Introduction%20to%20Renal%20Failure%20and%20Acute%20Renal%20Failure

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Introduction to Renal Failure and Acute Renal
Failure

• Jeffrey T. Reisert, DO
• University of New England
• Physician Assistant Program
• 20-27 JAN 20010

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Contact Information

• Jeffrey T. Reisert, DO
• Jeffrey.T.Reisert_at_Hitchcock.org
• 103 Boulder Point Rd., Suite 3
• Plymouth, NH 03264
• 603-536-6355
• 603-536-6356 (fax)

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Genitourinary Section-Part 1

• Male urogenital disorders/Impotence
• Nephrolithiasis
• Urinary Tract Infections

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Genitourinary Section-Part 2

• Introduction to Renal Failure
• Acute Renal Failure
• Chronic Renal Failure
• Glomerulopathies (builds on prior topics)
• Tubular disorders (builds on prior topics)
• Hematuria
• Proteinuria

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Introduction

• Two syndromes of renal failure
• Acute
• Chronic
• Diagnosis-2 Patterns
• Clinical suspect with signs and symptoms
• Found incidentally on lab screen (serum or urine)

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Agenda

• General evaluation of renal failure
• Definitions
• Acute Renal Failure (ARF)
• Etiology
• Diagnosis/Evaluation
• Treatment
• Chronic Renal Failure (CRF)
• Pathogenesis
• Complications
• Treatment of the complications

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Definition-Renal failure

• Spectrum of disease with declining kidney
  function
• Decreased glomerular filtration rate
• Resultant increase in nitrogenous waste products
  in the blood (azotemia)
• Alteration in fluid an electrolytes

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Definitions-Part II

• OliguriaUrine output (UOP) of less than 400 or
  500 cc/24 hours
• AnuriaNo UOP
• Uremia
• Decreased renal function
• Azotemia
• Symptoms

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Definitions-Part III

• Polyuria
• Excessive or frequent urination
• Excessive water intake
• Medical conditions?
• Diabetes insipidus (Inability to concentrate
  urine)
• Renal disease
• Hematuria-blood in urine
• Proteinuria-protein in urine

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Assessment

• Labs
• Urine
• Serum
• Radiographic

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Assessment-Labs I

• Blood urea nitrogen-BUN
• Creatinine
• BUN/Creatinine ratio
• gt40 in prerenal azotemia
• lt20 in intrinsic renal failure
• Electrolytes
• Potassium especially!

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Creatinine

• Goes up quickly in ARF due to ischemia and radio
  contrast (complication of x-ray dye studies such
  as IVP, CT scans)
• Peaks 3-5d after contrast
• Peaks 7-10d after ischemia
• Not correlative with symptoms

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Electrolytes

• Sodium reflects volume status
• Potassium, phosphate, and uric acid increase

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Assessment-Labs II

• Urine output (UOP)-Monitor Is and Os
• Urine sodium (reflects concentrating ability of
  kidneys)
• Body weight
• Toxin levels (i.e. CPK-MM fraction in
  rhabdomyolysis)

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Glomerular filtration rate

• Collectively, the measure of renal function
• If low, leads to azotemia
• Can be estimated by serum creatinine
• Affected by age, sex, weight, fluid status, and
  medical condition (illnesses, nutritional status,
  drugs on board, etc.)
• Creatinine used as a surrogate marker as levels
  vary little day-to-day.
• Creatinine is secreted in the proximal tubule

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Assessment-Labs III

• Creatinine clearance
• ml/min/1.73 per square meter
• Reflects the glomerular filtration rate
• Normal 85-125
• Lower in premies
• Measured or Calculated methods (next slides)

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Creatinine Clearance

• (Urine volume (ml/min) x Urine Creatinine)
• Divided by Serum Creatinine x
• 1.73/Body Surface Area
• -Involves 24 hour urine test mated with serum
  creatinine
• -Fairly accurate and easy
• -Once a year?
• Can be measured accurately by inulin (Usually in
  research)..Is filtered but not reabsorbed or
  secreted in the renal tubules.
• Also by radionuclide markers such as I125
  iothalamate or EDTA (uncommon use) because

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Creatinine Clearance Estimates

• Cockcroft-Gault equation
• Men(140-age) x (wt in kg) divided by 72 x serum
  creatine
• For women multiply by 85 to account for smaller
  muscle mass (0.85 of mens estimate)
• Use in hospitals with IV antibiotic dosing

