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Acute Renal Failure Pathogenesis and Treatment Lestariningsih Subbag Nefrologi/Hipertensi Bagian Penyakit Dalam FK UNDIP/RS Dr. Kariadi Semarang

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Acute Renal FailurePathogenesis and


Subbag Nefrologi/Hipertensi Bagian Penyakit Dalam

FK UNDIP/RS Dr. Kariadi Semarang

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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

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• Acute or acute on chronic• Single organ or multi-organ failure• Oliguric or polyuric• Mild or severe

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• Pre-renal ARF • Intrinsic ARF• Post-renal ARF

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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

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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

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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

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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,


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Cockcroft Gault equation

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

(corrected for males x 1.23, females x 1.04)

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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

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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

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

sounds, central pressures, blood pressure• Bladder and kidneys• Signs of systemic disease

– rashes, anaemia,

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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


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

scanning, renal angiography, isotope renography

• Renal biopsy

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Treatment• Correct renal perfusion

– Optimise volume status– Inotropes ( dopamin 3 ug/kgBB/jam )

• Remove nephrotoxins• Relieve obstruction - Bladder catheter

– Nephrostomies

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• Make the patient safe• Hyperkalaemia

– Volume overload– Uraemia– Acidosis

• Specific treatments– Antibiotics, steroids

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Methods of treatmentDRUG

Calcium Gluconate

Glucose + Insulin

IV Na Bicarbonate

Ventolin Nebuliser




10 ml of 10%

50 ml 50% + 8U

1l of 1.4%

5 ml

30 - 60 g (po/pr)



30 minutes

1 - 4 hours

1 - 8 hours

1 - 4 hours



and there is always dialysis!

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• Acute intermittent haemodialysis• Continuous dialysis treatments• Peritoneal dialysis

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

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