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Acute Renal Failure

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Title: Acute Renal Failure


1
Acute Renal Failure
  • Anthony R Mato, MD

2
Basic Facts
  • Renal failure over the course of hours to days.
  • The result will be failure to excrete nitrogenous
    waste and electrolyte imbalance.
  • Hard to define in 26 studies, no two used the
    same definition!!!

3
Classic laboratory definition
  • Cr increase of .5 mg / dl.
  • Increase in more than 50 over baseline Cr.
  • Decreased in calculated Cr Clearance by more than
    50.
  • Any decrease in renal function that requires
    dialysis.

4
Basic Differential Diagnosis
  • Pre-Renal Decreased renal perfusion without
    cellular injury.
  • 70 of community acquired cases.
  • 40 of hospital acquired cases.
  • 1 cause of Intra-Renal failure.
  • Intra-Renal
  • ATN Ischemic, toxic insult to the renal tubule.
    Tubular
  • AIN Inflammation and edema.
  • GNInjury to the filtering mechanism.
  • Post-Renal obstruction the urinary outflow
    tract.  

5
Prerenal Failure
  • Often rapidly reversible if we can identify this
    early.
  • The elderly at high risk because of their
    predisposition to hypovolemia and renal
    atherosclerotic disease.
  • This is by definition rapidly reversible upon the
    restoration of renal blood flow and glomerular
    perfusion pressure.
  • THE KIDNEYS ARE NORMAL.
  • This will accompany any disease that involves
    hypovolemia, low cardiac output, systemic
    dilation, or selective intrarenal
    vasoconstriction.

6
Differential Diagnosis
  • Hypovolemia
  • GI loss Nausea, vomiting, diarrhea
  • Renal loss diuresis, hypo adrenalism, osmotic
    diuresis (DM)
  • Sequestration pancreatitis, peritonitis,trauma,
    low albumin.
  • Hemorrhage, burns, dehydration.

7
Differential Diagnosis
  • Renal vasoconstriction hyper Ca, norepi, epi,
    cyclosporine, tacrolimus, ampho B.
  • Systemic vasodilation sepsis, medications,
    anesthesia, anaphylaxis.
  • Cirrhosis with ascites
  • Hepato-renal syndrome
  • Impairment of autoregulation NSAIDs, ACE, ARBs.
  • Hyperviscosity syndromes MM, WM, PCV

8
Differential Diagnosis
  • Low CO
  • Myocardial diseases
  • Valvular heart disease
  • Pericardial disease
  • Tamponande
  • Pulmonart HTNPE
  • Pos pressure mechanical ventillation

9
  • Reduced arterial stretch and activated
    baro-receptors ?
  • Neuro-humoral responses activated to maintain
    blood volume and pressure ?
  • Sympathetic nervous system
  • AT II system
  • AVP system
  • They will act together to maintain flow to the
    heart and the brain at the expense of other
    non-essential vascular beds.
  • Renal afferent vaso-dilation is triggered via
    PGE2 (afferent), Local myogenic reflex,
    ATII(efferent)
  • We have maximum dilation at SBP of 80 mm Hg.

PHYSIOLOGY OF HYPOVOLEMIA
10
Intrinsic Renal Disease
  • Anatomic organization seems to work best. ARF
    DOES NOT EQUAL ATN.
  • 30 of cases of intrinsic renal failure will not
    show any evidence of ATN on UA.
  • Glomerulus
  • Vessels
  • Interstitum
  • Tubules

11
THE DIFFERENTIAL DIAGNOSIS
12
Differential Diagnosis
13
Tubules ATN
  • Ischemic Injuries to the renal tubule
  • Takes 1-2 weeks to recover from after perfusion
    has been normalized.
  • In the extreme form this can lead to bilateral
    renal cortical necrosis
  • Three phases
  • Initiation phase
  • Tubuloglomerular feedback afferent arteriole
    constriction triggered by an increase in the salt
    delivery sensed by the macula densa.
  • Recovery phase tubular epithelial cell repair
    and regeneration. This may be associated with a
    marked diuretic phase.

