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ACUTE RENAL FAILTURE

ACUTE RENAL FAILTURE. LIJI VINCENT. Acute renal failure (ARF) refers to a sudden and usually reversible loss of renal function, which develops over a period of days or weeks and is usually accompanied by a reduction in urine volume. Reversible Pre-Renal Acute Renal Failure. Pathogenesis.

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ACUTE RENAL FAILTURE

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  1. ACUTE RENAL FAILTURE LIJI VINCENT

  2. Acute renal failure (ARF) refers to a sudden and usually reversible loss of renal function, which develops over a period of days or weeks and is usually accompanied by a reduction in urine volume.

  3. Reversible Pre-Renal Acute Renal Failure Pathogenesis

  4. Clinical Features • Hypotension and signs of poor peripheral perfusion • Postural hypotension fall in SBP/DBP >20/10 mmHg early sign of hypovolaemia. • The cause of reduced renal perfusion may be obvious or concealed • Metabolic acidosis and hyperkalaemia may be (+)

  5. Management • Establish and correct the underlying cause of the ARF. • If hypovolaemia (+) replace with blood, plasma or isotonic saline • Optimise systemic haemodynamics. Monitor CPU or pulmonary a wedge pressure. • Correct metabolic acidosis - Restoration of blood volume will restore kidney function - Isotonic sodium bicarbonate

  6. Established Acute Renal Failure Following severe or prolonged under perfusion of the kidney. Histology: Acute tubular necrosis Acute Tubular Necrosis: Cause (1) Ischaemia (2) Nephrotoxicity

  7. Nephrotoxic ATN Direct toxicity of the causative agent to the tubular cells.

  8. Recovery From ATN • Tubular cells can regenerate • If the patient is supported during the regeneration phase. • Kidney function restores • Recovery phase-Diuretic phase

  9. Other feature • Uraemic features- anorexia, nausea and vomiting drowsiness, apathy, confusion, muscle twitching • Respiratory rate increased – Acidosis, pulmonary oedema, infection. • Anaemia – Blood loss, haemolysis disordered platelet function and disturbances of the coagulation cascade.

  10. Clinical Features of Established ARF Reflect the causal condition – trauma, septicemia or systemic diseases + 1. Alterations in urine volume Oliguric (<500ml/daily) Anuria Non Oliguric - Normal or Increased • Disturbances of water, electrolyte and acid – base balance Hyperkalaemia - massive tissue breakdown, haemolysis Dilutionalhyponatraemia.

  11. URINARY TRACTOBSTRUCTION • SUGGESTED BY LOIN PAIN, RENAL COLIC OR DIFFICULTY IN MICTURITION • INVES- USG • PROMPT RELIEF OF OBSTRUCTION RESTORES KIDNEY FUNCTION

  12. VASCULAREVENT • MAJOR VASCULAR OCCLUTION OR SMALL VESSEL DISEASE • URINE SHOW MINIMAL ABNORMALITIES • MAY BE PRECIPITATED BY ACE INHIBITORS

  13. RPGN • SIGNIFICANT DIP STICK HAEMATURIA • ASSOSIATED WITH SYSTEMIC FEATURES • BLOOD TESTS-ANA, ANCA, ANTI-GBM ANTIBODIES • DIAGNOSIS- RENAL BIOPSY

  14. ACUTEINTERSTITIALNEPHRITIS • CAUSED BY ADVERSE DRUG REACTION • SMALL AMOUNT OF BLOOD AND PROTIEN IN URINE • KIDNEYS NORMAL IN SIZE • Tt-CESSATION OF DRUG AND PREDNISOLONE

  15. DRUGS • HAEMODYNAMIC EFFECTS- NSAIDs , ACE INHIBITORS • DIRECT TOXICITY TO THE TUBULES- AMINOGLYCOSIDES

  16. Screening Tests • Hematology Full blood count Blood film Clotting screen, Group and save • Biochemistry Urea, electrolytes and creatinine calcium Urinalysis Urine Microcopy Quantitative urinary protein measurement

  17. 3. Microbiology Blood culture CRP Mid-stream urine Other cultures 4. Imaging Renal USG Chest X ray ECG

  18. Immunoglobulin and protein electrophoresis • Urinary Bence Jones Protein • Complement • ANA and ds DNA • Extractable nuclear Antigen (ENA) • Rheumatoid factor

  19. Management 1.Emergency resuscitation • Hyperkalaemia – treated immediately • Circulating blood volume restoration • Acidosis-Isotonic sodium bicarbonate 2.Addressing the underlying cause • USG showing urnary tract obstruction. • ATN - restoring renal perfusion. • Postrenal obstruction :Due to Pelvic or ureteric dilatation – Percutaneousnephrostomy

  20. Fluid and electrolyte balance • Daily fluid intake should = prev. day urine output + 500ml to cover unsensible loss. • Abnormal loses like diarrhea – electrolyte replacement. • Since Na+ and K+ are retained their intake should be restricted • Protein and energy intake • In patients where dialysis is avoided – protein restriction to 40g/day • In patients with dialysis – more dietary protein

  21. Infection control Regular clinical examination and microbiological investigation required. • Drugs Vasoactive drugs NSAIDs & ACE inhibitors are to be avoided. • Renal Replacement therapy This may be required as supportive management in ARF.

  22. Increased Plasma urea andcreatinine urea >30mmol/l Creatinine >6.8mgdl At lower level – Progressive biochemical deterioration. Hyperkalaemia – K+ >6mmol Metabolic acidosis raise the plasma potassium further. Fluid overload and pulmonary oedemaUraemic pericarditis/ uraemic encephalopathy.

  23. Intermittent haemodialysis Best rate of small solute clearance.1 hour tt is prescribed. Subsequently when haemodyamically stable 3 – 4 hours 3 – 4 times a week. Haemodialysis 2 – 3 hrs every day – severly catabolic

  24. Haemofiltration Intermittent 15 – 30 liters of plasma ultra filtrate exchanged for replacement fluid over 3 – 5 hours. Continuous 1 – 2 liters of filtrate replaced higher rate of filtration MODS sepsis.

  25. Intermittent haemodiafiltration

  26. Peritoneal dialysis Seldom achieves adequate biochemical control

  27. Difference BetweenHD&PD

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