Renal Flashcards
Causes of AKI
Pre- renal (decreased vascular flow)
Renal (damage to glomerulus, intersitium or vessels)
Post-renal- blockage of urinary tract
Pre-renal causes of AKI
- hypovolaemia (dehyd, haemorrhage, D+V, burns, shock)
- reduced CO- HF, MI, sepsis
- Meds- ACEI, ARB, NSAIDs, loop diuretics, aminoglycosides
Renal Causes of AKI
- acute tubular necrosis
- *- vasculitis
- Glomerulonephritis
- *- infiltration- amyloidosis, myeloma, renal cancer
Post-renal causes of AKI
- Intrinsic- stones, clot, UT tumour
- Extrinsic- prostate, neurogenic bladder, blocked catheter
Presentation of AKI
- reduced UO
- colour change of urine (dark, brown)
Fluid overload
- Peripheral oedema
- pulm oedema- SOB, orthopnoea, PND, cough, crackles)
Uraemia
- confusion
- fatigue
- drowsiness, GCS
- N+V
- seizures
Diagnostic criteria fro AKI
1 of:
- raised Cr >=26 in 48hrs
- > =50% rise in Cr above baseline
- UO <0.5ml/kg/hr for at least 6 hours
definition of oliguria
<1ml/kg/hr infants
<0.5ml/kg/hr children
Adults:
<400-500ml daily in adults
17-21ml/hour
0.3-0.5ml/kg/hr
ix for ?AKI
- UO
- FBC, UE, CRP, Coag, LFT, CK
- *- urinalanysis
- *- immunology (autoantibs)
- renals USS
what urinanalysis results would suggest different causes of AKI
- negative- pre-renal
- blood and protein- glomerular
- white cell- infection/intersitital nephritis
what clasificaiton is used for AKI (stages)
- KIDGO
complications of AKI
- anaemia (EPO lacking)
- hyperkalaemia
- metabolic acidosis
- pulm oedema
- uraemia pericarditis
- total renal failure
Management of AKI
Pre-renal cause
- IV fluids
- Sepsis 6
- major haemorrhage protocol
Renal
- stop meds
- steroids
Post-renal
- catherterise
- surgery
General
- fluid balance (BP, skin turgor, JVP, fluid chart)
- monitor Na, K, Ca, Cr, glucose
- tx hyperkalaemia
- refer if no ID cause/moderate AKI
severe- haemodialysis
what is acute tubular necrosis
- ischaemic or nephrotoxic injury to tubular epithelial cells causing AKI
- results in detachment from BM
sx of acute tubular necrosis
- *- hypotension, fluid depletion
- exposure to nephrotoxic substances- contrast, aminoglycoside, abx, CT
- oligo/anuria
- *- poor oral intake, anorexia
- dizziness, malaise
ix ?acute tubular necrosis
- urinanalysis- muddy brown casts (epithelial cells)
* *****- urine Na conc, urine osmolality (ie conc)– high
management of acute tubular necrosis
- fluid balance
- remove toxic agents
definition of anuria
<100ml/day
what is the most common cause of CKD
diabetes
causes of CKD
diabetes
hypercholesterolaemia
HTN
glomerular disease
presentation of CKD
- asx in stages 1-4
- N+V, diarrhoea, anorexia, wt loss
- **- polyuria, nocturia, haematuria
- oedema, pleural effusions (SOB, cough, chest pain, orthopnoea)
- HTN
- *- bone pain, # (Ca, phosphate reab issues)
- *- prox muscle weakness (Ca, reabs issues)
- neuro- polyneuropathy, confusion
- uraemic pericarditis- chest pain worse on insp and lying), coughing
- skin pigmentation/darkening- pigments that are usually excreted are retained
ix ?CKD
- UE
- FBC- anaemia
- HbA1c, lipids
- PTH, Ca, Phosphate, vit D
- urinanalysis- proteinuria, haematuria
- urine albumin-Cr ratio– >3mg/mmol clinically relevant pronteinuria
- renal USS- obstruction, FH PCKD
Classification of CKD
1- eGFR >90 plus kidney damage (strctural/haematuria/proteinuria >3m) 2- eGFR 60-89 plus kidney damage 3a- eGFR 45-59 3b- eGFR 30-44 4- eGFR 15-29 5- eGFR <15
management of CKD
