Presentation is loading. Please wait.

Presentation is loading. Please wait.

Acute Renal Failure for the Intern

Similar presentations

Presentation on theme: "Acute Renal Failure for the Intern"— Presentation transcript:

1 Acute Renal Failure for the Intern

2 Background and Epidemiology
Affects 5%-7% of all hospitalized patients 20%-70% mortality rate overall ARF in ICU – 50%-70% mortality rate Mortality rate unchanged over past 50 years

3 Anatomy 1 Renal Arteries Kidneys Glomerulus Collecting system Ureter
Bladder Urethra Renal Vein

4 Anatomy 2 Glomerulus PCT Loop of Henle DCT Collecting system
130 to 180 liters is filtered across the glomerulus every day. 98 to 99 % of that filtrate is reabsorbed.

5 Estimations of Renal Function
What do the kidneys do? How can we measure the function of the kidneys? What is the “ideal” substance to measure? What do we commonly use to measure renal function? Filter the blood Completely filtered Not secreted Not reabsorbed / transported Measure the glomeular filtration of a substance within the kidneys Serum Creatinine Concentration

6 Creatinine Water soluble breakdown product of creatine from skeletal muscle (and ingested meat, suplements). Creatinine is released into the circulation at a relatively constant rate. Creatinine is freely filtered in the glomerulus, and is not metabolized by the kidney. Approximately 15% of the urinary creatinine is secreted in the proximal tubule (in normally functioning kidney). Remember: Not all individuals will have the same amount of creatinine in their blood. Different drugs can affect the concentration of serum creatinine (without affecting a patient’s renal function). Cimetidine Trimethoprim Decrease Creatinine Secretion  Rise in serum level by up to 0.5 mg/dl

7 Effects on Serum Creatinine
Decreased Creatinine Secretion Cimetidine >> Ranitidine & Famotidine Trimethoprim Interfere with the Assay Acetoacetate (Diabetic Ketoacidosis) Cefoxitin Flucytosine Enhanced Creatinine Production Large meat meal Creatine containing supplements Rhabdomyolysis

8 Serum Creatinine and Renal Function
Glomerular Filtration Rate Cockcroft-Gault Method Jelliffe Method MDRD (140 – age) * weight (kg) 72 * serum Creatinine (multiply by 0.85 for female) [98 – 0.8 * (age – 20)] * BSA 1.73 * serum Creatinine (multiply by 0.9 for female) 186 * sCr ^ (-1.154) * Age ^ (-0.203) Multiple by for female Multiply by 1.21 for African American Assumes albumin = 4.0 Assumes patient is ~ 1.73 m2 95 +/- 20 ml/min in women 120 +/- 25 ml/min in men

9 Which formula should you use?
Strengths & Weaknesses MDRD Underestimates patients with normal renal function Overestimates patients with severe renal impairment. Cockcroft-Gault Underestimates patients at older ages Overestimates patients at younger ages All of these formulas are best used in patient’s with stable renal function. It takes time for the serum creatinine level to accurately reflect renal function. We usually use the Modification of Diet in Renal Disease (MDRD) forumula. Levey et al. Ann Intern Med. Mar 1999.

10 What is Acute Renal Failure?
Increase in sCr > 0.5 mg/dl (44 umol/l) Increase in sCr > 2-fold Decrease in GFR > 50% Decrease in GFR requiring dialysis Depends on who you talk to!

11 Classification of ARF Etiology Urine Output Pre-Renal Intrinsic Renal
Post-Renal Urine Output Polyuria > 3 liters / day Oligouria: 400 – 100 cc/day Anuria: < 100 cc / day

12 Urinalysis Intrinsic Renal ARF usually has an abnormal urinalysis.
Are there casts present? Is there proteinuria present? If hematuria is present, are the RBC’s dysmorphic? YOU SHOULD KNOW HOW TO SPIN A PATIENT’S URINE!

13 Urinalysis Collect 10 – 20 ml of freshly voided urine in a sterile specimen container. Take the sample to the laboratory. Centrifuge the specimen at 2,500 rpm for 5 minutes. Decant the supernatent. Place the specimen on a UA microscope slide.

