SOAP – Chronic Kidney Disease

Chronic Kidney Disease

Adult-Gerontology Acute Care Practice Guidelines

Definition

A.Reduction of kidney function: An estimated glomerular filtration rate (GFR) less than 60 mL/min/1.73 m² for greater than 3 months.

OR

B.Evidence of kidney damage, including persistent albuminuria—defined as greater than 30 mg of urine albumin per gram of urine creatinine for greater than 3 months.

1.Anatomical abnormalities including, but not limited to, polycystic kidneys, kidney transplant, and genetic abnormalities.

2.Chronic kidney disease (CKD) versus acute kidney injury (AKI). A 3-month time frame is used to distinguish CKD from AKI.

C.Classification.

1.CKD stages are defined by a presence of albuminuria and the GFR (see Table 5.1).

2.The GFR requires age, race, gender, and serum creatinine for calculation.

TABLE 5.1 Stages of CKD

Notes: ACR, albumin-to-creatinine ratio; CKD, chronic kidney disease; ESRD, end-stage renal disease; GFR, glomerular filtration rate.

Incidence

A.It is estimated that approximately 14.8% of the adults in the United States have CKD.

B.Approximately 96% of those with mild to moderate reduced kidney function are unaware that they have CKD.

C.Approximately 48% of those with severely reduced kidney function are unaware that they have CKD.

D.Approximately 661,000 individuals in the United States have end-stage renal disease (ESRD); of these, 468,000 are on dialysis and 193,000 have a functioning kidney transplant.

Pathogenesis

A.Initial kidney injury or insult leads to the loss of functioning nephrons (nephron loss).

B.Hyperfiltration of the remaining intact nephrons occurs (glomerular hypertrophy).

C.Initial beneficial, adaptive response leads to ongoing damage (interstitial inflammation, fibrosis, and endothelial/vascular injury).

D.This injury eventually leads to further nephron loss (disease progression).

Predisposing Factors

A.General risk factors.

1.Diabetes mellitus.

2.Hypertension.

3.Cardiovascular disease (CVD).

4.History of kidney disease.

5.Family history of CKD.

6.Race/ethnicity.

a.African Americans.

b.Hispanics.

c.Native Americans.

d.Asians.

7.AKI.

8.Older age.

9.Smoking.

10.Exposure to nephrotoxins.

11.Obesity.

B.Risk factors for progression of CKD to next stage.

1.Male gender.

2.African American race.

3.Diabetes mellitus.

4.Hypertension.

5.Proteinuria.

6.Prior trajectory of kidney function.

Subjective Data

A.Common complaints/symptoms.

1.Often silent.

2.Lethargy due to low hemoglobin.

3.Metallic taste due to uremia.

4.Increased incidence of confusion with uremia.

5.Edema.

B.Medication history.

1.Medication review.

a.Prescription drugs.

b.Over-the-counter drugs.

c.Herbal supplements.

2.Medication-associated risk.

a.Clearance by kidney.

b.Narrow therapeutic window.

c.High risk in older population.

d.Potential central nervous system (CNS) effects.

e.Drug dosing data availability.

C.Review of systems.

1.Constitutional: Change in activity, appetite changes.

2.Head, ear, eyes, nose, and throat (HEENT): Changes in vision, facial swelling, nosebleeds.

3.Cardiovascular: Any pain in chest.

4.Respiratory: Difficulty breathing.

5.Gastrointestinal: Nausea or vomiting, hiccups, blood in stool.

6.Genitourinary: Difficulty urinating or pain on urination.

7.Musculoskeletal: Back pain, muscle cramps.

8.Neurological: Dizziness or balance problems.

9.Integumentary: Dry skin, itching, or rash.

10.Psychiatric: Confusion or difficulty concentrating, sleep disturbance.

11.Endocrine: Cold intolerance.

12.Hematologic: Bruising easily.

Physical Examination

A.Vital signs, including orthostatic signs.

B.Constitutional.

C.Eyes: Funduscopic examination.

1.Look for retinopathy secondary to diabetes mellitus.

D.Cardiovascular: Palpitations, dysrhythmia, tachycardia, heart sounds (S3 and S4, murmurs, rubs), distal pulses, lower extremity edema, carotid bruit, jugular venous distension (JVD).

E.Pulmonary: Breath sounds, effort (use of accessory muscles), wheezing.

F.Abdominal: Abdominal palpation, bowel sounds, dysgeusia, melena.

G.Genitourinary: Dysuria, flank pain, proteinuria, hematuria, oliguria, anuria.

H.Musculoskeletal: Arthralgias, gait disturbances, myalgias.

I.Integumentary/nails: Rash, pruritus, uremia.

J.Confusion, asterixis.

K.Endocrine: Polydipsia, polyphagia, polyuria.

L.Hematologic/lymphatic: Bruising, petechiae, ecchymosis.

Diagnostic Tests

A.Renal function panel.

B.Complete blood count (CBC) with differential.

C.Serum albumin.

D.Fasting lipid panel.

E.Urinalysis.

F.Urine albumin to creatinine ratio (UACR).

G.Urine culture and sensitivity (C & S; if indicated).

H.Renal ultrasound with post void residual.

I.Specialty serologic studies if indicated: Antinuclear antibody (ANA), C3, C4, hepatitis B and C serologies.

J.CKD mineral bone disorder: Calcium, phosphorus, intact parathyroid hormone (PTH), 25(OH) vitamin D.

K.Anemia.

1.Microcytic: Iron studies (iron, total iron-binding capacity [TIBC], ferritin).

2.Macrocytic: Folate and B12 levels.

L.Multiple myeloma/paraprotein.

