety of organs including brain, liver, heart, kidney, pancreas, nerve and other tissues as a consequence of certain inherited and acquired disorders
name 3 ischaemic causes of tubular damage + 4 toxic causes
ischaemic:
- hypotension (eg shock)
- blood vessel damage (eg vasculitis, HTN)
- glomerular damage
toxic:
- direct toxins
- hypersensitivity reactions
- crystal deposits (eg urate)
- abnormal protein deposition (eg Igs)
ischaemic causes result in reduced perfusion which leads to tubular damage (tubules are very sensitive to ischaemia!)
toxic causes directly result in tubular damage
name 4 types of drug which are nephrotoxic
- NSAIDs
- ACEi
- diuretics
- some antibiotics
name 5 non-drug compounds which are nephrotoxic
- contrast medium
- ethylene glycol (antifreeze)
- organic solvents
- pesticides
- heavy metals
nephrotic syndome:
- pathophysiology?
- 3 main features?
- 2 other possible features
- possible complications? 2
always due to damage to GLOMERULUS
- proteinuria
- oedema
- hypoalbuminaemia
(nb proteinuria results in other 2!)
+/- hypertension
+/- hyperlipidaemia
complications:
- infection
- thrombosis (as antithrombin lost in urine)
nephrotic syndrome:
- commonest cause in adults?
- 2 other common adult causes?
- 3 rarer causes in adults?
membranous nephropathy (commonest)
- idopathic primary glomerular disorder
- get thickening of basement membrane
- affect adults <60
- M>F
focal segmental glomerulosclerosis (FSGS)
- various causes (usually idiopathic, but also genetics, heroin use, HIV)
- M>F
minimal change disease
- normal histology
- diagnosis of exclusion
- M=F
(diabetes, lupus nephritis, amyloid)
what is the most common cause of nephrotic syndrome in children?
minimal change disease
- normal histology
- diagnosis of exclusion
- usually excellent prognosis
nephritic syndrome:
- alternative name?
- symptoms? 4
acute nephritis
- HAEMATURIA (norm macroscopic)
- proteinuria (less than in nephrotic)
- hypertension (slight)
- low urine output
what are 4 common causes of nephritic syndrome in adults?
post-infective glomerulonephritis:
- weeks after strep throat infection
- good recovery
IgA nephropathy
- common primary glomerular disease
- usu young adults
- 20-50% renal failure over 20 years
vasculitis
- autoimmune
lupus nephritis (caused by SLE)
- autoimmune
- usually young women
what other symptoms would someone with vasculitis have, alongside nephritic syndrome? 5
- unwell
- fever
- rash
- myalgia
- arthralgia
what are the 4 main causes of nephritic syndrome in children?
Henoch-Schönlein purpura
- a specific IgA nephropathy
- often follows throat infection
- most recover completely
haemolytic-uraemic syndrome
- typically children with e. coli gastroenteritis
post infective glomerulonephritis
IgA nephropathy
Henoch-Schönlein purpura:
- who norm affects?
- symptoms? 4
boys/teenagers
- arthralgia
- abdo pain
- purpuric rash
- proteinuria/haematuria -> acute kidney injury
haemolytic-uraemic syndrome:
- symptoms? 3
- pathophysiology?
- nephritic syndrome/acute nephritis
- haemolysis
- thrombocytopenia
norm caused by a toxin produced by e coli
- toxin damages vascular wall -> clots + haemolysis -> thrombocytopenia
get GI symptoms first, renal stuff follows
acute kidney injury (aka acute renal failure)
- definition?
- symptoms? 8
anuria/oliguria (<400ml/24hr)
+ raised plasma creatinine + urea
- malaise
- fatigue
- nausea
- vomiting
- high BP
- oedema
- confusion
- arrythmias
acute kidney injury:
- most common pre-renal causes? 2
- most common post-renal causes? 4
- when is a renal biopsy helpful?
pre-renal (norm reduced blood flow -> kidneys):
- severe dehydration
- hypotension (bleed, septic shock, LVF)
post-renal (urinary tract obstruction):
- urinary tract tumours
- pelvic tumours
- calculi (kidney stones)
- prostatic enlargement
only helpful for intra-renal causes of AKI
- imaging better for post-renal stuff
acute kidney injury:
- most common intra-renal causes in adults? 2
- most common intra-renal causes in children? 3
adults:
- vasculitis (autoimmune or inflammatory)
- acute interstitial nephritis (aka tubulointerstitial nephritis)
children:
- Henoch-Schönlein purpura
- haemolytic-uraemic syndrome
- acute interstitial nephritis
acute interstitial nephritis/tubulointerstitial nephritis:
- usual cause?
