Accurate staging of CKD is essential for determining a patient’s prognosis, follow-up recommendations, and referral guidelines.2 CKD is staged on the basis of eGFR and albuminuria levels.2 The 3 A stages are based on albuminuria level, which is determined by either albumin excretion rate or albumin-to-creatinine ratio. The 6 G stages (G1-G5) categorize patients based on eGFR. Stage G3 was split into G3a and G3b after meta-analyses revealed a significant difference in prognosis between the 45 to 59 mL/minute/1.73 m3 (G3a) and 30 to 44 mL/minute/1.73 m3 (G3b) eGFR ranges.3 An eGFR <60 mL/minute/1.73m3 is considered decreased, which corresponds to G stages G3a to G5. Patients in stages G1 to G2 have conserved eGFR, but can still meet requirements for CKD if other manifestations such as proteinuria or structural abnormalities are present.2

In addition to staging CKD, clinicians must identify possible metabolic and electrolyte imbalances by ordering a complete blood count and a complete metabolic panel. Anemia may be present as a result of impaired erythropoietin production in the kidneys. Hyperphosphatemia and hyperkalemia can result from impaired excretion. Hypocalcemia may be present because of the damaged kidneys’ inability to activate vitamin D. An arterial blood gas may also be indicated if signs of metabolic acidosis are present.5

The diagnostic process is not complete until the cause of CKD has been identified. To determine the etiology of a CKD case, a urinalysis, urine sediment examination, and imaging should be performed. Possible urine sediment findings include the characteristic broad, waxy casts of dilated nephrons; red blood cell casts suggestive of proliferative glomerulonephritis; white blood cell casts of pyelonephritis and interstitial nephritis; or oval fat bodies of nephrotic syndrome.13

On ultrasonography, damaged kidneys may appear small (9-10 cm) and echogenic, but normal-sized or large kidneys may be found in certain etiologies such as polycystic kidney disease and diabetic nephropathy.5 Other useful imaging studies include computed tomography and magnetic resonance imaging with and without contrast, isotope scans, and angiography.13 A renal biopsy can also distinguish the etiology and severity of CKD, but this procedure is not standard and should only be performed in cases in which the diagnostic value of the procedure outweighs the risks.14


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How Do I Manage a Patient With CKD?

To slow down the progression of CKD and prevent complications, managing the underlying causes of the disease is essential. Diabetes mellitus treatment goals should be adjusted according to the stage of CKD. Although patients with early CKD should follow strict diabetes treatment goals to limit hyperglycemia, patients with advanced CKD should follow goals aimed toward preventing hypoglycemia.5

Hypertension control can also reduce the rate of CKD progression and prevent cardiovascular events. The recommended medications for hypertension in a patient with CKD are angiotensin-converting enzyme inhibitors or angiotensin receptor blockers with a loop diuretic.5,15 The Eighth Joint National Committee’s target blood pressure recommendation for patients with CKD is 140/90 mm Hg. Studies assessing benefits of even lower blood pressure treatment goals for patients with CKD have yielded mixed results.16-18 Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers also have renoprotective properties and reduce proteinuria.5,15 The management of other cardiovascular risk factors, such as obesity, smoking, hyperlipidemia, and inactivity also plays a role in slowing renal decline.5 If applicable, the provider should also discontinue nephrotoxic drugs, treat infections of the urinary tract or kidneys, and correct renal obstructions.15

Because of the high rate of cardiac morbidity and mortality in patients with CKD, prevention and management of cardiorenal syndrome is essential.6,19 The cardiovascular and renal systems have a close, bidirectional relationship mediated by neurohormonal factors, renal perfusion, and renal venous pressure. Patients with cardiorenal syndrome may have a reduced GFR as a result of 1 or more of the following: CKD, decreased renal perfusion secondary to left-sided heart failure, or increased renal venous pressure secondary to right-sided heart failure. Regardless of the primary cause, a decrease in GFR activates the renin-angiotensin-aldosterone system, which causes downstream sodium and water retention, thus exacerbating volume overload and congestive heart failure. Antihypertensives that inhibit this signaling pathway (angiotensin-converting enzyme inhibitors and angiotensin receptor blockers) can prevent the perpetuation of this cycle.19

Symptomatic treatment can reduce the patient’s discomfort and prevent further damage caused by CKD. Patients who have anemia can be treated with erythropoietin and iron supplements. Although homeostatic mechanisms maintain normal blood volumes until late in disease, patients with CKD are at risk for hypervolemia after rapid ingestion of sodium. Diuretics help alleviate the swelling and hypervolemia associated with CKD.15 Vitamin D is often decreased in CKD because of the kidneys’ inability to convert vitamin D to its active form; therefore, vitamin D supplements can be used to prevent secondary bone disease.5

Personalized dietary interventions may be implemented to reduce the symptoms and progression of CKD.5 Access to nutritional counseling from a registered dietician with experience in kidney disease should be available to all patients with progressive CKD.2 Animal protein restriction to 0.6 to 0.8 mg/kg/d can slow rates of CKD progression and is safe in an otherwise well-nourished patient.

Because of the diseased kidneys’ diminished ability to secrete sodium, fluid and sodium intake restrictions may be indicated in patients with advanced disease. Goals of 2 g/day sodium and 2 L fluid per day prevent hypervolemia while still maintaining hydration. A potassium intake limitation to 50 to 60 mEq/day is necessary in hyperkalemic patients. Phosphorus also can be elevated in CKD, and a phosphorus restriction to 800 to 1000 mg/day can help control this. Phosphorus binders are often necessary in advanced disease.5 In addition, increasing total fiber intake has been shown to decrease inflammation and mortality in patients with CKD.20

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Providers must take a patient’s CKD status into account when prescribing and adjusting medications that are excreted by or toxic to the kidney. Table 1 lists commonly used medications that require caution or dose adjustment in patients with CKD; however, this list is not comprehensive.8

Table 1. Medications That Must Be Adjusted or Used With Caution in Patients With CKD8

ClassMedication
Antihypertensive and cardiac● RAAS antagonists
● Hydrophilic beta blockers
● Digoxin
Analgesics● NSAIDs
● Opioids
Antimicrobials● Macrolides
● Fluoroquinolones
● Tetracycline
● Antifungals
● Trimethoprim
Hypoglycemics● Sulfonylureas
● Insulin
● Metformin
Lipid-lowering agents● Lovastatin, pravastatin, rosuvastatin
Anticoagulants● Low-molecular-weight heparin
● Warfarin
● Direct-acting anticoagulants
Other ● Lithium
● Bisphosphonates
● Oral sodium phosphate-containing bowel preparations
● Gabapentin

NSAID; nonsteroidal anti-inflammatory drug; RAAS, renin-angiotensin-aldosterone system