11/3/24, 20:20 Chronic kidney disease (newly identified): Clinical presentation and diagnostic approach in adults - UpToDate

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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

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

Literature review current through: Feb 2024.

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:

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● 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

Patients with chronic kidney disease (CKD) 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 kidney 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

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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 patients with CKD 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 chronic kidney disease (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 kidney 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

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The initial assessment for all patients who present with suspected chronic kidney disease
(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-

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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

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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 patients with CKD, 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 chronic kidney disease (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
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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 "Focal segmental glomerulosclerosis: Genetic causes" and "Fabry disease:
Kidney manifestations" and "C3 glomerulopathies: Dense deposit disease and C3
glomerulonephritis", section on 'Pathogenesis' and "IgA nephropathy: Pathogenesis",
section on 'Genetic susceptibility'.)

● 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 kidney 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 "Nephrotoxicity of molecularly targeted

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agents and immunotherapy" 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
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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

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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's disease" 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.)

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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

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● 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.)

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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

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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) versus acute kidney disease or injury – 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). 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. Acute kidney injury (AKI)
is defined by a rise in the serum creatinine level that has developed within hours to
days ( table 2). (See 'Introduction' above and "Diagnostic approach to adult patients
with subacute kidney injury in an outpatient setting" and "Evaluation of acute kidney
injury among hospitalized adult patients".)

● Clinical presentation – Patients with CKD 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 kidney cysts with enlarged kidneys suggestive of
polycystic kidney disease) may be observed on imaging performed for some other
reason. (See 'Clinical presentation' above.)

● Initial assessment and triage – The initial assessment for patients who present with
suspected CKD starts with triage of those who may need urgent dialysis based upon

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symptoms or life-threatening laboratory abnormalities ( algorithm 1).

• Identification of patients needing urgent dialysis – Patients 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.)

• Evaluation of disease duration – 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.)

● 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. (See 'Evaluation to identify cause' above.)

• Indications for a nephrology evaluation – 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.)

Use of UpToDate is subject to the Terms of Use.

REFERENCES

1. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic
Kidney Disease. Kidney Int Suppl 2013; 3:1.

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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 York 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.
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GRAPHICS

Definition and criteria for chronic kidney disease

Definition:
Chronic kidney disease is defined based on the presence of either kidney damage or decreased
kidney function for three or more months, irrespective of cause.

Criteria Comment

Duration ≥3 months, Duration is necessary to distinguish chronic from acute kidney diseases.
based on Clinical evaluation can often suggest duration
documentation or Documentation of duration is usually not available in epidemiologic
inference studies

Glomerular filtration GFR is the best overall index of kidney function in health and disease.
rate (GFR) <60 The normal GFR in young adults is approximately 125 mL/min/1.73 m 2 ;
mL/min/1.73 m 2 GFR <15 mL/min/1.73 m 2 is defined as kidney failure
Decreased GFR can be detected by current estimating equations for
GFR based on serum creatinine (estimated GFR) but not by serum
creatinine alone
Decreased estimated GFR can be confirmed by measured GFR,
measured creatinine clearance, or estimated GFR using cystatin C

Kidney damage, as Pathologic abnormalities (examples). Cause is based on underlying illness

defined by structural and pathology. Markers of kidney damage may reflect pathology.
abnormalities or Glomerular diseases (diabetes, autoimmune diseases, systemic
functional infections, drugs, neoplasia)
abnormalities other Vascular diseases (atherosclerosis, hypertension, ischemia, vasculitis,
than decreased GFR thrombotic microangiopathy)
Tubulointerstitial diseases (urinary tract infections, stones, obstruction,
drug toxicity)
Cystic disease (polycystic kidney disease)

History of kidney transplantation. In addition to pathologic abnormalities

observed in native kidneys, common pathologic abnormalities include the
following:
Chronic allograft nephropathy (non-specific findings of tubular atrophy
interstitial fibrosis, vascular and glomerular sclerosis)
Rejection
Drug toxicity (calcineurin inhibitors)
BK virus nephropathy
Recurrent disease (glomerular disease, oxalosis, Fabry disease)

