Acute kidney injury

AKI, Acute renal failure

1. Acute Kidney Injury Dr Rajesh K Mandal MD,Internal medicine

2. Introduction Acute kidney injury (AKI), previously known as acute renal failure, is characterized by the sudden impairment of kidney function resulting in the retention of nitrogenous and other waste products normally cleared by the kidneys . The term AKI has largely replaced acute renal failure (ARF), reflecting the recognition that smaller decrements in kidney function that do not result in overt organ failure are of substantial clinical relevance and are associated with increased morbidity and mortality.

3. Epidemiology AKI complicates 5–7% of acute care hospital admissions and up to 30% of admissions to the intensive care unit, particularly in the setting of diarrheal illnesses, infectious diseases like malaria and leptospirosis, and natural disasters such as earthquakes. The incidence of AKI has grown by more than fourfold in the United States since 1988 and is estimated to have a yearly incidence of 500 per 100,000 population, higher than the yearly incidence of stroke.

4. Diagnostic Criteria   The Kidney Disease: Improving Global Outcomes (KDIGO) definition and staging system is the most recent and preferred definition . Other criteria include the RIFLE criteria and a subsequent modification proposed by the Acute Kidney Injury Network (AKIN) and others .

5. These criteria are The KDIGO guidelines define AKI as follows ●Increase in serum creatinine by ≥0.3 mg/ dL  (≥26.5  micromol /L) within 48 hours, or ●Increase in serum creatinine to ≥1.5 times baseline, which is known or presumed to have occurred within the prior seven days, or ●Urine volume <0.5 mL/kg/hour for six hours The KDIGO criteria allow for correction of volume status and obstructive causes of AKI prior to classification. Before diagnosing and classifying AKI, one should assess and optimize volume status and exclude obstruction.

6. STAGING CRITERIA   Using the Kidney Disease: Improving Global Outcomes (KDIGO) criteria, AKI is staged as follows: ●Stage 1 – Increase in serum creatinine to 1.5 to 1.9 times baseline,  or  increase in serum creatinine by ≥0.3 mg/ dL  (≥26.5  micromol /L),  or reduction in urine output to <0.5 mL/kg/hour for 6 to 12 hours. ●Stage 2 – Increase in serum creatinine to 2.0 to 2.9 times baseline,  or  reduction in urine output to <0.5 mL/kg/hour for ≥12 hours. ●Stage 3 – Increase in serum creatinine to 3.0 times baseline,  or  increase in serum creatinine to ≥4.0 mg/ dL  (≥353.6  micromol /L),  or reduction in urine output to <0.3 mL/kg/hour for ≥24 hours,  or  anuria for ≥12 hours,  or  the initiation of renal replacement therapy,  or , in patients <18 years, decrease in estimated glomerular filtration rate ( eGFR ) to <35 mL/min/1.73 m 2 .

7. The KDIGO criteria differ from the RIFLE classification in that the KDIGO criteria only utilize changes in serum creatinine and urine output, not changes in GFR for staging, with the exception of children under the age of 18 years, for whom an acute decrease in eGFR to <35 mL/min/1.73 m 2  is included in the criteria for stage 3 AKI. As with the RIFLE and Acute Kidney Injury Network (AKIN) staging systems, KDIGO suggested that patients be classified according to criteria that result in the highest ( ie , most severe) stage of injury.

8. Etiology and Pathophysiology  Patients who are hypotensive due to surgery, sepsis, bleeding, or other causes are at risk of developing ischemic acute tubular necrosis (ATN), especially if the impairment in renal perfusion is either severe or prolonged in duration. Patients may also suffer ischemic injury to the kidney due to interruptions in renal blood flow such as from cross-clamping of the renal artery during surgery for removal of renal cell carcinoma. 

9. Acute tubular necrosis (ATN) — 45 % Prerenal disease — 21 % Acute superimposed on chronic kidney disease — 13 % Urinary tract obstruction — 10 % Glomerulonephritis or vasculitis — 4% Acute interstitial nephritis — 2 % Atheroemboli — 1 % Liaño F, Pascual J. Epidemiology of acute renal failure: a prospective, multicenter, community-based study. Madrid Acute Renal Failure Study Group.

10. BPKIHS S epsis/MODS 35% H ypovolaemia/Bleed 28% M yocardial/Pericardial disease 11% D ecreased intake 11% O thers 14% P. Koirala et al . Outcomes of Acute Kidney Injury: A Hospital Based Study , 2010

11. Diagnostic Evaluation careful history taking, and physical examination often narrow the differential diagnosis for the cause of AKI. Prerenal azotemia should be suspected in the setting of vomiting, diarrhea, glycosuria causing polyuria, and several medications including diuretics, NSAIDs , ACE inhibitors, and ARBs. Physical signs of orthostatic hypotension , tachycardia, reduced jugular venous pressure, decreased skin turgor, and dry mucous membranes are often present in prerenal azotemia. A history of prostatic disease, nephrolithiasis, or pelvic or paraaortic malignancy would suggest the possibility of postrenal AKI .

12. Colicky flank pain radiating to the groin suggests acute ureteric obstruction. Nocturia and urinary frequency or hesitancy can be seen in prostatic disease. Abdominal fullness and suprapubic pain can accompany massive bladder enlargement .

13. Idiosyncratic reaction to wide variety of drugs can lead to allergic interstitial nephritis, which may be accompanied by fever, arthralgias , and a pruritic erythematous rash. The absence of systemic features of hypersensitivity, however, does not exclude the diagnosis of interstitial nephritis.

