1. Acute renal failure (ARF)  acute kidney injury AKI is a sudden and usually reversible loss of renal function which develops over days or weeks and is usually accompanied by a reduction in urine volume.  A rasied creatinine level can be due to acute, acute on chronic of chronic kidney disease.

2.  Two small kidneys on ultrasound indicate chronicity.

3. Causes of ARF  Pre renal Systemic Heart failure Blood/ fluid loss/ shock called hypovolemia Local Renal artery stenosis Disease affecting arterioles  Under perfusion initially causes rapidly reversible changes,. Subsequently, acute tubular necrosis that may lead to intrinsic renal failure.

4. Intrinsic renal disease  Toxic /septic renal failure 85%  glomerular diseases 5% Primary Component of systemic disease  Interstitial disease 10%

5. Post renal causes  Obstruction  Stones  Tumor  Enlarged prostate

6.  Reversible pre renal acute renal failure

7. Pathogenesis  The kidneys can regulate its own blood flow and GFR over a wide range of perfusion pressure  When the perfusion pressure falls—as in hypovolaemia, shock, heart failure or narrowing of renal arteries—the resistance vessels in kidneys dilate. It is mediated by prostaglandins.  (this is impaired by NSAIDS)

8.  if autoregualtion of blood is fails, the GFR can stillbe maintained by selective constriction of efferent arteriols by rennin angiotensin mechanism ( it is inhibited by ACE inhibitors)

9.  More sever or prolonged under perfusion of kidneys may lead to failure of these compensatory responses, and acute fall in GFR. This leads to formation of low volume concentrated urine (osmolality >600mOsm/kg) but low in sodium (<20mmol/l)  Note these changes may be absent in patient with pre existing renal impairment or those who received diuretics

10. Clinical features:  Marked hypotension  Signs of hypoperfusion such as delayed capillary return, cool peripheries etc.  Postural hypotension is reliable sign of early hypovolemia.

11. The causes reduces renal hypo perfusion  The sign suggesting following may be present  Shock  Blood loss  Crush injuries  Burns  Sepsis These causes should be assessed

12. Management  Establish and correct the under lying causes is very important step.  Treat hypovolemia with restore blood volume as soon as possible ( with blood, plasm, isotonic saline 0.9%)  Optimize systemic haemodynamics. Monitoring the central venous pressure and pulmonary wedge pressure is necessary for fluid administration.  Note: Meta analysis trials do not support the role of low dose dopamine in ARf.  Correct the metabolic acidosis  Restoring the blood volume will correct the acidosis by restoring the kidney function.  Sodium bi carbonate (50 ml of 8.4%) may be used severe acidosis.

13. Prognosis  Good full recovery of renal function if early treatment is given.  In some case treatments is ineffective and renal failure becomes established.

14. Established acute renal failure (ARF)  Acute renal failure (ARF) may develop follwing severe and prolonged underperfusion of kidneys when the histological pattern of acute tubular necrosis is usually seen.  Acute tubular necrosis (ATN)  It is necrosis of renal tubular cells may result from ischemia of nephrotoxicity caused by chemicals, bacterial toxins or combination.

15.  Drugs includes  Aminoglycosides antibiotics like gentamicin, the cytotoxic drugs cisplastin, anti fungal amphotericin B.

16.  Fortunately there is good recovery because renal tubular cells can regenerate and reform basement membrane.

17. Features of established ARF  These show the causal conditions  Urea and creatinine Raised urea and creatinine  Alterationin urine volume Oliguria/ anuria

18.  Disturbance in fluid, electrolytes and acid base balance  Hyperkalaemia Due massive tissue breakdown, hemolysis, and metabolic acidosis.  Dilutional hyponatraemia Oliguric patient continue to drink of excessive fluid is given

19.  Metabolic acidosis  Hypocalcaemia Reduced renal production of 1,25 dihydroxychlocalciferol

20. Uremia  Uremic features:  Anorexia  Nausea and vomiting  Drowsiness  Apathy, confusion  Hiccups  Fits, coma and death.

21. Respiratory features  Inc resp. rate  due to acidosis  infection  pulmonary edema due to excessive fluid administration

22. Blood  anemia Bloold loss Hemolysis Dec.erythropoetin secretion.  Platelets and cogulation dysfunctions.  Severe infection Depressed immunity.

23. Management  Initial Management is targeted at following priorities:  Hyperkalemia  Pulmonary edema  Infection  Uremia itself

24. Hyperkalemia  i.v calcium gluconate (10ml of 10% solution)  Inhaled β2 agonist e.g salbutamol  i.v glucose (50ml of 50% solution)  Insulin 5 U actrapid  Intravenous sodium bicarbonate.  Iv lasix and normal saline.  Ion exchange resin ( resonium) orally or rectally  Dialysis

25. Immediate fluid management  Volume replacement  CVP monitoring  Pulmonary edema may require dialysis to remove water and sodium from the body.  Temporary respiratory support CPEP IPPV Severe acidosis may require sodium bi carbonate if volume status allows

26. Addressing the underlying causes of ARF  Remove post renal obstruction Uretric dilation Prostate surgery Percutaneous nephrostomy

27.  No specifis treatment of ATN  immuno suppressive drugs for rapidly progressive glomerulo nephritis.  Plasma exchange in micro angiopathic disease.

28. FlUID AND ELECTROLYTE BALANCE  After initial resusitation, Maintain I/O chart Daily weight  Daily intake should equal the urinr out put plus 500 ml to cover insensible loss.

29. Protein and energy intake  By dietary protein restriction ( 40g per day), in whom dialysis is likely to be avoided.  Patients on dialysis may require more dietary proteins ( 1 g / kg proteins daily and 10-12g nitrogen).  Adequate energy is needed in hypercatabolic states like sepsis and burns.

30. Infection control  Treated accordingly with porper antibiotics.  dose adjustment is required.  Drugs like NSAIDS and ACE inhibitors should usually be avoided.

31. Renal replacement therapy  This may be required as supportive management in ARF.

32. Prognosis  In uncomplicated ARF, due to blood loss, hypovolemia, mortality is low.  In ARF associated with serious infection/ sepsis and multi organ failure, mortality is 50 to 70 %.

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