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Acute and Chronic Renal Failure
Courtney Bunevich, DO
December 19, 2007
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Acute Renal Failure
Rapid decline in the GFR over days to weeks
Serum Cr increases by >0.5 mg/dL GFR <10mL/min, or <25% of normal
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DefinitionsAnuria: No urine output
Oliguria: Urine output <400-500 mL/d
Azotemia: Increase in Serum Cr and BUN May be prerenal, renal, or postrenal Does not require any clinical findings
Chronic Renal Insufficiency Deterioration over months to years GFR 10-20 mL/min, or 20-50% of normal
ESRD: GFR <5% of normal
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ARF: Signs and Symptoms
Hyperkalemia Nausea/Vomiting HTN Pulmonary edema Ascites Asterixis Encephalopathy
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Causes of ARF in Hospitalized Patients 45% ATN
Ischemia, Nephrotoxins 21% Prerenal
CHF, volume depletion, sepsis 10% Urinary obstruction 4% Glomerulonephritis or vasculitis 2% AIN 1% Atheroemboli
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ARF: Focused History
Nausea? Vomiting? Diarrhea? Hx of heart disease, liver disease, previous renal
disease, kidney stones, BPH? Any recent illnesses? Any edema, change in urination? Any new medications? Any recent radiology studies? Rashes?
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Physical Exam
Volume Status Mucus membranes, orthostatics
Cardiovascular JVD, rubs
Pulmonary Decreased breath sounds Rales
Rash (Allergic interstitial nephritis) Large prostate Extremities (Skin turgor, Edema)
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Workup for ARF
BMP or RFP Urine
Urine electrolytes and Urine Cr to calculate FeNa
Urine eosinophilsUrine sediment: casts, cells, proteinUosm
Kidney U/S to rule out hydronephrosis
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FeNa = (urine Na x plasma Cr) (plasma Na x urine Cr)FeNa <1% PRERENAL
Urine Na < 20 because functioning tubules reabsorb lots of filtered sodium
ATN (unusual) Postischemic disease: most of UOP comes from few normal
nephrons, which handle sodium appropriately ATN + chronic prerenal disease (cirrhosis, CHF)
Glomerular or vascular injury Despite glomerular or vascular injury, pt may still have well-
preserved tubular function and be able to concentrate Na
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FeNa
FeNa 1%-2% Prerenal-sometimes ATN-sometimes AIN will have a higher FeNa due to tubular damage
FeNa >2% ATN
Damaged tubules cannot reabsorb sodium
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Calculating FeNa after Patient Has Recieved Lasix Caution with calculating FeNa if pt has gotten
loop diuretics in past 24-48 h Loop diuretics cause natriuresis that raises U
Na-even if the patient is prerenal So if FeNa>1%, you do not know if this is
because patient is euvolemic or because lasix increased the U Na
So, helpful if FeNa still <1%, but not if FeNa >1%
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Prerenal ARF
Hyaline casts can be seen in normal pts NOT an abnormal finding
UA in prerenal ARF is normal Prerenal: causes 21% of ARF in hospitalized
patients Reversible Prevent ATN with volume replacement
Fluid boluses or continuous IVF Monitor Uop
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Prerenal causes Intravascular volume depletion Hemorrhage
Vomiting, diarrhea “Third spacing” Diuretics
Reduced Cardiac output Cardiogenic shock, CHF, Tamponade Systemic vasodilation Sepsis Anaphylaxis, Antihypertensive drugs
Renal vasoconstriction Hepatorenal syndrome
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Intrinsic ARF
1. Tubular (ATN)
2. Interstitial (AIN)
3. Glomerular (Glomerulonephritis)
4. Vascular
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You evaluate a 57yo man with oliguria and rapidly increasing BUN and Serum Cr
A. ATNB. Acute glomerulonephritisC. Acute interstitial nephritisD. Nephrotic Syndrome
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ATN Muddy brown granular casts (last slide) Renal tubular epithelial cell casts (below)
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More ATN
•Broad casts (form in dilated, damaged tubules)
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ATN Causes Hypotension
Relative low BP May occur immediately after low BP episode or up to
7 days later Post-op Ischemia Post-aortic clamping, post-CABG Crystal precipitation Myoglobinuria Contrast Dye
ARF usually 1-2 days after IV contrast load Aminoglycosides
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ATN Treatment
