Renal Disorders: Chapter 74

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Renal Disorders Chapter 74

• Goodwin College
• Nursing 200

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Renal Disorders

• Interfere with kidneys ability to filter wastes,
  to balance fluid solutes
• Renal disorder(s) can significantly affect
  systemic health and lead to life-threatening
  outcomes
• Disorders can be categorized as
• congenital
• obstructive
• infectious,
• glomerular
• degenerative

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Inherited Polycystic Kidney Disease

• Most common inherited disorder affects
  250,000500,000 people in US
• Inherited autosomal dominant trait or as an
  autosomal recessive trait
• Recessive form of Polycystic Kidney Disease
  usually results in death in early childhood
• Polycystic Kidney Disease is more common in
  Caucasians than in other races
• Abbreviation PKD

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Pathophysiology - PKD

• Characterized by fluid filled cysts in epithelial
  cells of nephron
• Dominant form only 5-10 of nephrons involved
  until 40s
• Autosomal recessive form nearly 100 of
  nephrons are involved at birth
• Cysts develop due to
• kidney cell proliferation
• altered secretion
• abnormal cell matrix biology

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Pathophysiology - PKD

• Cysts develop anywhere in nephron can become
  progressively larger and more widely distributed
• Damage both glomerular tubular membranes
• As cysts grow and become filled with fluid
  nephron functions decrease

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Pathophysiology - PKD
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Pathophysiology - PKD

• Nonfunctioning cysts, which look like a cluster
  of grapes, eventually replace kidney tissue
• Kidneys become grossly enlarged (2-3x normal)
  causing other organs to become displaced posing
  considerable discomfort to client
• Fluid-filled cysts are prone to
• infection
• rupture
• bleeding

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Pathophysiology - PKD

• More than 60 of clients with PKD also have
  hypertension
• Possible cause of hypertension is renal ischemia
  caused from enlarging cysts
• Top priority in PKD is to control hypertension
  decrease vasoconstriction that leads to renal
  ischemia

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Etiology/Incidence - PKD

• 2 inherited forms men women have equal chance
  of inheriting PKD gene responsible for PKD is
  not found on sex chromosomes
• 5-10 incidence in clients with no family history
  - occurs as result of spontaneous genetic
  mutation
• Children of parents who have PKD have a 50
  probability of inheriting the gene that causes
  autosomal dominant form of PKD

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Etiology - ADPKD

• Autosomal dominant polycystic kidney disease
  (ADPKD) manifestations vary by age of onset and
  severity
• Half of those affected develop renal failure by
  age 50 yrs
• ADPKD 1 is most severe form both in progression
  and mortality.
• ADPKD 2 has slower rate of cyst formation

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Etiology Genetic Risk

• Presently, no way to prevent PKD early
  detection of and treatment of HTN may slow
  progression of renal impairment
• Genetic counseling and evaluation may be helpful
  to offspring whose parent(s) have PKD
• Age at which time signs and symptoms of PKD
  developed in parent(s) and any other related
  complications may have significance in their
  prognosis of PKD

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Clinical Manifestations Assessment

• Pain is usually first/presenting symptom
  (abdominal or flank pain) can be dull or sharp
  will vary depending on cause
• Dull, aching pain is caused by increased kidney
  size with distension or from infection within
  cyst(s)
• Sharp, intermittent pain occurs in response to
  ruptured cyst or presence of stone(s)

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Clinical Manifestations Assessment

• Distinctive factor between infectious process vs
  PKD is distended abdomen.
• Cystic Kidneys swell push abdominal contents
  forward and displace other organs
• Cystic kidneys are easily palpated because of
  their size be careful very tender use
  gentle palpation!

