ACUTE RENAL FAILURE
BY
PROF. WALE AKINSOLA
Deparment of Medicine,
Obafemi Awolowo University,
Ile-Ife
ACUTE RENAL FAILURE
DEFINITION:
RAPID DECREASE OF RENAL FUNCTION
INCREASE SCr &Urea
Oligo-Anuria ~ 20ml/hr (Non 0liguric in ~ 30%)
Etiology
a. Post Renal – Mainly obstructive uropathy
b. Pre –Renal - decreased Arterial BP
- decreased Blood Volume
- decreased Circulating Vol.
[Shock state, infection)
c. Renal –as in b.
- Hemepigments
- Haemolysis
- Rhabdomyolysis
- Nephrotoxins;Chemicals
Drugs
Pregnancy –related – Abruptio placenta
- Haemorrhage
- Eclampsia
- Postpartum
Others: GN etc
Pre-renal Renal
[Link] < 10mmol/L > 30mmol/L
[Link] high (>500mOs low
Osm.U/serum > 2.0 < 1.1 approaching 1
U/P Urea > 20 <3
U/P Creat. > 40 < 10
SG. > 1020 < 1020
Pre-renal:
Hypotension
Reduced Cardiac Output
Reduced Circulation Vol. - Septicaemia
- Endotoxic Shock
- Anaphylactic Shock
Hypovolaemia
Haemorrage
GIT Loss (Diarrhoea & Vomitting) Aspiration
Burns, peritonis, severe NS
Urinary loss (Diuretics, Diabetes insipidus)
Vascular Disease:
Arterial Thrombosis, Embolism
Aortic Aneurysm
Renal:
Arterial or ateriolar disease
Malignant HT
Vasculitis (polyart, DIC, HUS)
Post-partum Renal Failure
Glomerulonephritis:
AGN
Crescentic GN
Tubular
Nephrotoxicity (Herbal prep.)
(Antibiotics)
Obstruct. (myeloma, urates, sulphonamides)
Rhabdomyolysis
Hepatorenal
Metabolic (Acidosis, Hypercalcaemia)
Acute Interstitial Nephritis (Antibiotics,
Diuretics)
Nephrotoxins
Infections (bacterial, viral)
Post-renal:
Obstruction
Luminal (calculi, [Link])
Mural (Tumours, TB, Prostatic hypertophy)
Extramural retroperitoneal fibrosis, malignancies)
INFECTION-INDUCED ARF
Protozoa - Malaria, Pneumocytostis
Spirochaetal - Leptospirosis
Bacteria - Salmonelia, Staph, TB,
Legionella, GR-ve Infections
Rickettsia - Q-fever
Chlamydia - Psittacosis
Viral - HIV-related,Cocksachie,
Hanta, CMV, .
RHABDOMYLOYSIS-INDUCED ARF
Direct muscle damage
Crush injury Prolonged combats
Eclampsia Severe muscle exertion Electroshock injury
Metabolic
Hypokalaemia CO poisoning DM Ketoacidosis
Hyperpyrexia
PATHOGENESIS
a. Underperfusion with shunting of blood
cortex [25 – 75%]
b. ? Renin-Angiotensin/prostagladin, ADH
c. Tubular factors
Blockade by casts
Rupture of tubules with increased back diffusion of gl.