- pathophysiology?
- prognosis?
drugs
tubular damage with inflammation
most recover
acute kidney injuey:
- complications? 5
- treatment? 2
- cardiac failure (fluid overload)
- arrythmias (electrolyte imbalance)
- GI bleeding (multifactorial)
- jaundice (hepatic venous congestion)
- infection (esp lung + urinary tract)
- depends on underlying cause
- short term dialysis may be needed
nb with any fluid overload there is a resulting risk of infection
how do the kidneys regulate the acid-base balance in the body?
- excrete acid
- reabsorb bicarbonate (to greater of lesser extents)
what are 4 main groups of effects that chronic renal failure has on the body?
reduced excretion of water/electrolytes:
- > oedema
- > hypertension
reduced excretion of toxic metabolites:
- > itchy
- > confusion
- > fatigue
reduced production of erythropoetin
-> anaemia
reduced activation of vit d
-> renal bone disease
what is isolated proteinuria?
what are the possible benign causes? 3
what could it also be due to?
proteinuria BUT less than nephrotic range
- no allied haematuria, renal failure or oedema
- postural
- related to pyrexia
- related to exercise
renal disease
what does urine sample tend to look like if there is proteinuria?
frothy
isolated haematuria:
- definition?
- possible causes? 4
- investigation needed?
haematuria +/- proteinuria with NORMAL renal function
- IgA nephropathy
- thin basment membrane disease (inherited condition causing abnormally thin glomerular BM - renal function norm normal)
- alport hereditary nephropathy
- malignancy
cystoscopy/urological investigations needed to exclude malignancy
acute pyelonephritis:
- risk factors? 4
- complication?
- female (ascending infection)
- instrumentation (ie catheter)
- diabetes
- urinary tract structural abnormalities
abscess formation
chronic pyelonephritis:
- main risk factor?
- main complication?
urinary tract obstruction -> reflux
- chronic renal failure
renal artery stenosis:
- most common cause?
- other cause?
- pathophysiology?
- long term effect?
most common = renal artery stenosis
- also: arterial dysplasia
ischaemic injury of affected kidney -> activation of renin-angiotensin-aldosterone system (as kidney thinks body is hypovolemic as narrow lumen means low blood flow to kidney) -> HTN -> further damage to kidney = damage spiral
loss of renal tissue -> reduced renal function
how does hypertension cause kidney damage?
HTN -> wall thickening + reduction in lumen size
this -> chronic hypoxia
-> loss of renal tubules + reduced renal function
reduced blood flow activates renin-angiotensin-aldosterone system -> exacerbates HTN
what are the two mechanisms of kidney damage seen in diabetes mellitus?
hyperglycaemia -> damaged/thickened BM
- therefore glomerulus produces excess extracellular matrix -> nodules in kidneys which reduces function
hyperglycaemia -> small vessel damage -> ischaemia -> tubular damage
If you have an elderly patient with acute renal failure and the cause is not pre-renal or due to drugs, what should you suspect and investigate for?
myeloma
what is the most common cause of interstitial nephritis?
adverse drug reactions
causes of urinary tract obstruction:
- within the lumen?
- abnormalities of the wall?
- external compression?
