TOPIC2: acute kidney injury

Question 1

Definition of AKI

Answer 1

• formerly known as acute renal failure
• it is a SYNDROME arising from the rapid reduction in kidney function over a period of hours to days
• it is NOT A DIAGNOSIS NOR A DISEASE but rather a SYNDROME that is caused by or complicates a wide range of disorders.
• as measured by serum urea and creatinine(retention factors)
• leading to failure to maintain fluid, electrolyte and acid base homeostasis.

-depending on the degree of injury pts present with a SPECTRUM OF DISEASE, from mild deterioration in function to severe injury requiring renal replacement therapy (RRT)

Question 2

KDIGO criteria for diagnosing AKI

Answer 2

1. increase is SCr by >26.5micromol/L within 48 hr
2. increase in SCr by > or equal 1.5xbaseline ( know or presumed to have occured within prior 7days)
3. urine volume <0.5mL/kg/h for 6hr

Question 3

KDIGO criteria for staging AKI

Answer 3

STAGE1:

• SCr is 1.5-1.9xbaseline or >26.5micromol/L within <48hr
• UrineOutput is <0.5mL/kg/hr for 6-12hr

STAGE2:

• SCr is 2-2.9xbaseline
• UO is <0.5mL/kg/hr for >12hr

STAGE3:

• SCr is >3xbaseline or >354micromol/L or initiation of RRT
• UO <0.3mL/kg/hr for >24hr or anuria for >12hr

NOTE: oliguria is >100ml/day but <400ml/day
anuria is <100ml/day

Question 4

Clinical presentation

Answer 4

• pts with mild to moderate AKI are asymptomatic & are identified on lab testing
• pts with severe cases can have: confusion,fatigue,anorexia,nausea,vomiting,weightgain or edema
• pts can present with oliguria,anuria or can be non oliguric (non oliguric AKI)
• uremic encephalopathy(decline in mental status, asterixis)
• anemia
• bleeding(uremic plt dysfunction)
• because a wide variety of diseases can cause the syndrome it is important to narrow the list and categorize AKI by 3 clinical syndromes in order to direct the diagnosis and therapy
  1. pre-renal
  2. post renal
  3. intrinsic

Question 5

Pre-renal AKI causes

Answer 5

• decrease in GFR due to hypoperfusion of the kidneys
• renal function may go back to normal after resolving the hemodynamic problem
• pts with baseline chronic kidney disease are at risk for this type of AKI (acute-on-chronic)

1. extracellular fluid loss: hemorrhage, diarrhea, vomiting, excessive diuresis ( uncontrolled DM)
2. decreased effective circulating volume with edema: CHF, nephrotic syndrome, liver cirrhosis
3. decreased effective circulating volume and vasodilation: sepsis, anaphylaxis
4. glomerular autoregulatory failure:
   - afferent arteriole vasoconstriction: NSAIDS, hepatorenal syndrome, adrenaline, hypercalcemia, sepsis
   - efferent arteriole vasoconstriction: ACEi, ARB

Question 6

Pre-renal AKI clinical features

Answer 6

1. decreased urine Na+ conc. (<20mmol/L) if person takes diuretics, it may be normal
2. FeNa <1%
3. urine osmolarity >500mosm/L
4. urine specific gravity >1.020
5. BUN increases usually more than SCr
6. no urinary sediment

–> basically diluting ability of the urine is lost

Question 7

intrinsic AKI causes

Answer 7

1. Tubular: ATN is the most common often as a result of:
   - pre-renal damage
   - nephrotoxins ( aminoglycosides,radiocontrast,myoglobinuria) -due to crystal damage (ethyline glycol or uric acid)
   - myeloma
   - hypercalcemia
2. Glomerular:
   - autoimmune disease (SLE,HSP)
   - Drugs
   - infections
   - primary glomerulonephritis
3. interstitial:
   - drugs
   - infiltration (lymphoma)
   - infection
   - tumor lysis syndrome (after chemo)
4. Vascular:
   - vasculitis
   - malignant HTN
   - thromboemboli or cholesterol emboli from angio
   - HUS/TTP
   - large vessel occlusion (dissection or thrombus)

Question 8

post-renal AKI causes

Answer 8

Caused by obstruction of the ureter, urinary bladder or urethra:

• extra ureteral obs:
  
  • tumor, lymphadenopathy, ligation
• intra ureteral obs:
  
  • lithiasis/ tumor
• bladder obs:
  
  • prostate hypertrophy, tumor, neurologic
• urethral obs:
  
  • stricture,phimosis

Question 9

Acute-on-chronic AKI

Answer 9

-usually in any kidney damage, there is increased retention factors, decreased eGFR, maybe oliguria so
differentiating true AKI from long-standing stable CKD or an acute exacerbation of pre-existing renal impairment is very imp.

the only two consistently useful discriminators are:
1. Previous measurements of renal function (BASELINE SCr level)

2. ULTRSOUND:
   - long standing renal disease leads to loss of renal parenchyma and decreased renal size. So small (<9-10cm), echo bright often cystic kidneys are characteristic of CKD

-normal sized kidneys should arouse suspicion of AKI (exc. is diabetic nephropathy)

NOTE:
- ANEMIA might suggest chronic under-synthesis of EPO by the scarred kideys but it can occur also in AKI!

• decreased Ca2+ and increased PO4 suggest establishes CKD but may be misleading as disturbances of MINERAL metabolism can occur rapidly in AKI

Question 10

Diagnostic steps

Answer 10

1. full medical history (pain, hematuria, systemic illness, drugs)
2. physical exam (assess IV volume or skin rashes for systemic disease)
3. Lab exam: urineanalysis (casts), urine and blood electrolytes (Na+)
   FBC, SCr (retention factors), FeNa
4. imaging: US
   
   • obstruction/ hydronephrosis (post-renal)
   • bilateral small kidneys suggest that the pt has CKD so this prob is an acute-on-chronic exacerbation
   • normal sized kidneys suggest renal-parenchymal disease, further steps needed:
     - cast analysis:
5. brown muddy casts–>ATN
6. RBC casts &proteinuria in GN &myeloma
   
   • ->BIOPSY!