Acute kidney injury - Internal medicine Flashcards
Nephrology in brief
Definition of Acute kidney injury and clinical picture
Abrupt severe deterioration of renal function over hours to days with the hallmark azotemia (increased BUN and creatinine [Cr]) and often oliguria.
C/P: The hallmarks are azotemia and abnormal urine volume: formally <0.5 ml/kg/h for >6 h but can manifest as anuria, oliguria, or polyuria.
Kidney Diseases: Improving Global Outcomes (KDIGO) criteria for AKI?
- Rise in creatinine ≥ 0.3mg/dl (≥26.5μmol/L) within 48h.
- Rise in creatinine >1.5 × baseline (i.e. before the AKI) within 7days.
- Urine output <0.5mL/kg/h for >6 hours.
KIDGO staging of AKI
Stage 1:
a) Serum Creatinine:
Increase by ≥ 0.3 mg/dL (≥ 26.5 μmol/L) within 48 hours, or
Increase to 1.5-1.9 times baseline
b) Urine Output:
< 0.5 mL/kg/h for 6-12 hours
Stage 2:
a) Serum Creatinine:
Increase to 2.0-2.9 times baseline
b) Urine Output:
< 0.5 mL/kg/h for ≥ 12 hours
Stage 3:
a) Serum Creatinine:
- Increase to 3.0 times baseline, or
- Increase in SCr to ≥ 4.0 mg/dL (≥ 353.6 μmol/L),or
- Initiation of renal replacement therapy, or
b) Urine Output:
- < 0.3 mL/kg/h for ≥ 24 hours, or
- Anuria for ≥ 12 hours
Risk factors of AKI
- Pre-existing chronic kidney disease (CKD).
- Old age, Male.
- Comorbidity (DM, cardiovascular disease, malignancy, chronic liver disease, complex surgery).
Rifle criteria of AKI
Risk (R): Increased serum creatinine level by 1.5 times or GFR decrease by >25%
Injury (I): Increased serum creatinine level by 2.0 times or GFR decrease by >50%
Failure (F): Increased serum creatinine level by 3.0 times, GFR decrease by >75% or serum creatinine level ≥354μmol/L
Loss (L): Persistent acute renal failure or complete loss of function for >4 weeks
ESKD (E): End-stage kidney disease (ESKD) for >3 months
Causes of Acute kidney injury
- Prenatal causes of Acute kidney Injury:
- Decreased vascular volume: e.g. Hemorrhage, Diarrhea & vomiting, burns, pancreatitis.
- Decreased cardiac output: e.g. Cardiogenic shock, myocardial infarction (MI)
- Systemic vasodilation: e.g. Sepsis, drugs
- Renal vasoconstriction: e.g. Nonsteroidal anti-inflammatory drugs(NSAIDs), Angiotensin-converting-enzyme inhibitors (ACE-I), Angiotensin receptor blockers (ARBs), hepatorenal syndrome.
- Renal artery stenosis - Intrinsic renal causes of Acute kidney Injury:
- Glomerular: Glomerulonephritis.
- Tubular: ATN
- Interstitial: Acute interstitial nephritis, pyelonephritis.
- Vascular: Vasculitis, Hemolytic uremic syndrome (HUS), Thrombotic thrombocytopenic purpura (TTP), Disseminated intravascular coagulation (DIC) and Malignant hypertension. - Postrenal causes of Acute kidney Injury:
- Urethral obstruction, Ureteral obstruction (bilateral, or unilateral if solitary kidney) e.g. Stone, renal tract malignancy, stricture, pelvic malignancy, prostatic hypertrophy, retro-peritoneal fibrosis.
Why careful history is essential in Acute kidney injury?
- Evidences of volume depletion: diarrhea, bleeding, burns.
- Exposure to nephrotoxins and drugs.
- Past and present use of medications.
- Skin rashes may indicate allergic nephritis
- Anuria may indicate post-renal causes
- Pelvic and per-rectal examination: look for evidence of abortion
- Recent surgical or radiologic procedures.
- Ischemia or trauma to the legs or arms may indicate rhabdomyolysis.
- Family history of renal diseases.
Physical examination of AKI
Should be focused to rule out possible differential diagnosis Prerenal AKI:
A) Suggested by clinical signs of:
* Intravascular volume depletion (e.g. ↓blood pressure, ↓urine volume,
non-visible Jugular Venous Pressure (JVP), poor tissue turgor, rapid
thread pulse)
* Congestive heart failure (e.g. raised JVP, S3, dependent edema, and
pulmonary rales).
* Acute allergic interstitial nephritis: Suggested by signs of allergy (e.g.
periorbital edema, eosinophilia, maculopapular rash, and wheezing).
* Lower Urinary tract obstruction: Suggested by suprapubic dullness or flank
mass, symptoms of bladder dysfunction (e.g. hesitancy, urgency).