Albuminuria as a marker of kidney damage (increased glomerular

permeability, urine albumin-to-creatinine ratio [ACR] >30 mg/g).*
The normal urine ACR in young adults is <10 mg/g. Urine ACR
categories 10-29, 30-300 and >300 mg are termed "mildly increased,

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moderately increased, and severely increased" respectively. Urine ACR

>2200 mg/g is accompanied by signs and symptoms of nephrotic
syndrome (low serum albumin, edema and high serum cholesterol).
Threshold value corresponds approximately to urine dipstick values of
trace or 1+, depending on urine concentration
High urine ACR can be confirmed by urine albumin excretion in a timed
urine collection

Urinary sediment abnormalities as markers of kidney damage, for example:

RBC casts in proliferative glomerulonephritis
WBC casts in pyelonephritis or interstitial nephritis
Oval fat bodies or fatty casts in diseases with proteinuria
Granular casts and renal tubular epithelial cells in many parenchymal
diseases (non-specific)

Imaging abnormalities as markers of kidney damage (ultrasound, computed

tomography and magnetic resonance imaging with or without contrast,
isotope scans, angiography).
Polycystic kidneys
Hydronephrosis due to obstruction
Cortical scarring due to infarcts, pyelonephritis or vesicoureteral reflux
Renal masses or enlarged kidneys due to infiltrative diseases
Renal artery stenosis
Small and echogenic kidneys (common in later stages of CKD due to
many parenchymal diseases)

* Albumin-to-creatinine ratio (ACR) conversion factor 1.0 mg/g = 0.113 mg/mmol.

Reproduced from: Levey A, Coresh J. Chronic kidney disease. Lancet 2011. DOI: 10.1016/S0140-6736(11)60178-5. Table used
with the permission of Elsevier Inc. All rights reserved.

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Criteria for acute kidney injury

RIFLE [1] AKIN [2] KDIGO [3]

Diagnostic criteria*

Increase in serum Increase in serum

creatinine of ≥0.3 creatinine of ≥0.3
mg/dL or ≥50% within mg/dL within 48 hours
48 hours or ≥50% within 7 days

OR OR

Urine output of <0.5 Urine output of <0.5

mL/kg/hour for >6 mL/kg/hour for >6
hours hours

Staging criteria

Risk (RIFLE) or stage Increase in serum Increase in serum Increase in serum

1 (AKIN/KDIGO) creatinine to 1.5 times creatinine of ≥0.3 creatinine of ≥0.3
baseline mg/dL or to 150 to mg/dL or 1.5 to 1.9
200% baseline times baseline
OR
OR OR
Urine output of <0.5
mL/kg/hour for 6 to 12 Urine output of <0.5 Urine output of <0.5
hours mL/kg/hour for 6 to 12 mL/kg/hour for 6 to 12
hours hours

Injury (RIFLE) or Increase in serum Increase in serum Increase in serum

stage 2 creatinine to 2 times creatinine to 200 to creatinine to 2 to 2.9
(AKIN/KDIGO) baseline 300% baseline times baseline

OR OR OR

Urine output of <0.5 Urine output of <0.5 Urine output of <0.5

mL/kg/hour for 12 to mL/kg/hour for 12 to mL/kg/hour for 12 to
24 hours 24 hours 24 hours

Failure (RIFLE) or Increase in serum Increase in serum Increase in serum

stage 3 creatinine to 3 times creatinine to >300% creatinine to ≥3 times
(AKIN/KDIGO) baseline baseline baseline

OR OR OR

Increase in serum Increase in serum Increase in serum

creatinine by >0.5 creatinine by >0.5 creatinine of ≥0.3
mg/dL to >4 mg/dL mg/dL to ≥4 mg/dL mg/dL to ≥4 mg/dL ¶

