AKI

recognize if AKI based change in SCr or UoP

nephrotoxic

renally adjust

Detection Of AKI only one meet 

• increase in SCr by at least 0.3 within 48 hours 

• Increase in Scr 1.5x from baseline within 7 days 

• Decrease in Urine Output (UoP) to < 0.5 mL/kg/hr for at least 6 hours 

  • normal 2L/day and typically changes faster than SCr, thus better to use for dose adjustment. 

  • Nonoliguria - UoP > 500 mL/day → intrinsic failure or incomplete block

  • Oliguria - UoP 50-500 mL/day → prerenal 

  • Anuria -  UoP < 50 mL/day → complete block or catastrophy 

• Clinical Presentation of AKI

  • rapid decrease in GFR and increase in SCr and BUN

  • dehydration and hypotension and edema/sudden weight gain 

  • severe abdominal/flank pain from infection, nephrolithiasis,  glomerular or interstitial nephritis 

  • bladder distension from obstruction 

  • cola-colored urine sign of blood and acute glomerulonephritis 

• Assessment based on trends -

  • PMH of CKD, DM, HTN since high risk medications needed over long-term usually hold then give back 

  • Onset of acute AKI, Acute or Chronic CKD 

  • eGFR Cockcroft-Gault often overestimates in worse and underestimates in resolving due to lagging behind 1-2 days 

  • Urinary analysis to determine type of AKI and infection 

  • CBC to see infection 

  • Electrolytes too see if any are toxic or near those levels 

  • BUN:SCr increased to 20:1 sign or prerenal AKI

• Fractional excretion of sodium (FENa) assess tubular integrity

  • low value means pre-renal AKI <1 % and renal > 2%

  • other conditions associated CHF, cirrhosis, nephrosis, contrast-induced nephropathy, rhabdomyolysis 

• Imaging of abdominal, CT, ultrasound, biopsy can reveal shrunken kidneys and obstructions when source unclear after labs 

Types Of AKI

• normal afferent arteriole dilates (widens) or efferent arteriole constricts (narrows) along with RAAS system to compensate for mild-moderate decreases or increases to renal perfusion 

• Pre-Renal - decreased blood flow to kidney caused by

  • less intravascular or circulating volume blood 

  • less perfusion due to medications or renal artery stenosis 

    • loop diuretics, NSAIDs/COX2, ACEi/ARBs, cyclosporine or tacrolimus 

• Intrinsic - injury to kidney anatomy of renal tubules, glomerulus, vascular structures, interstitium 

  • tubular - from prerenal damage like prolonged HTN or nephrotoxic causing acute tubular necrosis (ATN) 

  • Interstitial - inflammatory infiltrates and edema in interstitium from nephrotoxic  medications and takes weeks to months to heal after stopping medication 

  • Vasculatures - occlusion of renal vessels from HTN or thrombus

  • Glomerular - nephrotic syndrome and glomerulopathies 

• Post-renal - caused by obstruction from constriction or crystallization

  • common in BPH, nephrolithiasis, malignancy from medications like acyclovir, methotrexate, sulfadiazine, triamterene, tenofovir, indinavir, foscarnet, anticholinergics 

• Contrast Induced nephropathy CIN - visualize atomic structures in CT and angiography, but directly toxic and can lead to ATN

  • often nonoliguric and typically returns within 14 days to serious AKI

  • preventable by anticipation and measures 

    • alternate CT with and without contrast in small volumes

    • avoid nephrotoxic agents and n-acetylcysteine 

    • hydrate before and after administration to dilute contrast 

    • LR/NS as 1 -1.5 mL/kg/hr started 3-12 hours before procedure then 6-24 hrs afterwards 

• Drug induced - increased SCr and BUN while decreasing GFR

  • shown by timing of drug or dose adjustment and recovery upon stopping

  • diuretics causing too much volume depletion lessening perfusion and being nephrotoxic 

  • tacrolimus elevates levels to increase SCR causing renal dysfunction

Nephrotoxic Drugs

• usually keep the life saving ones like antibiotics, antivirals, immunosuppressants 

General Management 

• prevention by avoid nephrotoxic agents in high risk, monitor patient closely, renally adjust doses and short duration 

• treat underlying problem and d/c offending agents 

• hydration and dialysis 

Supportive Care Treatment 

• Generally treat identifiable causes which can reverse pre-renal/post-renal AKI and prevent further damage 

  • mange fluids, electrolytes, d/c offending agents, treat non-renal complications while recovering 

    • hyperkalemia (Na 135-145 mEq/L),

    • hyperphosphatemia (Phos 2.5-5 mg/dL),

    • hypermagnesemia (Mg 1.5-2.0 mEq/L),

    • acid-base abnormalities 

  • hydrate PO or NS/LR given as 250 mL- 1L boluses then re-evaluate

    • if overloaded or pulmonary edema use furosemide or (torsemide, bumetanide, ethacrynic acid), but monitor electrolytes again and renal dysfunction caution

  • blood products if low Hgb, Hct, anemic, active bleeding  

  • Monitor SCr, BUN, fluid input and output, electrolytes, vitals, weight, medications

  • Correct: electrolytes, acid-base disorders, fluid status, etc

  • Even if dopamine increases kidney perfusion not for AKI

Dose Adjustment 

Contrast Induced Nephropathy

• IV contrast used to improve visualization of atomic structures within the body during coronary angiography and CT

• Leading cause of AKI, but often nonoliguria and typically returns within 14 days and can progress to serious AKI needing dialysis

• Risk factors with conditions that decrease renal perfusion (DM, CKD, sepsis, hypotension, dehydration, frequent administration, concurrent nephrotoxic agents)

• Prevent by

  • alternate CT with and without contrast in small volumes,

  • hydration 1-1.5 mL/kg/hr before and after administration to dilute

  • avoid nephrotoxic agents in sepsis, ESLD, HIV, CHF, Transplant

  • use lower doses and renally adjust

  • monitor patient closely and treat underlying problems

  • dialysis

Renal Replacement Therapy (RRT)

• short (AKI or AEIOus) or long term (CKD) replacement of patients own kidneys due to bad kidney function for inpatient, outpatient, clinics, and at home

• Once started survival rate goes down due to CV related or infection IV dialysis 

• Initiate and plan for stage 4 CKD based on patient and nephrologist input

Dialysis 

• determines rate and efficacy of removal by modifying rate, speed, target

  • can go between large and small pores to change flux and filter molecules

• dialysate creates osmotic gradients to clean the blood by changing concentration i.e hyperkalemic  dialysate low [K] to diffuse out patient

Hemodialysis 

• commonly done 3 days/week for 3-4 hours with heparin in circuit to anticoagulate blood 

• Needs vascular access so arteriovenous (AV) fistula (abnormal connection) connects artery and vein to increase blood flow for a dialysis machine  

  • lasts longer, less infection and thrombosis risk preferred for Long term

  • takes 3 - 4 months to mature before use 

• AV graft and CVC in emergency (tunneled or not tunneled) have higher risks 

Peritoneal Dialysis 

• Blood is filtered out by the peritoneal cavity by a indwelling catheter across a semipermeable membrane lining abdominal wall and covering organs 

  • dwelling - hookup, infusion, and fresh diffusion of dextrose

  • exchanging - waste diffusion is drained 

• same result as hemodialysis

  • less efficient and safe due to constant therapy 

  • more stable due to slower filtration rate 

Continuous Renal Replacement therapy (CRRT)

• reserved for critically ill hemodynamically unstable patients who cannot tolerate HD, but has same mechanism as HD over 24 hours