RENAL DISORDERS AND THEIR DENTAL MANAGEMENT IN A CONCISE FORM.

1. PRESENTED BY:
DR DIVYA RANA
PG 2nd
YEAR
MGDCH

2. Bones can break, muscles can atrophy, glands can
loaf, even the brain can go to sleep without
immediate danger to survival. But -- should
kidneys fail.... neither bone, muscle, nor brain
could carry on.
Homer Smith, Ph.D.

3.  Renal circulation receives 20 - 25 % of
cardiac output under normal physiologic
conditions.
 The bodies blood volume circulates through
the kidney every 6 minutes (12 times/hour).

4.  Renin secretion and
the regulation of
volume and
composition of
extracellular fluid.
 Excretion
 Blood pressure control
 Vitamin D activation
 Acid-base balance
regulation.
 Erythropoietin
production
 Urine formation

5.  Renin is important in the regulation of
blood pressure.
 It is released from the granular cells of
the efferent arteriole in response to
decreased arteriole blood pressure, renal
ischemia, extracellular fluid depletion,
increased norepinephrine, and increased
urinary Na+
concentration.

6. 4 mechanisms are involved
 Volume control
 Aldosterone effect
 Renin-angiotensin-aldosterone
 Renal prostaglandin

7. Prostoglandins (PGs)- synthesized by most
body tissues. In the kidney, PGs are
synthesized in the medulla and have a
vasodilating action and promote Na+
excretion. PGs counteract the
vasoconstrictor effect of angiotensin and
norepinephrine. Renal PGs systemically
lower blood pressure by decreasing systemic
vascular resistance.

8.  Acquired by the body through diet or through
synthesis by ultraviolet radiation on the
cholesterol in the skin.
 The liver and the kidney make the vitamin
active in the body.

9.  Erythropoietin is produced and released by
the kidneys in response to decreased oxygen
tension in the renal blood supply that is
created by the loss of red blood cells.
 Erythropoietin stimulates the production of
RBCs in the bone marrow.
 Erythropoietin deficiency leads to anemia in
renal failure.

10. Kidney secrete Erythropoietin, it stimulates
the bone marrow to produce RBC’s
  in oxygen delivery simulates release
 in response the RBC count rises in 3 - 5 days
 speeds the maturation of RBC’s

11. Kidneys regulate acid-base balance by
stabilizing body fluid volume & flow rate to
enhance the reabsorption or excretion of
bicarbonate & hydrogen ions

12.  Sodium
 Potassium
 Calcium Need to Know:
 Phosphate Normal Values
 Magnesium Functions
 Chloride Factors affect

13.  Over 200 waste products excreted
 Only 2 are used for clinical assessment
 BUN
 Creatinine

14.  Over 200 waste products excreted
 Only 2 are used for clinical assessment
 BUN
 Creatinine

15.  Normal 8 - 20 mg/dl
 Nitrogenous waste product of protein
metabolism
 Unreliable in measurement of renal function
 Relevance is assessed in conjunction with
Creatinine

16.  Urine flow
 low renal perfusion
 Volume depletion
 Metabolic rate
 Protein metabolism
 Drugs

17.  A waste product of muscle metabolism
 Normal value 0.6 - 1.2 mg/dl
 2 times normal = 50% damage
 8 times normal = 75% damage
 10 times normal = 90% damage
 Exception - severe muscular disease can
greatly  Creatinine levels

18.  Blood Tests
BUN elevated (norm 10-20)
Creatinine elevated (norm 0.6 - 1.2)
K elevated
PO4 elevated
Ca decreased
 Urinalysis
Specific gravity
Protein
Creatinine clearance

19.  Biopsy
 Ultrasound
 X-Rays

20.  Sudden onset - hours to days
 Often reversible
 Severe - 50% mortality rate overall; generally
related to infection.