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Assessment-Labs III

• Fractional excretion of Na
• (Urinary Na x Plasma Creatinine x 100) divided
  by (Plasma Na x Urinary Creatinine)

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Azotemia

• Defined as excess of urea and nitrogenous
  compounds in blood
• Due to breakdown of protein
• (Metabolism of carbohydrates and fats yields
  water and CO2)
• If symptoms, use term uremia

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Assessment-Radiographic

• Ultrasound
• Excludes obstruction
• ?Small kidneys---gtCRF
• Advantages
• Non invasive
• No risky contrast dye
• Readily available

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Assessment-Radiographic II

• Plain x-Ray
• Flat plate (?stone)
• Pyelogram-Inject a dye, cleared through kidney
• Retrograde pyelogram-Inject dye inside urinary
  collection system (intravesicular, using
  cystoscope)
• CT
• Probably better but dye risk in face of rising
  creatinine
• MRI

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Assessment-Wrap up

• Avoid contrast in ARF or CRF not on dialysis
• Biopsy may be needed in ARF for intrinsic disease
• Ultrasound is easy and helpful

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Complications of ARF

• Volume overload
• Decreased sodium and water excretion
• Resultant weight gain, heart failure, and edema
• Hyponatremia
• Hypocalcemia
• Paresthesias, cramps, seizures, confusion

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Complications of ARF II

• Hyperkalemia, phosphatemia, magnesemia
• Potassium increases 0.5mmol/l/d in uremia
• Treat hyperphosphatemia with calcium or aluminum
• Metabolic acidosis
• Hypertension (Moreso in CRF)

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General treatment of ARF

• Prevention!!! (Avoid nephrotoxins, diabetes
  control, etc.)
• Reverse poisons (ETOH in ethylene glycol,
  bicarbonate in acidosis)
• Restore fluid volume and electrolyte balance
  (Saline/crystalloids, colloids, blood)
• Dialysis when needed (Acute if responsive (i.e.
  dialyzable toxin) or in CRF)
• Relieve obstruction (Easiest way to fix ARF!)

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Acute renal failure

• Definitions
• Classifications/Types
• Treatment

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Defined

• Renal failure of recent onset (hours to days to
  weeks)
• Typically little symptoms
• Can be found on random lab test or when suspect
• If acute obstruction, symptoms (below)

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Classification

• Prerenal renal failure (Renal hypoperfusion)-55
• Renal/Parenchymal/Intrinsic-45
• Post renal (Obstructive)-5

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Outcome

• Usually reversible
• Can recover even if almost no function
• Nephrology opinion?

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Prerenal azotemia

• Due to renal hypoperfusion
• Usually reversible if restoring renal blood flow
  (RBF)
• Parenchyma usually not damaged
• In severe cases, ischemia/injury

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Etiology

• Hypovolemia
• Fluid loss
• Decreased cardiac output
• Decreased systemic vascular resistance
• Renal hypoperfusion
• See next slides

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Fluid or blood loss

• Dehydration
• GI bleeds
• Burns
• Osmotic diuresis (i.e. diabetes)
• Sequestration (i.e. pancreatitis)

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Decreased Cardiac Output

• Acute MI
• CHF (perhaps most common among hospital patients)
• Arrhythmias
• Pulmonary embolism (PE)
• Mechanical ventilator

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Altered systemic vascular resistance

• Sepsis, antihypertensives, anesthetics,
  anaphylaxis

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Hypovolemia

• Leads to epinephrine release and subsequent
  vasoconstriction
• Also activations of renin angiotensin
  system--gtVasoconstriction
• Release of arginine vasopressin (AVP)

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Renal hypoperfusion

• Renal vasoconstriction due to epinephrine
• ACE inhibitors
• Cyclooxygenase inhibitors (i.e. NSAIDs)-Also
  lead to volume depletion
• Hyperviscosity syndromes

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Hepatorenal syndrome

• Cirrhosis leads to intrarenal vasoconstriction
• Sodium retention
• Precipitated by bleeding, paracentesis,
  diuretics, vasodilation, cyclooxygenase inhibitors

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Prerenal azotemia-Assessment