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Clinical Manifestations Assessment

• Nocturia(excessive night-time urination) may be
  early sign occurs because of decreased renal
  concentrating ability
• As renal function declines, other symptoms
  include increasing hypertension and edema
• Other key features of PKD
• increased abdominal girth
• constipation
• bloody or cloudy urine
• kidney stones

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Diagnostic Assessment PKD

• BUN and serum creatinine levels rise as kidney
  function deteriorates
• With decreasing function may also see changes
  in renal handling of Na
• Urinalysis
• Proteinuria present once glomeruli are involved
• Hematuria gross or microscopic
• Bacteria may be found -signifying infection
• Urine culture needed if UA for bacteria

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Diagnostic Assessment PKD

• Renal Sonography, CT scan and MRI are among
  diagnostic studies utilized
• Small cysts are detected via sonography, CT scan
  or MRI
• Renal sonography provides the diagnostic evidence
  of PKD with minimal risk

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Common Nursing DiagnosisPKD

• Acute Pain r/t cyst rupture or stones
• Chronic Pain r/t enlarging kidneys or compressed
  organs
• Constipation r/t intestinal tract compression
• Collaborative Problems include
• Potential for Infection
• Potential for Hypertension
• Potential for Stone Formation
• Potential for Renal Failure

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Interventions Pain management

• Pain Management analgesic administration
• Comfort measures include pharmacologic and
  complementary medicine
• NSAIDs are used cautiously due to their tendency
  to adversely affect renal function
• Aspirin-containing compounds are avoided to
  prevent increased potential for bleeding

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Interventions Pain management

• Cyst Infection-pain source lipid-soluble
  antibiotic I.e.Bactrim, Septra, Trimpex or Cipro
  (which penetrate cyst wall)
• Monitoring serum Cr levels is important because
  antibiotic therapy can be nephrotoxic
• Cysts may be aspirated, dry heat to abdomen if
  pain is severe
• Relaxation methods (deep breathing, guided
  imagery) may be useful as comfort measures

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Interventions Constipation

• Constipation teach client about adequate fluid
  intake, increased dietary fiber and need for
  regular exercise
• Advise client about appropriate use of stool
  softeners and bulk agents
• Nurse lets client know that pressure from
  enlarged kidneys on large intestine may also
  impede peristalsis so changes in bowel
  management might be necessary as disease
  progresses

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Interventions Renal Failure HTN

• Renal Failure when renal impairment is evident
  through decreased concentrating ability (nocturia
  low specific gravity) encourage client to
  drink at least 2L fluid/day to prevent
  dehydration which can lead to further renal
  impairment
• Hypertension Restrictions on sodium intake may
  help to control blood pressure

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Interventions HTN

• Meds for HTN include diuretics
  anti-hypertensive agents review with client how
  to take meds, how to take and record BPs and
  monitoring daily weights
• Low sodium diet may/may not be prescribed can be
  helpful to reduce HTN clients may experience
  salt-wasting and protein intake may be restricted
  to slow development of renal failure

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Hydronephrosis- Pathophysiology

• Usually associated with obstruction of urine
  outflow
• Hydronephrosis kidney becomes enlarged as urine
  accumulates in renal pelvis and kidney tissue
• Accumulating urine causes increasing renal
  pressure-eventually causing damage to blood
  vessels and renal tubules
• Caused by an obstruction in upper part of ureter

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Hydronephrosis- Pathophysiology
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Hydronephrosis - Pathophysiology

• Disorder(s) that cause hydronephrosis include
• tumors
• stones
• trauma
• congenital structural defects
• retroperitoneal fibrosis
• Early treatment of causes can prevent
  hydronephrosis and prevent permanent renal
  damage, specific time needed to prevent permanent
  damage varies-depends on clients underlying
  renal status may occur lt48 hours in some and
  after several weeks for others

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Assessment Hydronephrosis

• History from client noting childhood urinary
  tract problems which may signal unidentified
  structural defects
• Ask about pattern of urination amount,
  frequency, color, clarity and odor.
• Client is asked about recent flank/abdominal
  pain. Also, client is asked about signs/symptoms
  of infection chills, fever or malaise.

