CONTRAST-INDUCED AKI

Defined as the impairment of renal function—measured as either a 25% increase in serum creatinine  from baseline or a 0.5 mg/dL  increase in absolute SCr value—within 48-72 hours after intravenous contrast administration.

  • SCr levels peak between 2 and 5 days and usually return to normal in 7 -10 days

CONTRAST-INDUCED AKI

  • Defined as the impairment of renal function—measured as either a 25% increase in serum creatinine from baseline or a 0.5 mg/dL increase in absolute SCr value—within 48-72 hours after intravenous contrast administration.
  • SCr levels peak between 2 and 5 days and usually return to normal in 7 -10 days.
  • Risk factors for contrast-induced nephrotoxicity: Patients related factors Procedure related factors Constrast related factors

Other causes of acute kidney injury

  • Hepatorenal syndrome: Renal failure in patients with advanced liver failure (acute or chronic) in absence of any other causes of renal pathology. • Rhabdomyolysis & Myoglobinuria: Large amount of myoglobin released from necrotic muscles in the setting of volume depletion causes ATN. • Tumor Lysis Syndrome: Caused by the rapid release of intracellular contents of tumor cells the systemic circulation.

Diagnosis

Pre-renal: • History: vomiting, diarrhea, and several medications including  NSAIDs, ACEI, and ARBs.

  • Examination: Physical signs of orthostatic hypotension, tachycardia, decreased skin turgor, and dry mucous membranes are often present in prerenal azotemia.

Post- Renal: • Colicky flank pain radiating to the groin suggests acute ureteric obstruction.

  • Nocturia and urinary frequency or hesitancy can be seen in prostatic disease.
  • Definitive diagnosis of obstruction requires radiologic investigations.

Acute kidney injury Diagnostic Tools • Urine macroscopic and  dipstic.

  • Urinary microscopic(urinary sediment)i.cell,cast &crystalls
  • Serum createnine & BUN
  • Radiologic studies.

Important Biomarkers

  • Cystatin C
  • Kidney injury molecule-1 a marker of severity of AKI

Radiologic studies

  • X-ray(KUB) useful for obstructive forms
  • Doppler (to assess renal blood flow)
  • Pyelography
  • Renal ultrasound
  • CT Scan/MRI

Lab findings

  • Rising creatinine and urea • Rising potassium • Acidosis • Hyponatraemia • Hypocalcaemia

Complication

  • Uremia (Bleeding, u frost, encephalopathy) • Hypervolemia and Hypovolemia • Hyponatremia/hypernatremia • Hyperkalemia • Hyperphosphatemia and Hypocalcemia • Cardiac Complications.

TREATMENT

General: • Optimization of systemic and renal hemodynamics through

volume resuscitation.

  • Elimination of nephrotoxic agents (e.g., ACEi, ARBs, NSAIDs,

aminoglycosides) if possible • Initiation of renal replacement therapy when indicated

VOLUME DEPLETION

  • Prompt reversal of volume depletion by IV fluids may

prevent or limit kidney injury.

  • Crystalloid solutions, such as isotonic saline are

preferred for initial therapy

  • Patient with pre-renal causes respond well to fluid therapy while those who do not respond by an increase in urine UOP or decrease in the serum Cr are unlikely to have prerenal disease and more likely to have established ATN or inadequate resuscitation

VOLUME OVERLOAD

  • Diuretics are used as temporizing agents to relieve volume overload, dialysis offers the most efficient for volume removal in patients with AKI from any cause.
  • Loop diuretics are the preferred agents as they provide a greater natriuretic effect than thiazide diuretics.

HYPERKALEMIA

  • Cardiac and neurologic complications may occur if serum K+ level is > 6.5 mEq/L
  • Restrict dietary K+ intake to ≤ 2g/day and potassium sparing duretics
  • Dialysis: If medial therapy fails or the patient is very toxic.

METABOLIC ACIDOSIS

  • The excretion of acid and regeneration of bicarbonate is impaired in AKI resulting in metabolic acidosis
  • Its not treated unless serum bicarbonate concentration falls below 15 mmol/L or arterial pH falls below 7.2.
  • More severe acidosis is corrected by oral or intravenous sodium bicarbonate. Provided no fluid overload • Most patients requiring sodium bicarbonate need emergency dialysis within days.

Indications for Dialysis

A – Acidosis (pH<7.1 in those with bicarbonate contraindication such   as volume overload) E – Electrolyte disturb., usually hyperkalemia of >6.5meq/l I – Intoxications (lithium, ethylene glycol, etc) O – Overload (volume overload that is refractory to deuretics) U – Uremia (symptoms & signs) Non-emergent dialysis may also be indicated for patients with prolonged AKI even in the absence of the indications listed above

Prognosis

  • Pre-renal and Post- renal better prognosis.
  • Kidneys may recover even after dialysis requiring AKI.
  • 10% of cases requiring dialysis develop CKD.

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