B) Uremia: Clinical syndrome resulting from the adverse effect of the AKI on other
organ systems (only very few develop in AKI).
Investigations used in AKI
- Serum Cr, Serum BUN and Serum BUN:Cr ratio
- CBC, electrolytes Na, K, Ca2+
, PO43–.
In pre-renal AKI:
- Urinalysis: Urine volume, specific gravity, pH, albumin, hemoglobin, glucose, leukocytes, urobilinogen, sediment, casts, crystals, Electrolytes, osmolality, Culture and sensitivity
- Foley catheterization (rule out bladder outlet obstruction)
- Imaging: U/S (assess kidney size, hydronephrosis, postrenal obstruction)
- Renal biopsy indicated in:
✓ Diagnosis is not certain
✓ Prerenal azotemia or ATN is unlikely
✓ Oliguria persists >2-4 d
✓ Rapidly progressive glomerulonephritis (RPGN), signs of significant
glomerular disease (proteinuria, RBC casts) despite normal kidney
size/echogenicity.
- Serum BUN : Cr ratio >20:1
- Fractional excretion of sodium [FENa] < 1%
- Urine osmolality > 500 mOsm/kg. (tubular function remains intact)
In ATN:
- Serum BUN: Cr ratio <15
- FENa >2%
- Urine osmolality < 500 mOsm/kg (inability to concentrate urine)
How to prevent AKI
- Many cases of ischemic AKI can be avoided by close attention to cardiovascular function and intravascular volume in high-risk patients, such as the elderly and those with preexisting renal insufficiency.
- Aggressive restoration of intravascular volume has been shown to reduce the incidence of ischemic AKI dramatically after major surgery or trauma, burns, or cholera.
- The incidence of nephrotoxic AKI can be reduced by tailoring the dosage of potential nephrotoxins to body size and GFR; for example, reducing the dose or frequency of administration of aminoglycoside drugs in patients with preexisting renal impairment.
Treatment of AKI
-Requires determination and treatment of the underlying cause.
-Exclusion of reversible causes: e.g. Obstruction should be relived.
1) Prerenal:
Correct volume depletion and/or improve renal perfusion via circulatory/cardiac support, treat any underlying sepsis.
- Assessment of volume status.
- Fluid resuscitation in case of Hypovolemia:
✓ Give 500mL crystalloid over 15min.
✓ Reassess fluid state.
✓ Further boluses of 250–500mL crystalloid with clinical review after each.
✓ Stop when euvolemic.
- Any crystalloid can be used e.g. normal saline.
- Blood components should be used in resuscitation due to hemorrhage.
- Human albumin solutions may be given in hepatorenal syndrome and
as second line to crystalloids in septic shock.
2) Fluid overload: Occurs due to aggressive fluid resuscitation, oliguria, and in sepsis due to ↑capillary permeability.
✓ Oxygen supplementation if required.
✓ Fluid restriction.
✓ Diuretics: Only in symptomatic fluid overload. They are ineffective and potentially harmful if used to treat oliguria without fluid overload.
AKI with fluid overload and oligo/anuria needs urgent referral to renal/critical care
3) Intrinsic renal:
- Address reversible renal causes: discontinue nephrotoxic drugs, treat infection, and optimize electrolytes, correct ECF volume.
- Specific treatment of intrinsic renal disease according to biopsy.
4) Post-renal:
- Management of post-renal AKI requires close collaboration between nephrologist, urologist, and radiologist.
- Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter, which provides temporary relief while the obstructing lesion, is identified and treated definitively.
How to treat hyperkalemia
Acute therapy is warranted if ECG changes are present or if patient is symptomatic
regardless of [K+]. Tailor therapy to severity of increase in [K+] and ECG changes.
- [K+] <6.5 and normal ECG: treat underlying cause, stop K+ intake, increase the loss of K+ via urine and/or GI tract
- [K+] between 6.5 and 7.0, no ECG changes: add insulin to above regimen
- [K+] >7.0 and/or ECG changes: first priority is to protect the heart, add calcium gluconate to above.
◆ Calcium gluconate 1-2 amps (10 mL of 10% solution) IV over 5–10min.
◆ Intravenous insulin (10U soluble insulin) in 25g glucose (50mL of 50% or 125mL of 20% glucose). Insulin shift K+ intracellular, lowering serum K+ .
◆ Salbutamol also causes an intracellular K+
shift but high doses are required (10–20mg via nebulizer) and tachycardia can limit use.
◆ Dialysis: If medial therapy fails or the patient is very toxic.
How to treat metabolic acidosis
- Mild metabolic acidosis can be treated with oral sodium bicarbonate.
- Severe acidosis (pH <7.2) can be temporized with IV sodium bicarbonate but requires monitoring for volume overload, rebound alkalosis, and hypocalcemia.
- Metabolic acidosis that is refractory to medical management is an indication for urgent dialysis.
- From a practical point of view, most patients requiring sodium bicarbonate need emergency dialysis within days.