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Assessment Hydronephrosis

• Palpate abdomen to identify areas of tenderness
  inspect each flank for asymmetry.
• Gentle pressure on abdomen may cause urine
  leakage signifying a full bladder or potential
  obstruction
• Urinalysis may show bacteria or WBCs

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Assessment Hydronephrosis

• Microscopic examination may reveal tubular
  epithelial cells in urine if a urinary tract
  obstruction has been prolonged
• Check BUN and serum Cr levels will increase if
  glomerular filtration rate decreases
• Serum electrolyte levels may also be altered
• hyperkalemia
• hyperphosphatemia
• hypocalcemia
• metabolic acidosis

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Diagnostic Assessment Hydronephrosis

• Intravenous urography (using a contrast medium)
  reveals ureteral or renal pelvis dilation
• Sonography or Computed tomography (CT) may reveal
  a urinary outflow obstruction.

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Interventions Hydronephrosis

• Primary problems
• Urinary retention
• Potential for infection
• Failure to treat urinary obstruction may lead to
  infection and renal failure
• See page 1710 chart 74-2 for interventions
• Urological intervention(s) may be required to
  remove or reduce cause of obstruction
• Worst case scenario involves a nephrostomy

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Infectious Disorders Pyelonephritis

• Pyelonephritis bacterial infection in upper
  urinary tract involving kidney and renal pelvis
• Acute Pyelonephritis a condition resulting from
  an active bacterial infection
• Chronic Pyelonephritis results from repeated or
  continued upper urinary tract infections or the
  effects of such infections

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Pathophysiology Pyelonephritis

• Urinary system normally excretes sterile urine
  unobstructed and complete passage of urine is
  critical in maintaining a sterile urinary tract
• Microorganisms usually ascend (flow upward) from
  lower urinary tract into renal pelvis
• Bacteria trigger inflammatory response and
  localized edema results

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Pathophysiology Chronic Pyelonephritis

• Associated with
• anatomic urinary tract anomaly
• urinary obstruction
• vesicoureteral urine reflux (most common)
• Vesicoureteral junction is point where ureter
  joins bladder
• Reflux refers to backward or upward flow of urine
  towards renal pelvis and kidney

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PathophysiologyChronic Pyelonephritis

• Chronic Pyelonephritis inflammation, fibrosis
  and deformity of renal pelvis and calices are
  evident
• Repeated or continuous infections produce
  additional scar tissue
• Vascular, glomerular and tubular changes within
  scars can occur impairing filtration,
  re-absorption and secretion, as well as
  diminishing renal function

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PathophysiologyAcute Pyelonephritis

• Acute Pyelonephritis involves
• acute interstitial inflammation
• tubular cell necrosis
• abscess formation (pockets of infection)
• Scar tissue or fibrosis develops from
  inflammation
• Pattern of infection within kidney is not uniform

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Etiology Pyelonephritis

• Acute may result from entry of bacteria
  associated with pregnancy, obstruction or reflux
• Chronic associated with structural
  abnormalities and/or obstruction causing reflux
  of urine often due to stones, obstruction, or
  neurogenic impairment involving voiding
  mechanisms.

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Etiology Pyelonephritis

• Reflux is more common in children - leading to
  chronic pyelonephritis as adults due to
  scarring
• If no history of reflux chronic pyelonephritis
  can be caused in adults by
• spinal cord injury
• bladder tumor
• prostatic hypertrophy
• urinary tract stones

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Etiology Pyelonephritis

• Acute/Chronic Pyelonephritis more likely to
  affect clients who have
• urinary catheters
• diabetes mellitus
• chronic renal calculi
• hx of overuse of analgesics
• NSAID use has been associated with papillary
  necrosis leading to reflux

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Etiology Pyelonephritis organisms

• Most common infection-causing organism
  responsible for pyelonephritis is E. Coli
• In hospitalized clients, it is Enterococcus
  faecalis
• Both organisms are commonly found in GI Tract
• Bloodborne infection commonly is caused by
  Staphlococcus aureus, Candida, and Salmonella
  species

