Acute Kidney Injury Flashcards
Sudden impairment of kidney function –> retention of nitrogenous and other waste products normally cleared by the kidneys
Acute Kidney Injury
Common Diagnostic Features of AKI
↑ in BUN concentration
↑ in plasma or serum creatinine concentration
↓ in urine volume
KDIGO 2012 Definition of AKI
↑ in SCr by >0.3 mg/dL (>26.5 mmol/L) w/n 48 hrs
↑ in SCr to >1.5 x the baseline - occured w/n the prior 7 days
urine volume <0.5 mL for 6 hrs
MC form of AKI
prerenal azotemia
Due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal glomerular filtration
prerenal azotemia
-NO parenchymal damage
MC causes of intrinsic AKI
sepsis
ischemia
nephrotoxins (endogenous and exogenous)
Very important cause of AKI in the developing world
sepsis
The site of one of the most hypoxic regions in the body
renal medulla
Intrinsic AKI
tubular damage
glomerular damage
interstitial damage
vascular damage
Small Vessels Damage (Intrinsic AKI)
Glomerulonephritis Vasculitis TTP/HUS DIC Atheroemboli Malignant HTN Calcineurin inhibitors Sepsis
Tubules (Intrinsic AKI)
Toxic ATN Endogenous (rhabdomyolysis,hemolysis) Exogenous (contrast, cisplatin, gentamicin) Ischemic ATN Sepsis
Intratubular (Intrinsic AKI)
Endogenous • Myeloma proteins • Uric acid (tumor lysis syndrome) • Cellular debris
Exogenous
• Acyclovir, methotrexate
MC clinical conditions associated with prerenal azotemia
hypovolemia
↓ cardiac output
medications that interfere with renal autoregulatory responses (NSAID and inhibitors of Angiotensin II)
Risk factors for nephrotoxicity
age
CKD
prerenal azotemia
Clinical course of contrast AKI
↑ in SCr beginning 24–48 h following exposure
peaking within 3–5 days
resolving within 1 week
Common findings in contrast AKI
low fractional excretion of sodium (FeNa) < 1
benign urinary sediment without features of tubular necrosis
MC protein in urine and produced in the THICK ascending limb of the loop of Henle
uromodulin
Occurs when the normally unidirectional flow of urine is acutely blocked either partially or totally
Postrenal Acute Kidney Injury
Complete anuria early in the course of AKI is uncommon EXCEPT in the following situations:
complete urinary tract obstruction
renal artery occlusion
overwhelming septic shock
severe ischemia (often with cortical necrosis)
severe proliferative glomerulonephritis or vasculitis
AKI leads to
hyperkalemia
hyperphosphatemia
hypocalcemia
The fraction of the filtered sodium load that is reabsorbed by the tubules measure of both the kidney’s ability to reabsorb sodium as well as endogenously and exogenously administered factors that affect tubular reabsorption
fractional excretion of sodium (FeNa)
Type 1 transmembrane protein that is abundantly expressed in proximal tubular cells injured by ischemia or nephrotoxins such as cisplatin
Kidney Injury Molecule-1 (KIM-1)
Highly upregulated after inflammation and kidney injury and can be detected in the plasma and urine within 2 h of cardiopulmonary bypass–associated AKI
Neutrophil gelatinase associated lipocalin (NGAL aka lipocalin-2 or siderocalin)
Hallmark of AKI
elevated BUN concentration
Major complication of oliguric and anuric AKI due to impaired salt and water excretion
expansion of extracellular fluid volume
An important complication of AKI particularly common in rhabdomyolysis, hemolysis, and tumor lysis syndrome due to release of intracellular potassium from damaged cells
Hyperkalemia
Major cardiac complications of AKI
arrhythmias
pericarditis
pericardial effusion
