Chronic kidney disease (CKD) is a commonly diagnosed condition, affecting approximately 30 million adults in the United States.1 CKD refers to a diverse group of pathologies that result in kidney function decline for at least 3 months.2,3 Kidney disease etiologies are generally classified into 3 categories: prerenal, intrinsic renal, and postrenal. Prerenal disease is marked by renal hypoperfusion, whereas postrenal disease results from a distal obstruction in the urinary tract. Intrinsic renal disease includes damage to the renal vasculature, glomeruli, tubules, and interstitium.4
In the United States, the most common cause of CKD is diabetic nephropathy. In addition to diabetes, hypertension, obesity, cardiovascular disease, family history of kidney disease, and advanced age are all risk factors for CKD.5
Patients with CKD have increased mortality rates (109.7 per 1000 patient-years), which is almost double that of healthy age- and sex-matched adults (45.6 per 1000 patient-years).1 Patients with CKD who are older than 65 years have an increased risk for mortality caused by associated cardiac risks factors. Unchecked, CKD will progress to end-stage renal disease, an advanced form of CKD that necessitates renal replacement therapy.6
To prevent the progression of CKD to end-stage renal disease, prompt identification and referral by primary care providers is essential.7
What Are the Symptoms of CKD?
Early stages of CKD are asymptomatic; therefore, many cases are first identified incidentally by an elevated creatinine level on a basic metabolic panel.8 The asymptomatic nature of early disease suggests that screening for CKD may be beneficial. However, a systematic review in 2014 concluded that screening for CKD by annual proteinuria or estimated glomerular filtration rate (eGFR) measurements is cost-effective only in patients with diabetes and hypertension, who are at an elevated risk for CKD.9
CKD causes a progressive loss of kidney function, but patients remain asymptomatic late into the disease because of the kidneys’ ability to compensate via hyperfiltration through the remaining healthy nephrons. Long-standing kidney dysfunction results in edema, hypertension, and decreased urine output, but not anuria, which indicates an acute injury.4 Depending on the severity and duration of disease, the kidneys may fail to excrete metabolic wastes, resulting in uremia. General uremic symptoms include fatigue, weakness, and anorexia.
Common gastrointestinal complaints related to CKD include nausea, vomiting, and a metallic taste in the mouth. Neurological and psychiatric issues such as irritability, memory impairment, insomnia, restless leg syndrome, paresthesias, and twitching may also prompt a patient with undiagnosed CKD to come to the clinic. Patients may also suffer from changes in the menstrual cycle, decreased libido, pruritus, pericarditis, and hypoglycemia. Associated bone disease may present as pathologic fractures.5
What Are Some Common Physical Exam Findings?
The most common physical examination finding in a patient with CKD is hypertension.5 This occurs because of the kidneys’ decreased ability to excrete sodium. Hypertension that does not decrease by at least 10% at bedtime, known as nondipping hypertension, has a strong association with CKD.10,11 Other features seen on physical examination may include an ill appearance, halitosis, signs of volume overload such as edema, and neurologic signs related to uremic encephalopathy. Signs of uremic encephalopathy include impaired cognition, asterixis, myoclonus, and seizures.5
Other physical examination findings may reflect the underlying etiology of CKD, including enlarged bladder or kidneys in obstructive disease, costovertebral angle tenderness from infection, renal artery bruits from renovascular disease, and characteristic changes on ophthalmoscopic exam as result of diabetes mellitus and hypertension.12
How Do I Work Up a Patient With CKD?
CKD is defined by abnormalities in kidney structure or function for at least 3 months. Abnormalities in kidney function can be represented by albuminuria, urinary sediment abnormalities, electrolyte imbalances, histological findings on biopsy, structural abnormalities on imaging studies, and decreased GFR.2
Serum creatinine level alone is not a sufficient indicator of kidney function, as this value is influenced by patient demographic factors such as race and sex. Therefore, equations that take such factors into account must be used to calculate an eGFR based on serum creatinine. The Modification of Diet in Renal Disease equation previously was the standard for measuring eGFR; however, this equation has been criticized for underestimating higher GFRs.3 The 2009 CKD Epidemiology Collaboration (CKD-EPI) equation uses the same variables as the Modification of Diet in Renal Disease equation, but is more accurate for a wider range of GFRs.3 If further confirmation is needed for diagnosis, clinicians can also estimate GFR using cystatin C, a filtrate that is less influenced by non-GFR factors than creatinine.2-3
This article originally appeared on Clinical Advisor