Kidneys: AKI, CKD (Alport, ADPKD, Amyloidosis) Flashcards

1
Q

What are the 6 main functions of the kidney

A

Electrolyte, fluid balance
Waste clearance
pH regulation
Hormone action site
-ADH, Aldosterone, PTH, ANP
Hormone production site
-renin, vitamin D, erythropoietin, prostaglandins
Gluconeogenesis

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2
Q

Describe the 3 stages of AKIs
- serum creatinine
- urine output

A

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

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3
Q

What are some causes of prerenal AKIs
- Volume depletion
- Drugs
-how to identify

A

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

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4
Q

What are some causes of intrinsic AKIs
- ATN
- Acute glomerulonephritis
- Acute interstitial nephritis
- Vascular
-how to identify renal causes

A

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

Glomerulonephritides
Urine dip - haematuria

Kidneys can no longer concentrate urine or retain Na
Serum urea:creatinine ratio normal

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5
Q

What are some causes of post renal AKIs
-how to identify post renal causes

A

Obstruction => hydronephrosis, loss of corticomedullary diff
- stones
- strictures
- BPH, cancers
- retroperitoneal fibrosis

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6
Q

What are the 4 consequences of AKIs

A

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

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7
Q

What are the 4 steps in managing AKIs

A
  1. Exclude life threatening complication
  2. Address cause
  3. Support
    • Nutrition
    • Ulcer prophylaxis
  4. Avoid progression
    • Aminoglycosides, gentamicin
    • hypotension, hypovolemia
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8
Q

AKI presentation

What investigations would you do for a suspected AKI?

A

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?

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9
Q

Which drugs are safe to continue in AKI?

A

Aspirin at cardiac dose 75mg
Bb
Clopidogrel
Statins
Paracetamol
Warfarin

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10
Q

Which drugs should you stop in AKI as renal function may deteriorate

A

NSAIDS except aspirin at cardiac dose
Aminoglycosides
ACEi, ARB
Diuretics

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11
Q

Which drugs should you stop due to an increased toxicity risk?

A

Don’t usually worsen AKI
Digoxin
Lithium
Metformin

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12
Q

Describe how kidney function changes in
- normal people
- AKI with recovery
- AKI without recovery
- CKD progressing to ESRF

A

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

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13
Q

What are the 5 stages of CKD
How frequently should you test each stage?
How would you judge the prognosis

A

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

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14
Q

CKD
-presentation
-risk factiors
-investigations

A

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

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15
Q

Conservative management of CKD

A

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

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16
Q

Conditions to look after in CKD

A

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

17
Q

How to differentiate between AKI and CKD

A

Renal US
CKD - bilaterally small unless
-ADPKD
-early diabetic nephropathy
-amyloidosis

Low Ca due to lack of VitD in CKD

18
Q

When to refer to nephrologist in CKD

A

eGFR Stage 4-5
Progressive fall by 15+ in a year

19
Q

Causes of CKD

A

Diabetic nephropathy
Chronic glomerulonephritis
Chronic pyelonephritis
HTN
ADPKD

20
Q

Hydronephrosis
-causes
-investigations
-management

A

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

21
Q

Alport Syndrome
-what is it
-inheritance
-presentation
-diagnosis
-management

A

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

22
Q

ADPKD
-what is it
-inheritance
-presentation
-diagnosis
-management

A

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

23
Q

Amyloidosis
-what is it
-presentation
-diagnosis
-management and subtypes

A

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

24
Q

Considerations for contrast in CKD
-what are the agents used
-what problems can they cause
-how to consider when contrast is needed

A

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