14 Urine Microscopy a

15 Urine Microscopy, cont. Renal Tubular Cast Dysmorphic RBC

16 Urinalysis Clinical Correlation
Nephritis: “active” urinary sediment with casts, RBC’s, WBC’s. May be accompanied by HTN, proteinuria, ARF. Implies inflammation and glomerular damage. Nephrotic Syndrome: proteinuria without casts. Proteinuria (GBM defect) Edema (low albumin) Hypoalbuminemia Lipid Abnormalities Hypercoagguable State (AT III depletion)

17 Pre-Renal ARF Is the patient dry? Treatment? Etiology
FENa < 1 % FEUrea < 35 % BUN / Cr ratio Urine Osm and SG Urine Volume Heart Rate & BP Pulse Pressure Skin Turgor Mucous Membranes Thirst Treatment? Etiology Acutely reduced renal perfusion Aortic dissection Thromboembolic disease Drugs (NSAID, ACEI) Volume Depletion Bleeding Third Spacing Fluid Dehydration Relative Hypotension Shock Cardiac failure (Volume depletion) Urine Na * Plasma Cr * 100 Plasma Na & Urine Cr

18 NSAID’s and ACE-I in the kidneys
ACE-I inhibit arteriolar constriction NSAID Inhibit PG-mediated dilatation

19 Post-Renal ARF Laboratory Evaluation Radiographic Evaluation
FENa – variable Urine Osm – variable Radiographic Evaluation Renal US: hydonephrosis, hydroureter. Unilateral obstruction often does not cause rise in serum creatinine (unless patient only has a single functional kidney). Etiology of Obstruction? Foley malfunction Prostatic obstruction Neurogenic bladder Post-surgical complication Retroperitoneal fibrosis / CA Bilateral Urolithiasis

20 Intrinsic Renal ARF “Active” Urine sediment implies renal involvement.
Categorized based on location of injury: Tubules Interstitium Glomerulus Vessels Less common systemic conditions Pre-eclampsia TTP – HUS Thadhani, R. et al. N Engl J Med 1996;334:

21 Acute Tubular Necrosis
Urinalysis Iso-osmolar (300 – 400 mOsms) Urine Na > 20 FENa > 1 % “Muddy brown casts” are nonspecific, but sensitive. Urine Output Oligouria: more tubular damage, longer recovery. Non-oligouria: less tubular damage, shorter recovery time. Still carries a high mortality. For those who improve 90% will do so within 3 weeks 99% will do so within 6 weeks Most common cause of ARF due to intra-renal causes (~ 75%) Many causes of ATN Transient ischemic episode Toxic injury to the kidneys Myoglobinuria (Rhabdomyolysis) Heavy metals Contrast exposure

22 Microscopy of ATN

23 Tubular Necrosis: Ischemia
Etiology Systemic Hypotension Cardiogenic Shock Distributive Shock (sepsis) Hypovolemia (burns, trauma, blood loss). Post-Surgical Anesthesia Distributive Hypoperfusion Thyroid Storm Heart Failure ? Hepato-Renal Syndrome Tubular cells have a high metabolism (i.e. are sensitive to states of low blood flow, hypoxia, or hypotension). Continuum with pre-renal azotemia

24 Tubular Necrosis: Nephrotoxins
Common Drugs: Amphotericin B toxicity is dependent on the total dose (>3 gram); can also cause an RTA. Aminoglycosides cause proximal tubule damage resulting in non-oligouric ATN. Cisplatin is directly toxic to the tubules; also causes a magnesuria and hypomagnesemia. Methotrexate Radiocontrast IVIG Thadhani, R. et al. N Engl J Med 1996;334:

25 Contrast Induced Nephropathy
Pathogenesis is not fully understood Renal vasoconstriction? Direct toxic effect of contrast? Tubular injury from oxygen radicals? Patient’s at highest risk Diabetes with renal insufficiency Baseline CKD (sCr > 1.5 mg/dl) High total dose of contrast (> 70 cc) Multiple Myeloma Hypovolemia (or distributive state) Concurrent Nephrotoxic Drugs Radiocontrast agents Osmolality First generation contrast agents had very high osmolality (1500 – 1800 mosm/kg) Second generation contrast agents have lower osmolality (600 – 800 msom/kg): iohexol Third generation agents have even lower osmolality (~290 mosm/kg): iodixanol Ionic versus non-ionic First generation were ionic compounds, newer products are non-ionic.

