Kidneys: AKI, CKD (Alport, ADPKD, Amyloidosis) Flashcards
What are the 6 main functions of the kidney
Electrolyte, fluid balance
Waste clearance
pH regulation
Hormone action site
-ADH, Aldosterone, PTH, ANP
Hormone production site
-renin, vitamin D, erythropoietin, prostaglandins
Gluconeogenesis
Describe the 3 stages of AKIs
- serum creatinine
- urine output
Stage 1
C 1.5-1.9x from baseline
+26.5umol/L in 2 days
U <0.5ml/Kg/h for 6+hrs
Stage 2
C 2-2.9x from baseline
U <0.5ml/Kg/h for 12+hrs
Stage 3
C 3x from baseline
+353.6umol/L
U <0.3ml/Kg/h for 24+hrs
anuria for 12+hrs
What are some causes of prerenal AKIs
- Volume depletion
- Drugs
-how to identify
Volume depletion
- hypovolemia
- renal artery stenosis
Drugs
- NSAIDs => low PGIs => no afferent VD
- ACEi => low Ang2 => no efferent VC
Kidneys still have ability to concentrate urine, retain Na
Urea:creatinine ratio disproportionately raised
What are some causes of intrinsic AKIs
- ATN
- Acute glomerulonephritis
- Acute interstitial nephritis
- Vascular
-how to identify renal causes
Intrinsic damage to kidney structures themselves
Most common - ATN from prolonged ischemia or toxins
-radiocontrast, aminoglycosides
-heme from rhabdomyolysis, hemolysis
-crystals
Urine dip - no inflammation, no WCC
Rarer - AIN
-drugs - penicillin, PPI, pain free (NSAIDs), pee (diuretics), rafamPicin
- infection
- systemic disease
Urine dip - WCC
Allergic type blood test picture
Systemic upset - fever rash, joint pain
STOP CAUSATIVE DRUG
SUPPORTIVE CARE
-diuretics
CS if needed
Glomerulonephritides
Urine dip - haematuria
Kidneys can no longer concentrate urine or retain Na
Serum urea:creatinine ratio normal
What are some causes of post renal AKIs
-how to identify post renal causes
Obstruction => hydronephrosis, loss of corticomedullary diff
- stones
- strictures
- BPH, cancers
- retroperitoneal fibrosis
What are the 4 consequences of AKIs
Supportive management and address underlying cause
Reduced urine output => pulmonary, peripheral edema
- diuretics
- ventilation/intubation if severe
Uraemia
-pericarditis, pleurisy, encephalopathy => RRT
Hyperkalaemia (5.5+)
- Ca gluconate
- Insulin dextrose/salbutamol neb
- Remove K (Ca resonium/loop/dialysis)
Metabolic acidosis
- abdo pain, N+V, muscle weakness
- palpitations
- SOB
If not responding => RRT
What are the 4 steps in managing AKIs
- Exclude life threatening complication
- Address cause
- Support
- Nutrition
- Ulcer prophylaxis
- Avoid progression
- Aminoglycosides, gentamicin
- hypotension, hypovolemia
AKI presentation
What investigations would you do for a suspected AKI?
Reduced urine output - U0.5ml/kg/hour
Fluid overload - pulmonary, peripheral edema
High K, U, C - uremia, arrythmias
Urgent ABG, U&E => high urea, creatinine with electrolyte imbalances
Urinalysis
AKI of unknown etiology - US within 24hrs
-renal or post renal?
Which drugs are safe to continue in AKI?
Aspirin at cardiac dose 75mg
Bb
Clopidogrel
Statins
Paracetamol
Warfarin
Which drugs should you stop in AKI as renal function may deteriorate
NSAIDS except aspirin at cardiac dose
Aminoglycosides
ACEi, ARB
Diuretics
Which drugs should you stop due to an increased toxicity risk?
Don’t usually worsen AKI
Digoxin
Lithium
Metformin
Describe how kidney function changes in
- normal people
- AKI with recovery
- AKI without recovery
- CKD progressing to ESRF
Normally GFR declines with age
AKI with recovery => GFR suddenly declines but recovers
AKI without recovery => GFR suddenly declines and stays low
CKD progressing to ESRF => rapid decline in GFR
What are the 5 stages of CKD
How frequently should you test each stage?
