Chronic Kidney Disease (Newly Identified) : Clinical Presentation and Diagnostic Approach in Adults
Chronic Kidney Disease (Newly Identified) : Clinical Presentation and Diagnostic Approach in Adults
Chronic Kidney Disease (Newly Identified) : Clinical Presentation and Diagnostic Approach in Adults
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Literature review current through: May 2023. | This topic last updated: Jun 24, 2022.
INTRODUCTION
CLINICAL PRESENTATION
CKD patients may present with symptoms and signs resulting directly from
diminished kidney function, such as edema or hypertension. However, many
have no clinical symptoms, and kidney disease is often detected in these
patients when an elevated serum creatinine, reduced estimated glomerular
filtration rate (eGFR), or an abnormal urinalysis is discovered incidentally
(when such tests are obtained as part of routine evaluation or for a possibly
unrelated disorder). In addition, radiographic findings (eg, small and
echogenic kidneys [by ultrasound] suggesting chronic damage, multiple
bilateral renal cysts with enlarged kidneys suggestive of polycystic kidney
disease) may be observed on imaging performed for some other reason.
Depending upon the duration and severity of CKD, patients may also present
with symptoms and/or signs of prolonged kidney failure, including weakness
and easy fatigability, anorexia, vomiting, pruritus, and, in very advanced
stages, with encephalopathy or seizures.
The most common laboratory findings in patients with CKD include increased
serum creatinine and blood urea nitrogen. Urine studies may show
proteinuria (or albuminuria) and/or abnormal red or white blood cells on
urine microscopy. (See "Assessment of kidney function" and "Urinalysis in the
diagnosis of kidney disease".)
The degree to which these abnormalities are present depends upon the
severity of CKD. Hyperphosphatemia is uncommon among CKD patients with
eGFR >45 mL/min/1.73 m2. PTH, on the other hand, may be mildly elevated
even with a mild reduction of eGFR (ie, 50 to 60 mL/min/1.73 m2). (See
"Overview of chronic kidney disease-mineral and bone disorder (CKD-MBD)",
section on 'Overview'.)
The most common causes of CKD are poorly controlled diabetes mellitus and
hypertension. These and other possible etiologies are discussed in detail
below. (See 'Subsequent Evaluation' below.)
The causes of kidney injury are classically divided into three categories:
prerenal; intrinsic renal; or postrenal. However, any cause of kidney injury, if
sufficiently severe or long-standing, may lead to persistently abnormal kidney
function and therefore CKD. As an example, a patient with severe heart failure
may have recurrent or prolonged acute kidney injury (AKI) due to reduced
effective arterial blood volume (ie, prerenal disease). Over time, even if
cardiac function and renal perfusion pressure improve, glomerular filtration
rate (GFR) may never fully recover to normal.
The initial assessment for all patients who present with suspected CKD starts
with triage of those who may need urgent dialysis based upon symptoms or
life-threatening laboratory abnormalities ( algorithm 1). In other patients,
the time course of their kidney disease should be established to determine
the role and timing of consultation with a nephrologist.
Even among patients not requiring urgent dialysis, most may benefit from
early referral to a nephrologist. (See 'Indications for a nephrology evaluation'
below.)
Along with the trend of any clinical symptoms, the trajectory of the laboratory
abnormalities will determine if and when additional evaluation or nephrology
referral is necessary. Recognition of a rapidly progressive process versus
stable disease permits early intervention to curtail an active process and to
preserve residual kidney function.
The determination of disease duration can also help distinguish between CKD
and subacute kidney injury (also called acute kidney disease), although this
distinction can be arbitrary. The clinical course of gradually progressive CKD is
commonly punctuated by transient, small "spikes" in serum creatinine, which
often improve to resume a prior long-term trajectory ( figure 1). However,
the pace of eGFR decline may increase and, if the rate of decline becomes
rapid, such patients may be more appropriately evaluated as subacute kidney
injury rather than CKD. (See "Diagnostic approach to adult patients with
subacute kidney injury in an outpatient setting", section on 'Evaluation'.)
SUBSEQUENT EVALUATION
Once the initial assessment and triage is complete, we perform an evaluation
to identify the cause of CKD and identify individuals who may benefit from a
nephrology consultation ( algorithm 1).
● Complete blood count with white cell differential ("CBC with diff").
Specific abnormalities in blood and urine studies guide the utility and timing
of further evaluation and referral. In addition to a rapidly declining eGFR,
other laboratory abnormalities may require directed evaluation and
management by a nephrologist. As an example, microscopic hematuria
and/or increased proteinuria (as detected by UPCR or UACR) often prompts
specific serologic testing to investigate possible glomerular disease. Sterile
pyuria, especially if coupled with peripheral eosinophilia, may direct further
testing for a hypersensitivity reaction or autoimmune disease or, in endemic
regions, renal tuberculosis. The combination of metabolic acidosis with
hyper- or hypokalemia may indicate the presence of a renal tubular acidosis,
which is a notable feature in some etiologies of CKD. Evidence of a
monoclonal gammopathy should prompt a referral to nephrology or
hematology for further evaluation of related kidney or plasma cell diseases.