Remove any offending agent IVFTry Lasix if a euvolemic patient is not having
adequate urine outputDialysis
Most patients return to baseline Serum Cr in 7 to 21 days
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ATN Prerenal
Cr increases at 0.3-0.5 /day
increases slower than 0.3 /day
U Na, FeNa
UNa>40
FeNa >2%
UNa<20
FeNa<1%
UA epithelial cells, granular casts
Normal
Response to volume
Cr will not improve much
Cr improves with IVF
BUN/Cr 10-15:1 >20:1
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Which UA is most compatible with contrast-induced ATN?A. Spec gravity 1.012, 20-30 RBC, 15-20 WBC,
positive for eosinophilsB. Spec gravity 1.010, 1-3 WBC, 5-10 renal
tubular cells, many granular casts, occasional renal tubular cell casts, no eosinophils
C. Spec gravity 1.012, 5-10 RBC, 25-50 WBC, many bacteria, occasional fine granular casts, no eosinophils
D. Spec gravity 1.020, 10-20 RBC, 2-4 WBC, 1-3 RBC casts, no eosinophils
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ATN
B. Spec gravity 1.010, 1-3 WBC, 5-10 renal tubular cells, many granular casts, occasional renal tubular cell casts, no eosinophils
Dilute urine: failure to concentrate urine No RBC casts or WBC casts in ATN Eosinophils classically in AIN or renal
atheroemboli, but nonspecific
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WBC Casts
Cells in the cast have nuclei(unlike RBC casts)
Pathognomonic for Acute Interstitial Nephritis
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Acute Interstitial Nephritis
70% Drug hypersensitivity 30% Antibiotics: PCN, Cephalosporins, Cipro Sulfa drugs NSAIDs Allopurinol
15% Infection Strep, Legionella, CMV
8% Idiopathic 6% Autoimmune Diseases
Sarcoid, Tubulointerstitial nephritis
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AIN from Drugs
Renal damage is NOT dose-dependent May take weeks after initial exposure to drug
Up to 18 months to get AIN from NSAIDS But only 3-5 days to develop AIN after second exposure to drug
Signs and Symtpoms Fever (27%) Serum Eosinophilia (23%) Maculopapular rash (15%)
Labs Bland sediment or WBCs, RBCs, non-nephrotic proteinuria WBC Casts are pathognomonic Urine eosinophils on Wright’s or Hansel’s Stain Also see urine eosinophils in RPGN and renal atheroemboli
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AIN Management
Remove offending agent Most patients recover full kidney function
in 1 year Poor prognostic factors
ARF > 3 weeksAdvanced age at onset
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You evaluate a 32yo woman with HTN, oliguria, and rapidly increasing Cr, BUN. You spin her urine:
A. ATNB. Acute glomerulonephritisC. Acute interstitial nephritisD. Nephrotic Syndrome
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Acute Glomerulonephritis
RBC casts: cells have no nuclei Casts in urine: think INTRINSIC renal disease If she has Lupus with recent viral prodrome,
think Rapidly Progressive Glomerulonephritis (RPGN)
If she had a sore throat 10 days ago, think Postinfectious Proliferative Glomerulonephritis
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Glomerular Disease
Hematuria: dysmorphic RBCs RBC casts Lipiduria: increased glomerular
permeability Proteinuria: may be in nephrotic range Fever, rash, arthralgias, pulmonary
symptoms Elevated ESR, low complement levels
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Type 1: Anti-GBM disease Type 2: Immune complex
IgA nephropathy Postinfectious glomerulonephritis Lupus nephritis Mixed cryoglobulinemia
Type 3: Pauci-immune Necrotizing glomerulonephritis Often ANCA-positive and associated with vasculitis
Can present with viral-like prodrome Myalgias, arthralgias, back pain, fever, malaise
Kidney biopsy : Extensive cellular crescents with or without immune complexes
Can develop ESRD in days to weeks Treat with glucocorticoids and cyclophosphamide
Rapidly Progressive Glomerulonephritis
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Usually after strep infection of upper respiratory tract or skin after a 8-14 day latent period Can also occur in subacute bacterial endocarditis,
visceral abscesses, osteomyelitis, bacterial sepsis Hematuria, hypertension, edema, proteinuria Positive antistreptolysin O titer (90% upper
respiratory and 50% skin) Treatment is supportive
Screen family members with throat culture and treat with antibiotics if necessary
Postinfectious Proliferative Glomerulonephritis
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A 19yo woman with Breast Cancer s/p chemo in the ER has weakness, fever, rash. WBC=15.4, Hct 24, Cr 2.9, LDH 600, CK 600. UA=3+ protein, 3+blood, 20 RBC. What next test do you order? What’s her likely diagnosis?
