Chronic Kidney Disease (Newly Identified) : Clinical Presentation and Diagnostic Approach in Adults

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Chronic kidney disease (newly identified):

Clinical presentation and diagnostic approach


in adults
Authors: Pedram Fatehi, MD, MPH, Chi-yuan Hsu, MD, MSc
Section Editors: Gary C Curhan, MD, ScD, Marcello Tonelli, MD, SM, FRCPC
Deputy Editor: Eric N Taylor, MD, MSc, FASN

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is
complete.

Literature review current through: May 2023. | This topic last updated: Jun 24, 2022.

INTRODUCTION

Chronic kidney disease (CKD) is defined by the presence of kidney damage or


decreased glomerular filtration rate (GFR) for three or more months,
irrespective of the cause ( table 1) [1]. This three-month duration
distinguishes chronic from acute kidney disease. Additional details on the
definitions and staging are presented at length elsewhere. (See "Definition
and staging of chronic kidney disease in adults" and "Definition and staging
criteria of acute kidney injury in adults".)

For patients being evaluated for elevated serum creatinine or reduced


estimated glomerular filtration rate (eGFR), it is important to distinguish
those who have relatively stable CKD from those who have acute or subacute
kidney injury, which may be ongoing and reversible. Acute kidney injury (AKI)
is defined by a rise in the serum creatinine level that has developed within
hours to days ( table 2). Subacute kidney injury (also called acute kidney
disease) informally refers to any decline in kidney function that evolves over
more than 48 hours but less than three months [2]. Diagnostic approach to
these patients is presented in detail elsewhere. (See "Diagnostic approach to
adult patients with subacute kidney injury in an outpatient setting" and
"Evaluation of acute kidney injury among hospitalized adult patients".)

An overview of the presentation and evaluation of patients with newly


identified CKD is presented in this topic ( algorithm 1). Specific aspects of
the evaluation are presented separately:

● Assessment of kidney function by eGFR. Estimation of the GFR requires


that the patient is in steady state. (See "Assessment of kidney function".)

● Careful examination of the urine by both qualitative chemical tests and


microscopic examination. The urinary findings narrow the differential.
(See "Urinalysis in the diagnosis of kidney disease".)

● Radiologic imaging of the kidneys. (See "Radiologic assessment of kidney


disease".)

● Serologic testing and tissue diagnosis with kidney biopsy if noninvasive


evaluation is insufficient for diagnosis. (See "Glomerular disease:
Evaluation and differential diagnosis in adults".)

The epidemiology and management of patients with CKD, as well as clinical


presentation and evaluation of CKD in children are discussed elsewhere:

● (See "Epidemiology of chronic kidney disease".)


● (See "Overview of the management of chronic kidney disease in adults".)
● (See "Chronic kidney disease in children: Clinical manifestations and
evaluation".)

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.

An abnormally reduced urine output (ie, oliguria or anuria) is seldom


observed with CKD alone and always indicates at least some component of
acute kidney injury (AKI). Oliguria or anuria may be present among patients
with AKI superimposed on CKD, such as may be observed in a patient with
chronic obstruction who develops acute urinary retention. Similarly, anuria as
a result of severe or prolonged shock, bilateral urinary tract obstruction,
pregnancy-related cortical necrosis, or bilateral renal arterial occlusion (eg,
due to a dissecting aortic aneurysm) may occur in patients with underlying
CKD. (See "Evaluation of acute kidney injury among hospitalized adult
patients", section on 'Clinical manifestations'.)

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".)

Other common laboratory abnormalities that may be part of the clinical


picture include anemia, hyperphosphatemia, hyperkalemia, metabolic
acidosis, hypocalcemia, and elevated parathyroid hormone (PTH).

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'.)

CAUSES OF CHRONIC KIDNEY DISEASE

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.

In addition, whatever the initial cause of kidney disease, a sustained decrease


in GFR can produce adaptive hyperfiltration within the remaining functional
nephrons, which may lead to further injury and worsening of CKD. (See
"Overview of the management of chronic kidney disease in adults", section on
'Natural history of kidney disease' and "Secondary factors and progression of
chronic kidney disease", section on 'Intraglomerular hypertension and
glomerular hypertrophy'.)