OR OR OR

Urine output of <0.3 Urine output of <0.3 Urine output of <0.3

mL/kg/hour for >24 mL/kg/hour for >24 mL/kg/hour for ≥24
hours or anuria for >12 hours or anuria for >12 hours or anuria for ≥12
hours hours hours

OR OR OR

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Initiation of kidney Initiation of kidney Initiation of kidney

replacement therapy replacement therapy replacement therapy

Loss (RIFLE) Need for kidney

replacement therapy
for >4 weeks

End stage (RIFLE) Need for kidney

replacement therapy
for >3 months

RIFLE: risk, injury, failure, loss, ESKD; AKIN: Acute Kidney Injury Network; KDIGO: Kidney Disease:
Improving Global Outcomes; ESKD: end-stage kidney disease.

* AKIN and KDIGO provided both diagnostic and staging criteria. RIFLE provided a graded definition
of AKI that is implicit in the staging criteria.

¶ In patients <18 years, stage 3 AKI is also defined by KDIGO as a decrease in estimated glomerular
filtration rate (eGFR) to <35 mL/min/1.73 m 2 .

References:
1. Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure-definition, outcome measures, animal models, fluid therapy and
information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative
(ADQI) Group. Crit Care 2004; 8:B204. Copyright © 2004 BioMed Central Ltd.
2. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute
kidney injury. Crit Care 2007; 11:R31. Copyright © 2007 BioMed Central Ltd.
3. Kidney Disease: Improving Global Outcomes (KDIGO). Acute Kidney Injury Work Group. KDIGO clinical practice
guidelines for acute kidney injury. Kidney Int Suppl 2012; 2:1.

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Newly identified chronic kidney disease (CKD)

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CKD: chronic kidney disease; eGFR: estimated glomerular filtration rate; SLE: systemic lupus
erythematosus; HCV: hepatitis C virus; HBV: hepatitis B virus.

* CKD is defined by the presence of kidney damage or decreased kidney function for 3 or more
months, irrespective of the cause. Kidney damage refers to pathologic abnormalities, whether
established with a kidney biopsy or imaging studies, or inferred from markers such as urinary
sediment abnormalities or increased rates of urinary albumin excretion. Decreased kidney function
refers to a decreased eGFR (eGFR <60 mL/min/1.73 m 2 ).

¶ Dialysis may be needed urgently if a patient with markedly impaired eGFR (ie, eGFR <15
mL/min/1.73 m 2 ) has severe and refractory hyperkalemia, acidosis, or hypervolemia; in addition,
severe uremic symptoms (encephalopathy, pericarditis, etc) often warrant initiation of dialysis. Most
patients presenting with CKD will not require dialysis at presentation. Refer to UpToDate topic on
indications for initiation of dialysis in patients with CKD.

Δ Urinary tract obstruction typically causes decreased eGFR if the obstruction is bilateral; unilateral
obstruction may lead to decreased eGFR if the obstructed kidney was the primary functioning kidney,
or if both kidneys are damaged due to another disorder such that neither kidney has functional
reserve. Kidney ultrasound may also corroborate the presence of CKD (revealing small echogenic
kidneys) or may suggest an alternate etiology of CKD, such as cystic kidney disease. Refer to
UpToDate topic on radiographic assessment of kidney disease.

◊ Rapid progression is defined as a decrease in eGFR >5 mL/min/1.73 m 2 over a year (or a
corresponding rate of decline over a shorter period of time), or a 25% decline in eGFR from baseline.
Rapid progression over 4 to 8 weeks should be viewed as subacute kidney injury and may warrant
urgent consultation with nephrology. Refer to UpToDate topic on subacute kidney injury.

§ Consultation with nephrology may result in directed medical management, kidney biopsy, and
dialysis planning when indicated.

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Creatinine trend in a patient with chronic kidney disease and superimposed

bouts of acute or subacute injury

Note the gradual rise in average serum creatinine over many years (progressive chronic kidney
disease) as well as stuttering course (ie, rise and fall) of individual creatinine values. A corresponding
graph of estimated glomerular filtration rate would reveal a similar but inverse temporal trend.