(See 'Indications for a nephrology evaluation' below and "Clinical
manifestations and diagnosis of acute interstitial nephritis" and "Glomerular
disease: Evaluation and differential diagnosis in adults" and "Kidney disease
in primary Sjögren syndrome" and "Kidney disease in sarcoidosis" and
"Urogenital tuberculosis", section on 'Renal and urologic tuberculosis' and
"Kidney disease in multiple myeloma and other monoclonal gammopathies:
Etiology and evaluation" and "Renal amyloidosis" and "Membranoproliferative
glomerulonephritis: Classification, clinical features, and diagnosis", section on
'Monoclonal gammopathies'.)
Patients who are at a high risk for renovascular disease should have
dedicated imaging to evaluate for renal artery stenosis. Vascular duplex
ultrasound of the renal arteries is often a first step. Depending upon each
institution's radiologic expertise, computed tomography angiography and/or
magnetic resonance angiography may be obtained. This imaging is used in
conjunction with vascular surgery or interventional radiology evaluation to
determine the possible role of revascularization versus medical management.
(See "Chronic kidney disease resulting from atherosclerotic renal artery
stenosis".)
● Resistant hypertension
● Pregnancy
Patients who have stable, mild to moderate kidney disease (ie, that is not
progressive) can be monitored every three to six months (or a longer interval
if laboratory studies and clinical status are clearly stable) for the development
of the following findings that would benefit from a nephrology evaluation
(see 'Indications for a nephrology evaluation' above):
● A change in the pace of eGFR decline, such that the patient is rapidly
losing kidney function (ie, loss of eGFR >5 mL/min/1.73 m2 per year or
>25 percent decline in eGFR).
SOCIETY GUIDELINE LINKS
UpToDate offers two types of patient education materials, "The Basics" and
"Beyond the Basics." The Basics patient education pieces are written in plain
language, at the 5th to 6th grade reading level, and they answer the four or
five key questions a patient might have about a given condition. These
articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are
longer, more sophisticated, and more detailed. These articles are written at
the 10th to 12th grade reading level and are best for patients who want in-
depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We
encourage you to print or e-mail these topics to your patients. (You can also
locate patient education articles on a variety of subjects by searching on
"patient info" and the keyword(s) of interest.)
● Basics topics (see "Patient education: Chronic kidney disease (The Basics)"
and "Patient education: Acute kidney injury (The Basics)")
● Beyond the Basics topics (see "Patient education: Chronic kidney disease
(Beyond the Basics)" and "Patient education: Dialysis or kidney
transplantation — which is right for me? (Beyond the Basics)" and
"Patient education: Hemodialysis (Beyond the Basics)" and "Patient
education: Peritoneal dialysis (Beyond the Basics)" and "Patient
education: Protein in the urine (proteinuria) (Beyond the Basics)" and
"Patient education: Split urine collection for orthostatic proteinuria
(Beyond the Basics)")
● CKD patients may present with symptoms and signs resulting directly
from diminished kidney function, such as edema or hypertension.
However, many have no clinical symptoms, and kidney disease is often
detected in these patients when an elevated serum creatinine, reduced
estimated GFR (eGFR), or an abnormal urinalysis is discovered
incidentally (when such tests are obtained as part of routine evaluation or
for a possibly unrelated disorder). In addition, radiographic findings (eg,
multiple bilateral renal cysts with enlarged kidneys suggestive of
polycystic kidney disease) may be observed on imaging performed for
some other reason. (See 'Clinical presentation' above.)
● Patients with CKD may have absolute or relative indications for dialysis at
the time that their kidney disease is discovered. Those who have
refractory pulmonary edema, life-threatening hyperkalemia or metabolic
acidosis, encephalopathy, or a pericardial rub should be referred to the
emergency department for rapid evaluation and possible initiation of
dialysis. (See 'Identifying patients needing urgent dialysis' above.)
● Among patients who do not require dialysis, we start by evaluating the
duration of the kidney disease. Typically, this entails assessing serial
serum creatinine values (and associated eGFRs) over time. If urine tests
or radiologic studies of the kidney are abnormal at the time of CKD
discovery, temporal changes in these data should also be assessed.
Establishing the duration and trajectory of the disease accurately is
fundamentally important and requires that older data be obtained for
comparison. In some cases, it may be necessary to acquire this
information from the patient's prior caregivers or from other health
centers. When prior serum creatinine values, urine studies, or
radiographic images are unavailable, certain findings from the history
and physical examination, or subsequent laboratory or radiographic
evaluation, may suggest the duration of disease. (See 'Determine the
duration of kidney disease' above.)