tammy harris, mpas, pa-c...as the end of this presentation, participants will be able to: identify...
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Chronic Kidney Disease
Tammy Harris, MPAS, PA-C
BCPAS Fall CME
November 1, 2019
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This presentation may contain images of clinical patients. In some cases the images have been obtained by direct consent for educational purposes only. In other cases the published material is used from the institution’s academic license with the copyright clearance center. Additional images may be considered fair use from public domain, or have been allowed directly from the publisher. Redistribution of this presentation may not comply with U.S. copyright law and should not be attempted.
DISCLAIMER…
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CKD Objectives
As the end of this presentation, participants will be able to:Be
Identify epidemiology and risk factors associated with chronic kidney diseasesIdentify
Differentiate the etiology and pathogenesis for the acute and chronic kidney injury/diseasesDifferentiate
Recognize the signs, symptoms and complications of the acute and chronic kidney injury/diseases Recognize
Ascertain differential diagnosis and correlate diagnostic tests with the etiology, pathophysiology and signs and symptoms of acute and chronic kidney injury/diseasesAscertain
Determine relevant diagnoses and treatments based on etiology, pathophysiology, physical findings, and diagnostic tests of acute and chronic kidney injury/diseasesDetermine
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CKD - Epidemiology
In 2016, ~753 million people globally
In US, ~ 1/10 people have CKD (16.8% of US)
AA > American Indians > Hispanics > South AsiansAA more likely to develop ESRD
Peak GFR ~120 mL/min per 1.73 m2 (3rd decade)
Gradual decline ~1 mL/min per year70 y/o GFR ~70 mL/min per 1.73 m2Death usually occurs when GFR less
than 5 ml/min
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Evaluation of Renal Disease
Incidental finding or patient is
symptomatic
Characterized by a loss of renal function which can progress
to renal failure/ESRD
Duration Urinalysis
Labs Imaging Biopsy
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Evaluation of Renal DiseaseUrinalysis:
Hematuria – 3 RBC per high-power field twice
• Functional proteinuria – benign• Overload proteinuria – overproduction• Glomerular protein – albumin• Tubular protein – immunoglobulin light chains
Proteinuria (>150 mg/24 hours)
• <1% if urine is being retained by kidney • >2% if urine is being overly excreted
Urine sodium excretion ~1%
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Evaluation of Renal Disease
Urine microscopy:
Sediments/Casts• Bland – early CKD• Urinary casts (Tamm-Horsfall protein in tubules)
• Waxy casts – late in CKD• Hyaline casts – concentrated urine, fever, exercise,
diuretics• RBC casts – GN• WBC casts – Pyelo, interstitial nephritis• Pigmented/muddy brown casts – acute tubular
necrosis (ATN)• Granular casts – ATN
Urine culture - infection
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Evaluation of Renal Disease
Labs:
Blood Urea Nitrogen (BUN): Normal range is 7-30 mg/dL
Creatinine: Normal range 0.7-1.2 mg/dL
Normal BUN/creatinine ratio is 10:1
Creatinine clearance: CC 100 mL/min/1.73 m2 females and 120 for males
Glomerular Filtration Rate (GFR): Normal range for females 90-120 mL/min/1.73 m2 of BSA and 100-130 for males
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Evaluation of Renal Disease
Imaging – Ultrasound, CT, MRI, Angiogram
Renal Biopsy
• Unexplained AKI, CKD, hematuria, proteinuria
• Acute nephritis syndromes• Guide treatments
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Chronic Kidney Disease
Decline of kidney function or kidney damage over three months:
Structural and/or functional abnormalities of the kidney
Destruction of nephrons leads to hypertrophy of remaining nephrons• Decline in GFR• Eventually leads to sclerosis and fibrosis• Proteinuria (albumin-to-creatinine ratio>30mg/g)• Abnormal urine sediment, imaging
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CKD –Pathogenesis
Mechanism of damage:• Acute seen with genetics (PCKD), autoimmune,
inflammatory, infectious, or toxins• Chronic seen with long-term GFR decline due to
medical conditions (DM, HTN)• Loss of nephrons leads to decreased renal function
• Remaining nephrons compensate for loss with hyperplasia and hyperfiltration
• Overuse eventually leads to fibrosis and sclerosis of kidneys
• Continue to lose functioning nephrons until unable to make urine and remove toxins from the body
• Multiple body systems are affected
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CKD –Risk Factors
Modifiable:
HTN
Medications
Proteinuria
Smoking
Salt intake
Obesity
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CKD –Risk Factors
Nonmodifiable:
Age
Gender
H/O pre-eclampsia
Ethnicity (AA)
FHx (renal, DM, CVS)
Type of renal disease
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CKD - Etiology
Diabetic nephropathy #1
Hypertension (cause and complication)
Glomerulonephritis
Autosomal dominant PCKD
Other cystic and tubulointerstitial nephropathies
Obesity
The prevalence is increasing because people are living longer
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CKD - Staging
Based on estimated glomerular filtration rate (eGFR)
Creatinine has to be stable (neither falling or rising)
Measurement of albuminuria (proteinuria)
Use to monitor injury and response to treatment24-hour urine is the Gold StandardAlbumin-to-Creatinine Ratio (ACR) is more practical (spot first-morning urine)
Microalbuminuria – not for staging, but good screening tool for early disease (not with urine dip)