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Retinal fundus photographs of hypertensive retinopathy

Representative digital retinal fundus photographs of mild (A,B), moderate (C,D), and severe (E,F)
hypertensive retinopathy, as graded with the simplified classification:

(A) Mild hypertensive retinopathy is indicated by the presence of generalized arteriolar narrowing,
arteriovenous (AV) nicking, and opacification of the arteriolar wall ("copper wiring").

(B) Mild hypertensive retinopathy with focal arteriolar narrowing.

(C,D) Moderate hypertensive retinopathy with multiple retinal hemorrhages and cotton wool patches.

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(E,F) Severe hypertensive retinopathy with swelling of the optic disk, retinal hemorrhages, hard
exudates, and cotton wool patches.

From: Downie LE, Hodgson LA, Dsylva C, et al. Hypertensive retinopathy: Comparing the Keith-Wagener-Barker to a simplified
classification. J Hypertens 2013; 31:960. DOI: 10.1097/HJH.0b013e32835efea3. Copyright © 2013. Reproduced with permission
from Wolters Kluwer Health. Unauthorized reproduction of this material is prohibited.

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Leukocytoclastic vasculitis

Leukocytoclastic vasculitis appearing as raised purpura. This lesion can occur with any vasculitic
syndrome and in the collagen vascular diseases.

Courtesy of Marvin I Schwarz, MD.

Graphic 78697 Version 2.0

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11/3/24, 20:20 Chronic kidney disease (newly identified): Clinical presentation and diagnostic approach in adults - UpToDate

Leukocytoclastic vasculitis of lower extremities with histology

Cutaneous vasculitis most often presents as palpable purpura that is typically a manifestation of
benign, localized, self-limited cutaneous disease, often triggered by preceding infection or drug
ingestion. Histologically, it is identified by a neutrophilic infiltrate surrounding and disrupting small
vessels (postcapillary venules) associated with fibrin deposits and nuclear debris (leukocytoclasia).
Extravasated red blood cells, purpura, will be found in the adjacent dermis.

From: Carlson JA, Chen KR. Cutaneous vasculitis update: Small vessel neutrophilic vasculitis syndromes. Am J Dermatopathol
2006; 28:486. Reproduced with permission from Lippincott Williams & Wilkins. Copyright © 2006 International Society of
Dermatopathology. Unauthorized reproduction of this material is prohibited.

Graphic 94489 Version 6.0

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Puffy hands and shiny skin in early systemic sclerosis

(A) Diffusely puffy fingers are a common initial presentation.

(B) Shiny skin suggests impending skin thickening.

Reprinted with permission from Systemic Sclerosis/Scleroderma: A Treatable Multisystem Disease, October 15, 2008, Vol 78, No
8, American Family Physician. Copyright © 2008 American Academy of Family Physicians. All Rights Reserved.

Graphic 96749 Version 2.0

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First web-space contracture in systemic sclerosis

This patient has a first web-space contracture associated with systemic sclerosis. The thumb MCP joint
exhibits a hyperextension deformity, and the thumb IP joint exhibits a flexion deformity. The resultant
contracture limits the patient's ability to bring the thumb out of the plane of the palm to grasp large
objects.

MCP: metacarpophalangeal; IP: interphalangeal

Courtesy of Philip E Blazar, MD.

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Contributor Disclosures
Pedram Fatehi, MD, MPH No relevant financial relationship(s) with ineligible companies to
disclose. Chi-yuan Hsu, MD, MSc No relevant financial relationship(s) with ineligible companies to
disclose. Gary C Curhan, MD, ScD Grant/Research/Clinical Trial Support: GlaxoSmithKline [Shingles]. All
of the relevant financial relationships listed have been mitigated. Marcello Tonelli, MD, SM, FRCPC No
relevant financial relationship(s) with ineligible companies to disclose. Eric N Taylor, MD, MSc,
FASN No relevant financial relationship(s) with ineligible companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

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