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Offic ial reprint from UpToDate


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2010 UpToDate

Diagnostic approach to the patient with acute or chronic kidney


disease
Authors
Theodore W Post, MD
Burton D Rose, MD

Section Editor
Gary C Curhan, MD, ScD

Last literature review version 18.3: Setembro 2010 |


2009

Deputy Editor
Alic e M Sheridan, MD

This topic last updated: Abril 30,

INTRODUCTION Patients with renal disease may have a variety of different c linical
presentations. Some have symptoms (or signs) that are direc tly referable to the kidney
(hematuria, flank pain) or to associated extrarenal symptoms (edema, hypertension, signs of
uremia). Many patients, however, are asymptomatic and are noted on routine examination to
have an elevated plasma creatinine c onc entration or an abnormal urinalysis (such as microscopic
hematuria or proteinuria). Spec ific disorders are more likely to be either ac ute or c hronic in
duration, thereby narrowing the differential diagnosis among patients presenting with similar
clinical findings related to the kidney.
An overview of the diagnostic approach to the patient with renal disease is presented in this
topic. There are two major components to this evaluation:
Assessment of renal func tion by estimation of the glomerular filtration rate (GFR), initially
by measurement of the plasma c reatinine concentration and (in those with stable renal
function) the application of formulas whic h provide reasonable, but not precise, estimates
of GFR. (See "Assessment of kidney function: Serum creatinine; BUN; and GFR".)
Careful examination of the urine (by both qualitative chemical tests and mic roscopic
examination), since the urinary findings narrow the differential (table 1). (See "Urinalysis in
the diagnosis of renal disease".)
The epidemiology of c hronic kidney disease and recommendations for screening are presented
separately. (See "Epidemiology of chronic kidney disease and screening recommendations".)
MAJOR CAUSES OF KIDNEY DISEASE The c auses of ac ute or c hronic kidney disease are
traditionally classified by that portion of the renal anatomy most affec ted by the disorder [1].
Renal function is based upon four sequential steps, which are isolated to specific areas of the
kidney or surrounding struc tures:
First, blood from the renal arteries and their subdivisions is delivered to the glomeruli.
The glomeruli form an ultrafiltrate, nearly free of protein and blood elements, which
subsequently flows into the renal tubules.
The tubules reabsorb and secrete solute and/or water from the ultrafiltrate.
The final tubular fluid, the urine, leaves the kidney, draining sequentially into the renal
pelvis, ureter, and bladder, from which it is excreted through the urethra.
Renal disease can be caused by any proc ess that interferes with any of these struc tures and/or
functions. Identifying prerenal (reduced renal perfusion) and postrenal (obstructive) diseases is
particularly important because they may be readily reversible.
There is also a variable time course. The distinction between ac ute, subac ute and chronic
kidney disease is arbitrary. Clearly, a rise in the plasma c reatinine concentration or an
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abnormality on the urinalysis that has developed within days to weeks represents an acute
process, whereas evidence of renal disease extending for months to years is a c hronic proc ess