- monitor eGFR and alb-Cr ratio
- smoking, alcohol, wt/diet
- avoid NSAIDs and other nephrotoxics
- pneumococcal and flu jabs
- bisphos, vit D and Ca supplements
- PO iron, IV iron, recombinant EPO/erythropoietic stimulatign agent
- manage HTN
- statins
- antiplatelets
- renal replacement
indications for renal replacement therapy
Severe AKI
- unresponsive acidosis
- unreposnsive electrolyte abnormalities, esp hyperkalaemia
- oedema
- uraemia, seizure, GCS, encephalopathy
- pericarditis
LT
- CKD stage 5
types of renal replacement therapy
Intermittent haemodialysis-
- AV fistula
- *- 3-4 times p/w, 3-4 hours
- infection, thrombosis, aneurysm in fistula, stenosis, STEAL syndrome (distal limb ischaemia), **high output HF (increased venous retrun to heart)
Peritoneal dialysis
- pt can do in own time, independence
- bacterial peritonitis, peritoneal sclerosis, wt gain, **LT ascites
Continuous-
- on ward, more unwell pts
- no toxin build up
what would suggest O/E of a renal transplant
- mass palpable in iliac fossa (usually R)
- Rutherford Morrison (reverse hockey stick ie long curved scar, usually in RIF).
- may have palpable AV fistula
- may have mutiple abdo scars due to dialysis insertion/exit sites (peritnoeal)
pathopysiology of renal arteyr stenosis
- atherosclerosis
- impaired renal BS
- juxtaglom apparatus detects
- renin released
- RAAS activated
- HTN
RAAS system
- low BP detected by juxtoglomerulus apparatus
- renin released
- angiotensinogen–> angiotensin I
- ACEI causes angio I–> II
- angio II causes aldosterone from adrenals plus vasoconstriction
- alosterone– reabs Na and water
where is angiotensinogen released from
liver
sx of renal artery stenosis
- **Flash pulm odema (recurrent)
- dyspnoea
- orthopnoea
- cough- frothy, blood
- wheezing
- weak, thirst, confusion, irritable (hypernatraemia)
- twitches, cramps, paralysis, arrhythmias (hypokalaemia)
- *- confusion, tremor (metabolic alkalosis)
- double vision, headaches
signs of renal artery stenosis
- sudden onset HTN
- tx resistant HTN
- worsening eGFR (ischaemia)- esp after starting ACEI
deranged U&Es - metabolic alkalosis
- HTN retinopathy on fundocscopy
ix ?renal artery stenosis
- UE, aldosterone to renin ratio
- renal USS
- duplex/doppler US
- CT/MRI angiography
tx renal artery stenosis
- diuretics
- angioplasty, stenting
- lifestyle
- manage diabetes
- antiplatelets, statins
presentation of glomerulonephritides
- asx
- nephritic or nephrotic syndromes
- chronic/end-stage- anaemia, bone disease
ix ?glomerulonephrtides
- bloods- inflam markers, protein levels, antibodies
- renal biopsy
What is Nephrotic Syndrome
- large proteinuria (>=3.5g/day)
AND - hypoalbuminaemia (<=30g/L)
- cause by non-proliferative glomerulonephritis
- also has hyperlipidaemia- liver compensates fro reduces albumin by also increasing lipid production
- loss of Ig proteins
- loss of antithrombotic proteins
sx nephrotic syndrome
- oedema- ascites, effusion
- immunosupression, recurrent infections
- clotting (urinary loss of antithrombotic proteins, increased prod of prothombotic factors)- renal vein thromb, PE, DVT
- frothy urine (proteinuria)
What is nephritis syndrome
- small proteinuria
- haematuria (micro or macro)
- reduced renal function– reduced UO– HTN
+- oedema - caused by proliferative glomerulonephritis
- red cell casts in urine (indicate glomerular damage)
Name some non-proliferative glomerulonephritis
