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ACUTE RENAL FAILURE. Carly Thompson MD, CCFP August 27, 2008. Objectives. Definitions Epidemiology Differential Diagnosis Investigations: Labs, Urinalysis, Imaging Treatment: Medications Renal Replacement Therapy. Case 1. Mrs. K. Bean 78 yo female
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ACUTE RENAL FAILURE Carly Thompson MD, CCFP August 27, 2008
Objectives • Definitions • Epidemiology • Differential Diagnosis • Investigations: Labs, Urinalysis, Imaging • Treatment: • Medications • Renal Replacement Therapy
Case 1 • Mrs. K. Bean 78 yo female • PMHx: liver cirrhosis, ascites, hepatic encephalopathy due to hepatitis C • Family is concerned that she is not drinking, not eating, and having recurrent diarrhea as she is getting sleepier • Labs: • Na 140 • BUN 20 • Cr 247
Case 1 Is she in renal failure?
Definitions: Acute Renal Failure • The deterioration of renal function over hours or days resulting in accumulation of toxic wastes and the loss of internal homeostasis • Indirect Measures: • 50% increase in serum Cr • 50% decrease in creatinine clearance / GFR • Highly variable across different studies
Definitions: Types of Acute Renal Failure • Non-oliguric • Better prognosis • Oliguria: • <1mL/kg/hr in infants • <0.5mL/kg/hr in children • <400mL / day in adults • <0.3mL/kg/hr OR 17mL / hour in 60kg x 24 hours • Anuria • <100mL / day in adults
Definitions: Acute Kidney Injury • RIFLE Criteria Mortality Risk 2.4 4.15 6.37
Definitions: AKIN Criteria Acute Kidney Injury Network
Quick Epidemiology Slide • Community-acquired ARF: • Only diagnosed in 1% of hospital admissions at presentation • Most commonly due to volume depletion • 90% may have reversible cause • Hospital-acquired ARF: • Up to 4% of admissions, 20% of critical care admissions • Multifactorial: elderly, nephrotoxic medications, often in ICU • Mortality: • 50% - minimal change since dialysis was invented! • 25% in children, but 45% if intrinsic renal failure • 75% for hospital acquired mortality • 7% community-acquired prerenal ARF • Causes of Death: • Sepsis, cardiac and pulmonary failure
Case 1 Follow-Up • Baseline Cr 165 -> Now 247 • 82 mmol/L increase, 150% increase • GFR 28 -> Now 21 • 25% decrease • Urine Output: Foley inserted • Diagnosis: AKIN Criteria - Stage 1 Acute Kidney Injury • Plan: Admitted for rehydration, monitoring, and placement issues.
Case 2 • Mr. Pastie 68 yo man • Hx – unwell x 5 days, vomiting, diarrhea, lightheaded, presents confused • PMHx – Htn, CHF • Meds – B-blocker, lasix
Case 2 What do you think is going on? What would you look for on physical exam?
Prerenal Failure • History • Clues to dehydration • Physical Exam • Volume status exam
Case 2 What investigations would you like to order?
Renal Failure Work-Up • Labs: • CBC, lytes, BUN, Cr • Urinalysis: R+M • Chest x-ray: Volume status • ECG: Screen for hyper / hypokalemia • Insert foley: input / output
Renal Failure Work-Up How helpful is the BUN and Cr?
Importance of BUN and Cr Creatinine • A patient with a low baseline Cr can lose more than ½ of functioning nephrons before developing and elevated Cr • Breakdown product of skeletal muscle protein creatine • Linked to muscle mass, thus women and elderly have lower GFR for any Cr level • Glomerulonephritis causes increased tubular secretion of Cr independent of GFR • Trimethoprim, cimetidine, salicylates cause decreased secretion BUN • Decreased in patients with malnutrition and hepatic synthetic dysfunction • Increased in setting of a protein load, GI hemorrhage, trauma
Does the ratio of BUN/Cr help determine if the patient is dry?
