-H&P: Review history for any recent procedures, IV contrast, nephrotoxic meds; thirst; volume status; vital signs; orthostatic vitals; s/s of obstruction, vascular or systemic dis.
–AKI stage:____
-DDx: Prerenal vs Intrinsic vs Postrenal causes.
-Eval for complications of AKI.
Diagnostic testing
-CMP (serum electrolytes, creatinine, etc.),
-Urinalysis (to look for cells, casts, protein) and urine sediment
-Serum Ca, phos, and mg to r/o AKI-related electrolyte abnormalities.
-CBC with diff and coagulation panel if a systemic dis assoc w/ AKI e.g HUS, TTP, and DIC) is a concern.
-Urine output (anuria, oliguria, normal UOP),
-Urine Na and Urine Cr at the same time as plasma Na and plasma Cr.
–FENA=_____, indicating____(prerenal/Intrinsic renal/post-renal).
-BUN/Cr ratio = ____, indicating _________
-Urine osmolality,
-Renal US (if CT not done in ED) within 24h to r/o obstructive uropathy (hydroureter and hydronephrosis) & evaluate kidney size to estimate chronicity of kidney disease.
-Orthostatic vitals
-Urine eosinophils if concerned for AIN.
-Consider ABG and ECG
-Creatinine Kinase if rhabdomyolysis is a concern.
-Serologies to eval for glomerular disease, if AKI doesn’t resolve.
-Renal biopsy: may be needed if the cause remains unclear especially if pt develops hematuria and or proteinuria. Involve nephrology by this point.
Treatment
-Call MD if UOP <30 mL/hr
-IVF based on volume status & UOP.
-Daily weights. Monitor fluid status.
-Strict I&Os (may need bladder cath if pt unable to accurately collect urine e.g. from incontinence, dementia, etc.
-D/C nephrotoxic medications (ACEI/ARBs / NSAIDs / metformin and do not restart until renal function stable at 48 – 72 hrs.
-Renal diet.
-Adjust doses of meds metabolized or excreted by the kidneys.
-Monitor and tx complications of AKI such as hyperkalemia, hyponatremia, hyperphosphatemia, hypermagnesemia.
-Consult nephrology, as needed
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Key Points
- NB: Ischemia (prerenal & ATN) accounts for > 50% of in-hospital AKI.
- Interpreting a Urinalysis.
- The Urine Sediment Examination.
- BUN/Creatinine ratio.
- Fractional Excretion of Sodium (FENa).
- The BUN/Creatinine ration is usually >20: 1 in pre-renal disease.
- FENA works well in oliguric pts
- Creatinine kinase=creatinine phosphokinase.
- AIN = Acute Interstitial Nephritis.
- Oliguric vs. Anuric AKI
- When to avoid fluids in AKI
“Both NSAIDs and ACE inhibitors reduce glomerular filtration and can precipitate AKI, especially in patients with other contributing factors, such as dehydration. NSAIDs reduce glomerular filtration by inducing vasoconstriction of the afferent arterioles through inhibition of cyclooxygenase, which leads to increased levels of thromboxane A2, a potent vasoconstrictor. ACE inhibitors reduce glomerular filtration by reducing levels of angiotensin II, which allows vasodilation of efferent arterioles and reduces glomerular hydrostatic pressure.
Radiocontrast media are known to be potentially nephrotoxic and are best avoided in patients with, or at risk for, AKI. However, if the use of contrast media for imaging studies or coronary angiography is justified, the risk of renal injury can be reduced by infusion of sodium bicarbonate prior to administration of the contrast media (SOR A).” theabfm.org
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Intrinsic include: Acute Tubular Necrosis (ATN), Acute Interstitial Nephritis (AIN), small-medium vessel disease, and glomerulonephritis