filtrate
d. Glomerular factors
decreased permeability of [Link]
decreased filtration area
CLINICAL FEATURES
Urine Volume: * Oliguria - < 20ml/hr or < 400ml/day
* Anuria - < 50ml/day
* Non-oliguric (normal or sed
volume)
Electrolytes disturbances
Hyperkalaemia – associated with metabolic acidosis
(may lead to cardiac arrhythmias & cardiac arrest
in dyastole
Hyponatraemia: Dilution from fluid overload
Hypocalcaemia: may connote a reduction of renal
α1-hydroxylase
Or
Hypocalcaemia: – may occur in Rhabdomyolysis
Fluid Balance: Hypovolaemia – with classical
features
Fluid Overload – Peripheral oedema or pulmonary
oedema
ACID-BASE Balance: Commonly metabolic acidosis
Or
metabolic alkalosis
in the presence of vomiting & ng aspiration
SYSTEMIC EFFECTS:
Uraemia: * a few days into illness
* clouding of consciousness
* confusion
* disorientation and coma
Cardiac Effects:
* cardiomegaly in fluid overload
* cardiac arrhythmias in electrolyte
disturbance
Respiratory Rate:
* Tarchypnoea -> acidosis / pulmonary oedema
* Tarchypnoea
* Pulmonary oedema
* Haemoptysis - pulm oedema – Good Pasture’s
syndrome
Common Anemia:
* blood loss, haemolysis reduced
erythropoesis, bleeding tendencies /
Other Effects:
* Gastro-intestinal – nausea / vomiting etc
* haemorrhage
Infections:
* may complicate the course
NEED TO DISTINGUISH ARF FROM CRF
Long standing history of HT
Repeated episodes of UTI
Previous history of proteinuria / frothy urine / haematuria
Previous history of oedema
Long standing history of analgesic abuse
Findings: * target damage from hypertension
* cardiomegaly,
fundoscopic changes
Presence of normochronic / normocytic anaemia
Presence of osteodystrophic changes
Presence of shrunken kidneys by USS
OR
Polycystic renal disease
DIAGNOSIS
History & Physical Examination
Signs of Dehydration, BP (Previous data)
Urine
Blood
Chest X-ray, ECG, X-ray Abdomen – stones, renal size
IVU, USS, Retrograde Pyelography
? Renal BX – indicated in intrinsic R F
Exclude ATN - ? Wegener’s
- ? AntiGBM
- Interstitial nephritis
DRUG-INDUCED ARF
Nephrotoxicity
Antibiotics – Aminoglycosides, Tetracycline,
Rifampicin,
Sulphonamides,
Cephalosporin, Amphotericin, Cy A
Metals - Hg, B. Ag. Pb.
Organic Solvents CCl4,
Acute Interstitial Nephritis
Antibiotics – Methicillin, Rifampicin, Sulph,
Erythromycin
Diuretics - Thiazides, Frusemide
Others - Cimetidine, Naproxen,
Allopurinol, Fenoprofen
Rhabdomyolysis / Haemolysis
Primaquine [G6PD], Phenytoin, Phencyclidine
Obstruction
Chemotherapy – Lymphoma / Leukaemia
GN: Organic solvents, Heroine abuse, Penicillamine
Polyarteritis Syndrome: Sulphonamides, Phenytoins,
Phenicillin, DIC Oral Contraceptives, Ergotrates
Ischaemic / Nephrotoxic Injury
Disruption in the integrity of cell membrane
- reduced intracellular PO2 – Rapid influx of Ca++
- Mitochondrial activity reduced – Uncoupling of oxidative
- increased anaerobic glycolysis
- increased lactate & H2+
- protein denaturing – cell necrosis / karyolysis
- regeneration – 10 – 20 days
U/P Osmolality
>2 Approaching 1
[Link] low
Hypovol. IVP, Renal Imaging (scans)
Appropriate Replacement Kidneys normal small kidney
Intrinsic Renal Failure
[Link] high [Link] low [[Link] flt. Na+ decrease
RBC casts in urine
Fractional excretion
of flt. Na increase
Vasomotor nephropathy GN
Bx.
Pre Renal ATN GN[Vasculitis] CRF
N. Urinary sed. Prot+ RBC+ Prot++
Tub. Cells Prot+ RBC
Low cast(graph)
Non-Oliguric
U/P – [1.1 – 1.5]
[Link] higher than in PreRenal
Fractional Excretion of flt. Na borderline
Usual causes – Drugs
Prognosis: dialysis infrequent
Mortality
General Clinical Course
Oliguric / Diuretic / Recovery
Fluid / electrolyte {overload}***
Azotaemia
Acidosis
K+ & Cardiac
GIT
Haemorrage
Infection. Neurological / Psychiatry
MANAGEMENT
Emergency Resuscitation – Dangerous K
increases, / Acidosis/Pulmonary edema
Rapid Diagnosis of underlying Aetiology
Correction of metabolic abnormalities
Prevention of further renal damage
Control of blood chemistry during established
phase
Careful fluid and electrolysis balance during
recovery phase
USEFUL HINTS
FLUID / ELECTROLYTE / ACID-BASE status
FLUID – OVERLOAD / DEHYDRATION? BP status?