14
ATN Ischemic
  • Hypovolemia
  • Low cardiac output
  • Renal vasoconstriction
  • Systemic dilation
  • Hemorrhage

15
ATN Toxic
  • Exogenous
  • Radiocontrast
  • CSP
  • TAC
  • Amino glycosides
  • Chemotherapy
  • Ethylene glycol
  • Tylenol
  • Endogenous
  • Myoglobin
  • Hemoglobin
  • Uric acid
  • Oxylate
  • Light chains

16
ATN Toxic facts
  • ATN Exacerbated in the elderly, CRI,
    hypovolemia, and exposure to multiple toxins.
  • Intrarenal vaso-constriction radiocontrast,
    cyclosporin, tacrolimus. Initially they will look
    prerenal.
  • Contrast toxicity is worst in patients with
    CRI, DM, MM, CHF, hypovolemia. This is dose
    related.
  • Direct toxicity to epithelial cells frequent
    offenders are acyclovir, foscarnet,
    aminoglycosides (30 of patients with therapeutic
    levels will have ARF), Ampho B (causes
    vasoconstriction as well as direct toxicity).
  • Cisplatin (mitochondrial injury).
  • Myoglobin and hemoglobin will both increase
    epithelial cell oxidative stress. They also
    inhibit NO ? vasoconstriciton.
  • Light chains can form intratubular casts and
    are directly toxic. UA crystal deposition.

17
Allergic AIN
Allergic reaction in the tubules. IT IS PARAMOUNT
TO IDENTIFY THE OFFENDING AGENT AND REMOVE IT.
There may be some role for steroids in the case
of AIN.
18
AIN Allergic
  • Beta lactams / Cephalosporins
  • Sulfinamides
  • TMP
  • NSAIDs
  • Diuretics
  • Captopril
  • Autoimmune diseases
  • Infiltrative diseases
  • Infections Legionella / Hanta virus

19
Others
  • Infection Pyelonephritis, CMV, Candida
  • Infiltration lymphoma, leukemia, sarcoid
  • Intratubular deposition and obstruction

20
Post Renal Causes
If we can identify this early, this can be
readily reversible. This accounts for fewer than
5 of cases of ARF.
21
Differential Diagnosis
  • BPH 1
  • Prostatitis
  • Prostate / Cervical cancer
  • Retroperitoneal fibrosis / disorders
  • Extraluminal malignancy
  • Neurogenic bladder / anticholinergic drug use
    functional obstruction
  • Bilateral renal calculi
  • Myeloma light chains
  • Papillary necrosis
  • Urethritis with spasm
  • Inadvertent surgical ligature
  • Intraluminal Thrombosis
  • Intraluminal (collecting system) crystal disease
  • Uric acid
  • Calcium oxylate
  • Acyclovir
  • Sulfonamide
  • MTX

22
Rickys Story
  • 50 year old man presents to the ED with a 1
    day history of RUQ pain, N/V. He also reports
    fever and chills and decreased urine output. PMH
    is a sore throat a week ago, tx w/ an antibiotic.
    He is on ibuprofen only. T 102, HR 123, BP
    80/60. In general, he is an ill-appearing. Abd
    tenderness RUQ no peritoneal signs remainder
    of exam is WNL.

23
Rickys Story
  • Labs
  • WBC 20 w/
  • 16 bands
  • Hgb 14
  • Plts 300
  • Na 140
  • K 4.1
  • Cl 111
  • HCO3 22
  • BUN 35
  • Cr 1.6 (baseline is 0.7) 

24
H and P Prerenal
  • Thirst, orthostatic dizziness, hypovolemia on
    exam, tachycarida, decreased JVP, poor skin
    turgor, dry mucous membranes, reduced axillary
    sweating.
  • Start of new medications NSAIDs, ACE, ARBs.
    Stigmata of chronic liver disease. Advanced CHF.
    Signs of sepsis.