BUN:Cr Ratio Quick Physiology Lesson: • Both Cr and BUN are passively filtered at the glomerulus • Cr remains in the tubule • BUN is permeable and passively reabsorbed with sodium • Therefore . . . In the setting of Na retention, urea clearance can be as low as 30% of GFR in a patient with normal concentrating ability BUN:Cr >20 can suggest hypovolemia
Fractional Excretion of Na • Fractional excretion of sodium • FeNa = Urine Na ÷ Urine Cr Plasma Na Plasma Cr • In normal kidneys under prerenal stress <1% • 1-2% either ATN or prerenal failure • >2% ATN due to loss of concentrating ability • Benefits: Most accurate test • Limitations: Intrinsic renal failure when tubular concentrating capacity is retained (i.e. glomerulonephritis), the Fe Na may be depressed
Urine Sodium • Less accurate measurement of prerenal failure • Urine Na concentration affected by the rate of water reabsorption -> a patient may have a relatively high urine sodium concentration (20 - 40 meq/L or more) but may be in prerenal failure • Urine Na < 20 meq/L
Urine Osmolality Cause Osmolality • Pre-renal > 500 • Renal • Tubular injury <350 • Acute Interstitial Nephritis <350 • Acute Glomerulonephritis >500 • Post-renal <350
Case 2 Summary Pre-Renal Failure • BUN:Cr >20 • FeNa <1% • Urine osmolality >500 • Urinalysis: May have hyaline casts • Secreted from tubular epithelial cells Treatment • Rehydration!
Case 3 Mrs. Buckley • 36 yo female • Nausea, vomiting, SOB x 1 week • Sore throat 3 weeks ago • Cr 300
What do you think is going on? What would you like to order?
Case 3 • Cr 300 • BUN 20 • BUN:Cr <20 • Osmolality >500 • Urine R+M – proteinuria and casts • Urine lytes – Na 20, Fe Na <1% • Renal U/S - normal What kind of cast is this?
Intrinsic Renal Failure • Tubular Disease • Glomerular Disease • Interstitial Disease • Vascular Disease
Glomerulonephritis • Post-infectious (strep) • IgA nephropathy • SLE, PAN, Hep C, HIV, Wegener’s, • Goodpasture’s • HSP • HUS/TTP • Rapidly progressive glomerulonephritis RPGN • Membranoproliferative glomerulonephritis • Drugs • Tumors (leukemia, lymphoma)
Work-Up • ASO Titer • Renal biopsy • ASA / ANCA / serologies • Anti-GBM antibodies • Medication Hx • CT Scan
Renal Biopsy • Should be considered in all causes of acute intrinsic renal failure • Significantly changed dx and tx in 40% of cases should be considered in all causes of intrinsic ARF: significantly changed the dx and tx in 40% of cases • Complications: • Common: Hematuria • Serious: Blood transfusions, nephrectomy, puncture of other organs, perinephric hematomas – 2% • Mortality: 0.1%
Post-Strep Glomerulonephritis • 6-14 days after pharyngitis with Group A Strep or after skin infection • Hypertension, edema, pulmonary congestion common presentation • Urinalysis: RBC, RBC casts • Prognosis: • 5% progress to RPGN • 70% recover • Antibiotics may be considered for contacts
Case 3 Summary Intrinsic Renal Failure: Glomerulonephritis • BUN:Cr <20 • FeNa <1% • Urine osmolality >500 • Urinalysis: RBC, RBC casts, protein
Case 3 Continued • You insert a foley for Mrs. Buckley. Finish your shift and go home for the night. • Your friend is on internal medicine call that night, and calls you to debate whether he should start a diuretic for Mrs. Buckley whose urine output has dropped to <0.5mL/kg/hr for the past 6 hours. • What should you tell your friend?
Diuretic Use in Renal Failure • Rationale: Pts with non-oliguric ARF have improved mortality and renal function recovery rates, therefore using a diuretic to “convert” oliguric to nonoliguric ARF may be beneficial. • Evidence: RCTs have failed to show a benefit in administering diuretics to patients with ARF. • Shilliday IR, Quinn KJ, Allison ME. Loop diuretics in the management of acute renal failure: a prospective, double-blind, placebo-controlled, randomized study. Nephrol Dial Transplant 1997 Dec;12(12):2592-6 • No change in recovery, hemodialysis, or death • Bottom-Line: Diuretics are only useful in the management of volume-overloaded patients.