1.Serum protein electrophoresis (SPEP), urine protein electrophoresis (UPEP).

2.Serum and urine for immunoelectrophoresis.

3.Serum for free light chains.

M.Renal biopsy: Reserved to guide management or when the cause of CKD is unclear.

Differential Diagnosis

A.AKI.

1.Prerenal.

2.Intrinsic.

3.Postrenal.

B.Multiple myeloma.

C.Nephrolithiasis.

D.Diabetic nephropathy.

E.Glomerulonephritis.

Evaluation and Management Plan

A.General plan.

1.Determine CKD stage (see Table 5.2).

a.CKD Stage 1: Manage comorbid conditions and identify CVD risk factors.

b.CKD Stage 2: Monitor CKD progression.

c.CKD Stages 3a and 3b: Treat CKD complications.

d.CKD Stage 4: Refer to nephrology.

e.CKD Stage 5: Start kidney replacement therapy (KRT).

2.Manage complications.

a.Acidosis.

b.Anemia.

c.Hypertension.

d.CKD mineral bone disorder.

e.Dyslipidemia.

f.Diabetic complications: Indications for initiation of dialysis.

i.Hyperkalemia.

ii.Uremic pericarditis.

iii.Refractory metabolic acidosis.

iv.Volume overload.

v.Pulmonary edema.

vi.Uremic encephalopathy.

vii.Refractory hypertension.

viii.Persistent nausea and vomiting.

ix.Blood urea nitrogen (BUN) greater than 100 mg/dL.

B.Patient/family teaching points.

1.Patient-centered educational efforts: A conceptual model.

a.Prevent kidney disease.

i.Awareness of risk.

ii.Knowledge of prevention.

b.Identify kidney disease.

i.Awareness of diagnosis.

ii.Knowledge of health implications.

c.Manage kidney disease.

i.Knowledge of management goals and how to achieve them.

d.Comprehensive conservative care for ESRD.

i.Knowledge of treatments, risks, benefits, and management goals.

2.Dietary modifications.

a.Sodium intake: Less than 2 g/day.

b.Potassium intake: 2 g/day.

c.Protein intake.

i.Avoid high protein intake.

ii.Lower protein intake to 0.8 g/kg/day in adults with diabetes or without diabetes and a GFR less than 30 mL/min/ 1.73 m².

d.Phosphorus intake: 800 to 1,000 mg/day.

e.Diabetes dietary guidelines: Target hemoglobin A1c (HbA1c) of ∼7.0%.

f.Target HbA1c can be extended above 7.0% (53 mmol/mol) in individuals with comorbidities or limited life expectancy and risk of hypoglycemia.

g.Hyperlipidemia dietary modifications.

i.Decrease intake of saturated and trans fat foods.

ii.Substitute with monounsaturated fats and moderate intake of polyunsaturated fats.

C.Pharmacotherapy: Targeted at preventing complications.

1.Acidosis: Maintenance of carbon dioxide/bicarbonate level with sodium citrate tablets.

2.Anemia: Performance of iron studies to determine iron supplementation plan.

a.Ferrous sulfate tablets.

b.Folic acid replacement tablets.

c.Cobalamin for vitamin B12 replacement/supplementation.

d.Erythropoiesis stimulating agents (not recommended in patients with active malignancy or recent history of malignancy).

3.Hypertension: CKD with or without diabetes: Use an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB).

a.Obtain a baseline serum creatinine and serum potassium and follow.

b.Recheck those levels 1 week after starting or increasing dose to avoid further decreases in GFR and/or hyperkalemia.

4.CKD mineral bone disorder: Follow common minerals and replace as needed.

a.Phosphate binders: Example of calcium-based binders is calcium acetate.

b.Vitamin D replacement.

c.Bisphosphonates (avoid in CKD with GFR less than 30 mL/min/1.73 m²).

5.Dyslipidemia: Lipid lowering agent.

6.Diabetic complications: Keep HbA1c ∼7%.

7.Malnutrition: High biologic value protein intake.

8.Proteinuria: ACE inhibitor/ARB or non dihydropyridine calcium channel blocker.

Follow-Up

A.Follow-up in CKD is important to mitigate progression of disease and to manage risk factors that may contribute to worsening of the patient’s clinical health.

B.A nephrologist should be consulted if there is an increase in urine protein or abrupt decline in GFR.

C.Regular visits with a primary provider are essential for long-term health maintenance.

Consultation/Referral

A.Consult nephrology in the acute care setting for patients with the following.

1.An estimated GFR less than 30 mL/min/1.73 m².

2.Significant albuminuria or overt proteinuria.

3.An abrupt decrease in estimated GFR/acute rise in serum creatinine.

4.Evidence of worsening kidney function/CKD progression.

5.Persistent hematuria.

6.Resistant hypertension.

Special/Geriatric Considerations

A.The incidence of cardiovascular death increases with each stage of CKD. Individuals are more likely to die than to reach the next stage of CKD. In addition, the incidence of death related to cardiovascular procedures increases with CKD stage.

B.The incidence of hospitalization increases with CKD stage, although in the past 10 years, the number of hospitalizations has decreased.

C.It is important to identify CKD in hospitalized patients because it is an important prognostic factor for increased risk of in-hospital AKI.

D.The incidence of CKD and AKI increase with age.

1.Polypharmacy is more common in the elderly. It is important to review medications regularly to identify medications that are actual or potential nephrotoxins that require dose or schedule changes, as these should be avoided.

E.Older individuals have an increased prevalence of decreased estimated GFR and increased ACR.

1.There is a debate concerning whether decreased GFR or increased urine albumin-to-creatinine ratio in older individuals represents disease or normal aging.

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