21.  Homeostatic functions affected most
 Electrolyte imbalances
 Volume regulation
 Blood pressure control
 Endocrine functions affected lease
 Require time to evolve
 Renal size is preserved
 Evidence of acute illness or insult exists

22.  Sudden fall in glomerular filtration rate
(GFR)
 Retention of nitrogenous (BUN and creatinine)
and other wastes
 Hours to days
 About 5% of all hospitalizations
 About 20% of ICU admissions
 Mortality 50 – 80%
 Independent risk factor for death – 5x
increase risk

23.  Slow progressive renal disorder related to
nephron loss, occurring over months to years
 Culminates in End Stage Renal Disease

24.  Cause & onset often unknown
 Loss of function precedes lab abnormalities
 Lab abnormalities precede symptoms
 Symptoms (usually) evolve in orderly
sequence
 Renal size is usually decreased

25.  Diabetes
 Hypertension
 Glomerulonephritis
 Cystic disorders
 Developmental - Congenital
 Infectious Disease

26.  Neoplasms
 Obstructive disorders
 Autoimmune diseases
 Lupus
 Hepatorenal failure
 Scleroderma
 Amyloidosis
 Drug toxicity

27.  24 hour urine for creatinine clearance
 Can estimate creatinine clearance by:
140 – {age x weight (kg)}
72 x serum creatinine

28.  Reduced Renal Reserve
 Renal Insufficiency
 End Stage Renal Disease (ESRD)

29. Stage 1: GFR > 90 ml/min despite kidney
damage

30. Stage 2: Mild reduction (GFR 60 – 89
ml/min)
1. GFR of 60 may represent 50%
loss in function.
2. Parathyroid hormones starts to
increase.

31.  No symptoms
 Serum creatinine doubles
 Up to 50% nephron loss

32. Stage 3: Moderate reduction (GFR 30 – 59
ml/min)
1. Calcium absorption decreases
2. Malnutrition onset
3. Anemia secondary to Erythropoietin
deficiency
4. Left ventricular hypertrophy

33. Stage 4: Sever reduction (GFR 15 – 29
ml/min)
1. Serum triglycerides increase
2. Hyperphosphatemia
3. Metabolic acidosis
4. Hyperkalemia

34.  Signs and symptoms worsen if kidneys are
stressed
 Decreased ability to maintain homeostasis

35.  75% nephron loss
 Decreased: glomerular filtration rate, solute
clearance, ability to concentrate urine and
hormone secretion
 Symptoms: elevated BUN & Creatinine, mild
azotemia, anemia

36. Stage 5: Kidney failure (GFR < 15 ml/min)
1. Azotemia

37.  Residual function < 15% of normal
 Excretory, regulatory and hormonal functions
severely impaired.
 metabolic acidosis
 Marked increase in: BUN, Creatinine,
Phosphorous
 Marked decrease in: Hemoglobin,
Hematocrit, Calcium
 Fluid overload

38.  Uremic syndrome develops affecting all body
systems
 can be diminished with early diagnosis &
treatment
 Last stage of progressive CRF
 Fatal if no treatment

40.  Mood swings
 Impaired judgment
 Inability to concentrate and perform simple
math functions
 Tremors, twitching, convulsions
 Peripheral Neuropathy
 restless legs
 foot drop

41.  Pale, grayish-bronze color
 Dry scaly
 Severe itching
 Bruise easily
 Uremic frost

42.  Visual blurring
 Occasional blindness

43.  Volume expansion and fluid overload
 Metabolic Acidosis
 Electrolyte Imbalances
 Hyperkalemia

44.  Uremic fetor
 Anorexia, nausea, vomiting
 GI bleeding

45.  Anemia
 Platelet dysfunction

46.  Muscle cramps
 Soft tissue calcifications
 Weakness
 Related to calcium phosphorous imbalances

48.  Hypertension
 Congestive heart failure
 Pericarditis
 Pulmonary edema
 Pleural effusions

49.  Erythropoietin production decreased
 Hypothyroidism
 Insulin resistance
 Growth hormone decreased
 Gonadal dysfunction
 Parathyroid hormone and Vitamin D3
 Hyperlipidemia

50.  Oral manifestations
 Enlarged (asymptomatic) salivary glands
 Decreased salivary flow
 Dry mouth
 Odor of urea on breath
 Metallic taste
 Increased calculus formation
 Low caries rate
 Enamel hypoplasia
 Dark brown stains on crowns
 Extrinsic (secondary to liquid ferrous sulfate therapy)
 Intrinsic (secondary to tetracycline staining)