INITIAL ASSESSMENT AND TRIAGE

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.

Identifying patients needing urgent dialysis — 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. These indications are discussed
at length elsewhere. (See "Indications for initiation of dialysis in chronic
kidney disease".)

Even among patients not requiring urgent dialysis, most may benefit from
early referral to a nephrologist. (See 'Indications for a nephrology evaluation'
below.)

Determine the duration of kidney disease — 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
estimated glomerular filtration rates [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.

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 importance of determining the trajectory of kidney disease is illustrated


by the following examples:

● Consider a patient with no significant medical history and a current


serum creatinine of 4 mg/dL (354 micromol/L) who had a creatinine of 0.6
mg/dL (53 micromol/L) one month earlier. This patient has acute or
subacute kidney injury. This patient needs urgent evaluation and
management to stop further injury and to optimize kidney recovery. (See
"Diagnostic approach to adult patients with subacute kidney injury in an
outpatient setting".)

● By contrast, consider a different patient who has an identical current


serum creatinine of 4 mg/dL (354 micromol/L). However, this patient has
had long-standing, poorly-controlled diabetes mellitus and had a serum
creatinine of 3.5 mg/dL (309 micromol/L) two years earlier, as well as
chronically increased albuminuria. This patient likely has slowly
progressive CKD. Although this patient will also benefit from nephrology
referral, these laboratory data alone, without concurrent significant
symptoms, would not justify urgent or extensive evaluation, since the
process is less likely reversible. (See 'Clinical presentation' above and
'Indications for a nephrology evaluation' below.)

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'.)

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 [3]. As examples:

● New symptoms or signs, such as sudden onset of anasarca and


discolored urine, suggest a more acute process.

● Oliguria (urine output <0.5 mL/kg/hour [often <500 to 600 mL/day]) or


anuria in a patient not on maintenance dialysis indicates an acute
process. Prolonged oliguria or anuria do not occur in slowly progressive
CKD (even if advanced).

● A daily increase in serum creatinine after the initial discovery of an


abnormal value indicates at least some component of an ongoing acute
process. Conversely, a serum creatinine that does not change, or changes
minimally, over weeks to months suggests the presence of CKD.
Distinguishing CKD progression from subacute kidney injury may be
difficult in the setting of a serum creatinine that is worsening gradually
( figure 1). The level of CKD, magnitude of eGFR decline, changes in
clinical symptoms, and other factors (such as reliability of patient follow-
up) should dictate the frequency of laboratory monitoring to clearly
establish a trend. Overall, a rate of decrease of eGFR >5 mL/min/1.73 m2
per year (or >25 percent decline in eGFR) should prompt early retesting
to establish a clear trajectory and to rule out ongoing subacute injury.

● Imaging that reveals small, echogenic kidneys provides definitive


evidence of chronicity of disease. However, the presence of normal-sized
kidneys does not exclude chronicity, since some causes of CKD (such as
diabetic kidney disease) are associated with preserved kidney size. Kidney
parenchymal echogenicity (normally kidneys are less echogenic than the
liver), if increased, suggests nonspecific diffuse kidney dysfunction [4-6].
(See "Radiologic assessment of kidney disease".)

● Radiologic evidence of renal osteodystrophy such as subperiosteal bone


resorption or loss of bone density at the distal third of the clavicles
suggests CKD. (See "Overview of chronic kidney disease-mineral and
bone disorder (CKD-MBD)".)

Other findings are less helpful. As an example, anemia due to erythropoietin


deficiency is a common (although not absolute) finding in CKD, but acute or
subacute kidney injury can also be associated with anemia (from either
hemolysis or bleeding). Although hyperphosphatemia commonly affects CKD
patients, it may also be seen in AKI or subacute kidney injury and, therefore,
does not help distinguish acute from chronic disease. The absence of anemia
or hyperphosphatemia does not exclude the presence of CKD.

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).

