1.62 CME

Approche de la lésion rénale aiguë

Conférencier: Dr. Nikhil Bhasin

Nephrologist & Renal Transplant Physician, Wockhardt Hospital, Mumbai

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Description

Acute kidney injury involves a sudden decline in kidney function, shown by a rise in serum creatinine level with or without reduced urine output, ranging from mild to severe and sometimes necessitating renal replacement therapy. Diagnostic evaluation categorizes this injury as prerenal, intrinsic renal, or postrenal, with initial workup including a patient history to identify potential causes like nephrotoxic medications or systemic illnesses impacting kidney function.

Résumé

  • Acute Kidney Injury (AKI) is a rapid decline in kidney function, defined by increased serum creatinine, decreased urine output, or both. It's a common issue in medical practice, important for medical students, physicians, and clinical residents, and can be community or hospital-acquired, with varying degrees of severity. AKI can progress to Acute Kidney Disease (AKD) or Chronic Kidney Disease (CKD).
  • AKI staging, according to KDIGO guidelines, involves three stages based on creatinine levels and urine output. Creatinine isn't an ideal AKI marker due to delayed response to injury and dependence on multiple factors like clearance, production rate, volume of distribution, and muscle mass. Biomarkers are researched for earlier detection but are currently expensive and lack validation in India.
  • Approaching an AKI patient includes differentiating between AKI, CKD, or AKI on CKD, identifying the cause (pre-renal, intrarenal, or post-renal), maintaining hemodynamics, adjusting drug dosages, correcting the underlying etiology, and managing complications like fluid overload and hyperkalemia. Iatrogenic factors are important differential.
  • Pre-renal AKI is often caused by intravascular volume depletion, systemic vasodilation, or drugs affecting glomerular microcirculation. Intrarenal AKI involves tubules, interstitium, glomerulus, or vessels. Post-renal AKI is related to obstruction in the urogenital system. Some medications can cause slight, but sometimes beneficial, creatinine elevations.
  • Investigation is key. A routine investigation like full hemogram helps to identify potential causes. Urine analysis is an inexpensive but very helpful diagnostic component. Imaging helps to evaluate a patient who is in AKI. In AKI management, nephrotoxic agents should be discontinued, volume status maintained, drug dosages adjusted, and complications managed. In some cases, specific managements are necessary like treating the underlying cause.
  • Fluid resuscitation is important. Volume status should be assessed before fluid administration. Lasix stress test is necessary if the patient is volume overloaded. Diuretics use should be reserved. Prevention of AKI is a great importance like adopting sick-day protocols. Dialysis is indicated for acidosis, volume overload, hyperkalemia and uremic symptoms.

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