51.  Dental malocclusions
 Pale mucosa with diminished color demarcation between
attached gingiva
 and alveolar mucosa
 Low-grade gingival inflammation
 Petechiae and ecchymosis
 Bleeding from gingiva
 Prolonged bleeding
 Candidal infections
 Burning and tenderness of mucosa
 Erosive glossitis
 Tooth erosion (secondary to regurgitation associated with
dialysis)
 Dehiscence of wounds

52.  Radiographic manifestations
 Demineralization of bone
 Loss of bony trabeculation
 Ground-glass appearance
 Loss of lamina dura
 Giant cell lesions, “brown tumors”
 Socket sclerosis
 Pulpal narrowing and calcification
 Tooth mobility
 Arterial and oral calcifications

54.  Hemodialysis
 Peritoneal Dialysis
 Transplant

55.  Removal of soluble substances and
water from the blood by diffusion
through a semi-permeable membrane.

56.  Blood removed from patient into the
extracorporeal circuit.
 Diffusion and ultrafiltration take place in the
dialyzer.
 Cleaned blood returned to patient.

59.  Arterio-venous shunt (Scribner External
Shunt)
 Arterio-venous (AV) Fistula
 PTFE Graft
 Temporary catheters
 “Permanent” catheters

60.  External- one end into
artery, one into vein.
 Advantages
place at bedside
use immediately
 Disadvantages
infection
skin erosion
accidental separation
limits use of extremity

61.  Patients own artery and vein surgically
anastomosed.
 Advantages
patients own vein
longevity
low infection and thrombosis rates
 Disadvantages
long time to mature, 1- 6 months
“steal” syndrome
requires needle sticks

62.  Synthetic “vessel” anastomosed into an artery
and vein.
 Advantages
for people with inadequate vessels
can be used in 7-14 days
prominent vessels
 Disadvantages
clots easily
“steal” syndrome more frequent
requires needle sticks
infection may necessitate removal of graft

63.  Dual lumen catheter placed into a central
vein-subclavian, jugular or femoral.
 Advantages
immediate use
no needle sticks
 Disadvantages
high incidence of infection
subclavian vein stenosis
poor flow-inadequate dialysis
clotting

64.  NO BP’s, needle sticks to arm with vascular
access. This includes finger sticks.
 Place ID bands on other arm whenever
possible.
 Palpate thrill and listen for bruit.
 Teach patient nothing constrictive, feel for
thrill.

65.  During dialysis
Fluid and electrolyte related
 hypotension
Cardiovascular
 arrythmias
Associated with the extracorporeal circuit
 exsanguination
Neurologic
 seizures
other
 fever

66.  Between treatments
 Hypertension/Hypotension
 Edema
 Pulmonary edema
 Hyperkalemia
 Bleeding
 Clotting of access

67.  Long term
Metabolic
 hyperparathyroidism
 diabetic complications
Cardiovascular
 CHF
 AV access failure
Respiratory
 pulmonary edema
Neuromuscular
 neuropathy

68.  Long term cont’d
 Hematologic
 anemia
 GI
 bleeding
 dermatologic
 calcium phosphorous deposits
 Rheumatologic
 amyloid deposits

69.  Long term cont’d
 Genitourinary
 infection
 sexual dysfunction
 Psychiatric
 depression
 Infection
 bloodborne pathogens

70.  Fluid restrictions
 Phosphorous restrictions
 Potassium restrictions
 Sodium restrictions
 Protein to maintain nitrogen balance
 too high - waste products
 too low - decreased albumin, increased mortality
 Calories to maintain or reach ideal weight

71.  Removal of soluble substances and water
from the blood by diffusion through a semi-
permeable membrane that is intracorporeal
(inside the body).