that may be assoc iated with acute exac erbations.
Prerenal disease The two major causes of reduced renal perfusion are volume depletion
and/or relative hypotension. This may result from true hypoperfusion due to bleeding,
gastrointestinal, urinary, or cutaneous losses, or to effective volume depletion in heart failure,
shock, or c irrhosis. (See "Chapter 8A: Effec tive c irculating volume and the steady state".)
Prerenal disease is most commonly assoc iated with an acute time course. However, among
patients with chronic kidney disease, the addition of a prerenal process may result in acute renal
dysfunction.
Vascular disease The vasc ular diseases affec ting the kidney c an be divided into those that
produce ac ute and chronic disease:
The major ac ute renal vasc ular disease is probably vasculitis (eg, Wegener's
granulomatosis). Less common etiologies include thromboembolic disease, hemolytic-uremic
syndrome or thrombotic thrombocytopenic purpura (HUS/TTP), malignant hypertension,
and scleroderma. (See "Renal manifestations of systemic vasc ulitis" and "Clinical
characteristics of renal atheroemboli".)
The major chronic renal vascular diseases are benign nephrosclerosis, unilateral or bilateral
renal artery stenosis, and cholesterol atheroembolic disease. (See "Clinic al features and
treatment of hypertensive nephrosclerosis" and "Chronic kidney disease associated with
atherosclerotic renovasc ular disease" and "Clinical c haracteristic s of renal atheroemboli".)
Glomerular disease There are numerous idiopathic and sec ondary (due to neoplasia,
autoimmunity, drugs, genetic abnormalities, and infec tions) disorders that produce glomerular
disease. Two general patterns (with considerable overlap in some diseases) are seen (table 2):
A nephritic pattern, which is associated with inflammation on histologic examination and
produces an ac tive urine sediment with red c ells, white c ells, granular and often red c ell
and other cellular c asts, and a variable degree of proteinuria.
A nephrotic pattern, whic h is not associated with inflammation on histologic examination
and is associated with proteinuria, often in the nephrotic range, and an inac tive urine
sediment with few c ells or casts.
Both patterns can present with an acute or insidious time c ourse, and elements of both may be
also seen in some patients simultaneously or sequentially. (See "Differential diagnosis of
glomerular disease".)
Tubular and interstitial disease As with vascular disease, the tubular and interstitial
diseases affec ting the kidney c an be divided into those that produce ac ute and chronic disease:
Hereditary, systemic , toxic, and drug-induced causes predominate.
The most c ommon acute tubulointerstitial disorders are acute tubular nec rosis, which
typically occ urs in hospitalized patients, acute interstitial nephritis, which is often druginduced, and cast nephropathy in multiple myeloma. Other c auses that should be
considered in the appropriate setting are acute phosphate nephropathy following a
phosphate-c ontaining bowel preparation prior to colonosc opy or surgery, and tumor lysis
syndrome following chemotherapy [2]. (See "Etiology and diagnosis of acute tubular
necrosis and prerenal disease" and "Clinic al manifestations and diagnosis of acute
interstitial nephritis" and "Types of renal disease in multiple myeloma" and "Acute
phosphate nephropathy" and "Tumor lysis syndrome".)

