ALTERED RENAL FUNCTION

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ALTERED RENAL FUNCTION
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Overview of Kidney Diseases

• Organized by site or cause of disease
• Organization by site
• Prerenal
• From inadequate blood flow to the kidney
• Examples
• Decrd intravascular volume
• Lesions in renal arteries
• Hypotension ? decrd perfusion at the glomerulus
• Would these patients Pcr be higher or lower than
  normal? Blood creatinine?

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• Intrarenal
• Result from direct damage to nephron
• Tubulointerstitial disorders
• Disorders of renal tubules or of interstitial
  cells that comprise rest of kidney and surround
  tubules
• Examples
• Glomerular injury
• Diseases of the tubules

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• Postrenal
• Commonly from urinary tract obstruction
• Examples
• Kidney stones
• Tumors/lesions of the bladder/ureters/etc.
• Further divided into chronic, acute

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Intrarenal Disorders

• Glomerular disorders
• Due to change or dysfunction of specialized
  glomerular capillary, or cells of Bowmans
  capsule
• Often see decrd GFR
• Chronic in patients w/ recurrent obstructions
• Persistent, recurrent autoimmune dysfunction of
  kidney
• Onset insidious, often asymptomatic until renal
  damage
• Inflammation ? scarring ? gradual obstruction of
  tubules
• Can cause chronic renal failure

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• Chronic glomerular disorders contd
• Clinical
• Pain, fever
• Wbcs in urine
• Possible bacteriuria
• Systemic hypertension
• Treatment
• Relieve obstructions
• Antibiotics

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• Glomerulonephritis (GN)
• Defined inflammation of the glomerulus
• KNOW THIS DEFINITION!
• Relatively common
• Causes vary most common abnormal immune
  response
• ? Immune complexes
• Precipitate out of blood, fall on walls of
  glomerular capillary
• ? Inflammatory response
• Body tries to get rid of these obstructions
• Wbcs attack complexes BUT also cause destruction
  of glomerular capillary walls
• ? Scar tissue formation

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• Overall, glomerulus altered ?
• Filtration of blood constituents (out of the
  blood) decrd
• Retention of blood constituents that would
  normally be excreted out
• What are the immune complexes composed of?
• What type of hypersensitivity is demonstrated?
• What type of wbc plays a role in this
  hypersensitivity reaction?

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• Three types of glomerulonephritis (GN)
• Acute commonly assocd w/ strep infection
• Abrupt onset usually 7-10 days after strep
  infection of throat or skin
• Immune complexes deposit in glomerulus
• ? Proliferation capillary endothelial cells
• ? Thickening of the glomerular membrane
• ? Decrd GFR
• Treatment antibiotics for strep
• Most patients recover without serious loss of
  renal function
• Commonly occurs in younger patients

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• Types of GN contd
• Chronic ? chronic renal failure
• May be asymptomatic
• Caused by altered immune response, either by
• Ag-Ab complexes deposit in the glomerulus
• Neutrophils attack, breaking down the capillary
  tissue OR
• Abs attack glomerular capillary cells as
  non-self
• Followed by proliferation of cells among
  connective tissue that supports the glomerular
  capillaries
• ? altered glomerular membrane permeability

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• Chronic GN contd
• At first, as glomerulus broken down
• Doesnt act as a good filter
• Cells/molecules needed by body filtered out into
  tubule filtrate
• Urinalysis shows
• Hematuria
• Proteinuria (high levels of protein in the urine)
  
• Tubular dilation, atrophy may also result
• Later, compensation ? clogged filter
• Treatment
• Treat primary disease if it triggered the immune
  response (so antibiotics, immunomodulators)
• Correct accompanying problems (volume disorders,
  changes in blood pressure)

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• Types of GN contd
• Rapidly progressive glomerulonephritis
  Goodpastures syndrome
• Mostly seen in adults 50-60 years
• Crescent formation
• Proliferating cells mixed with fibrin accumulate
  in Bowmans space
• What changes in fluid pressures in the glomerulus
  would you expect? Would GFR go up or down?
  Would blood pressure go up or down?
• Rapid decline in glomerular function, possibly ?
  renal failure w/in months, weeks.