26 Contrast Induced Nephropathy Prevention & Treatment
Don’t use contrast (MRI?) Use smallest amounts possible of non-ionic, low-osmolar contrast media. Avoid volume depletion Avoid NSAID’s Sodium Bicarbonate D5W + 3 amps NaHCO3/liter (~130 MEQ) Run at 3.5 cc/kg*hour (ideal body weight) for 1 hour prior to study, and 1.2 cc/kg*hour for 6 hours after exposure N-acetylcysteine (Mucomyst) 600 mg PO BID Administer 2 doses prior to study, and 2 doses after study.

27 In Reality… ATN is commonly multifactorial – nephrotoxic drugs exposed to kidneys with decreased perfusion Thadhani, R. et al. N Engl J Med 1996;334:

28 Interstitial Nephritis
Antibiotic AIN Classic Triad = fever, rash, eosinophilia. Presentation is acute Common Agents Beta-Lactams (esp Methicillin) TMP/SMX Cephalosporins Rifampin FQ NSAID AIN Classic triad often absent Presentation subacute, or after months of use of NSAID. Acute Interstitial Nephritis Slight proteinuria +/- Renal tubular acidosis +/- Urine Eosinophils +/- RBC, WBC, and WBC Casts Caused by allergic reaction to medication / exposure Chronic Interstitial Nephritis Chronic analgesic abuse Heavy Meatals (lead, cadmium) Sjogren’s Disease Chronic Renal Outlet Obstruction Sickle Cell Anemia Multiple Myeloma

29 Glomerulonephritis Low Complement Renal Presentation PIGN MPGN Systemic Presentation SLE SBE Cryoglobulinemia Normal Complement ANCA + RPGN IgA Nephropathy Alport’s Syndrome Goodpasture’s Syndrome TTP – HUS Vasculitis First determine patient has glomerulonephritis (not just nephrotic syndrome). If active sediment What are the serum complement levels? Does the patient have systemic symptoms? Wegener’s PAN Idiopathic ANCA Any of the nephritic syndromes can be considered an RPGN, if it becomes rapidly progressive!

30 Consultation… If the patient has glomerulonephritis, you should be talking to nephrology!

31 Vascular Etiology Atheroembolic Small Vessel Disease
Recent intravascular intervention Livedo reticularis Low complement Eosinophilia Blue toes Small Vessel Disease Scleroderma TTP/HUS DIC Malignant HTN

32 Acute Indications for Hemodialysis
AEIOU: Acidosis: Which is not responsive to medical therapy Electrolytes: Hyperkalemia Toxic Ingestion: Lithium, TCA, Ethylene Glycol, Methanol, Salicylates, (many others) Fluid Overload: Especially in heart failure patients Symptomatic Uremia: Bleeding, encephalopathy, pericarditis.

33 What do you need to do as the Intern?
Learn about the patient’s history PMHx (CKD, CHF, Cirrhosis). Hospital Course Recent Surgery? Contrast exposures? Hypoxic episode? Hypotensive episode? New drugs? Labs Repeat the P2 Check a UA with micro (look at the microscope slide yourself!) Estimate proteinuria (spot protein/creatinine ratio) Is the patient making urine? Post-obstruction (foley, BPH, atonic bladder, etc) Hypovolemia or Pre-renal Examine the Patient Vital signs Fluid status (S3, JVD, edema) Mental Status (uremia?) Bleeding (uremia? hypovolemia?) GU Exam +/- Rectal Bladder scan and/or renal US What is the patient’s volume status?

34 Intern Evaluation, cont…
What category of renal failure is present? Pre-renal Intrinsic renal Post-renal Is there an indication for acute hemodialysis? AEIOU What can you do to support the patient? Fluid challenge if oligouric / anuric Remove potential nephrotoxins Dose medications for patient’s GFR Ensure adequate renal perfusion (BP) Electrolyte management Fluid management (especially if h/o CHF, and/or if patient is anuric!) Remember that ARF is usually not a disease in itself, but rather the final common pathway of a variety of disease states.

35 Review of ARF

36 Questions?

Download ppt "Acute Renal Failure for the Intern"

Similar presentations

Ads by Google