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The major chronic tubulointerstitial disorders are polycystic kidney disease, hypercalcemia,
and autoimmune disorders (such as sarc oidosis and Sjgren's syndrome). Reflux
nephropathy should be c onsidered in children and young adults, medullary cystic kidney
disease in families with a pattern of autosomal dominant inheritance, and nephrocalcinosis
should be considered in patients with one of the known causes of this disorder, such as
hypercalcemia. (See "Course and treatment of autosomal dominant polycystic kidney
disease" and "Renal disease in Sjgren's syndrome" and "Presentation, diagnosis, and
clinical course of vesicoureteral reflux" and "Medullary cystic kidney disease" and
"Nephrocalc inosis".)
Obstructive uropathy Obstruction to the flow of urine can occ ur anywhere from the renal
pelvis to the urethra. The development of renal insuffic iency in patients without intrinsic renal
disease requires bilateral obstruction (or unilateral obstruc tion with a single functioning kidney)
and is most c ommonly due to prostatic disease (hyperplasia or canc er) or metastatic cancer.
The time c ourse can be acute or c hronic. (See "Diagnosis of urinary tract obstruc tion and
hydronephrosis".)
Relative frequency There are limited data on the relative frequenc y of the different c auses
of acute renal failure (which is now commonly called acute kidney injury [AKI]) [3-6].
Furthermore, the distribution may vary with the type of hospital (community versus referral) and
geographic region.
A report from Madrid, for example, evaluated all 748 c ases of acute renal failure at 13 tertiary
hospital centers [4]. The most frequent causes were:
Acute tubular necrosis 45 percent
Prerenal 21 percent
Acute on chronic kidney disease 13 percent (mostly due to acute tubular necrosis and
prerenal disease)
Urinary trac t obstruction 10 percent (most often older men with prostatic disease)
Glomerulonephritis or vasc ulitis 4 percent
Acute interstitial nephritis 2 percent
Atheroemboli 1 percent
Data from the Program to Improve Care in Acute Renal Disease (PICARD) examined the etiology
of acute renal failure in a sicker population: 618 patients in five intensive care units in the United
States [5]. Over 70 percent of the c ases were asc ribed to isc hemic ac ute tubular necrosis
(including sepsis and hypotension); prerenal ac ute renal failure (hypovolemia, hemorrhage),
nephrotoxic ity (radioc ontrast nephropathy, rhabdomyolysis), ac ute renal failure with cardiac
disease (heart failure, shock), acute renal failure with liver disease (hepatorenal syndrome,
cirrhosis), and multifac torial etiologies ac counted for the remainder.
The incidence also varies because the definition of ac ute renal failure is unclear. The definition
of acute renal failure (also known as ac ute kidney injury [AKI]) is disc ussed separately. (See
"Definition of acute kidney injury (ac ute renal failure)".)
Little is known concerning the etiology of acute renal failure oc curring in patients with chronic
kidney disease. In a retrospective Chinese study of 104 patients with CKD, acute renal failure
was attributed to drug-related ATN/ac ute interstitial nephritis, prerenal disease, lupus nephritis
flare, and malignant hypertension in 36, 24, 20, and 9 percent of patients, respec tively [7].
The etiology of end-stage renal disease, although not verified histologically, is reported in
multiple databases. In the United States, the principal causes of ESRD are diabetes,
hypertension, glomerulonephritis, and tubulointerstitial disease.
PRESENTING MANIFESTATIONS Patients with renal disease may present in a variety of
ways:
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Signs and symptoms resulting directly from alterations in kidney function, inc luding
decreased or no urine output, flank pain, edema, hypertension, or disc olored urine.
Laboratory findings, inc luding elevations in the plasma c reatinine conc entration,
hyperkalemia, and an abnormal urinalysis.
Symptoms and/or signs of renal failure, including weakness and easy fatiguability (from
anemia), anorexia, vomiting, mental status changes or seizures, and edema.
Systemic symptoms and findings, such as fever, arthralgias, and pulmonary lesions,
suggestive of a concurrent systemic disease, such as vasculitis.
Incidental findings (eg, renal c yst or mass) on radiographic testing performed for some
other reason. (See "Simple and complex renal cysts in adults".)
The presence of c ertain symptoms or signs may suggest an underlying diagnosis. As examples,
unilateral flank pain is most consistent with a renal stone, renal infarction, infection, or
obstruc tion, while the total absence of urine (anuria) is primarily observed with bilateral ureteral
or renal arterial obstruction or shock.
A constellation of symptoms and signs may also favor a particular set of disorders. A patient
with edema, hypertension, red to brown colored urine due to hematuria (with red cell c asts), and
a rapidly rising plasma creatinine c oncentration almost certainly has acute glomerulonephritis or
vasculitis. Other manifestations, however, are relatively nonspecific and can be observed with a