What about “renal dose” dopamine? • Low-dose “renal” dose dopamine (1-5ug/kg/min) was used for many years to treat ARF • Rationale: Increases urine output • Evidence: No evidence that it improves renal recovery or mortality • Side effects: Pro-arrhythmic, and may cause increased medullary O2 consumption without increased O2 delivery • Bottom Line: Say NO to “renal dose” dopamine!
Case 4 Mr. Dye • 50 year old male • CC: Not peeing • HPI: 4 days of minimal urine output • Cardiac catheterization 1 week ago • PMHx: 15 years of DM II, lisinopril, insulin • O/E: BP 190/110 • JVP 9cm • Bibasilar crackles • Edema • Labs: • BUN: 20 • Cr: 450 (Baseline = 150)
Intrinsic Renal Failure Tubular Disease • Ischemic acute tubular necrosis • Nephrotoxins • Heme pigments: rhabdomyolysis, massive hemolysis Interstitial Disease • Acute interstitial nephritis (drug reaction) • Infiltrative disease • Autoimmune disease: SLE • Infectious: Legionnaire, hanta virus Vascular Disease • Malignant hypertension • Scleroderma • TTP, HUS, PAN • Renal Vein Thrombosis Glomerular Disease
Nephrotoxins Drugs that alter blood flow • NSAIDs, ACEI, cyclosporine, tacrolimus, contrast, amphotericin B, interleukin-2 Drugs that are toxic to tubules • Aminoglycosides, contrast, cisplatin, cyclosporine, tacrolimus, amphotericin B, methotrexate, solvents, heavy metals, IVIG Heme-Pigment-Induced toxicity • Cocaine, EtOH, lovastatin Drugs that precipitate and cause tubular obstruction • Acyclovir, sulfonamides, ethylene glycol, chemo drugs, methotrexate Allergic interstitial nephritis • Penicillins, cephalosporins, sulfonamides, rifampin, cipro, NSAIDs, TZDs, furosemide, cimetidine, phenytoin, allopurinol Hemolytic-Uremic Syndrome • Cyclosporine, tacrolimus, cocaine, quinine, conjugated estrogens
What puts Mr. Dye at risk for renal failure? (i.e. What are the risk factors for contrast-induced renal failure?)
Contrast-Induced Renal Failure • Course: • Increasing Cr for 3-5 days, then resolution • Risk Factors: • Chronic renal insufficiency • DM (Approximately 40% risk!) • Age • Hypovolemia • Hypoalbuminemia • Myeloma • Type and Dose of Contrast
Prevention • Alternative studies – MRI, ultrasound • Low-dose contrast, avoid repetitive studies (<72 hours), low or iso-osmolal nonionic contrast • Avoid hypovolemia • IV NS or NaHCO3 • Avoid NSAIDs • N-Acetylcysteine • Minimizes vasoconstriction and free radicals? • Much heterogeneity in trials, largest meta-analysis showed RR 0.62 (.44 - .88) • NAC 600 - 1200mg po bid day before and of procedure • IV NAC for emergent scans? Risk of anaphylaxis, unclear data.
What if Mr. Dye had just been started on his ACE inhibitor? What condition would you be concerned about?
ACE Inhibitors • Dilate postglomerular capillaries -> increase renal blood flow and decrease GFR -> natural increase in serum Cr 10-20% • ARF after ACEI initiation -> bilateral renal artery stenosis • ARBs may also cause ARF • Check Cr, lytes 2 weeks after starting ACE
NSAIDs / COX Inhibitors • Risk Factors for Renal Failure: • Age • Chronic Renal Failure • CHF • DM • Hypovolemia • Diuretics • ACEI
Aminoglycosides • Trough concentration is relevant • Once daily dosing can reduce toxicity
Heme-Pigment Induced Acute Renal Failure History: • Crush injuries Exam: • Pigmented granular casts, heme pigment in urine Pathophysiology: • Deposited in and concentrated in tubules • Obstruction and direct toxicity depending on acidic urine Treatment • Volume Replacement • Normal saline 1-2L / hour • Urine output 200 – 300 mL/hour • Forced Alkaline-Mannitol Diuresis • Urine pH >6.5 • Once diuresis established 75mmol/L of NaHCO3 • Caution re: hypercalcemia • Consider mannitol / diuretic if not effective diuresis