• Symptoms
• Thirst, dizzy
• Signs
• Low blood pressure, tachycardia, orthostasis
• Low UOP

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Lab evaluation

• Urine volume
• Urine microscopy
• Hyaline/bland casts due to concentrated urine

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Intrinsic renal failure

• Renovascular obstruction-Large vessel disease
• Glomerular or microvascular diseases

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Renovascular obstruction

• Obstructed renal artery (Atherosclerosis,
  thrombus)
• Renal vein obstruction (Thrombosis, external
  compression)

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Glomerular diseases

• Glomerulonephritis
• Vasculitis
• Acute tubular necrosis
• Ischemic or nephrotoxic
• Interstitial nephritis
• Renal allograft rejection
• Will expand in later section

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Vasculitis

• Kidneys are one of several very vascular organs
• Hemolytic uremic syndrome
• Thrombotic thrombocytopenic purpura
• Disseminated intravascular coagulation
• Toxemia
• Accelerated HTN
• Lupus
• ?Include sickle cell disease

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Acute tubular necrosis

• Most susceptible area of the nephron to ischemia
  is the renal tubule
• Ischemia from prerenal azotemia (Most common)
• Prerenal azotemia is the most common cause of
  intrinsic renal failure
• Toxin induced
• Often see casts (covered later)

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Ischemia

• Hypoperfusion
• Resultant injury or ischemia
• Cortical necrosis
• Either recover (tubules regenerate) or develop
  irreversible failure

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Nephrotoxins

• Radiocontrast (Intrarenal vasoconstriction)
• Aminoglycosides (Decrease GFR)
• Cyclosporin
• Chemotherapy (Cisplatin)
• Solvents (ethylene glycol)
• Others

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Endogenous nephrotoxins

• Rhabdomyolysis (Due to crush, injury, ETOH)
• Hemolysis (toxic to renal tubule)
• Uric acid (Same thing that causes gout)
• Myeloma (Plasma cell malignancy)
• Hypercalcemia (Causes renal vasoconstriction)

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Interstitial Nephritis

• Allergic (Antibiotics such as beta-lactams),
  NSAIDs, diuretics
• Infection (Bacterial-pyelonephritis, viral-CMV,
  Fungus-Candidiasis)
• Infiltration (Lymphoma, leukemia, sarcoidosis)
• Idiopathic

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Intrinsic renal failure

• Symptoms-Often none
• May have history of nephrotoxin exposure
• Signs-Azotemia on lab testing
• Nephritic syndrome (Oliguria, edema, HTN, Urine
  sediment)
• This suggests a glomerulonephritis or vasculitis

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Intrinsic renal failure-Lab evaluation

• Microscopy
• Muddy brown casts (ischemia and nephrotoxic)
• Red cell casts (acute glomerular injury or
  nephritis)
• White cell casts (interstitial nephritis)
• Eosinophilic casts (allergic nephritis)
• Often no casts
• Hematuria

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Intrinsic renal failure-Lab evaluation

• Proteinuria due to impaired reabsorption at the
  proximal tubules
• Guided by etiology (i.e. sedimentation rate if
  vasculitis)

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Intrinsic renal failure-Treatment

• Treat cause
• Remove insult
• Support, hope, and pray

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Examples

• Glucocorticoids in vasculitis and allergic
  interstitial nephritis)
• Control blood pressure

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Postrenal renal failure

• Urinary outflow obstruction
• Single kidney or urethral obstruction--gtAnuria

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Etiologies of postrenal azotemia

• Prostate disease
• Neurogenic bladder
• I.e. spinal cord injuries
• Anticholinergics
• Blood clots
• Stones
• Tumor or other extrarenal obstruction

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Postrenal signs and symptoms

• Bladder distension
• Abdominal pain-colic
• Renal distension (ultrasound)
• History of risk factors (prostate disease,
  stones, etc.)

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Treatment of obstruction

• Urologist
• Fix plumbing
• May need nephrostomy tube or suprapubic catheter
  placed

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Miscellaneous treatment wrap-up

• Loop diuretics may restore diuresis
• Dopamine may promote sodium and water excretion
• Dialysis when needed

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Wrap-up II--Dialysis Use

• ?BUN gt 100
• Uremia
• Hypervolemia
• Hyperkalemia
• Acidosis
• Toxins
• Multiple
• Include digoxin, others

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More

• to come in next slide set