Chronic Kidney Disease and Dialysis

Kidney Functions

• Regulate fluid volume and acid-base balance → ultrafiltrate produced at 125ml/ min

• Excrete nitrogenous waste

• Synthesize Erythropoietin (to produce RBCs) and 1,25-dihydroxycholecalciferol (active vit D) and renin

• Metabolizes drugs

• Target organ for parathormone and aldosterone

Chronic Kidney Disease (CKD)

• Define

• Stages

• Define: Progressive loss of kidney function that persists for more or equal to 3 months → from direct damage to nephrons

• Stage Classifications:

  • Stage 1: Normal or slightly decreased GFR associated with some kidney damage

  • Stage 2: Mildly decreased GFR

  • Stage 3: Moderately decreased GF to 50% of normal renal function\

  • Stage 4: Severely decreased GFR

  • Stage 5: Renal failure; More than 75% of renal function loss

What problems develop due to Renal failure

• Azotemia: due to buildup of nitrogen compounds such as urea → not detectable yet

  • Use BUN test to detect

• Uremia: urea in blood due to inability of kidneys to concentrate and filter sodium → decreased urine output, fluid overload

  • Hypertension due to urine output drop and NaCl retention

    • Hyperlipidemia, atherosclerosis and arterial hypertension, congestive heart failure

• Insulin resistance

• Metabolic Acidosis → sepsis

• Hematologic abnormalities: anemia, leukocyte dysfunction and platelet dysfunction and coagulopathy

• Impaired immunity

• Renal osteodystrophy → no vit D synthesized → causes reduced intestinal absorption of calcium → leads to low serum calcium and increased serum phosphate → PTH increases

  • Secondary parathyroidism → decreased osteoblast activity and increased bone remodeling→ osteomalacia, osteitis fibrosa, osteosclerosis

What are the primary etiologic diseases that can cause CKF?

1. Diabetes

2. Hypertension

3. Chronic glomerulonephritis

4. Polycystic kidney disease

Pathophysiology of CKD

1. Various diseases can affect different segments of the nephron but eventually the entire nephron is lost and cannot be replaced

2. Early renal failure is usually asymptomatic due to compensatory hypertrophy of remaining nephrons

• There might be underlying azotemia

• Sodium pump loses effectiveness and sodium is excrete, polyuria occurs

3. As disease progresses, the compensatory mechanisms become overwhelmed, then signs and symptoms such as uremia appear

Clinical presentation

Few until Stage 3

• Malaise, fatigue, headaches, nausea, loss of appetite and weight loss

• Further progression →

  • Leg cramps, insomnia, nocturia, anemia (lethargy and dizziness)

  • Skin:

    • Hyperpigmentation (brown-yellow) due to retention of carotene-like pigments normally excreted by the kidney

    • Whitish coating on skin of trunk and arms is urea crystals left when perspiration evaporates→ “uremic frost”

      

  • Bone pain

  • Gastrointestinal: anorexia, nausea, vomiting, generalized gastroenteritis, peptic ulcer disease, malnutrition and diarrhea (from uremic syndrome)

  • Neurologic: mental slowness, depression, psychosis, peripheral neuropathy, muscular hyperactivity

  • Hemorrhagic episodes: occult GI bleeding, mucous membrane bleeding, skin manifestations, skin ecchymoses/petechiae, purpura

  • CV manifestations: congestive heart failure, hypertension, pericarditis

CKD Laboratory tests

• GFR: Overall kidney function

  • Not detected until 20mL /minute

• Urinalysis

  • Special emphasis on specific gravity

  • Principal marker of kidney damage is persistent protein in urine

• BUN: Not as specific as creatinine clearance or serum creatinine level

  • Not detected until over 20mg/dL

• Serum creatinine: Measure of muscle breakdown & filtration capacity of nephrons

• Creatinine clearance: Proportional to the glomerular filtration and tubular excretion rates in a 24-hour urine collection

  • Not detected until 20mL/min

• Serum electrolytes involved in acid-base regulation

• Protein electrophoresis

Medical management for each Stage of CKD

• Stage 1&2:

  • Decrease retention of nitrogenous waste

    • Low-protein diet

  • Control fluid and electrolyte imbalances

  • Maintain fluid, sodium and potassium intake

  • Correct and control comorbid conditions such as diabetes, htn, chf and hyperparathyroidism