wide variety of disorders.
Disease duration An important aspect of the evaluation of the patient with renal disease is
the determination of disease duration. As noted above, the differential diagnosis c an frequently
be narrowed if the disease duration is known.
The distinction between acute, rapidly progressive (subacute), and c hronic kidney disease is
arbitrary. Clearly, a rise in the plasma creatinine concentration or an abnormality on the
urinalysis that has developed within hours to days represents an acute process, whereas
evidence of renal disease extending for weeks represents a rapidly progressive proc ess and one
whic h extends over months to years is a chronic process that may be associated with acute
exacerbations.
This assessment is best performed by c omparing the current urinalysis or plasma creatinine
concentration with previous results. A patient with a c urrent plasma c reatinine of 4.0 mg/dL
(354 micromol/L) but a plasma level of 1.0 mg/dL (88 micromol/L) one month previously has
acute or rapidly progressive disease, while the same patient with a prior plasma creatinine
concentration of 3.0 mg/dL (265 micromol/L) two years ago has slowly progressive chronic
disease or an ac ute event in a patient with chronic disease.
When a previous urinalysis, plasma creatinine c onc entration, or radiographic study is unavailable,
certain c linical elements, including findings from the history and physical examination, may
suggest the duration of disease. These inc lude [1]:
The recent onset of symptoms or signs, such as fever and discolored urine, suggests an
ac ute proc ess.
Little or no output also suggests an acute component, since prolonged oliguria (output less
than 500 mL/day) is assoc iated with advanced renal failure.
An increasing plasma creatinine concentration after the initial evaluation is indicative of at
least an acute or rapidly progressive component to the disease, while a stable value
suggests a chronic disease. In addition, the rate of rise in the plasma creatinine
concentration may help distinguish among possible disorders. As an example, the plasma
creatinine c onc entration tends to rise progressively and usually at a rate greater than 0.3
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to 0.5 mg/dL (26 to 44 mic romol/L) per day in acute tubular nec rosis. In comparison, a
slower rate of rise with periodic downward fluctuations (due to variations in renal
perfusion) is suggestive of prerenal disease. (See "Etiology and diagnosis of acute tubular
necrosis and prerenal disease".)
Radiologic examination, most commonly by renal ultrasonography, showing small, echogenic
kidneys is most c onsistent with a chronic disease because of the progressive loss of renal
parenchyma and increased interstitial fibrosis with time. However, the presence of normalsized kidneys does not exclude chronic disease.
Other findings are less helpful. Although most patients with chronic kidney disease develop
anemia (due primarily to erythropoietin defic iency), a variety of acute diseases also can be
associated with anemia due to hemolysis or bleeding. Similarly, although the absence of anemia
in a patient with substantial renal insuffic iency is more compatible with acute disease, some
patients with chronic kidney disease are not anemic.
In-hospital acute renal failure Among patients who develop acute renal failure in the
hospital, the date of onset can be precisely timed in patients in whom the plasma c reatinine
concentration is measured frequently as part of routine blood testing. Suppose, for example,
that a patient has had a stable plasma creatinine concentration, which then begins to rise
progressively on day five. In suc h a patient, there must have been some insult on day four or a
cumulative insult that has bec ome clinic ally apparent (such as aminoglycoside therapy, a
hypotensive episode, or administration of radiographic contrast media). Careful perusal of the
patient's chart may identify the precipitating event on day four (eg, hypotension, radioc ontrast
exposure, c essation of intravenous hydration in a patient treated with intravenous acyclovir).
ASSESSMENT OF RENAL FUNCTION Once renal disease is disc overed, the presence or
degree of renal dysfunc tion is assessed and steps are taken to identify the cause. The history
and physic al examination are frequently helpful (eg, ac ute renal failure developing after
radiocontrast exposure or a course of aminoglycoside therapy). Initial testing must include an
estimation of the glomerular filtration rate and examination of the urine.
Glomerular filtration rate Estimation of the glomerular filtration rate (GFR) gives an
approximate measure of the number of func tioning nephrons. A reduction in GFR implies either
progression of the underlying disease or the development of a superimposed and often reversible
problem, such as decreased renal perfusion due to volume depletion. An increase in GFR, on the
other hand, is indic ative of improvement in renal function, whereas a stable GFR in patients with
renal disease implies stable disease.
The most common methods utilized to estimate the GFR in adults are the serum creatinine
concentration, the creatinine c learance, and estimation equations based upon the serum