- functional obstruction?
within the lumen:
- kidney stones (calculi)
- strictures (post-procedural, post-infective, congenital)
- neoplasm
abnormalities of the wall:
- congenital anatomical abnormalities
- neoplasm (benign or malignant)
external compression:
- inflammatory conditions (retroperitoneal fibrosis)
- pregnancy
- enlarged prostate (BPH, prostitis, neoplasm)
- tumour outside urinary tract
functional obstruction:
- neurological conditions
- severe reflux
what are the 3 main sequelae of a urinary tract obstruction?
infection
- cystitis, ureteritis, pyelitis, ascending pyelonephritis
stone/calculi formation
kidney damage (acute or chronic)
what is a complication of urethral obstruction?
bladder hypertrophy
what can occur due to chronic ureteric obstruction?
hydroureter
- ureter is distended proximal to obstruction
can then -> hydronephrosis
- dilated calyces, pelvis + cortical atrophy
what are the clinical features of:
- acute bilateral obstruction? 3
- chronic unilateral obstruction? 2
acute bilateral obstruction:
- pain
- anuria
- acute kidney injury
chronic unilateral obstruction
- asymptomatic initially
- often get recurrent UTIs
nb takes a loonnng time for symtpoms to present
renal calculi/urolithiasis:
- M or F?
- peak onset age?
- most common cause?
- other causes? 2
male predominance
peak onset 20-30 years
hypercalciuria
- gout (forms a core for Ca2+ crystal formation)
- hyperoxaluria (hereditary or excess dietary intake)
types of causes of hypercalciuria? 4
- hypercalcaemia
- excessive absorption of intestincal calcium
- inability to reabsorb tubular calcium
- idiopathic
causes of hypercalcaemia? 3
- bone disease
- parathyroid hormone excess
- sarcoidosis
struvite renal stones:
- cause?
- pathogenesis?
- typical appearance on imaging?
urease producing bacterial infection
- urease converts urea -> ammonia
- > rise in urine pH
- > precipitation of magnesium ammonium phosphate salts -> calculi
large ‘staghorn’ calculi
causes of urate renal stones? 3
cause of cystine stones?
urate stones
- hyperuricaemia (caused by gout)
- hyperuricaemia (caused by patient’s with high cell turnover eg leukaemia)
- idiopathic
cystine stones (rare!) - inability of kidneys to reabsorb amino acids
what is the gold standard test for renal calculi?
- test if not available?
non-contrast CT scan
- ultrasound in pregnancy or where CT not available
commonest type of kidney cancer?
norm age of onset?
main risk factor?
- other risk factors? 5
renal cell carcinoma (95%)
- arises from proximal convoluted tubules
- norm ‘clear cell’ tumours
65-80 years
SMOKING
- obesity
- hypertension
- oestrogens
- acquired cystic kidney disease (due to chronic renal failure)
- asbestos exposure
von-hippel lindau syndrome:
- gene mutated?
- type of cancers caused?
inherited mutated VHL gene -> oncogene
- kidneys
- blood vessels
- pancreas
renal cell carcinoma:
- signs/symptoms? 3
- % present with systemic symptoms +/or metastases?
- haematuria
- costovertebral pain (along ribs + back)
- palpable abdominal mass (if big)
25%
name 3 paraneoplastic syndromes associated with renal cell carcinoma (RCC).
what % of people with RCC have a paraneoplastic syndrome?
cushing syndrome
- ACTH
hypercalcaemia
- parathyroid hormone related peptide
polycythaemia
- erythropoietin
1%
most common type of bladder cancer?
urothelial cell carcinoma (aka transitional cell carcinoma)
- 95% of bladder tumours
nb most common in bladder but may arise anywhere from renal pelvis to urethra
urothelial cell carcinoma risk factors? 6
- old age
- male
- smoking
- arylamines (dye used in dye factories)
- Cyclophosphamide (chemo drug)
- radiotherapy
symptoms of urothelial cell carcinoma? 3
- HAEMATURIA (most common)
- urinary frequency
- pain on urination (dysuria)
urine volumes per 24 hrs in:
- healthy people?
- oliguria?
- anuria?
- polyuria?
healthy people: 750-2000ml
oliguria: <400ml
anuria: <100ml
polyuria: >3000ml (+ is not drinking, norm caused by diabetes insipidus)
what things can cause high plasma urea? 4
- high dietary protein
- lots of tissue protein breakdown (eg post surgery or trauma or GI bleed)
- renal problems
- post-renal problems
is more urea reabsorbed into the blood when the kidneys are hypoperfused or hyperperfused? why?
what does this mean clinically?