Evaluation to identify cause — We obtain a cause-specific history, perform a


targeted physical examination, and, if not done recently, we obtain urine
studies and an ultrasound to determine the cause as follows:

Targeted history — We specifically determine if there is a history of any of


the following:

● Long-standing diabetes and hypertension commonly lead to CKD. The


duration of disease (diabetes and/or hypertension) and the degree of
control should be determined in such patients. In addition, the presence
of diabetic or hypertensive retinopathy should be ascertained because
patients with retinopathy have a higher likelihood of having CKD from
diabetes and/or hypertension. (See "Clinical features, diagnosis, and
treatment of hypertensive nephrosclerosis" and "Diabetic kidney disease:
Pathogenesis and epidemiology" and "Overview of hypertension in acute
and chronic kidney disease".)

● Renovascular disease should be suspected among patients who have


peripheral arterial disease in other vascular beds or who have multiple
vascular risk factors, such as age over 50 years, hyperlipidemia, or
cigarette smoking. Renovascular disease can present as CKD. Features
that suggest CKD due to renovascular disease include resistant
hypertension, recurrent flash pulmonary edema, or a reversible increase
in serum creatinine after receiving antihypertensive therapy, particularly
angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor
blockers (ARBs), which improves after withdrawal of the drug. (See
"Chronic kidney disease resulting from atherosclerotic renal artery
stenosis".)
● Patients should be asked about a history of prior severe or prolonged
acute kidney injury (AKI) to determine if it could have contributed to their
CKD. Prior AKI, particularly if dialysis-requiring, may lead to CKD. CKD
may have developed even if the patient had sufficient recovery to stop
dialysis. (See "Kidney and patient outcomes after acute kidney injury in
adults", section on 'Determinants of kidney outcomes'.)

● Histories of obesity, heart failure, liver failure, autoimmune disease,


recurrent and complicated urinary tract infections, and reduced kidney
mass (eg, nephrectomy, renal agenesis) should be elicited due to their
associations with CKD. (See "Overweight and obesity in adults: Health
consequences", section on 'Chronic kidney disease' and "Cardiorenal
syndrome: Definition, prevalence, diagnosis, and pathophysiology" and
"Hepatorenal syndrome" and "Lupus nephritis: Diagnosis and
classification" and "Overview of and approach to the vasculitides in
adults".)

● Inherited disorders, such as some cystic, interstitial, and glomerular


kidney diseases, are relatively common causes of CKD. Thus, it is
important to ask specific questions about kidney disease in family
members, including their history of abnormal kidney imaging (eg, large
kidneys with many cysts seen in polycystic kidney disease) or abnormal
urine studies (eg, hematuria or proteinuria found in glomerular
diseases). (See "Autosomal dominant polycystic kidney disease (ADPKD)
in adults: Epidemiology, clinical presentation, and diagnosis" and
"Autosomal dominant tubulointerstitial kidney disease" and "IgA
nephropathy: Pathogenesis and etiology", section on 'Genetic
predisposition' and "Focal segmental glomerulosclerosis: Genetic causes"
and "Fabry disease: Kidney manifestations" and "C3 glomerulopathies:
Dense deposit disease and C3 glomerulonephritis", section on
'Pathogenesis'.)
● Patients who have a history of cancer (eg, myeloma or renal cell
carcinoma) and treatment with chemotherapy or radiotherapy may
develop CKD from the cancer itself or from its treatment. Many patients
with multiple myeloma, for example, have AKI at the time of diagnosis;
such patients often develop CKD as a result of incomplete recovery from
AKI. Patients with renal cell carcinoma often require a partial or complete
nephrectomy, which can lead to CKD from decreased renal mass. In
addition, patients who are treated with chemotherapy using cisplatin,
ifosfamide, immune checkpoint inhibitors, or newer molecular-targeted
agents may develop CKD as an adverse consequence of their treatment.
(See "Overview of kidney disease in patients with cancer" and "Kidney
disease in multiple myeloma and other monoclonal gammopathies:
Etiology and evaluation" and "Chemotherapy nephrotoxicity and dose
modification in patients with kidney impairment: Molecularly targeted
agents and immunotherapies" and "Cisplatin nephrotoxicity" and
"Ifosfamide nephrotoxicity".)