25
H and P Intrinsic Renal
  • Recent history or hypovolemia / septic shock.
    Careful review of clinical data, pharmacy,
    nursing, and radiology records for evidence of
    toxin exposure. History of myeloma. Recent
    rhabdo.
  • Flank pain (worry for arterial occlusion) SC
    nodules, livedo reticularia, hollenhorst plaques,
    digital ischemia with palpable pulses. Fevers,
    arthralgias, pruritis erythemetous rash AIN.

26
H and P Post renal
  • Presence of suprapubic and flank pain. Pain
    radiating to the groin. History of nocturia,
    frequency, hesitancy.
  • History of anticholinergic medication use.  

27
What is your differential?
28
What additional workup do you want to diagnose
the etiology of his ARF / abdominal pain?
29
Urinalysis
  • Dip pH, SG, glucose, protein, nitrite, leuk
    esterase, bili, heme.
  • Micro RBCs, WBCs, casts, crystals, bacteria.
  • Normal 0-2 RBCs, 0-4 WBC, occasional hyaline
    cast.

30
Urinalysis Prerenal / Post-renal
  • Sediment is acellular and may contain hyaline
    casts
  • This is protein that is normally part of the
    urine (Tamm-Horsfall Protein).
  • Post renal Sediment is classically acellular
    and bland.
  • May also see pyuria and hematuria. No casts.

31
Renal ATN
  • Muddy brown casts
  • (contain tubular-epithelial cells).
  • They are usually associated with microscopic
    hematuria and mild tubular proteinuria (lt 1 g /
    d) from impaired re-absorption.
  • CASTS ARE ABSENT IN 30 OF THE CASES OF ATN.

32
Renal GN
  • Red blood cell casts are the classic finding.
  • Dysmorphic RBCs.
  • These indicate glomerular injury.
  • These are rarely seen in acute ATN.
  • May also see proteinuria gt 1 g / day.

33
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34
Renal AIN
  • White cell / granular casts.
  • KEEP IN MIND THAT BROAD GRANULAR CASTS REFELCT
    CHRONIC RENAL DISEASE (fibrosis).
  • Eosinophiluria (gt 5) is a classic finding
    (Hansels Stain) especially in antibiotic
    associated AIN.

35
Common UA Patterns
  • Rhabdo dip is pos for heme, neg for RBCs
  • MM dip is neg for protein, for light chains on
    UPEP
  • EG look for calcium oxylate crystals, elevated
    AG, elevated osm gap.
  • TLS uric acid crystals (can also be a normal
    variant of concentrated urine)

36
URINE BLING
37
Results
  • Tbili 2.0
  • Alk 269
  • ALT 44
  • AST 44
  • UA SG 1.02, trace ketones
  • Micro No cells, No casts, No crystals
  • Urine Na 10
  • Urine Cr 80

38
Renal Failure Indices
  • Fractional excretion of Na this will relate the
    clearance of Na to that of Cr.
  • In the case of prerenal disease Na is actively
    reabsorbed to restore intravascular volume.
  • This is not the case in renal injury (absorptive
    mechanisms are broken). In either case Cr is NOT
    reabsorbed. So we have the makings of a
    comparative ratio. The cut off is 1.
  • U Na / P Na
  • __________ x 100 .14 (Prerenal)
  • U Cr / P Cr

39
Keep in mind
  • Keep in mind that when pre renal patients are
    receiving diuretics or have bicarbonaturia all
    bets are off.
  • Also salt wasting states such as CRI and adrenal
    insufficiency will also alter results.
  • In 15 if patients with ATN FeNa can be lt 1
    reflecting patchy injury with partially preserved
    function.
  • In GN, acute urinary post renal obstruction, and
    vascular diseases the FeNa will often be lt 1.
  • Urine sodium, specific gravity, urine osm, BUN
    Cr ratio are less sensitive and of limited value
    in differentiating this differential.