72.  CAPD: Continuous ambulatory peritoneal
dialysis
 CCPD: Continuous cycling peritoneal dialysis
 IPD: Intermittent peritoneal dialysis

73.  Catheter into peritoneal cavity
 Exchanges 4 - 5 times per day
 Treatment 24 hours; 7 days a week
 Solution remains in peritoneal cavity except
during drain time
 Independent treatment

75.  Fill: fluid infused into peritoneal cavity
 Dwell: time fluid remains in peritoneal cavity
 Drain: time fluid drains from peritoneal
cavity

76.  Infection
peritonitis
tunnel infections
catheter exit site
 Hypervolemia
hypertension
pulmonary edema
 Hypovolemia
hypotension
 Hyperglycemia
 Malnutrition

77.  Obesity
 Hypokalemia
 Hernia
 Cuff erosion

78.  Independence for patient
 No needle sticks
 Better blood pressure control
 Some diabetics add insulin to solution
 Fewer dietary restrictions
 protein loses in dialysate
 generally need increased potassium
 less fluid restrictions

81.  Vitamins - water soluble
 Phosphate binder - (Phoslo, Renagel,
Calcium, Aluminum hydroxide) Give with
meals
 Iron Supplements - don’t give with phosphate
binder or calcium
 Antihypertensives - hold prior to dialysis

82.  Erythropoietin
 Calcium Supplements - Between meals, not
with iron
 Activated Vitamin D3 - aids in calcium
absorption
 Antibiotics - hold dose prior to dialysis if it
dialyzes out

83.  Many drugs or their metabolites are excreted
by the kidney
 Dosages - many change when used in renal
failure patients
 Dialyzability - many removed by dialysis
varies between HD and PD

84.  Alleviate fear
 Dialysis process
 Fistula/catheter care
 Diet and fluid restrictions
 Medication
 Diabetic teaching

88.  Restoration of “normal” renal function
 Freedom from dialysis
 Return to “normal” life

89.  Life long medications
 Multiple side effects from medication
 Increased risk of tumor
 Increased risk of infection
 Major surgery

90.  Major surgery with general anesthesia
 Assessment of renal function
 Assessment of fluid and electrolyte balance
 Prevention of infection
 Prevention and management of rejection

91.  ATN? (acute tubular necrosis)
 50% experience
 Urine output >100 <500 cc/hr
 BUN, creatinine, creatinine clearance
 Fluid Balance
 Ultrasound
 Renal scans
 Renal biopsy

92.  Accurate I & O
CRITICAL TO AVOID DEHYDRATION
Output normal - >100 <500 cc/hr, could be
1-2 L/hr
Potential for volume overload/deficit
 Daily weights
 Hyper/Hypokalemia potential
 Hyponatremia
 Hyperglycemia

93.  Major complication of transplantation due to
immunosuppression
 HANDWASHING
 Crowds, Kids
 Patient Education

94.  Hyperacute - preformed antibodies to donor
antigen
 function ceases within 24 hours
 Rx = removal
 Accelerated - same as hyperacute but
slower, 1st week to month
 Rx = removal

95.  Acute - generally after 1st 10 days to end of
2nd month
 50% experience
 must differentiate between rejection and
cyclosporine toxicity
 Rx = steroids, monoclonal (OKT3), or polyclonal
(HTG) antibodies

96.  Chronic - gradual process of graft dysfunction
 Repeated rejection episodes that have not been
completely resolved with treatment
 Rx = return to dialysis or re-transplantation

97.  Prednisone
 Prevents infiltration of T lymphocytes
 Side effects
 cushnoid changes
 Avascular Necrosis
 GI disturbances
 Diabetes
 infection
 risk of tumor

98.  Azathioprine (Imuran)
 Prevents rapid growing lymphocytes
 Side Effects
 bone marrow toxicity
 hepatotoxicity
 hair loss
 infection
 risk of tumor

99.  Cyclosporin
 Interferes with production of interleukin 2 which
is necessary for growth and activation of T
lymphocytes.
• Side Effects
– Nephrotoxicity
– HTN
– Hepatotoxicity
– Gingival hyperplasia
– Infection

100.  Cytoxan - in place of Imuran less toxic
 FK506 - 100 x more potent than Cyclosporin
 Prograf
 Cellcept

101.  OKT3 - monoclonal antibody used to treat
rejection or induce immunosuppression
decreases CD3 cells within 1 hour
 Side effects
anaphylaxis
fever/chills
pulmonary edema
risk of infection
tumors
 1st dose reaction expected & wanted, pre-treat
with Benadryl, Tylenol, Solumedrol

102.  Atgam - polyclonal antibody used to treat
rejection or induce immunosuppression
decreased number of T lymphocytes
 Side effects
anaphylaxis
fever chills
leukopenia
thrombocytopenia
risk of infection
tumor