● Urinary tract obstruction should be suspected among patients who have


a history of prior urological surgery, prior pelvic or retroperitoneal
surgery, a known or suspected abdominal or retroperitoneal malignancy,
neurologic disease involving the bladder, gross hematuria, lower
abdominal, pelvic, or flank pain, or in men with lower urinary tract
symptoms. (See "Clinical manifestations and diagnosis of urinary tract
obstruction (UTO) and hydronephrosis" and "Chronic urinary retention in
females" and "Lower urinary tract symptoms in males".)

● Clinicians should inquire about risk factors for human immunodeficiency,


hepatitis C, or hepatitis B virus infections, such as a history of intravenous
drug use or sexually transmitted disease. Patients with risk factors should
be tested for the presence of these viruses. Because these viruses may
cause a variety of kidney diseases, these etiologies should also be
considered when the underlying cause of CKD is not clear. (See "Overview
of kidney disease in patients with HIV" and "Kidney disease associated
with hepatitis B virus infection" and "Overview of kidney disease
associated with hepatitis C virus infection".)

● Medications should be reviewed, including for potentially nephrotoxic


medications that the patient used in the past (even if not currently using).
As examples, prolonged use of lithium for psychiatric conditions, certain
Chinese herbs from "slimming clinics," or analgesic combination agents
may each cause chronic interstitial injury that leads to CKD. In addition,
drugs that can precipitate allergic interstitial nephritis may lead to CKD
since such patients often do not have complete recovery of kidney
function. (See "Renal toxicity of lithium" and "Nephropathy induced by
aristolochic acid (AA) containing herbs" and "Clinical manifestations and
diagnosis of analgesic nephropathy".)

● Geography may be a clue to the cause of CKD. A history of agricultural


work in hot environments or history of exposure to pesticides and other
agrochemicals is associated with CKD of unknown cause (ie, "CKDu," also
called Mesoamerican nephropathy). Such a history should raise suspicion
for this disorder as the cause of CKD. Patients who lived for many years in
particular regions of the Balkans may be at risk for a different chronic
tubulointerstitial nephropathy that is slowly progressive. In endemic
regions, infections such as schistosomiasis and tuberculosis may be
common causes of CKD. (See "Mesoamerican nephropathy" and "Balkan
endemic nephropathy" and "Schistosomiasis and glomerular disease"
and "Urogenital tuberculosis".)

● A review of toxic environmental or occupational contaminants may reveal


exposure to lead, which is associated with CKD. A history of lead mining,
plumbing, auto-repair work, or shipbuilding may be associated with
significant lead exposure. (See "Lead nephropathy and lead-related
nephrotoxicity".)

Targeted physical examination — We perform a physical exam to elicit the


following signs that may suggest a specific etiology of kidney disease:

● Signs of volume overload may indicate the presence of heart failure or


cirrhosis, which are associated with CKD.

● Signs of volume depletion, such as may occur with a chronic diarrheal


syndrome or a high-output bowel stoma, may suggest a longstanding
state of prerenal azotemia with risk of recurrent AKI, thereby leading to
CKD.

● The presence of arteriovenous nicking or retinopathy on funduscopic


examination can be seen in chronic hypertensive microvascular disease
( image 1), which may also involve the kidney.

● An abdominal bruit or abnormal distal pulses may be detected in patients


with renal artery stenosis.

● Enlarged kidneys that are palpable on examination may suggest


polycystic kidney disease.

● Peripheral neuropathy may be associated with diabetic microvascular


disease or another disorder that causes dysautonomia (such as a
paraproteinemia).

● Rashes and skin lesions, such as may occur with leukocytoclastic


vasculitis or purpura, suggests that small vessel vasculitis may be the
cause of CKD ( picture 1 and picture 2).

● Skin thickening and hardening as may be seen with systemic sclerosis


(scleroderma), an uncommon cause of CKD ( figure 2 and picture 3).
Targeted laboratory assessment — Initial testing for all patients should
include:

● Basic metabolic panel that includes serum creatinine for calculation of


the estimated glomerular filtration rate (eGFR).

● Complete blood count with white cell differential ("CBC with diff").

● Urinalysis using reagent test strips (dipstick) and automated urine


microscopy.