ELECTROLYTE K increase – Cardiac Arrhythmias
Immediate correction – Glucose / insulin, Calcium
resin
HYPOXIA – Shock / Pulm Oedema
METABOLIC ACIDOSIS: PH < 7 – infusion 1.4%
NaHCO3
LACTIC ACIDOSIS [Shock]
Any PMH of Renal Disease
OR
Evidence of pre-existing Renal Disease
Is Renal Failure Established? – Trial of
Diuretics – Mannitol
Is there poor Renal Perfussion? – Dopamine
– 2ug/kg/min
Correct Fluid / Cal. / Protein Intake?
+ Electrolytes
MORTALITY
35 – 65% are saved
Worse in surgical cases
DIET
DRUGS
DIALYSIS
Worsening clinical picture + prolonged
oliguria
Urea > 260
K < 6.5
Overhydration – pulmonary congestion
Acidosis
Rising Blood Urea > 100mg/day
PROGNOSIS
35 – 65% - mortality
Worse – Surgical cases
Dialysis
PRERENAL AZOTAEMIA
True volume depletion or Hypovolaemia
• Correct volume deficit but with caution
• 0.9% NaCl – 250 – 1.0 lit over 1 hour
Evaluate for signs of Hypovolaaemia or Overload
• BP or Pulse improving, JVP getting visible
• Lung signs ( crackles) + 3rd Heart sound
• Monitor & correct associated electrolyte deficits
• If there is cardiovascular instability- install CVP
line; CVP – 2-12cm of water
• Swan-Ganz catherter measures directly
PAWP,and reflects LVED pressure- its gives
critical infor about fluid balance
ARTERIAL UNDERFILLING WITH ECF
EXCESS
Even though pre-renal, but not a true fluid
deficit
Treat underlying causes
A) Heart failure-direutics/digitals/ACE
inhibitors when refractory treat with CRRT
B) Liver disease
Reduce symptoms/treat ascites & oedema
Sodium restricted diet 1-2g salt/day
• Aldosterone Antagonist/furosemide
Diuretic Resistance – Quite Common
B) POST RENAL
Bladder catheterisation
Ureteric drainage catheterisation/stents
C) PRIMARY RENAL DISEASE
Treat as for specific renal disease steriods/immunosuppresives
D) Acute interstitial nephritis
Withdrawal of offending drugs
Treat infections
Steriod ( a short course)
E) INTRINSIC RENAL DISEASE(ATN)
• Masterly inactivity
i) Nephrotoxic drugs
» Aminoglycosides xxx
» Radioconstrast agents etc
» NSAIDS, ACEI, Cyclosporin
ii) Adjust dose based on GFR
Cockcroft/Guault
{(140 – Age) x wt}x 0.85 if FM
{plasma creat x 72)
iii)Caution with renal –dose dopamine
Established benefit in incipient renal failure
Dose: 2ug/kg/min
Effect: b-adrenergic on heart +vasodilator on
renal vessels.
May cause arrythmias and bowel ischaemia
iv) Prevent volume overload
Supportive therapy for ATN
• Drug dosages– watch out
• Nutritional support
– Basis: ARF is a hypercatabolic state
• -Nitrogen balance is negative
• Protein 1-1.5g/kg
• Cal:3kc
• Dialysis
i) Don’t delay – initiate Dialysis early
ii) General guidelines
Persistent Oliguria ( <400ml/day)
Serum creatinine > 6mg/dl
Serum ureat > 200mg%
Rapidly rising area
Hyperkalaemia > 6.5mmol/l
Severe metabolic acidosis
• Modalities: Intermittent HD
Continuous Renal Replacement Theraphy
(CRRT)
Mandatory for Heamodynamically unstable
patients)
Peritoneal Dialysis
THANK YOU
FOR YOUR
ATTENTION