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–Nephrotic: proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia, and edema

Minimal change disease, membranous nephropathy, focal segmental

glomerulosclerosis

Amyloidosis, diabetic nephropathy

Vascular: HTN, thrombotic microangiopathies, vasculitis (Wegener), scleroderma

Interstitial-tubular: infections, obstruction, toxins, allergic interstitial nephritis, multiple myeloma, connective tissue disease, cystic disease

Postrenal: obstruction (benign prostatic hyperplasia), neoplasm, neurogenic bladder

Genetics

Alport syndrome, Fabry disease, sickle cell anemia, SLE, and autosomal dominant polycystic kidney disease can lead to CKD.

Polymorphisms in gene that encodes for podocyte nonmuscle myosin IIAare more common in African Americans than Caucasians and appear to increase risk for nondiabetic ESRD.

RISK FACTORS

Type 1 or 2 diabetes mellitus (DM); most common

Age >60 years

Cardiovascular disease (e.g., HTN [common], renal artery stenosis, atheroemboli)

Previous kidney transplant

Urinary tract obstruction (e.g., BPH)

Autoimmune disease, vasculitis/connective tissue disorder

Family history of CKD

Nephrotoxic drugs (lithium, salicylate, high-dose or chronic NSAIDs, sulfonamide)

Congenital anomalies, obstructive uropathy, renal aplasia/hypoplasia/dysplasia, reflux nephropathy

Hyperlipidemia

Low income/education/ethnic minority status

Obesity/smoking/heroin use

Chronic infection (hepatitis B, hepatitis C, HIV)

GENERALPREVENTION

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Treat reversible causes: hypovolemia, infections, diuretics, drugs (NSAIDs, aminoglycosides, IV contrast).

Treat risk factors: DM, HTN, hyperlipidemia, smoking, and obesity; adjust medication doses to prevent renal toxicity.

COMMONLYASSOCIATED CONDITIONS

HTN, DM, cardiovascular disease

DIAGNOSIS

HISTORY

Patients with CKD stages 1 to 3 are usually asymptomatic; can present with

Oliguria, nocturia, polyuria, hematuria, change in urinary frequency

Bone disease

Edema, HTN, dyspnea

Fatigue, depression, weakness

Pruritus, ecchymosis

Metallic taste in mouth, anorexia, nausea, vomiting

Hyperlipidemia, claudication, restless legs

Erectile dysfunction, decrease libido, amenorrhea

PHYSICALEXAM

Volume status (pallor, BP/orthostatic; edema; jugular venous distention; weight)

Skin: sallow complexion, uremic frost

Ammonia-like odor (uremic fetor)

Cardiovascular: Assess for murmurs, bruits, pericarditis.

Chest: pleural effusion

Rectal: enlarged prostate

CNS: asterixis, confusion, seizures, coma, peripheral neuropathy

DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (lab, imaging)

GFR can be estimated using the Modification of Diet in Renal Disease (MDRD) and Chronic Kidney Disease-Epidemiology Collaboration (CKDEPI) equations. Arecent meta-analysis found the MDRD has greater accuracy

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at GFR 60, whereas the CKD-EPI is more accurate at GFR >60 (1)[A].

Cr clearance (CrCl) can be calculated using Cockcroft-Gault formula to determine medication adjustments.

Urine analysis to assess for evidence of damage

–Urine microscopy: WBC casts in pyelonephritis, RBC casts in glomerulonephritis/vasculitis

–Urine electrolytes: sodium, Cr, urea (if on loop diuretics)

–Albuminuria is more sensitive than proteinuria at detecting disease (2)[B]. Meta-analyses link CVD mortality with albuminuria (2)[A].

Report as a ratio of albumin concentration to Cr concentration (mg/mmol

or mg/g)

Ultrasound (initial imaging test of choice): small, echogenic kidneys; may see obstruction (e.g., hydronephrosis); cysts; kidneys may be enlarged with HIV and diabetic nephropathy.