● If an experienced operator is available for manual review of urine


microscopy, such a detailed examination of the urine may further guide
the evaluation. Urine microscopy is especially helpful if there are cellular
elements (red blood cells and/or white blood cells), cellular or granular
casts, or crystals in the urine. In the absence of an experienced urine
microscopist, or if the urinalysis and automated microscopy are normal,
manual review may generally be deferred. (See "Urinalysis in the
diagnosis of kidney disease".)

● Quantification of urine protein and albumin by random (or "spot")


protein-to-creatinine ratio (UPCR) and albumin-to-creatinine ratio (UACR);
each provides slightly different but related information. Our practice is to
check both UPCR and UACR concurrently, and, in some cases, a 24-hour
urine collection for protein and creatinine at least once early in the
evaluation and to follow one of the values over time. A more detailed
discussion of proteinuria is presented elsewhere. (See "Assessment of
urinary protein excretion and evaluation of isolated non-nephrotic
proteinuria in adults".)

● In addition, in patients older than 40 years of age who have


hypercalcemia, severe anemia, bony lesions suggestive of multiple
myeloma, or a progressively worsening eGFR without an obvious cause,
we also obtain a serum and urine protein electrophoresis with
immunofixation and a serum free light chain assay. (See "Kidney disease
in multiple myeloma and other monoclonal gammopathies: Etiology and
evaluation", section on 'Evaluation'.)

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'.)

Depending upon further testing by a nephrologist, a kidney biopsy may be


warranted. (See 'Indications for a nephrology evaluation' below.)
In some cases of newly identified CKD with stable, mild laboratory
abnormalities, expectant management with watchful waiting, and without
nephrology referral, is reasonable. A patient, for example, with stable eGFR
>45 mL/min/1.73 m2, normal urine microscopy, UPCR <500 mg/g and UACR
<300 mg/g may not require extensive serologic testing or kidney biopsy. (See
'Stable patients not in need of a nephrology evaluation' below.)

Targeted radiologic assessment — Unless recent abdominal imaging is


available, we obtain a kidney ultrasound in all patients at the time of their
initial evaluation for CKD. Abnormalities in kidney imaging may warrant
urologic evaluation and urodynamic studies. (See "Radiologic assessment of
kidney disease".)

Patients who have evidence of urinary tract obstruction (ie, hydronephrosis)


on ultrasound require further investigation to determine the cause and
duration, and to establish reversibility of kidney injury. Early recognition and
correction of urinary obstruction can help salvage kidney function. (See
"Clinical manifestations and diagnosis of urinary tract obstruction (UTO) and
hydronephrosis".)

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".)

Indications for a nephrology evaluation — Based upon the targeted


history, physical examination, laboratory testing, and imaging discussed
above, further evaluation with additional tests and kidney biopsy may be
warranted. (See "Definition and staging of chronic kidney disease in adults",
section on 'Referral to a specialist' and "Overview of the management of
chronic kidney disease in adults", section on 'Referral to nephrologists'.)

With increasing accessibility of telehealth visits and electronic consults that


can often be completed more efficiently than traditional in-office patient
visits, a subspecialty referral may now include a spectrum of possible
scenarios. In some cases, a nephrologist may review the electronic medical
record for the history, medications, and laboratory data and determine that a
formal referral for full evaluation is appropriate. In other cases, she or he may
simply render education and guidance to a primary care clinician on further
evaluation, if necessary, and on issues of surveillance and management of
stable disease. Local practice may vary along this spectrum. In an adult with
newly identified CKD, indications for consultation with a nephrologist include:

● eGFR <30 mL/min/1.73 m2

● Persistent UACR ≥300 mg/g (34 mg/mmol)

● Persistent UPCR ≥500 mg/g (56.5 mg/mmol)

● Abnormal urine microscopy (cellular casts, nonurologic hematuria, sterile


pyuria)

● Personal history of systemic autoimmune disease

● Large cystic kidneys by kidney imaging or examination

● Known history of multiple myeloma or monoclonal gammopathy

● Evidence of relatively rapid loss of kidney function (reduction in eGFR >5


mL/min/1.73 m2 per year or decline >25 percent); because there is
common physiologic variability, repeat lab testing within one to two
months (or sooner in some cases) may be warranted to clearly establish
trajectory of eGFR change ( figure 1)