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• Rapidly progressive GN contd
• Clinical
• Hematuria
• Proteinuria
• Edema
• Hypertension
• Treatment - prednisone, immunosuppressants,
  anticoagulants, dialysis, eventual transplant

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• GN, regardless of cause, ? common systemic
  effects
• Nephrotic syndrome
• Excretion gt3.5g protein/day in urine
• So glomerulus too permeable
• Pathophysiology related to loss of plasma
  proteins
• Hypoalbuminemia (or loss of albumins)
• What might loss of these proteins do to fluid
  pressures throughout the body? (Hint think
  COP)
• Susceptibility to infection
• Due to loss of immunoglobulins

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• Nephrotic syndrome pathophys contd
• Edema
• COP reduced ? GFR changed ? plasma volume
  decrd
• ? Hormonal compensation response ? Na and water
  retention
• Over time, see incrd fluid volume, which spills
  into interstitium
• Increased plasma lipid levels
• Bodys feedback response to decrd protein
  concentrations by increasing lipoprotein
  synthesis
• Vitamin D deficiency
• Due to loss of proteins needed for proper Ca2
  absorption
• In turn affects Vitamin D metabolism

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• Nephrotic syndrome pathophys contd
• Treatment
• Diet patient must be monitored for sufficient
  nutrition (loss of proteins, other important
  molecules through urine)
• Diuretics, Na restriction
• Protein supplements

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• Nephritic syndrome
• Alteration of filtration ? rbcs excreted out of
  the body (so hematuria)
• Also decrd GFR ?
• Decrd urinary output and
• Incrd water retention
• Azotemia (increased nitrogenous wastes in blood)
• What would BUN and Pcr results be?
• As GFR is chronically decreased, renal tubules
  undergo disuse atrophy ? scarring of tubules

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• Tubulointerstitial Disorders
• Tubulo of the renal tubule interstitial
  cells surrounding the nephrons
• Pyelonephritis infection of interstitium and
  renal pelvis
• May be by bacteria in blood, or bacteria
  ascending from genitourinary tract
• Acute - caused by bacteria ascending from ureters
• Second most common infectious disease
• Common risk factors
• Female
• Urinary obstruction
• Disorders that lead to reflux urine from the
  bladder

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• Acute Pyelonephritis contd
• Inflammn ? wbcs in kidney medulla ? edema,
  purulent urine
• If severe form ? local abcesses
• May affect renal tubules
• Glomerulus seldom affected
• With healing, may get scar tissue formation
  tubule atrophy poss
• Rarely causes renal failure, BUT may progress ?
  chronic form, so ? renal failure
• Clinical fever, chills, groin pain, increased
  pain/frequency of urination
• Treatment antibiotics

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Pus in tubules appears as yellow streaks in the
cortex and medulla.
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Renal Obstructions

• Kidney stones urinary calculi
• Affect about 1 of the U.S. population
• Composition of crystals
• Ca2 or Mg2 OR
• Uric acid (gout) OR
• Ammonium or phosphate
• Get incrd concentrations in urine, with
• Incrd renal excretion of these (so higher
  concents in normal volume of filtrate) OR
• Decrd urine volume (so decrd amount of filtrate
  ? incrd concents) OR
• Change in urine pH (may ? precipitation of salts
  out of urine)

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• Usually grow in renal tubules, calyces, ureter,
  bladder
• Back pressures may ? renal damage and/or
  secondary infection
• Symptoms
• Pain (renal colic) if in tubules, ureter
• Nausea/vomiting
• Chills, fever
• Hematuria
• Treatment
• Removal by surgery, instrumentation
• Drugs to dissolve stones
• Treatment to prevent further stone formation

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Urinary Tract Infection

• Caused by bacteria
• Retrograde movement from outside environment
• Urethra ? bladder ? ureter ? kidney
• Affect 10-20 of all females in the U.S.
• Risk factors as for pyelonephritis

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• Cystitis - bladder inflammation
• Generally uncomplicated
• Resolves spontaneously
• BUT, if advanced form develops, can ? hemorrhage,
  pus formation in the tubules
• Clinical
• Urination painful, may increase in
  frequency/urgency
• Low back pain
• Hematuria possible

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• Nonbacterial cystitis
• Symptoms same as cystitis, but patient
  demonstrates negative urine culture
• Due to dysfunction or infection of tissues/organs
  surrounding bladder
• May be autoimmune dysfunction
• Treatment
• Relieve inflammation

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Consequences of Renal Disorders

• Acute Renal Failure (ARF)
• Abrupt decrease in renal function ? decrd
  urinary output
• See incrd BUN, Pcr
• Reversible with early diagnosis and treatment
• Many causes (including drugs/toxins, disease,
  trauma, etc.)
• Most common acute tubular necrosis
• May be due to problems within kidney or
  anatomically pre- or post-kidney