creatinine concentration: the Coc kcroft-Gault equation and Modification of Diet in Renal Disease
(MDRD) study equation. Since all renal disorders variably affec t renal func tion, estimation of the
GFR has no diagnostic utility. In addition, serum creatinine and GFR estimation equations can
only be used in patients with stable kidney function. (See "Assessment of kidney function:
Serum creatinine; BUN; and GFR".)
The United States K/DOQI working groups have published guidelines rec ommending that patients
with c hronic kidney disease (CKD) should be classified by disease stage, with each stage being
defined in part by GFR estimation. The classification of CKD by stage is discussed elsewhere.
(see "Epidemiology of c hronic kidney disease and screening recommendations").
In adults with CKD, the GFR should be estimated from the MDRD Study and Cockcroft-Gault
equations, which take into account the serum c reatinine concentration and some or all of the
following variables: age, gender, race, and body size. Since the MDRD Study equation was
derived from patients (largely white) with nondiabetic renal disease (mean GFR of 40 mL/min per
1.73 m2) in the United States, it can be reliably used in such patients with significant kidney
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disease. It also appears to be ac curate in Afric an-Americans and those with diabetic kidney
disease.
However, the estimation equations have not been validated, and may be less ac curate, in some
populations. These include individuals with high, normal, or near-normal renal func tion, children,
certain ethnic groups, pregnant woman, and those with unusual musc le mass, body habitus, and
weight (eg, morbid obesity or malnourished). Some therefore rec ommend measuring the
creatinine clearance to estimate the GFR in these patients with stable renal func tion.
Serum creatinine and GFR estimation equations c an only be used in patients with STABLE kidney
function. With ac ute renal failure, for example, the GFR is initially markedly reduced but there
has not yet been time for c reatinine to accumulate and for the serum c reatinine concentration
to reflec t the degree of renal dysfunc tion.
It is important to apprec iate, however, that in most c linical settings (other than dose
adjustment for medications), exact knowledge of the GFR is not required. As an example,
knowing that the GFR is 40 mL/min rather than 30 or 50 mL/min provides little useful information
to help determine therapy. What is important to know in the patient with kidney disease is
whether the GFR (and therefore disease severity) is c hanging or is stable. This can usually be
determined by monitoring c hanges in the serum creatinine or the estimated GFR in patients with
a relatively c onstant body mass and diet. (See "Assessment of kidney function: Serum
creatinine; BUN; and GFR".)
URINARY FINDINGS
Urinalysis The microsc opic examination of the urinary sediment urinalysis is the most
important noninvasive test in the diagnostic evaluation, since characteristic findings strongly
suggest c ertain diagnoses (table 1). As an example, the presence of muddy brown granular
casts and epithelial cell casts in a patient with ac ute renal failure is highly suggestive of acute
tubular necrosis. However, the absence of these urinary findings does not exc lude the diagnosis.
(See "Urinalysis in the diagnosis of renal disease" and "Etiology and diagnosis of acute tubular
nec rosis and prerenal disease".)
The finding of one red cell c ast is diagnostic of vasculitis or glomerulonephritis (either acute or
chronic), while the presence of signific ant proteinuria is generally indicative of some form of
glomerular disease. Evaluation of red cell morphology also may be helpful in the patient with
hematuria. The red c ells are typically uniform and round (as in a peripheral blood smear) with
extrarenal bleeding, but usually have a dysmorphic appearance with renal lesions, partic ularly
glomerular diseases.
Among patients who have glomerular disease, the urinalysis c an help subclassify patients into
those with glomerulonephritis, who have an active "nephritic" sediment, and those with a
nephrotic pattern in which moderate to heavy proteinuria is associated with a generally inactive
sediment (table 2). (See "Differential diagnosis of glomerular disease".)
Even a normal urinalysis has diagnostic utility. The finding of normal or near-normal urinalysis,
characterized by few cells with little or no c asts or proteinuria, suggests different disorders
based upon disease duration:
With an ac ute proc ess, prerenal disease, urinary tract obstruc tion, hyperc alcemia, cast
nephropathy in multiple myeloma, acute phosphate nephropathy, tumor lysis syndrome,
and some cases of acute tubular nec rosis.
With c hronic disease, prerenal disease due to advanced heart failure or cirrhosis,
nephrosclerosis, urinary tract obstruction, and tubulointerstitial disease are the most
frequent c auses.
In addition to microscopic examination, the urine is also tested via dipstick for protein, pH,
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concentration, glucose, hematuria and pyuria.