40
Additional Labs
  • Peak Cr
  • In prerenal disease may fluctuate with
    hemodynamics. Rise will be rapid. This is true
    for contrast (5 days to peak and 7 to normal)
  • Atheroembolization (later peak and return to
    baseline), and ischemia (later peak and return to
    baseline).
  • Rise will be delayed in toxin exposure.
  • Rhabdo elevated K, Phos, hypocalcemia with
    elevations in CK and UA.
  • TLS elevated UA, K, Phos, low Ca, elevated Cr
    and elevated LDH (intracellular enzyme).
  • Elevated anion gap elevated osm gap suggests
    ethylene glycol / methanol exposure.
  • Anemia may suggest hemolysis, MM, or TTP.
  • Eosinophillia may suggest AIN, atheroembolic
    disease, PAN.

41
Back to Ricky
  • An abdominal CT with contrast shows acute
    cholecystitis. He is given an intravenous dose of
    ampicillin and gentamycin, along with normal
    saline.
  • The next morning you note LE edema and bibasilar
    crackles. His blood pressure has improved to
    110/70 and fever has resolved. His overnight
    urine output was 150cc.
  • Na 137, K 6.7, Cl 100, H2CO3 15, BUN 37, Cr 2.7

42
Why is he hyperkalemic?What is the
management?Does need dialysis?
43
Hyperkalemia
  • Plasma Potassium gt 5.0
  • Pseudohyperkalemia
  • Prolonged tourniquet use
  • Hemolysis
  • Leukostasis / Thrombocytosis

44
Physiology
  • A large meal has enough potassium to kill us. How
    will the body handle this load initially.
  • Buffering system will stimulate liver / muscle
    N-K ATPase
  • Insulin
  • Epinephrine
  • Aldosterone

45
The Kidney to the Rescue
  • Kidney handles it in a unique way.
  • It virtually reabsorbs 100 of the K in the
    proximal tubule (70) and the loop of henle
    (30).
  • Solvent Drag
  • Single Effect / Paracellular pathway
  • We reabsorb almost all of the K before we reach
    the distal segments.

46
The Principal Cell
  • BL membrane we have a Na/ K ATPase
  • On the apical side we have amilloride Na channels
    and other channels that allow the movement for K.
  • Tight junctions - the potential across the apical
    membrane is 30. The BM is at - 70mv.
  • The common denominator intracellular K will
    raise electrochemical gradient for K inside of
    the cell will cause an increase in K secretion
    into the urine.

47
The Key Players
  • 1. K concentration
  • 2. Aldosterone
  • 3. Flow
  • 4. Distal Na
  • 5. ADH
  • 6. Acid base status of the blood

48
Differential Diagnosis
  • Increased intake rare except in iatrogenesis
  • Cellular release
  • TLS, Rhabdomyolysis, exercise, trauma
  • Metabolic acidosis
  • Insulin deficiency
  • Hyperkalemic periodic paralysis
  • Digoxin toxicity, beta blockers
  • Adrenal insufficiency
  • Succinylcholine

49
Differential Diagnosis
  • Impaired excretion
  • Renal failure
  • Primary hypoaldosteronism
  • Secondary hypoakdosteronism
  • ACE, NSAIDs, Heparin, Type 4 RTA
  • Aldo resistance
  • K sparing diuretics, bactrim, pentamidine, sickle
    cell disease, multiple myeloma.
  • Gordons syndrome (enhanced Cl reabsorption, less
    K secretion, HTN)
  • Ureter Diversion to Jejunum.

50
Symptoms / Signs
  • Flaccid paralysis
  • Arrhythmia
  • Peaked T waves
  • PR / QRS prolongation
  • AV conduction delay
  • Loss of P waves
  • Sine wave
  • V fib

51
Treatment Keep the Physiology in mind.
  • EKG changes necessitate treatment
  • Calcium gluconate stabilized myocardium
  • Insulin / Glucose intracellular shift
  • Bicarbonate intracellular shift
  • Beta 2 agonists intracellular shift
  • Diuretics IV Lasix
  • Kayexylate exchanges K for Na
  • Dialysis

52
Dialysis Needs
  • A acidosis
  • E electrolytes
  • I intoxication (methanol, ethylene glycol,
    isopropanol, theophylline, lithium, salicylates)
  • O volume overload
  • U uremia (pericarditis, seizures,
    encephalopathy)