Doppler ultrasound to assess for renovascular disease, thrombosis

Noncontrast CT scan: obstruction, calculi, cysts, neoplasm, renal artery stenosis

MRI/MRA: Avoid gadolinium because of the risk of nephrogenic systemic fibrosis.

Renal arteriogram for renal artery stenosis can be therapeutic (angioplasty or stenting).

Renal scan to screen for differential function between kidneys

Retrograde pyelogram: if strong suspicion for obstruction despite negative finding on ultrasound

Follow-Up Tests & Special Considerations

Additional evaluation may be indicated to assess for complications or cause, as clinically indicated:

Hematology: normochromic, normocytic anemia; increased bleeding time

Chemistry: elevated BUN, Cr, hyperkalemia, metabolic acidosis, increased PTH, HLD, hyperphosphatemia, decreased 25-(OH) vitamin D, hypocalcemia, decreased albumin

Serology: antinuclear antibody (ANA); double-stranded DNA, antineutrophil cytoplasmic antibody; complements (C3, C4, CH50); anti-glomerular basement membrane (GBM) antibodies; hepatitis B, C; and HIV screening

Serum and urine immunoelectrophoresis

Follow-Up Tests and Special Considerations

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Monitoring the parameters with frequency based on GFR and risk of progression:

–Urine albumin and GFR at least annually

–Hb: clinically indicated for GFR ≥60, annually for 30 to 59, twice per year for <30 (3)[B]

–Calcium, phosphate, PTH, alkaline phosphate actively beginning at CKD Stage G3a (4)[C]

–25(OH)D (calcidiol) levels with repeated testing determined by baseline values and therapeutic interventions (4)[C]

Therapeutic decisions should be based on trends rather than on a single laboratory value, taking into account all available CKD-MBD assessments (4) [C].

ALERT

Drugs that may alter lab result:

Cimetidine: inhibits Cr tubular secretion

Trimethoprim: inhibits Cr and K+ secretion and may cause/worsen hyperkalemia

Cefoxitin and flucytosine: increases serum Cr

Diltiazem and verapamil (like ACE/ARBs) have significant antiproteinuric effects in patients with CKD.

Diagnostic Procedures/Other

Biopsy: hematuria, proteinuria, acute/progressive renal failure, nephritic or nephrotic syndrome

TREATMENT

GENERALMEASURES

Lowering salt intake to <2 g/day of sodium in adults, unless contraindicated (5)[C]

Minimize radiocontrast exposure; prehydrate; N-acetylcysteine use is controversial. Avoid nephrotoxins (NSAIDs, aminoglycosides, etc.).

Encourage smoking cessation, encourage weight loss (if applicable), and limit alcohol consumption (5)[C].

Protein restriction to 0.8 g/kg/day is recommended in CKD G4 to G5 (2)[B]. CKD at risk of progression should avoid dietary protein >1.3 g/kg/day to

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avoid accelerating progression (2)[B].

MEDICATION

HTN: Goal in adults is BP<130/80 mm Hg if urine albumin excretion is ≥30 mg/24 hr and <140/90 mm Hg if urine albumin excretion is <30 mg/24 hr. Goal in children is <90th percentile for age, sex, weight (5)[B].

–ACE-I or ARB recommended for diabetic and nondiabetic adults with albumin excretion >30 mg/24 hr based on evidence of reductions in proteinuria, improved CVD outcomes, and decreased progression of CKD (5)[A]. Monitor potassium and serum Cr (tolerate up to 30% rise unless hyperkalemia develops).

–Additional antihypertensive agents should be selected based on the type of

CKD and comorbid factors.

Secondary hyperparathyroidism

–For GFR <45, monitor for hyperphosphatemia, hypocalcemia, and vitamin D deficiency if intact PTH is elevated beyond lab normals (2)[C].

–Cinacalcet, paricalcitol (decrease PTH levels)

Hyperphosphatemia: Maintain phosphate according to reference lab normals (2)[C]. Recommended serum phosphate maintenance levels for CKD patients:

–Stages 3 to 5 CKD (not on dialysis): Restrict dietary phosphate to 800 to 1,000 mg/day.