(See "Urinalysis in the diagnosis of renal disease".)
The diagnostic evaluation of the patient with isolated hematuria or proteinuria and a normal
plasma creatinine concentration is discussed in detail separately. (See "Evaluation of hematuria
in adults" and "Evaluation of isolated proteinuria in adults".)
Urine sodium excretion The urine c an be rendered virtually sodium-free (urine sodium
concentration as low as 1 meq/L) in the presence of volume depletion and normal renal function.
Acute renal failure With acute renal failure, measurement of the urine sodium
concentration is helpful in distinguishing acute tubular nec rosis from effective volume depletion.
The urine sodium concentration is usually above 40 meq/L and below 20 meq/L in the former and
the latter conditions, respec tively. However, sinc e the urinary sodium c onc entration is influenced
by the urine output, there is substantial overlap due in part to variations in the urine volume. As
an example, a given rate of sodium exc retion will be assoc iated with a lower urine sodium
concentration by dilution in patients who have a high urine output.
The effect of variations in urine volume can be eliminated by calc ulating the fractional excretion
of sodium (FENa). This is defined by the following equation:

FENa, percent

UNa x PCr

PNa x UCr

100

where UCr and PCr are the urine and plasma creatinine concentrations, respectively, and UNa
and PNa are the urine and plasma sodium conc entrations, respectively.
The FENa is the most ac curate screening test to differentiate between prerenal disease and
acute tubular nec rosis. A value below 1 percent suggests prerenal disease, where the
reabsorption of almost all of the filtered sodium represents an appropriate response to decreased
renal perfusion; in comparison, a value between 1 and 2 percent may be seen with either
disorder, while a value above 2 percent usually indicates ATN.
The FENa is most useful in patients with severe renal failure. It is less ac curate in those with a
normal or moderately reduced GFR because the value determining a prerenal state c hanges
continuously with the GFR. Why this occurs is discussed in detail separately. (See "Frac tional
excretion of sodium in ac ute kidney injury (acute renal failure)".)
A low FENa is not unique to prerenal disease, sinc e it can occ ur in disorders assoc iated with
normal tubular function but a low GFR. These include acute glomerulonephritis, vasculitis, and
acute urinary tract obstruction. It can also be seen when ac ute tubular necrosis is superimposed
upon a chronic sodium-retaining state (eg, aminoglycoside therapy in a patient with cirrhosis).
Chronic kidney disease Among patients with chronic kidney disease, the addition of a
prerenal process may not result in a low urine sodium conc entration or FENa since the renal
tubules may be unable to maximally c onserve water and sodium. In suc h patients, the prerenal
state may be strongly suggested from the history (eg, vomiting, diarrhea, diuretic therapy) and
physical examination (eg, relative hypotension, reduced skin turgor). A judicious trial of fluid
repletion may result in recovery of renal func tion.
Urine volume Although the glomerular filtration rate is very low in patients with renal failure,
the urine output is variable, ranging from oliguria to normal or even above normal levels. These
findings are related to the fact that the urine output is determined, not by the GFR alone, but by
the difference between the GFR and the rate of tubular reabsorption. If, for example, a patient
with advanced ac ute or chronic kidney disease has a GFR of 5 L/day (versus the normal of 140
to 180 L/day), the daily urine output will still be 1.5 L if only 3.5 L of the filtrate is reabsorbed.
(See "Urine output and residual renal func tion in renal failure".)
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This suggests that the urine output is of little diagnostic value. However, little or no output is
diagnostically useful in the acute setting. Causes of this finding inc lude shock, complete bilateral