    • Adjust drug dosage: increase if drug does not bind strongly to protein (may be cleared by hemodialysis), decrease if GFR is below 60 (both antibiotics and analgesics but not anesthetics), single dose diazepines

  • Provide tx day after dialysis or at least 6 hrs after

  • Avoid bp cuff on arm with shunt

  • Avoid narcotics

• Stage 3:

  • Manage anemia, malnutrition, bone disease

• Stage 4

  • Care by nephrologist recommended and begin preparation for renal replacement therapy

• Stage 5

  • Start dialysis and consider if eligible for renal transplant

Dialysis

• Define

• Types: proas and Cons of each

• Define: A medical procedure that artificially filters blood necessary when the number of nephrons diminishes to the point that azotemia is uncontrollable

• Types

  • Peritoneal: hypertonic solution instilled into the peritoneal cavity through a permanent catheter and eventually the solution and urea are drawn out

    • Can be continuous at night or manually 4-5 times a day

    • Pros: low initial cost, ease of performance, reduced disease transmission and no need for anticoagulants

    • Cons: Frequent sessions needed due to lesser effectiveness, risk of peritonitis, common development of abdominal hernias

  

  • Hemodialysis: Method of choice, permanent surgically-created arteriovenous graft or fistula to which patients are plugged into and machine filters blood

  • Pros: only needed every 2-3 days

  • Cons: Heparin anticoagulant needed, still provides only about 15% of normal function → anemia, amyloidosis, improper calcium (m tetany and high PTH);

    • Increased risk of infection (HBV and HCV)

    • Staph aureus infection of fistula that can result in sepsis

    • Risk of antibiotic resistant infections

    • Bleeding tendencies due to anticoagulant and mechanical destruction by machine

Dental management of Patients with CKD 

• General considerations:

  • Monitor bp before and during tx

  • Alterations in drug dosages may be needed

  • May be taking large doses of corticosteroids so ensure they take them before tx to avoid adrenal crises

  • For invasive procedures, screen for bleeding disorders, obtain platelet count, hematocrit and hemoglobin to assess anemia

    • Anticoagulants may be needed: topical thrombin, microfibrillar collagen or systemic agents such as desmopressin

  • Antianxiety agents need little modifications: nitrous oxide and diazepam

  • Intravenous sedation: hematocrit or hemoglobin should be measured to ensure adequate oxygenation

  • CNS depressant drugs such as barbiturates and narcotics should be avoided in pts with uremia due to bbb not being intact and sedation may be excessive

• Stage 3 and below:  can be treated i an outpatient setting, conservative medical care and well controlled disease

• Stage 4 or Higher: consult with physician first

  • Defer tx if uncontrolled disease or comorbidity

  • Consult with physician to assess if they need antibiotics after surgical procedure

CKD Oral manifestations

• Mucosal anemia (oral pallor)

• Red-orange discoloration due to carotene-like pigment deposition

• Salivary flow may be diminished → causing xerostomia and parotid infections

• Candidiasis

  

• Uremic Stomatitis: adherent white plaques on buccal mucosa, tongue, floor of the mouth

  

• Altered pH due to high urea, ammoniac/urine breath odor

• Altered or metallic taste: bleeding tendency in labial, buccal, soft palate, tongue margins and gingival bleeding

• Poor oral hygiene, gingivitis and periodontal disease in pt over stage 3

• Increased incidence of lesions: ulcers, lichen planus, lichenoid-like lesions, hairy tongue, hairy leukoplakia, pyogenic granulomas

• Osseous changes in Triad: loss of lamina dura, demineralized bone (ground glass appearance), localized radiolucent jaw lesions (central giant cell granulomas from secondary hyperthyroidism)

• If ESRD begins at an early age: enamel hypoplasia, tooth erosion from vomiting, red-brown discoloration of enamel, slight delay on eruption, pulp narrowing, caries

CKD Secondary Hyperparathyroidism  Oral manifestations

• Dental abnormalities: widened pulp chamber, developmental defects, eruption alteration, weak teeth, 

• Brown tumor

• Loss of bone density

• Soft tissue calcification