A. Nephrotic Syndrome
B. ATNC. Acute
GlomerulonephritisD. Thrombotic
Thromboctyopenic Purpura
E. Rhabdomyolysis
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TTP
Order blood smear to rule out TTP TTP associated with malignancy and
chemotherapy TTP may mimic Glomerulonephritis on UA
(RBCs, WBCs) Thrombocytopenia and anemia not consistent
with nephrotic or nephritic syndrome Need CK in the thousands to cause ARF
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Microvascular ARF
TTP/HUS HELLP syndrome Platelets form thrombi and deposit in
kidneys leading to glomerular capillary occlusion or thrombosis
Plasma exchange, steroids, IVIG, and splenectomy are possible treatments
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Macrovascular ARF Aortic Aneurysm Renal artery dissection or thrombosis Renal vein thrombus Atheroembolic disease
New onset or accelerated HTN?Abdominal bruits, reduced femoral pulses?Vascular disease? Embolic source?
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A. Renal Artery Stenosis
B. Contrast-Induced Nephropathy
C. Abdominal Aortic Aneurysm
D. Cholesterol Atheroemboli
Your 68yo male inpatient with baseline Cr=1.2 had negative cardiac cath 4 days ago, now Cr=1.8 and blanching rash.
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Why do his toes look like this?
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Renal Atheroembolic Disease
1% of cardiac caths can cause atheromatous debris scraped from the aortic wall will embolize Retinal Cerebral Skin (Livedo Reticularis, Purple toes) Renal (ARF) Gut (Mesenteric ischemia)
Unlike in Contrast-Induced Nephropathy, Serum Cr will NOT improve with IVF
Diagnosis of exclusion: will NOT show up on MRI or Renal U/S; WILL show up on renal biopsy
Treatment is supportive
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Post-Renal ARF
• Urethral obstruction: prostate or urethral stricture• Bladder calculi or neoplasm• Pelvic or retroperitoneal neoplams• Bilateral ureteral obstruction• Retroperitoneal fibrosis
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“Doc, your patient has not peed in 5 hrs....what do you want to do?” Examine patient: Dry? Septic? Flush foley: sediment can obstruct outflow Check I/Os: Has she been drinking? Give IV BOLUS (250-500cc IVF), see if patient has
urine output in next 30-60 min If yes, then patient was dry If no, then patient is either REALLY dry or in renal failure
Check UA, Labs Consider Renal U/S if reasonable
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You are called to the ER to see... A 35yo woman with previously normal
renal function now with BUN=60, Cr=3.5. Do you call the Renal fellow to dialyze this pt?
What if her K=5.9? What if her K=7.8?
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Indications for acute dialysis
AEIOUAcidosis (metabolic)Electrolytes (hyperkalemia) Ingestion of drugs/IschemiaOverload (fluid)Uremia
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You admit this patient to telemetry and aggressively hydrate her
You recheck labs 6h later and BUN=85, Cr=4.2. Suddenly the patient starts to seize.
Now what?
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Patient is Uremic
General Fatigue, weakness Pruritis
Mental status change Uremic encephalopathy Seizures Asterixis
GI disturbance Anorexia, early satiety, nausea and emesis
Uremic Pericarditis Platlet dysfunction and bleeding
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A patient with chronic lung disease has acute pleuritic pain and O2 saturation of 87%. You want to rule out PE but her Cr is 1.4. Can you get a CT with IV contrast?
A. Send her for Stat CT with IV contrast
B. Send her for Stat CT without IV contrast
C. Just give her heparin
D. Begin IV hydration
E. Begin pre-procedure Mannitol
F. Get a VQ scan instead
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Contrast-Induced Nephrotoxicity
Cr increases by 25% post-procedure Contrast causes renal vasoconstriction
leading to renal hypoxia Iodine itself may be nephrotoxic If Cr>1.4, use pre-procedure prophylaxis
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Pre-Procedure Prophylaxis
IVF 0.9NS 1-1.5 mg/kg/hour x 12 hours prior to procedure and 6-12
hours after Mucomyst (N-acetylcysteine)
Free radical scavenger; prevents oxidative tissue damage 600mg po BID x 4 doses (2 before procedure, 2 after)
Bicarbonate (JAMA 2004) Alkalinizing urine should reduce renal medullary damage D5W with 3 amps HCO3; bolus 3.5 mL/kg 1 hour
preprocedure, then 1mL/kg/hour for 6 hours postprocedure Small study and not reduplicated in larger trial thereafter
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Chronic Renal Failure
Definitions
• Chronic Renal Failure (CRF) - irreversible kidney dysfunction with azotemia >3 months
• Creatinine Clearance (CCr) - the rate of filtration of creatinine by the kidney (GFR marker)
• Glomerular Filtration Rate (GFR) - the total rate of filtration of blood by the kidney
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Episodes of ARF (usually acute tubular necrosis) often lead, eventually, to CRF • Over time, combinations of acute renal
