Chronic Kidney Disease

Tammy Harris, MPAS, PA-C

BCPAS Fall CME

November 1, 2019

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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

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

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%

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

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

Evaluation of Renal Disease

Imaging – Ultrasound, CT, MRI, Angiogram

Renal Biopsy

• Unexplained AKI, CKD, hematuria, proteinuria

• Acute nephritis syndromes• Guide treatments

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

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

CKD –Risk Factors

Modifiable:

HTN

Medications

Proteinuria

Smoking

Salt intake

Obesity

CKD –Risk Factors

Nonmodifiable:

Age

Gender

H/O pre-eclampsia

Ethnicity (AA)

FHx (renal, DM, CVS)

Type of renal disease

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

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)

CKD - Staging

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

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)

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

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

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

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

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

CKD –Complications and Treatments

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)

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

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

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

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

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

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