- focal segmental glomerulosclerosis
- minimal change
- membranous glomerulonephritis
what type of renal syndrome do non-proliferative glomerulonephritides cause
- nephrotic
who does focal segmental glomerulosclerosis affect
adults
pathophysio of focal segmental glomerulosclerosis
- non proliferative
- segmental scarring of glomeruli and fusion of foot processes
- idiopathic
- HIV, lupus, reflux nephro
who does minimal changes disease tend to affect
2-6yo
causes of minimal change disease
- idiopathic
- paraneoplastic- Hodgkins
- drugs
sx of minimal change disease
- oedema / wt gain
- in a child
pathophysio of membranous glomerulonephritiis
- non-proliferative
- IgG deposition, thickening of glomerular cap wall
- glomerular PLA2R antigen targetting
- mostly caused by autoimmune disease
- can also be caused by infection, drugs, tumour
presentation of focal segmental glomerulosclerosis and membranous glomerulonephritis
- facial swelling
- oedema
- HTN
- renal failure (reduced UO)
who does membranous glomerulonephritis tend to affect
adults, slow
ix of non-proliferative glomerulonephritides/nephrotic syndromes (focal segmental glomerulosclerosis, minimal change, membranous)
- urinanalysis- large proteinuria
- PLAR2 ab in urine (membranous)
- renal biopsy
management of non-proliferative glomerulonephritides/nephrotic syndromes (focal segmental glomerulosclerosis, minimal change, membranous)
- prednisolone
cyclophosphamide/ciclosporin - salt/fluid restriction
- correct cause (infection, drug, autoimmune disease)
what would yuo see on renal biopsy of the different non-proloferative glomerulonephritides
focal segmental glomerulosclerosis
- segmental scarring of glomeruli
- fusion of foot processes
minimal changes
- no changes on light micro
- effacement of podocyte foot process on electrone
- no deposits or ig complements
Membranous
- Ig deposits on immunofluoresent staining
- thickened BM
Name proliferative glomerulonephritis
- IgA (berger’s)
- post- strep
- anti-glomerular BM
- rapidly progressive
what renal syndrome do proliferative glomerulonephritides tend to cause
nephritic
what is igA nephropathy
- igA deposits
- proliferative glomerulonephritis
- occurs post- URTI
sx of igA nephropathy
- frank haematuria
- after URTI
- can cause henoch-schonlein purpura in children- deposits in skin, GI tract
management f igA nephropathy
- ARB, ACEI (BP control)
- low cholesterol diet
- immunosupresison- steroids, cyclophosphamide, azathioprine for remission
most common proliferative glomerulonephritis
igA nephropathy/Berger’s
most common non-proliferative glomerulionephritis
adult- focal segmental glomerulosclerosis
children- minimal change
ix for any cause of ?nephritic syndrome/proliferative glomerulonephritis (frank haematuria)
- dipstick
- renal biopsy- to find cause
- serology for autoab
what is post-strep glomerulonephritis
- proliferative glomerulonephritis
- immune glomerular injury triggered by strep infection (2w following)
- generally self limiting
what is the specific antibody found in post- strep glomerulonephritis
anti-streptococcal antibody titres
management of post-strep glomerulonephritis
fluid balance
supportive
self limiting
what is anti-glomerular basement membrane disease
- autoimmune attack of basemement membrane antigens located in glomeruli and alveoli
sx anti-glomerular BM disease
- nephritic syndrome- haematuria, HTN, oedema
- haemoptysis, cough, SOB- Goodpasture’s syndrome!