Pre-Renal Disease Flashcards by Aarya Sumesh

Clinical and morphological presentation of renal diseases:

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Acute Kidney Injury (AKI):

occurs when sudden decrease in
GFR
GFR maintained by sufficient blood
flow to the kidneys and nephron
usually reversible
GFR dependent on a pressure
gradient between the incoming
blood at the afferent capillaries and
pressure in the Bowman’s space: net
filtration pressure

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AKI: Pre-Renal Disease:

hypoperfusion: reduced perfusion
to the kidneys in afferent arteriole
occurs whether a patient has
hypovolaemia, euvolaemia,
hypervolaemia

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5 causes of pre-renal injury:

intravascular volume depletion:
absolute hypovolaemia (most
common)
decreased cardiac output
renal vasoconstriction
renovascular diseases (anatomical)
drugs that impair autoregulation
and GFR in specific setting by
affecting vascular tone of afferent
and efferent arterioles

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Pre-Renal Injury: Intravascular Volume Depletion- Absolute Hypovolaemia:

Haemorrhage: trauma, surgical, GI
GI losses: diarrhoea, vomiting
Renal losses: drug induced/osmotic
diarrhoea, diabetes
insipidus, adrenal
insufficiency
Skin/Mucous Membrane: burns,
hyperthermia
Third Space losses: pancreatitis,
hypoalbuminaemia

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Causes of Pre-Renal Injury: Decreased Cardiac Output:

Diseases of myocardium,
pericardium, valves, conducting
system
Pulmonary hypertension, PE,
positive pressure mechanical
ventilation
systemic vasodilatation: sepsis, liver
failure, anaphylaxis
Drugs: antihypertensives,
anaesthetics, drug overdose

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Causes of Pre-Renal Injury: Renal Vasoconstriction (4):

noradrenaline (sepsis treatment
when BP drops, too much NA causes
contraction)
liver disease
sepsis
hypercalcaemia

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Causes of Pre-Renal Injury: Renovascular Diseases - Anatomical:

atheroscleorsis (lipid deposition in
tunica media spills over into intima
narrowing blood vessels, rupture
results in thrombosis and narrowing
of renal arteries.
thromboembolic disease
renal artery dissection

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Causes of Pre-Renal Injury: Drugs:

ACE inhibitors
- inhibition of prostaglandin
synthesis by NSAIDs during renal
hypoperfusion
Angiotensin II receptor blockers:
candesartan

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AKI causing Drugs: PCT:

tubular cell toxicity
aminoglycosides
amphotericin B
cisplatin

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AKI Causing Drugs: Interstitial Nephritis:

NSAIDs
Rifampicin

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AKI Causing Drugs: Renal Tubules/Blood Vessels:

acyclovir
ampicillin

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ACE Inhibitor Therapy Worsening Renal Function:

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efferent arteriole constricted to maintain pressure for GFR
ACE inhibitor dilates efferent arteriole, reducing intravascular pressure, reduces GFR.

NSAIDs:
constriction of afferent arteriole and therefore reduce GFR

Long term ACE inhibitor protects the small blood vessels from high blood pressure or high intra-glomerular pressure from glomerular sclerosis = renoprotective

only stop in acute situations

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Acute Kidney Injury: Renal:

develops when there is a disruption
to the anatomy or function of the
nephron
can occur independently or as a
consequence of pre-renal AKI
defined by the area of nephron
disruption

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Acute Kidney Injury: Renal Causes:

Acute Tubular Necrosis:
- most common
- ischaemia/ toxic injury to PCT
Acute Interstitial Nephritis:
- Drug induced: NSAIDs, penicillin
- Infection: TB
- Immune-mediated: SLE, sarcoid
Glomerular Disease:
- Nephrotic/Nephritic Syndrome
- primary: antiglomerular
basement membrane
disease
- secondary: immune complex
mediated: IgA
nephropathy
Tubular Obstruction:
- Meyloma
- Rhabdomyolysis

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Acute Kidney Injury: Post-Renal:

following acute obstruction of
urinary flow
increased intra-tubular pressure
and reduction in GFR
acute urinary tract obstruction leads
to impaired renal blood flow and
inflammatory processes
contributing to diminished GFR

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Acute Kidney Injury: Post-Renal Causes:

Ureter: stones, RFP, ureterocoele
Bladder: malignancy
Prostate: cancer, BPH
Urethra: stricture disease, posterior
urethral valve
Extrinsic compression of ureters:
pelvic malignancy, lymph nodes

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Causes of Acute Kidney Injury:

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Pre-Renal AKI Symptoms:

severe dehydration symptoms:
- sunken eyes
- dry skin
- decreases skin elasticity
- dry mouth and eyes
- tachycardia
- dizziness standing or sitting up:
orthostatic hypotension

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AKI: Diagnosis: Pre-Renal:

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Pathophysiology of Pre-Renal AKI:

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Pre-renal insult and renal injury both result in AKI but pre-renal is

reversible
renal is often reversible but can lead to CKD

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Distinguishing Pre-renal insult from acute tubular necrosis

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Renal Disease involves

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parenchymal changes

Acute Kidney Injury

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Chronic Kidney Disease occurs how many days after the acute kidney injury

>90 days

AKI Staging:

- stage 1: serum creatinine 1.5-1.9x reference value - stage 2: 2.0-2.9x reference value - stage 3: 3.0x reference value

Pre-Renal Acute Kidney Injury can lead to acute tubular necrosis. true or false?

true pre-renal can lead to parenchymal changes seen in renal disease

Chronic Kidney Disease:

- kidney waste filtration becomes worse over time - gradually develops - result of chronic illnesses like diabetes and hypertension - patients often asymptomatic and often discovered incidentally

Causes of chronic kidney disease:

- diabetes mellitus (type 1& 2) - uncontrolled hypertension - chronic glomerulonephritis - hereditary renal diseases - chronic tubulointerstitial nephritis - congenital kidney anomalies - chronic pyelonephritis - renal stones and obstructive uropathy - chronic infection of kidney: TB

Stages of chronic kidney disease

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Staging of CKD:

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Relationship between GFR and Creatinine in early stages of AKI

- reduction in GFR may coexist with normal serum creatinine

Renal Vascular Disease:

- affects blood flow to and from kidneys - causes kidney damage, failure and high BP - manifestation of renal vascular disease: - Renal Artery Stenosis (RAS) - Renal Artery Thrombosis

Renal Artery Stenosis:

- manifestation of renal vascular disease - causes kidney injury and high BP - smokers - high cholestrol, triglycerides, diabetes, obesity, heart disease family history

Renal Artery Thrombosis:

- manifestation of renal vascular disease - blood clot in the renal artery

AKI Investigations:

- bloods: FBC (high urea, creatinine) (anaemia if loss of blood) (WBC high if sepsis) - serological: U&E, CRP, multiple myeloma screen (blood and urine) - Blood and Urine Cultures (bacteraemia) - Urine Microscopy - urine Dipstick: blood, proteins, WBC CRP = inflammation - immunological tests: - ANCA, ANA, dsDNA (serum) - Viral serology: Hep B/C, HIV - Imaging: CXR, USS Kidney Ureter Bladder, Ct KUB - Renal Biopsy: intrinsic renal disease ABG: - metabolic acidosis: low pH, low pCO2, low bicarb

Management of AKI

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Treatment of Pre-renal AKI:

- fluids - maintain sufficient BP - antibiotics for sepsis - renal replacement therapy (RTT): - fluid overload - hyperkalaemia - metabolic acidosis - uraemia