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• Prerenal ARF due to impaired blood flow
• Examples
• Vasoconstriction
• Hypotension
• Hemorrhage, burns
• All may ? renal ischemia
• See decrd GFR due to decrd pressures of
  filtration

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• Intrarenal ARF due to diseases, dysfunctions
  within kidney itself, most commonly within
  nephron
• Possible causes
• Acute glomerulonephritis
• Acute tubular necrosis, occurring
• After surgery
• With sepsis
• With severe burns
• With obstetrical complications
• Regardless of cause ? decreased GFR

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• Postrenal ARF usually with urinary obstruction
• Affects both kidneys
• Characteristic - several hours anuria, then flank
  pain, then polyuria
• Anuria no urine output
• Polyuria increased urine output

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• Clinical symptoms of ARF divided into 3 stages
• First stage -- Oliguria
• Decrd urine volume to anuria
• About 25 of normal about 400 mL/day
• Lasts 1-3 weeks, depending on severity
• BUN, Pcr increased (with decr'd GFR)
• Clinical
• Increased K in body (hyperkalemia)
• How might this be a problem?
• Other electrolyte imbalances
• Fluid retention ? edema
• Congestive heart failure
• May require maintenance dialysis

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• Second stage of ARF Symptoms Diuresis
• Body beginning to recover, now attempts to
  compensate
• 3-4 L/day urine excretion possible
• Tubules still damaged early in phase, but
  gradually recovering
• Na, K lost in incrd urine volume
• Electrolyte imbalances occur (now in opposite
  direction)
• May see ECF volume depletion
• Closely follow electrolytes

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• Third stage -- Recovery
• May be 3-12 months for normal Pcr
• About 30 of all ARF patients never regain normal
  kidney function
• Treatment
• Prevention if possible (ex planned surgeries,
  monitoring obstetrical patients)
• Maintain fluid volume
• Mannitol
• ? Incrd renal vasodilation, so incrd GFR
• Also ? decrd Na/water reabsorption
• Other diuretics

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• ARF Treatment contd
• Maintain life functions until kidneys can take
  over
• Correct fluid imbalances
• Treat any infections
• Maintain nutrition, cardiac function
• Dialysis if necessary

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Chronic Renal Failure

• A progressive condition with slow development
  (may be years)
• Common causes
• Chronic glomerulonephritis
• Chronic pyelonephritis
• Diagnosed with loss of 50-70 of functional
  nephrons, then
• Renal insufficiency GFR lt 25 of normal
• Clinical BUN, Pcr steeply increase
• Then

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• End-stage renal failure GFR lt 10 of normal
• So GFR approx 5-10 mL/min
• BUT still excess water loss because tubules lose
  ability to reabsorb water
• Now may lead to uremic syndrome
• At first, remaining (healthy) nephrons
  hypertrophy
• ? Incrd GFR, tubular reabsorption and secretion
  in these nephrons
• BUT compensation breaks down at GFR 25 of
  normal
• Now, diet and fluid intake are crucial
• Note Removal of one kidney causes hypertrophy
  of other kidney, allowing the body to maintain
  function (can maintain gt25 GFR)

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• Uremic syndrome GFR5-10 of normal, regardless
  of cause
• Accumulation of toxins in plasma
• Most common toxins urea, creatinine
• ? Cecline in renal function, so
• ? Varied dysfunctions and symptoms
• Metabolic acidosis
• Impaired ability to excrete H and/or reabsorb
  HCO3-
• So blood pH decrd and blood buffer
  concentrations deviate from 201 ratio
• How will the ratio now differ?
• Deep respirations to blow off excess CO2
• What will this do to blood acid? How will that
  change the 201 ratio?

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• Dysfunctions, symptoms of uremic syndrome
  contd
• Sodium imbalance
• Some compensation from hypertrophied tubules,
  BUT
• At terminal stages, compensation fails, so
• Na retention problems
• Hypertension
• Edema
• Cardiovascular difficulties related to
  electrolyte imbalances
• K retained
• Ca2 lost (with tubule failure to reabsorb)
• Na/water retained
• Leads to
• Hypertension
• Congestive heart failure

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• Dysfunctions, symptoms of uremic syndrome
  contd
• Hematologic problems
• Kidneys produce erythropoietin
• Anemia possible
• Blood coagulation problems possible
• Probably due to K, Ca2 imbalances
• CNS dysfunctions
• Decreased nerve conduction with electrolyte
  imbalances ?
• Weakness
• Confusion
• Convulsions ? ? ? coma