14. Urine Findings Complete anuria early in the course of AKI is uncommon except in the following situations: complete urinary tract obstruction, renal artery occlusion , overwhelming septic shock, severe ischemia (often with cortical necrosis), or severe proliferative glomerulonephritis or vasculitis . A reduction in urine output (oliguria, defined as <400 mL/24 h) usually denotes more severe AKI (i.e., lower GFR) than when urine output is preserved. Oliguria is associated with worse clinical outcomes . Preserved urine output can be seen in nephrogenic diabetes insipidus characteristic of longstanding urinary tract obstruction, tubulointerstitial disease, or nephrotoxicity from cisplatin or aminoglycosides, among other causes . Red or brown urine may be seen with or without gross hematuria; if the color persists in the supernatant after centrifugation, then pigment nephropathy from rhabdomyolysis or hemolysis should be suspected

15. Urine sediments Analsis

16. Blood I nvestigations Assessment of kidney function Estimation of glomerular filtration rate Creatinine U rea C ystatin C

17. Urinary finding Fractional excretion of sodium R adiologic studies USG Helical CT

18.   F ractional excretion of urea ( FEurea ) Lithium U ric acid

19. RENAL BIOPSY Isolated glomerular hematuria with proteinuria Nephrotic syndrome Acute nephritic syndrome Unexplained acute or rapidly progressive kidney disease

20. PROGNOSTIC BIOMARKER Urinary angiotensinogen ratio of urinary angiotensinogen to urinary creatinine correlated with the maximum serum creatinine and the maximum percent change in serum creatinine higher risk of worsening AKI

21. COMPLICATIONS U remia H ypervolemia and hypovolemia H yponatremia H yperkalemia A cidosis H yperphosphatemia H ypocalcemia B leeding I nfections C ardiac complications M alnutrition

22. SUPPORTIVE MANAGEMENT M aintenance of fluid and electrolyte balance A voidance of nephrotoxic medications A dequate nutrition T reatment of infections C orrection of reversible factors C lose monitoring P roper dosing of medications

23. NUTRITION KDIGO guidelines, patients with AKI: total energy intake of 20–30 kcal/kg per day . Protein intake: 0.8–1.0 g/kg per day in noncatabolic AKI without the need for dialysis; 1.0–1.5 g/kg per day in patients on dialysis; m aximum of 1.7 g/kg per day if hypercatabolic and receiving continuous renal replacement therapy.

24. MONITORING   D aily weights F luid intake U rine output 

25. MANAGEMENT Treatment of the cause T reatment of complications

26. HAEMODIALYSIS I NDICATIONS Refractory fluid overload Hyperkalemia (plasma potassium concentration >6.5  meq /L) or rapidly rising potassium levels Signs of uremia , such as pericarditis , neuropathy, or an otherwise unexplained decline in mental status Metabolic acidosis (pH less than 7.1) Certain alcohol and drug intoxications: ethylene glycol

27. TIMING A large multicenter observational study found that early initiation of dialysis may be associated with a survival advantage . T he risk of death was correlated with the BUN level at the start of dialysis among 243 patients with acute renal failure (low and high degree of azotemia defined by BUN ≤76 mg/ dL  and >76 mg/ dL , respectively).

28. TIMING I ncreased risk of death at 60 days from the diagnosis of acute renal failure for those begun on dialysis at the high BUN level (RR 1.97). Liu KD et al. Timing of initiation of dialysis in critically ill patients with acute kidney injury. Clin J Am Soc Nephrol 2006; 1:915

29. Initiating dialysis in acute kidney injury (AKI) in an intensive care unit (ICU) remains a subjective clinical decision. They examined factors and practice patterns that influence early initiation of dialysis in ICU patients . Severely ill patients were more likely to be subjected to early dialysis initiation, but its utility is not clear. Rank-order analysis indicates dialysis initiation is still influenced by "imminent" indications rather than a "proactive" decision based on the severity of AKI or azotemia . Charuhas V Thaka r, Timing of dialysis initiation in AKI in ICU: international survey , Critical Care  2012, 16:R237  

30. ACUTE KIDNEY INJURY IN PREGNANCY H yperemesis gravidarum S eptic abortion- acute tubular necrosis T hrombotic thrombocytopenic purpura S evere preeclampsia R enal cortical necrosis A cute pyelonephritis U rinary tract obstruction

31. Nonsteroidal Antiinflammatory Drugs I nduce two different forms of acute kidney injury: Hemodynamically mediate d Acute interstitial nephritis - accompanied by the nephrotic syndrome

32. PROGNOSIS Most patients recover Prerenal azotemia, with the exception of the cardiorenal and hepatorenal syndromes, and postrenal azotemia carry a better prognosis than most cases of intrinsic AKI I ncreased chance of chronic kidney disease and end stage renal disease, 10% I ncreased morbidity and mortality

33. PROGNOSIS Follow up with renal function and urinary albumin to creatinine ratio L ong term outcomes not well documented

34. REFERENCES Harrison’s Principles of internal Medicine 19 th edition UP TO DATE 2018 ACUTE RENAL FAILURE IN A TERTIARY CARE CENTER IN NEPAL J Nep Med Assoc 2005; 44: 32-35 Khakurel S*, Satyal P R*, Agrawal R K*, Chhetri P K*, Hada R * P. Koirala et al . Outcomes of Acute Kidney Injury: A Hospital Based Study , 2010

35. Thank You