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Acute Kidney Injury - Mini Lecture

Acute Kidney Injury - Mini Lecture. Updated 02/2013. Quickly and easily identify and workup acute kidney injury. Objectives. The incidence of AKI is estimated at 1% of patients that present to the hospital and 7-50% of patients in the ICU.

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Acute Kidney Injury - Mini Lecture

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  1. Acute Kidney Injury - Mini Lecture Updated 02/2013

  2. Quickly and easily identify and workup acute kidney injury. Objectives

  3. The incidence of AKI is estimated at 1% of patients that present to the hospital and 7-50% of patients in the ICU. Part of the initial history should be determining every patients baseline Cr. May present as Uremia (malaise, anorexia, nausea, vomiting), but is usually asymptomatic. Acute Kidney Injury Network (AKIN) Criteria Background

  4. AKI can be Prerenal, Intrinsic or Postrenal

  5. Prerenal azotemia is the most common cause of acute kidney injury in the outpatient setting Look for patients with decreased PO, diarrhea, vomiting, tachycardia, orthostasis…. Order: UA, Uosm, Una, Ucr, BMP, Uurea (if on diuretics) The kidney functions properly in patients with prerenal azotemia. True volume depletion can be treated with normal saline. Decreased effective arterial blood volume can be present in CHF, Cirrhosis or nephrotic syndrome. Treatment should focus on the underlying disease. Prerenal Azotemia

  6. ATN - Acute Tubular Necrosis Usually occurs after an ischemic event or exposure to nephrotoxic agents. Look for muddy brown casts and FeNa>2% AIN - Acute Interstitial Nephritis Classic presentation is fever, rash, eosinophilia and Cr bump 7-10 days after drug exposure. Urine may show leukocytes, leukocyte casts and erythrocytes, cultures will be negative. CIN - Contrast Induced Nephropathy Increased Cr of 0.5mg/dl or 25% 48hrs after contrast administration. Prevent with NS or isotonic fluid+sodium bicarb, hold NSAIDs, metformin and diuretics (in patients without fluid overload). Others – Glomerular Disease, Pigmented Nephropathy, Thrombotic Microangiopathy Intrinsic Kidney Diseases

  7. Obstruction anywhere in the urinary tract Bladder outlet obstruction can be seen with bladder scan and relieved with catheterization Ureteral obstruction and hydronephrosis may be seen on ultrasound and noncontrast CT Order: Order: UA, Uosm, Una, Ucr, BMP, Uurea (if on diuretics) Patients often have a history of pelvic tumors, irradiation, congential abnormalities, kidney stones, genitourinary, procedures or surgeries, and prostatic enlargement. Postrenal Disease

  8. AKI can be Prerenal, Intrinsic or Postrenal

  9. A 74 year old man was hospitalized 3 days ago with cellulitis. He has a history of HTN, HLD, PVD and has been non-compliant with his medications. At presentation, his vitals were T-37, BP-170/90, HR-90, RR-20 and Cr was 1.5. He was started on Cefazolin and his home meds (Lisinopril, Metoprolol, HCTZ, Amolodipine, Pravastatin and ASA) were restarted. Today, his vitals are T-37, BP-110/55, HR-60, RR-16 and his Cr is 2.7, FeNa-2.3%, FeUrea-51%, UA shows trace protein and occasional Granular casts. UOP has been stable. What is the most likely cause of his AKI? A. Acute Interstitial Nephritis B. Benign Prostate Hypertrophy C. Acute Tubular Necrosis D. Prerenal Azotemia Practice Question

  10. Identify AKI early on Monitor serum Cr for at risk patients Make sure I/Os are recorded correctly Diagnose as Prerenal, Intrinsic or Postrenal Detailed history Order routine labs including BMP, UA, Uosm, Ucr, Una (Urine Urea if on diuretics) Imaging studies as necessary Begin appropriate treatment Stop offending agent Fluids if appropriate Relieve obstruction Renal dosing of meds Take Home Points

  11. Thank You

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