MORE urea REabsorbed if kidneys are HYPOperfused
- as there is more time for urea to diffuse back into the peritubular capillaries
therefore an early clinical sign of hypovolemia is high blood urea
what is the relationship between plasma creatinine + renal function
not-proportional
GFR can decline hugely and only see a small change in creatinine
- creatinine increases in an exponential fashion
change within individual patient is usually more important than absolute value
how do renal physicians predict when a patient with chronic renal failure will need dialysis or transplantation?
plot graph of the reciprocal of their plasma creatinine over time and extrapolate it to work out when they will need renall replacement therapy (RRT)
When is glomerular filtration rate measured in practise? 2
how is this done?
- kidney donors
- to work out dose of drug needed for some chemo drugs
radioactive substances are used to work it out
what is the formula used to work out creatinine clearance?
when is this used in practise?
(urine creatinine conc, mmol/L x urine volume, ml/24hrs) / plasma creatinine conc, umol/L
very very rarely!!
- hard and complicated to measure practically and different units of measurement make maths hard too
what changes in blood plasma chemistry are seen during the progression of chronic renal failure?
about 50% kidney function:
- increased creatitine
- increased urea
then:
- increased potassium
- decreased bicarbonate
then:
- increased phosphate
- increased uric acid
what four factors are used to calculate eGFR?
- plasma creatinine
- age
- gender (male = worse)
- ethnicity (black = worse)
what would you expect to happen to:
- urine volume?
- urine conc?
- plasma values: Na/urea/creatinine?
- urine values: Na/urea?
in:
- pre-renal kidney failure
- intra-renal kidney failure
pre-renal kidney failure:
- urine volume: low
- urine conc: high
- plasma values of Na/urea/creatinine: all raised
- urine values of Na: low
- urine values of urea: high
intra-renal kidney failure:
- urine volume: low
- urine conc: low
- plasma values of Na/urea/creatinine: all raised
- urine values of Na: high
- urine values of urea: low-ish
nb kidneys aren’t working so can’t concentrate urine or reabsorb Na
what should you always look at in any patient who you suspect kidney damage in?
urine volume!!
define the stages of kidney failure?
stage 1:
- eGFR >90
- normal kidney function but urine findings/structural abnormalities indicate kidney disease
stage 2:
- eGFR 60-90
- mildly reduced kidney fuinction (+stuff in stage 1)
stage 3:
- eGFR 30-60
- moderately reduced kidney func
stage 4:
- eGFR 15-30
- severley reduced kidney func
- planning for RRT
stage 5:
- eGFR <15 or on dialysis
- end-stage kidney failure
- needs transplant/dialysis
symptoms of prostatic enlargement?
known as: lower urinary tract symptoms (LUTS)
- urgency
- hesitancy
- diminished stream size + force
- increased frequency
- incomplete bladder emptying
- nocturia
what is the difference in where BPH (benign prostatic hyperplasia) and where prostate cancer tends to affect the prostate
prostate cancer normally affects peripheral zone
- so can be detected using a digital PR
BPH is more likely to affect the central zone, around the urethra, so is more likely to cause urinary symptoms
what are the 3 pathological changes that occur during the development of BPH?
what is another name for BPH?
- nodule formation
- diffuse enlargement of the transition zone + periurethral tissue
- enlargement of nodules
nodular hyperplasia of the prostate
what are the majority of prostate cancers?
what are the main 5, assumed, risk factors for prostate cancer?
adenocarcinomas
- AGE
- race (african more at risk)
- family history
- hormone levels (high testosterone)
- environmental influences (eg increased consumption of fats)
what is the histological scoring system for prostate cancer?
gleason scoring system
testicular cancer:
- most common type?
- age group norm affected?
- 3 main risk factors?
- ethnicity more likely to be affected?
- symptoms? 3
germ cell testicular cancer
15-50 years
- cryptorchidism (+ other probs with testes)
- family history
- previous testicular cancer in other testes
caucasian
- lump in the scrotum
- dull ache in scrotum
- feeling of heaviness in the scrotum
what is cryptorchidism?
