Acute Kidney Injury Year 4 Paediatrics Notes OmpathStudy

Acute Kidney Injury Year 4 · Paediatrics Collection: 4TH YEAR ALL NOTES / PAEDS / PAEDS 4.2 / MUNGE / RENAL PAEDS -- Slide 1 Acute Kidney Injury Dr Rose Munge Slide 2 Introduction Acute kidney injury (AKI) has been traditionally defined as an abrupt loss of kidney function leading to a rapid decline in the glomerular filtration rate (GFR), accumulation of waste products such as blood urea nitrogen (BUN) and creatinine, and dysregulation of extracellular volume and electrolyte homeostasis.\n The term AKI has largely replaced acute renal failure (ARF).\n AKI embodies a continuum of renal dysfunction that ranges from a small increase in serum creatinine to complete anuric renal failure. Slide 3 AKI is a common problem afflicting all ages, the leading reason to seek inpatient nephrology consultation, and associated with serious consequences and unsatisfactory therapeutic options.\n The incidence of AKI varies from 2–5% of all hospitalizations to 25% in critically ill infants and children. Slide 4 The etiology of AKI varies widely according to age, geographic region, and clinical setting. Functional AKI induced by dehydration is usually reversible with early fluid therapy.\nHowever, the prognosis for patients with structural AKI in the intensive care setting with multiorgan failure remains guarded. A classification system proposed by the Kidney Disease Improving Global Outcomes (KDIGO) AKI Consensus Conference takes both serum creatinine and urine output criteria into account to define and stage AKI Slide 6 Pathogenesis AKI has been conventionally classified into three categories: prerenal, intrinsic renal, and post-renal Slide 7 PRERENAL Dehydration Gastroenteritis Hemorrhage Burns Sepsis Capillary leak Hypoalbuminemia Cirrhosis Abdominal compartment syndrome Cardiac failure Anaphylaxis Prerenal AKI, also called prerenal azotemia, is characterized by a diminished effective circulating arterial volume, which leads to inadequate renal perfusionand a decreased GFR.\nEvidence of structural kidney damage is absent.\nCommon causes of prerenal AKI include dehydration, sepsis, hemorrhage, severe hypoalbuminemia, and cardiac failure. If the underlying cause of the renal hypoperfusion is reversed promptly, renal function returns to normal.\nIf hypoperfusion is sustained, intrinsic renal parenchymal damage can develop. Slide 8 Intrinsic renal AKI includes a variety of disorders characterized by renal parenchymal damage, including sustained hypoperfusion and ischemia. Ischemic/hypoxic injury and nephrotoxic insults are the most common causes of intrinsic AKI in the United States and are more common with an underlying comorbid condition; most are associated with cardiac, oncologic, urologic, renal, and genetic disorders or prematurity.\nMany forms of glomerulonephritis, including postinfectious glomerulonephritis, lupus nephritis, Henoch-Schönlein purpura nephritis, membranoproliferative glomerulonephritis, and anti–glomerular basement membrane nephritis, can also cause intrinsic AKI. Severe and prolonged ischemic/hypoxic injury and nephrotoxic insult lead to acute tubular necrosis (ATN), seen most often in critically ill infants and children. INTRINSIC RENAL Glomerulonephritis Postinfectious/poststreptococcal Lupus erythematosus Henoch-Schönlein purpura Membranoproliferative Anti–glomerular basement membrane,Hemolytic-uremic syndrome Acute tubular necrosis Cortical necrosis, Renal vein thrombosis,Rhabdomyolysis Acute interstitial nephritis Tumor infiltration, Toxin and drugs\nTumor lysis syndrome, Vasculitis Slide 9 Mechanisms leading to ischemic AKI include hypotension/intravascular volume depletion (hemorrhage, third-space fluid losses, diarrhea), decreased effective intravascular volume (heart failure, cirrhosis, hepatorenal syndrome, peritonitis, abdominal compartment syndrome), vasodilation/vasoconstriction (sepsis, hepatorenal syndrome), renal artery obstruction (thrombosis, embolization, stenosis), intrarenal artery disease (vasculitis, hemolytic-uremic syndrome, sickle cell anemia, transplant rejection), and impaired renal blood flow (cyclosporine, tacrolimus, angiotensin-converting enzyme [ACE] inhibitors, angiotensin-receptor blocking agents, radiocontrast agents). Slide 10 The typical pathologic feature of ATN is tubular cell necrosis, although significant histologic changes are not consistently seen in patients with clinical ATN. The mechanisms of injury in ATN can include alterations in intrarenal hemodynamics, tubular obstruction, and passive backleak of the glomerular filtrate across injured tubular cells into the peritubular capillaries. Tumor lysis syndrome is a specific form of AKI related to spontaneous or chemotherapy-induced cell lysis in patients with lymphoproliferative malignancies. This disorder is primarily caused by obstruction of the tubules by uric acid crystals.\nAcute interstitial nephritis is another common cause of AKI and is usually a result of a hypersensitivity reaction to a therapeutic