53
Why did his renal failure worsen?
54
Additional Labs
  • U OSM 300
  • Muddy brown casts
  • U Na 80
  • U Cr 40

Calculate FeNa? What is highest on your
differential? How does this alter your treatment
plan?
55
Treatment
  • Prevention is the key.
  • Appropriate volume resuscitation.
  • Renal dosing of potentially toxic meds
  • To estimate GFR Cockcroft-Gault Formula takes
    weight and age into account. (ONLY IN STABLE
    CREATININE) MULTIPLY BY .85 IN WOMEN.
  • When appropriate follow serum drug levels for
    dosage adjustment.
  • Use of NSAIDS, ACR, ARBs, diuretics should be
    used sparingly in patients who are hypovolemic or
    have renovascular disease.
  • Allopurinol / IVFs use in patients high risk for
    TLS.
  • Ethanol for EG toxicity / NAC for tylenol
    toxicity.
  • Alkalinization of urine to prevent MTX
    toxicity.

56
Prerenal disease
  • IVFs keep in mind where the loss is coming from
    and administer fluids accordingly.
  • Inotropes, preload / after-load reduction,
    anti-arrythmics, mechanical aids in CHF.
  • Large volume paracentesis to decrease
    intra-abdominal pressure and increase venous
    return from the kidneys.

57
Post Renal Treatment
  • Foley catheter
  • Nephrostomy tube
  • Stenting
  • 5 will develop a salt wasting diuresis.

58
Intrinsic Renal Disease
  • Intrinsic renal disease NO SPECFIC REVERSING
    THERAPIES FOR ISCHEMIC AND NEPHROTOXIC DISEASE.
    SUPPORTIVE CARE.
  • Follow electrolytes. Avoid further insult.
  • GN may respond to steroids, alkylating agents,
    plasmapheresis.
  • AIN glucocorticoids may be of use.
  • Malignant HTN control of blood pressure.
  • Scleroderma HTN and ARF may responsive to ACE.

59
Case 2 Fred
  • 85 year old man with a PMHx significant for
    osteoarthritis is admitted to the hospital for
    confusion. Physical exam reveals a thin,
    disoriented man T 98, HR 80, BP 120/80, wt
    75 kg, and a suprapubic mass. He takes no
    medication except for naproxen.
  • Labs Na 131, K 4.8, Cl 98, HCO3 15
  • BUN 65, Cr 7.3 (baseline on computer 1.3)

What is the FeNa? What is the baseline Cr
clearance?
Cockcroft-Gault (140-age) x wt/(Cr x 72)
60
What is your differential?
61
The Intervention
  • The next morning the creatinine is 2.5 and his
    mental status has cleared.

62
Geraldine
  • 45 yr old female with a PMH for HTN presents
    with HEADACHE, low back pain, and left should
    pain. You decide to order labs and discover
    discover a Cr 2.0 (baseline 1.0), Calcium 10.0,
    and mild pan-cytopenia (Hb 10.0, Pts 144). FeNa
    is 2.0. UA dip is bland (no protein, no leuks,
    no nitrites)

63
What additional tests would you like?
64
Multiple Myeloma

65
Multiple Myeloma
  • The minimal criteria for the diagnosis of
    multiple myeloma include a bone marrow usually
    containing more than 10 percent plasma cells (or
    presence of a plasmacytoma) plus at least one of
    the following
  • A monoclonal protein (M-protein) in the serum
    (usually gt3 g/dL)
  • An M-protein in the urine
  • Lytic bone lesions.
  • Additionally, at least some of the following
    Anemia, hypercalcemia, azotemia, hypoalbuminemia,
    bone demineralization (THE MINOR CRITERIA)

66
Sams Case
30 year old man with diabetes, hypertension and
chronic renal insufficiency (baseline creatinine
of 2.5) presents to VA clinic for routine
follow-up. His medications are captopril, HCTZ
and insulin. Physical exam is unremarkable. Na
138, K5.8, Cl110, HCO320, BUN30,
Cr2.4,Glu129  
67
What is your differential for elevated Potassium?
68
What is your plan management plan?
69
Acid / Base Basics
  • The normal renal response to acidemia is to
    reabsorb all of the filtered bicarbonate and to
    increase hydrogen excretion primarily by
    enhancing the excretion of ammonium ions in the
    urine. Each hydrogen that is secreted results in
    the regeneration of a bicarbonate ion in the
    plasma.