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CKD - Staging
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CKD – Clinical Presentation
Initial symptoms: nonspecific
Asymptomatic, weight loss, pruritus, fatigue, weakness, anorexia, nausea, vomiting, headaches, frequent hiccups
Advance symptoms:
Increase or decrease in urine output, nocturia, easy bruising, anemia, edema (ankles/legs), ascites/anasarca, SOB, DOE,
Late symptoms: Uremic Syndrome*
Uremic fetor (metallic or urine taste), frost (uremic coating), Severe DOE, metabolic acidosis, pulmonary edema, GI bleeding, pericardial/pleuritic CP, polyneuropathy, insomnia, HA, asterixis, restless leg syndrome, AMS, seizures, and coma
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CKD - Diagnosis
History:
HTN, DM, RA, SLE, MM, PTH, PCOS, BPH, FHx of renal disease
Surgeries
Urine abnormalities (foaming), stones, nocturia, sexual dysfunction
Medications (NSAIDS, chemo, abx, laxatives, herbals)
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CKD - Diagnosis
PE:• Vital signs: BP and Orthostatic, pulse, pulse
ox• Gen: complexion• Skin: ecchymosis, epistaxis (PLT dysfxn)• Neuro: stupor, asterixis, myoclonus• Eye: pale conjunctiva; fundoscopic• Cardio: rubs, murmurs, S3, S4 (fluid overload)• Pulm: crackles, dec breath sounds• Abd: palpate kidneys• Ext: edema
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CKD - Diagnosis
PE:
Stage 1-4: ◦ HTN, mild extremity swelling, asymptomatic
Stage 5: ◦ Severe HTN, pallor, skin pigmentation, pruritis, dry skin, metallic
taste, edema, abnormal lung sounds, brown nails, paresthesia
Pre-terminal symptoms:◦ Red eyes, evidence of bleeding (oral and GI), severe tachypnea,
pulmonary edema, abnormal respiratory pattern, myoclonic jerks, asterixis, pericardial and pleuritic rubs, AMS, coma
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CKD - Diagnosis
Labs:
BUN and CRT – elevated; confirms dx (acute or chronic)
GFR – decreased
Abnormal ACR (< 30, 30-300, >300 mg/g)
Magnesium, phosphorus, potassium – elevated
Calcium – decreased
CBC – normocytic, normochromic anemia
Imaging: Classic finding
Renal US – bilateral small kidney or singular small kidney*• Exception: DM
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CKD –Treatment Goals
Preserve renal function
Reduce blood pressure and proteinuria• Uncontrolled SBP most important predictor of
progressive renal loss• Goal < 130/80 (lower if have proteinuria)
High cardiovascular risk!!!• Proteinuria is a marker and promoter of CKD
progression• Treat with ACE inhibitors, ARBs
Must monitor potassium
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CKD –Treatment Goals
Treat reversible causes first:• Infections, obstructions, volume depletion, HTN, CHF
Monitor I/Os
Prevent and/or treat hyperkalemia and hyperphosphatemia
Control HTN and DM
Sodium restriction
Treat hyperlipidemia
Treat anemia
Uremic bleeding
Dialysis for emergencies and ESRD
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CKD –Complications and Treatments
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Cardiovascular
HTN is the most common complication• Treat with ACEi or ARB; must check serum Cr and
K+ • Wt loss, low salt diet, exercise, lipid meds, reduce
alcohol, avoid NSAIDS
CAD and CHF: • Treat with diuretics
• Loop diuretics if GFR < 30; ACE and ARBs; Lifestyle changes
Pericarditis• Treat the cause (NSAIDS, steroids, antibiotics, rare
need for surgery)
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Mineral Bone DisorderControl hyperphosphatemia with phosphate binders:◦ Calcium carbonate or acetate (OTC calcium or Tums) (monitor
calcium levels) ◦ Non-calcium binders:
◦ Sevelamer and lanthanum◦ Aluminum hydroxide good for acute setting only (3 weeks)
◦ Calcitriol (closely monitor Ca+2 and phosporus)◦ Cinacalcet (if calcium or phosphate are elevated)◦ Once phosphate normal, start vitamin D supplements
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AnemiaDecrease erythropoietin production◦ Must assess for other etiologies first◦ Iron stores need to be replenished before starting erythropoietin◦ Treat with erythropoietin or darbepoetin◦ HTN must be controlled (<160/100)
◦ Erythropoietin can raise blood pressure causing HTN encephalopathy
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Hyperkalemia
Can occur earlier due to other medical issues
EKG if potassium > 6.0
Treatment:• Dietary restriction, review meds• Acute > 6.5 with or without EKG changes• Immediate: Insulin, bicarb, albuterol, IV calcium• Urgent: loop diuretic, kayexalate, hemodialysis,
peritoneal dialysis• Monitor potassium levels
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Metabolic Acidosis
Kidneys cannot excrete acid so bicarb is low
Treat with Sodium bicarb or sodium citrate (avoid aluminum-containing antacids)
Maintain serum bicarb at 22
Reduce consumption of animal proteins
If cannot correct or severe, start dialysis
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Uremic Encephalopathy
GFR between 5-10
Mild symptoms: • Neuropathies, RLS
Severe symptoms:• Difficult concentrating, lethargy,
confusion, seizure, and coma• AMS, weakness, and asterixis• Treat with dialysis
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Renal Replacement Therapy (RRT)
RRT includes dialysis or renal transplant
Once ESRD is inevitable, must start planning for RRT
Referral to nephrology in Stage 4, definitely by 5
• Stage 3 if GFR declining rapidly
Need to initiate RRT when GFR declines to 5 to 10 (with or without uremic symptoms)
Patient must be physically and psychologically prepared
Can take 3-6 months of preparation before starting RRT
Team approach:
• Nephrology, dietary, social workers, and PCP
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