Acute Kidney Injury - Mini Lecture Updated 02/2013

Objectives Quickly and easily identify and workup acute kidney injury.

Background 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 Stage Cr Criteria UOP Criteria 1 Cr↑by 1.5-2x baseline or Cr↑by 0.3 mg/dl < 0.5 ml/kg/hr for 6hr 2 Cr↑by 2-3x < 0.5 ml/kg/hr for 12hr 3 Cr↑by more than 3x or Cr↑by 0.5 if baseline >4mg/dl < 0.3 ml/kg/hr for 24hr Or anuria for 12h Other points to consider: 1) Can occur over hours to weeks (presence for >3 months meets definition of CKD) 2)While we typically measure the serum Cr to determine kidney function, it is not a great marker as some individuals can lose ~50% of their GFR before the level becomes abnormal. It is important to be aware that the rise in Cr lags behind the time of injury. 3) A patient’s Cr going for 0.6 to 0.9 can potentially be much more concerning that going from 3 to 4 4) A rise in Cr is not always pathogenic (ex. Bactrim and H2-blockers decrease tubular secretion of creatinine)

AKI can be Prerenal, Intrinsic or Postrenal The whole talk can be given from this slide, so take time to go over each box Audience Participation: Sodium is not a good marker of kidney function in patients on diurectics. What test should you use? - FeUrea (replace sodium with urea in the equation above). FeUrea<35% suggests prerenal AKI

Prerenal Azotemia 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. Audience Participation: Why do you get an elevated BUN-creatinine ratio? In patients with prerenal azotemia, both BUN and Creatinine can increase, but BUN often increases disproportionately more than creatinine. In the setting of decreased effective blood volume, slow flow through the tubules allows more time for BUN to be reabsorbed and creatinine to be secreted. In other words, BUN clearance goes down lower than Cr.

Intrinsic Kidney Diseases 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 If you don’t identify Prerenal Azotemia, it will progress to ATN Other types of disease to consider are: Pigmented Nephropathy from hemoglobin or myoglobin Thrombotic Microangiopathy- TTP/HUS And the whole topic of glomerular disease

Postrenal Disease 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.

AKI can be Prerenal, Intrinsic or Postrenal This is a repeat of the earlier slide to review

Practice Question 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 Correct answer is C. The patient is suffering from iatrogenic ATN. His history suggests CKD and vascular disease. If he is chronically hypertensive and has his BP dropped to the normal range, he becomes effectively hypotensive if his kidneys cannot compensate to increase renal blood flow. A – AIN usually manifests a week after starting the offending agent B – There is nothing in the question stem to indicate that this patient without a history of BPH is suffering from it acutely D – His FeNa and FeUrea are elevated making ATN more likely

Take Home Points 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

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