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.

4. Reversible Pre-Renal Acute Renal Failure
Pathogenesis

5. 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 (+)

6. 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

7. 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

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

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

12. 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.

13. 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
Dilutional hyponatraemia.

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

17. VASCULAR EVENT MAJOR VASCULAR OCCLUTION OR SMALL VESSEL DISEASE
URINE SHOW MINIMAL ABNORMALITIES
MAY BE PRECIPITATED BY ACE INHIBITORS

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

19. ACUTE INTERSTITIAL NEPHRITIS
CAUSED BY ADVERSE DRUG REACTION
SMALL AMOUNT OF BLOOD AND PROTIEN IN URINE
KIDNEYS NORMAL IN SIZE
Tt-CESSATION OF DRUG AND PREDNISOLONE

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

21. 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

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

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

24. 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 – Percutaneous nephrostomy

25. 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

26. 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.

27. 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 oedema Uraemic pericarditis/ uraemic encephalopathy.

28. 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

29. 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.

30. Intermittent haemodiafiltration

31. Peritoneal dialysis
Seldom achieves adequate biochemical control

32. Difference BetweenHD&PD
Efficient
Less efficent
4hours 3 times a week
4 exchanges per day each min. – CAPD or hrs Automated PD
2-3 day between
Few hrs between tt
Requires visit to hospital
Performed at home
Requires adequate venous acces
Requires an intact peritoneal cavity

33. Careful compliance to diet and fluid restriction
Diet & fluid less restricted
Fluid removal compressed during tt period - haemody instability
Slow continous fluid removal - asymptomatic
Infection reld to vascular access
Infection – Peritonitis,catheter reld infections
Patients are, to some extent dependent on others
Patients can take full reponsibility of their tt