insults are additive and lead to CRF • The definition of CRF requires that at least
3 months of renal failure have occurred Causes of Acute Renal Failure (ARF)
• Prerenal azotemia - renal hypoperfusion, usually with acute tubular necrosis
• Intrinsic Renal Disease, usually glomerular disease • Postrenal azotemia - obstruction of some type
Etiology
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Common Underlying Causes of CRF Causes of CRF
• There are about 50,000 cases of ESRD per year • Diabetes: most common cause ESRD
Over 30% cases ESRD are primarily to diabetes • CRF associated HTN causes about 23% ESRD cases • Glomerulonephritis accounts for ~10% cases • Polycystic Kidney Disease - about 5% of cases• Rapidly progressive glomerulonephritis (vasculitis) - about 2%
of cases • Renal (glomerular) deposition diseases • Renal Vascular Disease - renal artery stenosis, atherosclerotic
vs. fibromuscular
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Causes of CRF
Additional Causes of CRF• Medications - especially causing
tubulointerstitial diseases (common ARF, rare CRF)
• Analgesic Nephropathy over many years • Pregnancy - high incidence of increased
creatinine and HTN during pregnancy in CRF
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Analgesic Nephropathy• Slow progression of disease due to chronic daily
ingestion of analgesics • Drugs associated with this entity usually contain two
antipyretic agents and either caffeine or codeine • More common in Europe and Australia than USA • Polyuria is most common earliest symptom• Macroscopic hematuria and papillary necrosis • Chronic interstitial nephritis, renal papillary necrosis,
renal calcifications • Associated with long-term use of non-steroid anti-
inflammatory drugs
Analgesic Nephropathy
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Patients at risk include DM, CHF, Hepatic disease, and the elderly
Pathophysiology: nonselective NSAIDS inhibit synthesis vasodilatory prostaglandin in the kidney inducing a prerenal state ARF
Analgesic Nephropathy
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Excretion of sodium is initially increased, probably due to natriuretic factors • As glomerular filtration rate (GFR) falls, FeNa rises • Maintain urine volume until GFR <10-20mL/min and
then edema begins• Cannot conserve sodium when GFR <25mL/min,
and FeNa rises with falling GFR• Tubular potassium secretion is decreased • Cannot handle bolus potassium • Do not use potassium sparing diuretics
Electrolyte Abnormalities
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Normally, produce ~1mEq/kg/day of Hydrogen ions When GFR <40mL/min, there is a decrease in NH4
excretion which adds to metabolic acidosis When GFR <30mL/min, then urinary phosphate
buffers decline and acidosis worsens Bone CaCO3 begins to act as the buffer and bone
lesions result (renal osteodystrophy) Usually will not have wide anion gap acidosis if patient
can still make urine Defect in renal generation of HCO3 as well as
retention of nonvolatile acids
Acid Base Balance
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Low GFR leads to increased phosphate, low calcium, and an acidosis
Other defects include decreased dihydroxy-vitamin D production
Bone acts as a buffer for acidosis, leading to chronic bone loss in renal failure
Low vitamin D causes poor calcium absorption and secondary hyperparathyroidism
Increased PTH maintains normal serum Calcium and Phosphorus until GFR <30mL/min
Chronic hyperparathyroidism and bone buffering of acids leads to severe osteoporosis
Bone Metabolism
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Slight hypermagnesemia with inability to excrete high magnesium loads
Uric acid retention occurs with GFR <40mL/min
Vitamin D conversion to dihydroxy-Vitamin D is severely decreased
Erythropoietin (EPO) levels fall and anemia develops
Accumulation of normally excreted substances
Other Abnormalities
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Immunosuppression • Patients with CRF are at increased risk for
infection • Cell mediated immunity is particularly impaired • Hemodialysis seems to increase immune
compromise • Complement system is activated during
hemodialysis • Patients with CRF should be vaccinated
aggressively
Complications
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Due to reduced erythropoietin production by kidney
Occurs when creatinine rises to >2.5-3mg/dL
Anemia management with Procrit and Arensp
Anemia
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Phosphorus
Hyperphosphatemia
• Decreased excretion by kidney • Increased phosphate load from bone metabolism• Increased PTH levels leads to renal bone disease • Eventually, parathyroid gland hyperplasia occurs • Danger of calciphylaxis
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PREVENTION Treat the underlying cause Chronic Hemodialysis Medications
• Anti-hypertensives - Labetolol, CCB, ACE inhibitors • Eythropoietin (Epogen®) for anemia in ~80% dialysis pts• Vitamin D Analogs - calcitriol given intravenously • Calcium carbonate • RenaGel, a non-adsorbed phosphate binder• DDAVP may be effective for patients with symptomatic platelet
problems
Treatment