Acute Renal Failure

Pathogenesis and Treatment

LestariningsihSubbag Nefrologi/Hipertensi

Bagian Penyakit DalamFK UNDIP/RS Dr. Kariadi Semarang

Definition• Abrupt sustained decline in GFR• Rising serum urea and creatinine• Loss of water and salt homeostasis• Life threatening metabolic sequelae• Occurs over hours or days• Incidence approximately 140 p.m.p. per

year• 5% of all surgical and medical admissions

Subtypes

• Acute or acute on chronic

• Single organ or multi-organ failure

• Oliguric or polyuric

• Mild or severe

Aetiology

• Pre-renal ARF

• Intrinsic ARF

• Post-renal ARF

Pre-renal ARF• Reversible fall in GFR due to renal hypoperfusion

– Hypovolaemia

• Haemorrhage, burns, GI fluid loss, renal fluid loss

– Hypotension

• Cardiogenic shock, sepsis

– Renal hypoperfusion

• renal vasoconstriction, drugs, liver disease, renal vascular disease

Renal ARF

• Disease of the renal parenchyma– ATN

• Ischaemia, direct toxicity, myoglobin, sepsis

– Vascular disease• Vasculitis, atheroemboli, infarction

– Diseases of glomeruli/arterioles• RPGN, myeloma, HUS, vasculitis, SLE

– Tubulo-interstitial nephritis• Drug related, paraneoplastic

Post-renal ARF

• Renal failure secondary to urinary tract obstruction– Ureteric

• Calculi, carcinoma, retroperitoneal fibrosis, stricture

– Bladder neck• prostatic hypertrophy/malignancy, carcinoma,

neuropathy, blocked catheter

Prevention• Identify at risk patients

– pre-existing CRF, diabetes, jaundice, myeloma, elderly

• Optimise renal perfusion– IV fluids, inotropes, central line

• Maintain adequate diuresis– Mannitol, frusemide, NOT dopamine

• Avoid nephrotoxic agents– ACE inhibitors, NSAIDS, radiological contrast,

aminoglycosides

Cockcroft Gault equation

(140-age in years) x weight in kgserum creatinine (μmol/L)

(corrected for males x 1.23, females x 1.04)

Principles of investigation

• Acute or acute on chronic?

• Exclude volume depletion

• Exclude renal tract obstruction

• Exclude major vascular occlusion

• Exclude renal parenchymal disease other than ATN

History

• When did it start?• What was the baseline renal function?

– Pre -existing medical conditions

• What were the likely insults?– Episodes of hypotension– Nephrotoxic agents– Sepsis

• Symptoms of other diseases

Examination

• Current volume status– Skin turgor, oedema, lung bases, heart

sounds, central pressures, blood pressure

• Bladder and kidneys

• Signs of systemic disease– rashes, anaemia,

Investigations

• Laboratory– U+E’s, Bone, Glucose, Urate, Bicarbonate– Urine urea, sodium, creatinine, protein– FBC, Clotting, ESR– Urine microscopy, MSU, blood cultures– CRP, ANA, ANCA, anti GBM, myeloma

screen

Investigation

• Radiology– Plain abdomen, renal U/S, IVU, CT

scanning, renal angiography, isotope renography

• Renal biopsy

Treatment

• Correct renal perfusion– Optimise volume status– Inotropes ( dopamin 3 ug/kgBB/jam )

• Remove nephrotoxins• Relieve obstruction - Bladder catheter

– Nephrostomies

Treatment

• Make the patient safe

• Hyperkalaemia– Volume overload– Uraemia– Acidosis

• Specific treatments– Antibiotics, steroids

Methods of treatment

DRUG

Calcium Gluconate

Glucose + Insulin

IV Na Bicarbonate

Ventolin Nebuliser

Resonium

Bendrofluazide

DOSE

10 ml of 10%

50 ml 50% + 8U

1l of 1.4%

5 ml

30 - 60 g (po/pr)

5mg

DURATION

30 minutes

1 - 4 hours

1 - 8 hours

1 - 4 hours

days

days

and there is always dialysis!

Dialysis

• Acute intermittent haemodialysis• Continuous dialysis treatments• Peritoneal dialysis

Outcome

• Full recovery• Partial recovery• No recovery - progress to ESRF• Death