Calcium-containing phosphate binders (with meals): calcium carbonate, calcium acetate (risk of hypercalcemia)

Noncalcium phosphate binders (with meals): sevelamer, lanthanum

Vitamin D: inactive vitamin D 25 (ergocalciferol or cholecalciferol), calcitriol (active vitamin D 1,25 [OH]): Vitamin D may increase absorption of phosphate by intestines and should not be started until serum phosphate concentration is controlled.

Anemia: Hb <13 g/dL in adult males or <12 g/dLin adult females. Treat with iron replacement therapy with or without erythropoietin-stimulating agents (ESAs) (3)[B]. Consider ESAif Hb >9 g/dL and <10 g/dL. ESAinitiation not recommended for Hb >10 g/dL. If using ESA, goal Hb range 10 to 11 g/dL, not to exceed 11.5 g/dL(3)[B].

Hyperlipidemia: Statins with low-density lipoprotein (LDL) goal is similar to coronary heart disease patients (LDL<70 to 100).

Glycemic control: Target for HbA1c should be adjusted based on risk of hypoglycemia, comorbid conditions, and life expectancy (2)[B]. HbA1c may be falsely low in patients with decreased RBC; glucose logs may be more

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accurate reflection of glycemic control (2)[C]. Metformin use should be reconsidered for GFR between 30 and 44 and discontinued if GFR <30

mL/min/1.73 m2 (2)[C].

Metabolic acidosis: Start treatment when bicarbonate <22 mEq/L with goal to maintain in normal range (2)[C].

ISSUES FOR REFERRAL

Nephrology consult: GFR <15: immediate

GFR 15 to 29: urgent

GFR 30 to 59: nonurgent referral

GFR 60 to 89: not required unless with comorbidities

Renal replacement: Prepare for dialysis or transplant when GFR <30 mL/min/1.73 m2.

SURGERY/OTHER PROCEDURES

Placement of dialysis access or transplantation

ADMISSION, INPATIENT, AND NURSING CONSIDERATIONS

Uremia: nausea/vomiting, fluid overload, pericarditis, uremic encephalopathy, resistant HTN, hyperkalemia, metabolic acidosis, hyperphosphatemia

ONGOING CARE

DIET

Nutrition consult for CKD diet (2)[C]

PATIENT EDUCATION

Annual influenza vaccine unless contraindicated (2)

Polyvalent pneumococcal vaccine if GFR <30 mL/min/1.73m2 and those at high risk of pneumococcal infection (2)

Hepatitis B vaccine with serologic confirmation if high risk of CKD progression and GFR <30 mL/min/1.73 m2 (2)

PATIENT EDUCATION

National Kidney Federation patient Web site at: http://www.kidney.org/patients

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PROGNOSIS

Risk of progression and complications is based on cause, GFR category, albuminuria category, and comorbid conditions (2)[B]. Progression defined as decline in GFR category with 25% decrease in GFR from baseline (2). Rapid

progression is decrease in GFR by >5 mL/min/1.73 m2/year (2). Patients with CKD gradually progress to ESRD, with bad prognoses. 5-year survival rate for U.S. patients on dialysis is ~35%.

COMPLICATIONS

HTN, anemia, secondary hyperparathyroidism, renal osteodystrophy, sleep disturbances, infections, malnutrition, electrolyte imbalances, platelet dysfunction/bleeding, pseudogout, gout, metabolic calcification, sexual dysfunction

REFERENCES

1.Earley A, Miskulin D, Lamb EJ, et al. Estimating equations for glomerular filtration rate in the era of creatinine standardization: a systematic review. Ann Int Med. 2012;156(11):785–795.

2.Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl. 2013;3(1):1–150.

3.Kidney Disease: Improving Global Outcomes (KDIGO) Anemia Work Group. KDIGO clinical practice guideline for anemia in chronic kidney disease. Kidney Int Suppl. 2012;2(4):279–335.

