1. Acute Renal Failure Niroj Obeyesekere 3 rd year student notes

2. Definition Clinical syndrome characterised by rapid (over hours to weeks) decline in GFR, perturbation of extracellular fluid volume, electrolyte and acid base homeostasis, and accumulation of nitrogenous waste products from protein catabolism such as urea or creatinine.

3. RIFLE criteria

4. Why is it important 1. Common 5% of all hospital admissions and 5-30% in ICU admissions complicated by ARF. 2. Community acquired ARF does better than hospital acquired. 2. Major cause of in-hospital morbidity and mortality. 3. But, most cases are reversible. 4. and, most cases can be prevented.

5. Diagnosis Serial measurement of urea and creatinine, but this has its limitations, 1. GFR may need to fall by 50% for Cr to be outside the “normal” level. 2. Reduced muscle mass. 3. Pre-existing chronic renal insufficiency. 4. Other substance e.g. drugs that interfere with lab Cr measurements.

6. Aetiology 1. Prerenal – physiological response to hypoperfusion in which integrity of the renal parenchyma is preserved. Less than 48 hrs. 2. Renal – diseases of the renal parenchyma 3. Postrenal – acute obstruction of the urinary tract. Prerenal most common. Prerenal and renal in terms of ATN is a spectrum of hypoperfusion.

7. Causes of ARF

8. Causes of prerenal ARF

9. Pathophysiology of prerenal renal failure 1.True intravacular hypovolaemia 2.Decreased effceyive circulatory volume 3.Intrarenal vasoconstriction 4.Renal artery disease and borderline hypovolaemia

10. Pathophysiology Kidney function is maintained by – afferent arteriole vasodilatation by local myenteric reflex, increased PGs, kallikerin and kinins and preferential efferent arteriole constriction by angII. Afferent arteriole dilatation is maximal at mean BP of 80. Lesser degrees of hypotension can ARF in HT, DM and elderly. Very high Ang II causes both afferent and efferent constriction. Esp with pts with marked circulatory failure.

11. Pathophysiology 1. NSAIDS– reduce Pg production 2. ACE inhibitors and ARBs- intraglomerular pressure is dependent on efferent vasoconstriction. 3. Diuretics 4. Nephrotoxics

12. Intrinsic renal failure 1. large renal vessels – artheroemboli, thromboemboli, thromobosis or dissection or vasculitis 2. microvasculature and glomeruli – GN, scleroderma, HT, TTP, HUS, 3. ischamic and nephrotoxic ATN 4. tubulointerstitium – interstitial nephritis, infections, infiltrative.

13. Post Renal Obstruction – only 5% of cases

14. Clinical approach

15. Some basic questions- 1.Is it acute, acute on chronic or chronic 2. is there obstruction 3. evidence of true hypovolaemia 4. has there been a major vascular occlusion 5. is there parenchymal disease other than ATN

16. Approach Usually blood tests but if not, anaemia, PO4, Ca, kidney size can help to differentiate between acute and chronic.

18. Clinical evaluation of volume status

19. Investigations Urine output – relatively unhelpful in OP setting. If IP can be useful. Urine microscopy - useful Hyaline casts or bland urine prerenal or obstruction. (blood and pyuria in obstruction) Muddy brown granular casts in ATN (can be absent in 20-30%) Dysmorphic red cells GN Eosinophiluria – interstitial nephritis Haemogloburia or myogloburia – haemolysis or rhabdo

20. Investigations Proteinuria – less than 1 g in prerenal or ATN more than 1 g glomerular proteinuria Pattern of Cr – Cr increases 24 to 48 hrs in renal ischaemia, radiocontrast, and atheroembolism. In contrast nephropathy peaks at 3- 5 days and returns to normal in 5 to 7. Normally ATN gets better 7 to 14 days post and artheroembolic usually irreversible. Gentamicin Cr increases 7 to 10 days.

21. Other lab findings Hyperkalemia - Hyperphosphatemia High K disproportionate might indicate obstruction or type IV rneal tubular acidosis. Severe anaemia – haemolysis, MM or TTP. Thrombocytopenia, dysmorphic red cells in blood film.

22. isomorphic

23. dysmorphic

24. Muddy casts

25. Urine microoscopy

26. Ix-Renal US

27. Other Ix CT KUB Renal biopsy

28. Complications of ARF

29. Complications 1. Fluid overload 2.Hyperkalemia – ECG changes Peaked t waves Prolongation of PR interval Widening of QRS Heart block, VT, VF asytole.

30. Complications 3. acid base balance- wide anon gap metabolic acidosis 4. uremia

31. Management

32. When you see a patient with ARF always think

33. Indications for dialysis