70
Proximal Tubule
  • Reabsorption of filtered bicarbonate
    predominantly occurs in the proximal tubules
    primarily by Na-H exchange.
  • Approximately 85 to 90 percent of the filtered
    load is reabsorbed proximally.
  • By comparison, 10 percent is reabsorbed in the
    distal nephron primarily via hydrogen secretion
    by a proton pump (H-ATPase).
  • Under normal conditions, virtually no bicarbonate
    is present in the final urine.

71
Distal Tubule
  • We need to deal with acid load from protein
    catabolism.
  • There must be sufficient buffering compounds
    available to bind hydrogen ions.
  • The principal buffers in the urine are ammonia
    (excreted and measured as ammonium) and phosphate
    (referred to and measured as titratable acidity).
  • Failure to excrete sufficient ammonium ? net
    retention of H and metabolic acidosis.
  • Impaired hydrogen ion secretion is the primary
    defect in distal RTA while impaired
    ammoniagenesis is the primary defect in type 4
    RTA and renal failure.

72
Renal Tubular Acidosis
  • Renal tubular acidosis (RTA) is a disorder of
    renal acidification out of proportion to the
    reduction in GFR.
  • RTA is characterized by hyperchloremic metabolic
    acidosis with a normal serum anion gap Na
    (Cl HCO3).
  • There are multiple forms of RTA, depending on
    which aspects of renal acid handling have been
    affected.

73
Type I (DISTAL)
  • Distal nephron does not lower urine pH normally
  • The collecting ducts permit back-diffusion of H
    from lumen to blood with inadequate transport of
    H.
  • Causes a reduction in ammonium excretion.
  • Urinary and K conservation can be impaired.
  • Chronic acidosis lowers tubule reabsorption of
    calcium ? hypercalciuria and mild 2nd
    hyperparathyroidism.
  • Hypercalciuria, alkaline urine, and urine citrate
    cause calcium phosphate stones.
  • Growth retardation is common and improves with
    correction of the acidosis by alkali.
  • Since the kidney does not conserve potassium or
    concentrate the urine normally, polyuria and
    hypokalemia occur. Sometimes fatal.

74
Diagnosis and Treatment
  • Normal AG acidosis
  • Urine pH gt 5.5
  • Nephrocalcinosis
  • Oral ammonium load will worsen acidosis.
  • Urine anion gap is positive (vs. GI)
  • Na K Cl
  • Treat with bicarbonate.

75
Type II RTA (Proximal)
  • Bicarb resorption in prox tubule is impaired.
  • Distal tubule resorption is overwhelmed at first.
  • Equilibrium is established at bicarb of 16.
  • Urine pH is normal / high.
  • Ammonium challenge does not affect urine
    acidification.
  • Expect bicarbonaturia. FE Bicarb.
  • Bicarbonate must be given in LARGE doses. Alkali
    therapy can worsen hypokalemia.

76
Type IV RTA
  • Distal secretion of K and H is abnormal
    producing a non AG acidosis with hyperchloremia.
  • Hypo aldosteronism DM, ACE, NSAIDs, TMP, adrenal
    disease (high Renin level).
  • Tubular inflammation (low Renin state) with
    interstitial inflammation (SSD), K sparing
    diuretics (aldactone, amilloride).
  • HYPERKALEMIA IS THE PRIMARY PROBLEM. K MAY INHIB
    IT AMMONIA EXCRETION.
  • Do not have bicarbonaturia (vs. Type II).
  • Urine is APPROPRIATELY acidic (pH lt 5.5)

77
Treatment
  • Lower potassium
  • Remove drugs that lower aldosterone production.
  • High dose mineralocorticoids (beware of CHF).
  • Liberal Na intake.
  • Exchange resins.

78
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