4.Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work Group. KDIGO 2017 clinical practice guideline update for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD–MBD). Kidney Int Suppl. 2017;7(1):1–59.

5.Kidney Disease: Improving Global Outcomes (KDIGO) Blood Pressure Work Group. KDIGO clinical practice guideline for the management of blood pressure in chronic kidney disease. Kidney Int Suppl. 2012;2(5):337–414.

SEE ALSO

Hydronephrosis; Nephrotic Syndrome; Polycystic Kidney Disease; Proteinuria Algorithm: Anuria or Oliguria

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CODES

ICD10

CLINICALPEARLS

CKD is defined based on >3 months of kidney functional or structural abnormalities and classified based on GFR and albuminuria.

ACE-I and ARB are first line for HTN treatment in CKD with albuminuria.

Care should be taken in prescribing medication in CKD due to reduced renal clearance of certain medications.

Consider nonurgent nephrologist referral for GFR ≤59 and urgent nephrologist referral for GFR ≤29.

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND EMPHYSEMA

Alan Cropp, MD, FCCP Michael A. Apostolis, MD

BASICS

DESCRIPTION

Chronic obstructive pulmonary disease (COPD) usually describes a mixture of chronic bronchitis and emphysema. It is characterized by airflow limitation that is not fully reversible, inflammation, and is progressive (1,2).

Chronic bronchitis is defined clinically by increased mucus production and recurrent cough present on most days for at least 3 months per year during at least two consecutive years without another cause.

Emphysema, the destruction of interalveolar septa, occurs in the distal or terminal airways and involves both airways and lung parenchyma.

EPIDEMIOLOGY

Incidence

Affects >5% of adults in the United States and is the 12th leading cause of morbidity (1)

Prevalence

Third leading cause of death in the United States (1)

Projected to be the third leading cause of death globally by 2020 (2); 3.2 million deaths worldwide (2)

ETIOLOGYAND PATHOPHYSIOLOGY

Cigarette and/or cannabis smoking, air pollution (including indoor), antiprotease deficiency (α1-antitrypsin), occupational exposure (firefighters), infection (viral),

occupational pollutants (cadmium, silica)

Impaired gas (carbon dioxide and oxygen) exchange

Chronic bronchitis: airway obstruction (3) Emphysema: destruction of lung parenchyma

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Genetics

Chronic bronchitis is not a genetic disorder.

Antiprotease deficiency (due to α1-antitrypsin deficiency) is an inherited, rare disorder due to two autosomal codominant alleles.

RISK FACTORS

Smoking: passive smoking, especially adults whose parents smoked; cannabis use (one joint is equivalent to 2.5 to 5 cigarettes) (1–3)

Severe pneumonia early in life including viral (4)

Aging

Lower level of education and poverty (4)

Airway hyperactivity

Indoor pollution (open fire for cooking or heating) (4)

Occupational organic or inorganic dusts (4)

GENERALPREVENTION

Avoidance of smoking is the most important preventive measure.

Early detection through pulmonary function tests (PFTs) in high-risk patients may be useful in preserving remaining lung function.

COMMONLYASSOCIATED CONDITIONS

Pulmonary: lung cancer, chronic respiratory failure, acute bronchitis, sleep apnea, pulmonary hypertension (HTN), asthma

Cardiac: coronary artery disease, arrhythmia

Ear/nose/throat (ENT): chronic sinusitis, laryngeal carcinoma Miscellaneous: malnutrition, osteoporosis, muscle dysfunction, depression

DIAGNOSIS

HISTORY

Discuss patient’s use of tobacco and cannabis.

Consider indoor pollution (coal furnace) (4).

Review possible causes of exacerbation (e.g., recent infection) and history of cough, sputum, dyspnea.

Chronic bronchitis: cough, sputum production, frequent infections, intermittent dyspnea, wheeze, hemoptysis, morning headache, pedal edema Emphysema: minimal cough, scant sputum, dyspnea, weight loss, occasional

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