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Incidence Pyelonephritis

• Acute urinary conditions of kidneys or urinary
  tract, nephritic syndrome, urethral stricture and
  cystitis account for gt7 million new cases
  annually in non-institutionalized Americans
• Higher in women until age 65, then mens risk
  increases greatly due to prostate problems
  (prostatitis)

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Clinical ManifestationsPyelonephritis

• Key features-Acute Pyelonephritis
• fever
• chills
• flank/back/loin pain
• chart 74-4 on page 1713
• Chronic pyelonephritis has less dramatic
  presentation s/s are usually related to
  infection or renal function (chart 74-5 pge 1713)

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Diagnostic AssessmentPyelonephritis

• Urinalysis reveals WBCs and bacteria. Urine is
  analyzed to determine whether bacteria is
  gram-positive or gram-negative
• Urine culture/sensitivity testing to determine
  susceptibility/resistance to various antibiotics
• More specific testing for recurrent infections of
  bacterial antigens may help determine cause

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Diagnostic AssessmentPyelonephritis

• X-ray examination (KUB) of kidney, ureters and
  bladder and Intravenous urography may be done to
  determine presence of stones or obstructions
• Cystourethrogram radiologic procedure used to
  define urinary tract structures and identify any
  structural defects

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Collaborative Problems/Management

• Acute Pain surgical management to correct
  structural abnormalities
• Pyelolithotomy stone removal from renal pelvis
• Nephrectomy kidney removal (last resort)
• Ureteral diversion or reimplantation of ureter to
  restore proper bladder drainage

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Immunologic Renal DisordersGlomerulonephritis

• Glomerulonephritis is 3rd leading cause of
  end-stage renal disease
• Most forms of glomerulonephritis are associated
  with accumulation of immune complexes in
  glomeruli (antigen/antibody effect). Immune
  complexes activate many mediators that result in
  renal tissue injury
• Categorized into primary or secondary types
  (table 74-1 and table 74-2 page 1716)
• Abbreviation GN

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Acute Glomerulonephritis

• Precipitated by infection symptoms occur in
  about 10 days from time of infection
• Effects of acute GN are severe but recovery is
  quick and complete
• Most caused by infection (Table 74-3 pge 1717 for
  infectious causes), or related to secondary
  source (table 74-2 pge 1717)
• Incidence of Acute GN is unknown
• Post-streptococcal systemic infection GN is more
  common in males

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AssessmentAcute GN

• Nurse asks about recent infections (particularly
  of skin and upper respiratory tract)
• Recent travel or activities that pose possible
  exposure to viruses, bacteria, fungi or parasites
• Recent illnesses, surgery or invasive procedures
  may suggest infections, as well as systemic lupus
  erythematosus, which can cause acute GN

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Assessment Acute GN

• Nurse inspects clients skin for lesions or
  recent incisions
• Inspect face, eyelids, hands and other areas for
  edema (seen in approx. 75 of clients)
• Assess for circulatory congestion and fluid
  overload (fluid and sodium retention) breathing
  difficulty, dyspnea, crackles in lungs, S3 heart
  sound (gallop) and neck vein distention

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Assessment Acute GN

• Nurse asks about changes in urination or color
  microscopic hematuria occurs 66 of time urine
  appears as smoky, reddish-brown, rusty or cola
  colored dysuria or even oliguria may be present
• Mild to moderate HTN may occur due to sodium and
  fluid retention
• See other symptoms on page 1717

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Diagnostic Assessment Acute GN

• Urinalysis reveals hematuria and proteinuria
• Examination of early morning specimen is
  preferred formed elements are more intact in
  acidic urine at this time
• Urine sediment assay is usually positive (red
  blood cells casts and casts from other
  substances)

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Diagnostic Assessment Acute GN

• Glomerular Filtration Rate may be decreased to 50
  mL/min (measured in 24 hr urine test for
  creatinine clearance)
• An older client may have greater decline in their
  glomerular filtration rate
• Serum BUN levels are usually increased
• Serum albumin may be decreased due to loss of
  protein in urine and due to fluid retention
  (causes dilution)