- how can it predispose to testicular cancer?
what is the treatment for it?
what other complications can it cause? 2
one or both testes fail to reach scrotum before birth (or within one year)
testicles need to be cold (are too hot is kept in abdo) -> cancer
orchidoplexy = surgery to move teste into scrotum + permenentley fix it there
- testicular atrophy
- infertility
hypogonadism:
- primary causes? 9
- secondary causes? 4
primary causes:
- undescended testes (cryptorchidism)
- varicocele
- cystic fibrosis
- klinefelter syndrome
- haemochromatosis
- mumps
- orchitis (inflammation of testes)
- trauma
- testicular torsion
secondary causes:
- pituatory failure
- drugs
- obesity
- aging
what types of drugs can cause hypogonadism in men? 4
- glucocoticoids (corticosteroids)
- ketoconazole (antifungal)
- chemo drugs
- opiods
define + name common symptoms of:
- cystitis? 3
- pyelonephritis? 3
- urethral syndrome?
cystitis: - inflammation of the bladder -- dysuria -- urinary frequency -- urgency (also supra-pubic pain/polyuria/nocturia/haematuria)
pyelonephritis:
- upper urinary tract infection
- symptoms of lower UTI
- PLUS abdo/loin pain
- +/- fever (or other signs of systemic infection)
urethral syndrome:
- aka abacterial cystitis
- symptoms of lower UTI without demostrateable infection
asymptomatic bacteruria:
- definition?
- 4 groups commonly affected?
significant bacteruria (with a single organism - WITHOUT symptoms of UTI
- people with catheter
- diabetics
- pregnant women
- elderly women
asymptomatic bacteruria:
- definition?
- 4 groups commonly affected?
- what groups should be treated with Abx? 2
significant bacteruria (with a single organism - WITHOUT symptoms of UTI
- people with catheter
- diabetics
- pregnant women
- elderly women
use Abx:
- pregnant women
- infants
name 5 causes of urinary stasis, which can lead to UTIs
- stones
- strictures
- prostatic hypertrophy
- neoplasm
- pregnancy
name a congenital abnormality which leads to increased likelihood of getting UTIs
vesico-ureteric reflux (VUR)
what is the definition of a complicated UTI, as opposed to an uncomplicated one?
complicated:
- underlying abnormality (structural/functional)
- presence of foreign body (catheter/renal calculi/biofilm)
- children <10
- men <65
uncomplicated UTI = absence of above
organisms causing UTIs:
- most common?
- common in adult women?
- associated with kidney stone?
most common = E. coli
common in adult women = staph saprohyticus
associated with kidney stone = proteus mirabilis
what is pyuria?
what are the causes of STERILE pyuria? 4
the presence of pus in the urine (norm due to a bacterial infection)
- inhibition of bacterial growth (eg already started w antibiotics or specimen contaminated w antiseptic)
- ‘fastidious’ (hard to grow) bacteria (eg TB, anaerobes)
- urinary tract inflammation (renal/bladder stones or other renal disease)
- urethritis (sexually transmitted pathogen - eg gonorrhoea or chlamydia)
for a urine sample looking for UTIs, what part of the stream should you ideal use?
mid-stream
prostatitis:
- 2 types?
- normal bacterial cause?
- normal predisposing factor?
- symptoms? 3
chronic:
- recurrent UTIs with same organism (norm e coli)
- asymptomatic in-between
acute bacterial
- post procedure (eg post-prostate surgery/biopsy)
e coli
- lower urinary tract symptoms
- fever
- tender tense prostate on PR palpation
what 4 things are tested for in a standard U+E blood test?
- urea
- creatinine
- sodium
- potassium
what are the possible complications of chronic kidney disease? 9
why do they occur?
Na + water retention -> HYPERTENSION + increased vascular volume -> HEART FAILURE
uraemia -> MALAISE, FATIGUE, SEXUAL DYSFUNCTION + CNS DEPRESSION (reduced GCS)
lack of vit D activation -> hypocalcaemia + hyperphosphatemia -> HYPERPARATHYROIDISM -> breakdown of bone -> OSTEOPOROSIS
lack of erythropoeitin -> NORMOCYTIC ANAEMIA
describe the effects of ACE inhibitors on the kidney and when they should be used and when they shouldn’t be used
angiotensin II (with ACEi inhibit) constricts the Efferent arteriole -> increased pressure in the glomerulus -> increased filtration
so want to use ACEi in chronic kidney disease to reduce the pressure of the kidneys
however, in AKI, you want to increase the filtration of the kidney so get rid of ACEi increase amount of angiotensin II
- but remember to put them back on it once the AKI is over!!!