How would you judge the prognosis
Stage 1 => 90+ + U&E/proteinuria changes
-0-1x
Stage 2 => 60-89 + U&E/proteinuria changes
-0-1x
Stage 3 => 30-59
-1-2x
Stage 4 => 15-29
-2-3x
Stage 5 => U15, ESRF
-4x
Cause
GFR
Albuminuria/proteinuria
CKD
-presentation
-risk factiors
-investigations
Asymptomatic until late stage
Edema
Polyuria
Tired
Uremia => itch, N/V
HTN, DM, high cholesterol
Kidney - infection, AKI, ADPKD
BPH
eGFR and ACR
-if eGFR U60, repeat within 2wks
-if no evidence of AKI, repeat in 3 months
Diagnosis made if persistent low eGFR and high ACR
Conservative management of CKD
Conservative
- smoking cessation, alcohol reduction
- healthy diet, weight
- annual vaccinations
- avoid NSAIDs, nephrotoxics where possible
- CV risk factor reduction
Manage conditions that affect kidneys
- lupus nephritis - immunosuppresion
- myeloma - chemo
Conditions to look after in CKD
ACE/ARB + STATIN!
BP
-ACEi => 25% fall in eGFR, 30% rise in creatinine ok
-furosemide if GFR U45
Proteinuria
-ACR - 1st morning urine
3-70 => retest to confirm
70+ => confirmed
Refer to nephrology
ACEi + SGLT2
Normocytic anemia - manage if symptomatic or HbU110
-Fe, B12, folate optimisation => EPO if needed
2ndary hyperPTH - dietary
-reduce PO4 dietary intake
increase Ca, VitD intake (alfacalcidol, calcitriol)
-PO4 binders - calcium based/sevelamer
- remove PT gland surgically
Metabolic acidosis => PO bicarbonate
How to differentiate between AKI and CKD
Renal US
CKD - bilaterally small unless
-ADPKD
-early diabetic nephropathy
-amyloidosis
Low Ca due to lack of VitD in CKD
When to refer to nephrologist in CKD
eGFR Stage 4-5
Progressive fall by 15+ in a year
Causes of CKD
Diabetic nephropathy
Chronic glomerulonephritis
Chronic pyelonephritis
HTN
ADPKD
Hydronephrosis
-causes
-investigations
-management
Pelvic ureteric obstruction
Aberrant renal vessels
Stones
Renal pelvis tumours
Vesicoureteric reflux
Prostate enlargement
US - identify hydronephrosis
CT KUB - identify stone
Remove obstruction and drain urine
Acute obstruction => nephrostomy tube
Chronic obstruction => stent or pyeloplasty
Alport Syndrome
-what is it
-inheritance
-presentation
-diagnosis
-management
Type IV collagen defect => abnormal GBM
X linked - so more severe in men
Triad of renal failure (microscopic hematuria) + bilateral sensorineural deafness + retinitis pigmentosa and lenticonus
Genetic testing
Renal biopsy - longitudinal splitting of GBM => basket weave appearance
Management aim - slow rate of CKD
-ACEi/ARB for HTN
-diuretics and Na restriction
ADPKD
-what is it
-inheritance
-presentation
-diagnosis
-management
Most common inherited kidney disorder - AD
Symptoms develop between 30-60 when cysts are large enough to affect kidney function
Renal, hepatic cysts
Aneurysms, aortic root dilation
Hameturia
Loin pain
HTN
Recurrent UTIs
Kidney stones
Signs of renal failure
Renal US
U&E - renal function
Management aim - slow progression to ESKF
-HTN
-rule out other causes of renal pain - stones?
-Tolvaptan (ADH antagonist) - may slow cyst development and renal failure
Amyloidosis
-what is it
-presentation
-diagnosis
-management and subtypes
Extracellular and intracelluar tissue deposition of insoluble amyloid fibrils => prevents normal functioning of tissues and organs affected
Non specific - SOB, weight loss, fatigue
Renal - nephrotic syndrome
Cardiac - heart failure, syncope from arrythmia, MI
GI - hepatosplenomegaly
-cholestatic picture
Neuro - ischemic stroke, peripheral/autonomic neuropathy
Gold standard - biopsy
-Congo red staining with apple green birefringence under polarised light
Renal involvement
-urindip - protein
-U&E - high creatinine
-FBC - anemia, low platelets
Cardiac
-ECG - poor R wave progression in limb leads
-echo - ventricular wall thickening
GI
-LFTs - cholestatic
-clotting - high INR
-film - howell jolly bodies (reduced splenic function)
Management depends on subtype
AA - complication of long term inflammatory conditions
AL - associated with MM
Considerations for contrast in CKD
-what are the agents used
-what problems can they cause
-how to consider when contrast is needed
CT - iodine based contrast
=> contrast induced nephropathy
-rapid decrease in renal function in 48-72hrs
-renal symptoms - anorexia, N/V, fluid retention, tired
-reversible condition
MRI - gadolinium based contrast
=> nephrogenic systemic fibrosis
-burning, itching, red/dark patches on skin
-joint stiffness, muscle weakness
-develops within 24hrs to 3 months
No specific treatments but symptoms may improve with time