103.  Signs of infection
 Prevention of infection
 Signs of rejection
 decreased urine output
 increased weight gain
 tenderness over kidney
 fever > 100 degrees F
 Medications
 time, dose, side effects

104. Indication Drug
 Magnesium content Antacids (Maalox, milk of
magnesia)
Laxatives
 Potassium content IV fluids
Salt substitutes
Massive penicillin therapy (1.7
mEq/million U)
 Sodium content Carbenicillin (4.7 mEq/g)
Alka Seltzer (23 mEq tablet)
IV fluid
 Acidifying effects Ascorbic acid
Ammonium chloride (in cough syrup)
Nonsteroidal anti-inflammatory
agents

105.  Catabolic effects
Tetracyclines
Steroids
 Nephrotoxicity Phenacetin
Ketorolac
Cephalosporins*
 Alkalosis effect Absorbed
antacids
Carbenicillin
(large doses
Penicillin
(large doses

106.  Before treatment
 Determine dialysis schedule and treat on day after dialysis.
 Consult with patient’s nephrologist for recent laboratory tests and discussion
 of antibiotic prophylaxis.
 Identify arm with vascular access and type; notate in chart and avoid taking
 blood pressure measurement/injection of medication on this arm.
 Evaluate patient for hypertension/hypotension.
 Institute preoperative hemostatic aids (DDAVP, conjugated estrogen) when
 appropriate.
 Determine underlying cause of renal failure (underlying disease may affect
 provision of care).
 Obtain routine annual dental radiographs to establish presence and follow
 manifestations of renal osteodystrophy.
 Consider routine serology for HBV, HCV, and HIV antibody.
 Consider antibiotic prophylaxis when appropriate.
 Consider sedative premedication for patients with hypertension

107.  During treatment
 Perform a thorough history and physical examination for
presence of oral
 manifestations.
 Aggressively eliminate potential sources of infection/bacteremia.
 Use adjunctive hemostatic aids during oral/periodontal surgical
procedures.
 Maintain patient in a comfortable uncramped position in the
dental chair.
 Allow patient to walk or stand intermittently during long
procedures

108.  After treatment
 Use postsurgical hemostatic agents.
 Encourage meticulous home care.
 Institute therapy for xerostomia when appropriate.
 Consider use of postoperative antibiotics for traumatic
procedures.
 Avoid use of respiratory-depressant drugs in presence of severe
anemia.
 Adjust dosages of postoperative medications according to extent
of
 renal failure.
 Ensure routine recall maintenance.

111. Recurrent herpes labialis in an
immunocompromised patient
Recurrent herpes labialis

112. Recurrent intraoral herpes in a
cardiac transplant recipient.
Chronic herpes simplex in a chronically
immunosuppressed transplant recipient

113. Pseudomembranous candidiasis
Hyperplastic candidiasis in a kidney transplant
recipient. This infection did not respond to
fluconazole

114. Graft-versus-host disease in a patient who had undergone
HCT. Note the clinical resemblance to erosive lichen planus

115.  Pre-transplantation considerations
 Significantly ill patient with end-organ damage
 Medical consultation required
 Consider postponing elective treatment
 Dental consultation prior to anticipated transplant:
 Rule out dental infectious sources, definitively
 Perform necessary treatment; this will require consultation with
transplantation
 physician to determine medical risk-to-benefit ratio
 Obtain laboratory information/supplemental information as
needed
 Become acquainted with specific management issues (eg, blood
products,
 prophylactic antibiotics) that may need to be employed if
treatment is rendered.

116.  Post-transplantation considerations
Immediate post-transplantation period
 No elective dental treatment performed
 Emergency treatment only with medical consultation and consideration of
 specific management needs
Stable post-transplantation period
 Elective treatment may be performed after medical consultation with the
 transplantation physician
 Issues of immunosuppression must be recognized
 Oral mucosal disease must be diagnosed and treated
 Supplemental corticosteroids (steroid boost) may be necessary
 Consideration of antibiotic prophylaxis needed
 Consideration of specific management needs
Post-transplantation chronic rejection period
 Only emergency treatment
 Patients are very ill as they are immunosuppressed and have organ failure

117.  Thank you.