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Diagnostic Assessment Acute GN

• Total Protein Assay (in 24 hr urine collection)
  is obtained protein excretion can be elevated
  from 500 mg to 3gms within 24 hr period in gt75
  of clients
• Cultures may be obtained from blood, skin and
  throat specimens, if indicated to determine
  infectious cause
• Renal biopsy is another option to determine
  precise diagnosis of pathologic condition to
  assist in making prognosis

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Interventions Acute GN

• Interventions focus on treating
• underlying infectious process
• prevention of complications
• client education
• Infections are treated with appropriate
  antibiotic
• Nurse stresses personal hygiene basic infection
  control principles, to control spread MD may
  prescribe anti-infectives for those in close
  personal contact

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Interventions Acute GN

• Diuretics and a sodium/water restriction for
  those with fluid overload, HTN, and edema
• Potassium and protein intake may be restricted to
  prevent hyperkalemia and uremic manifestations of
  the elevated BUN levels
• Nausea, vomiting or anorexia in a client is
  indicative of uremia interfering with nutrition

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Interventions Acute GN

• Dialysis is necessary when uremic symptoms or
  fluid volume excess cannot be controlled
• Plasmapheresis the filtering of plasma to
  eliminate antibodies may also be attempted
• Restful environment is helpful to conserve energy

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Client Education

• Instruction on purpose/desired effects of
  prescribed medications
• Dosage and route of medications and potential
  adverse side effects
• Understanding of dietary or fluid modifications
• Weight and blood pressure monitoring to detect
  increases in either

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Nephrotic Syndrome NS

• Condition of increased glomerular permeability
  that causes massive proteinuria, edema and
  hypoalbuminemia
• Glomerular membrane changes from immune processes
  permitting protein loss into urine
• As a result of this loss, plasma albumin levels
  decrease and edema develops

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Pathophysiology NS

• Altered liver activity results in elevated lipid
  production hyperlipidemia
• Possible causes many agents, diseases and
  physiologic processes
• Primary Feature severe proteinuria (gt3.5g of
  protein in 24 hours)
• Other features chart 74-6 pge 1719

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Interventions NS

• Treatment varies depending on cause kidney
  biopsy is done to determine
• Some immunologic processes may respond to
  steroids or cytotoxic agents dietary
  modifications may be prescribed protein intake
  is decreased if the Glomerular Filtration Rate
  (GFR) is decreased

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Interventions NS

• If Glomerular Filtration Rate is normal or near
  normal, an increase in dietary protein may be
  needed to match increased protein loss associated
  with NS
• This increase in protein loss can lead to
  hypoalbuminemia and edema formation

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Interventions NS

• Other interventions mild diuretics (chart 74-7
  pge 1720) or dietary sodium restrictions to
  control edema and HTN
• Nephrotic Syndrome may progress to End Stage
  Renal Disease, but progression is not inevitable
• Hemodynamic changes and acute renal failure may
  be avoided if renal perfusion can be maintained

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Diabetic Nephropathy Pathophysiology

• Microvasular complication of diabetes defined by
  persistent albuminuria without evidence of any
  other renal disease
• Diabetic renal disease is progressive DM is
  leading cause of end-stage renal disease among
  Caucasians in US
• Can result from either Type 1 or Type 2 DM

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Diabetic Nephropathy Pathophysiology

• Severity of diabetic renal disease related to
  extent, duration, and effects of
• Atherosclerosis
• HTN
• Neuropathy which promotes bladder atony, urinary
  stasis, and UTIs
• Diabetic clients are always considered to be at
  risk for renal failure. Avoid if possible
  nephrotoxic agents and dehydration.

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Diabetic Nephropathy Pathophysiology

• As renal function worsens, clients may experience
  hypoglycemic episodes resulting in decreased
  need for insulin or oral anti-hyperglycemic
  agents
• Kidneys normally metabolize and excrete insulin
  as renal function worsens, insulin is available
  in body longer to control glucose levels (needing
  less insulin is NOT good sign)