● Single kidney with eGFR <60 mL/min/1.73 m2

● Inability to identify a presumed cause of CKD, especially in younger


patients

● Difficult to manage laboratory abnormalities such as hyperkalemia,


metabolic acidosis, anemia requiring erythropoietin therapy,
hyperphosphatemia, or hypocalcemia

● Resistant hypertension

● Recurrent or extensive nephrolithiasis

● Pregnancy

● Confirmed or presumed hereditary kidney disease, such as polycystic


kidney disease, Alport syndrome, or autosomal dominant interstitial
kidney disease

● Difficult to manage complications of various medications, such as


chemotherapeutic agents that may cause kidney injury or increase
proteinuria

Other patients do not require nephrology evaluation. As an example, patients


who have an eGFR that does not change over sequential measurements, who
have minimal or no proteinuria, and who have absence of cellular elements
on urine microscopy undergo a limited evaluation. A kidney biopsy is rarely
performed in such patients and the cause of CKD may not be identified with
certainty. (See 'Stable patients not in need of a nephrology evaluation' below.)

Stable patients not in need of a nephrology evaluation — Many patients


will have the cause of their kidney disease become apparent with the
evaluation described above. (See 'Evaluation to identify cause' above.)

However, the cause may not be apparent in some despite a thorough


evaluation. Among such patients, further evaluation and management
depends in part upon whether the kidney disease is progressive or stable. We
monitor serum creatinine within six weeks after CKD was initially recognized.
In some cases, the test should be repeated even sooner to determine if there
is evidence of rapid progression (ie, an eGFR decline of >5 mL/min/1.73 m2
per year or decline >25 percent). Those with rapid progression need to be
evaluated by nephrology. (See 'Indications for a nephrology evaluation'
above.)

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 decline in the eGFR to <30 mL/min/1.73 m2.

● A persistent increase in either the UACR to ≥300 mg/g (34 mg/mmol) or


the UPCR to ≥500 mg/g (56.5 mg/mmol).

● Development of new clinical evidence of autoimmune disease or


monoclonal gammopathy. This may be detected by new rash, arthritis,
bone pain, cytopenias, or other clinical changes that are otherwise
unexplained and were not present at initial evaluation.

● 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

Links to society and government-sponsored guidelines from selected


countries and regions around the world are provided separately. (See "Society
guideline links: Chronic kidney disease in adults".)

INFORMATION FOR PATIENTS

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)")

SUMMARY AND RECOMMENDATIONS


● Chronic kidney disease (CKD) is defined by the presence of kidney
damage or reduced glomerular filtration rate (GFR) for three or more
months, irrespective of the cause ( table 1). This three-month duration
distinguishes chronic from acute kidney disease. (See 'Introduction'
above.)

● 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.)

● 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. We obtain a cause-specific
history, perform a targeted physical examination, and, if not done
recently, we obtain urine studies and an ultrasound to determine the
cause ( algorithm 1). (See 'Evaluation to identify cause' above.)

● Based upon the targeted history, physical examination, laboratory


testing, and imaging, further evaluation with additional tests and kidney
biopsy may be warranted. Some adults with newly identified CKD should
be referred to a nephrologist. (See 'Indications for a nephrology
evaluation' above.)
REFERENCES

1. KDIGO 2012 Clinical Practice Guideline for the Evaluation and


Management of Chronic Kidney Disease. Kidney Int Suppl 2013; 3:1.
2. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury
Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury.
Kidney Int Suppl 2012; 2:1.
3. Rose BD. Pathophysiology of Renal Disease, 2nd ed., McGraw-Hill, New Yo
rk 1987. p.41.
4. Moghazi S, Jones E, Schroepple J, et al. Correlation of renal histopathology
with sonographic findings. Kidney Int 2005; 67:1515.
5. Manley JA, O'Neill WC. How echogenic is echogenic? Quantitative
acoustics of the renal cortex. Am J Kidney Dis 2001; 37:706.
6. Platt JF, Rubin JM, Bowerman RA, Marn CS. The inability to detect kidney
disease on the basis of echogenicity. AJR Am J Roentgenol 1988; 151:317.

Topic 102837 Version 18.0

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