urinary trac t obstruction, renal cortic al necrosis, and bilateral vascular occlusion (as with a
dissec ting aneurysm or thrombotic thrombocytopenic purpura-hemolytic uremic syndrome).
RADIOLOGIC STUDIES A number of radiologic studies are used to evaluate the patient with
renal disease. These tests are performed alone or in combination for the detec tion, diagnosis,
and/or the evaluation of multiple conditions. They are principally required to assess urinary tract
obstruc tion, kidney stones, renal c yst or mass, disorders with c haracteristic radiographic
findings, renal vascular diseases, and, in c hildren and young adults, vesicoureteral reflux.
Bec ause of safety, ease of use, and the information provided, the most commonly used
radiographic technique in patients presenting with renal disease is renal ultrasonography. Sinc e
obstruc tion is a readily reversible disorder, all patients presenting with acute or chronic kidney
disease of unknown etiology should undergo ultrasonography, the modality of c hoic e to assess
possible obstructive disease. Helical CT sc an is generally preferred with patients with flank pain
and possible urolithiasis. (See "Radiologic assessment of renal disease" and "Diagnosis and acute
management of suspected nephrolithiasis in adults".)
Among patients with moderate to advanc ed renal failure (dialysis-dependent or estimated GFR
less than 30 mL/min), the administration of gadolinium has been associated with the potentially
severe syndrome of nephrogenic systemic fibrosis. In such patients, gadolinium-based imaging
should be avoided if possible. This issue is disc ussed separately. (See "Nephrogenic systemic
fibrosis/nephrogenic fibrosing dermopathy in advanced renal failure".)
RENAL BIOPSY A renal biopsy is most commonly obtained when noninvasive evaluation has
been unable to establish the correct diagnosis [8,9]. (See "Indications for and complications of
renal biopsy".)
The major indications for renal biopsy inc lude:
Isolated glomerular hematuria with proteinuria
Nephrotic syndrome
Acute nephritic syndrome
Unexplained ac ute or rapidly progressive renal failure
Renal biopsy is most often performed percutaneously. Bleeding is the most common complication
with the perc utaneous tec hnique. The incidence can be minimized by documenting that the
partial thromboplastin time, prothrombin time, and platelet c ount are normal. To help ensure
normal c oagulation, patients should refrain from taking aspirin or nonsteroidal antiinflammatory
drugs at least one week prior to a scheduled elective biopsy, and heparin should be stopped the
day prior to the procedure.
Even with these precautions, transient microsc opic hematuria occurs in almost all patients and
transient gross hematuria in 3 to 10 perc ent [8-10]. Bleeding severe enough to cause
hypotension occ urs in 1 to 2 percent, and transfusions are required in approximately 0.1 to 0.3
percent. (See "Indications for and complications of renal biopsy".)
Percutaneous renal biopsy is generally c ontraindic ated in the following settings [8,9]:
Unc orrectable bleeding diathesis
Small kidneys which are generally indicative of chronic irreversible disease
Severe hypertension, whic h cannot be controlled with antihypertensive medications
Multiple, bilateral cysts or a renal tumor
Hydronephrosis
Active renal or perirenal infection
An unc ooperative patient
An open renal biopsy (or a modified open biopsy performed under loc al anesthesia) should be
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considered when there is an unc orrectable bleeding diathesis, after failed attempts at
percutaneous biopsy, and perhaps when there is a solitary native kidney. However, it has been
suggested that the likelihood of requiring surgery and nephrectomy after percutaneous biopsy is
so low that it may be less than the risk of general anesthesia [8,10,11]. As a result,
percutaneous biopsy may be considered in selected cases with a solitary native kidney.
SUMMARY AND GENERAL RECOMMENDATIONS
The approach to the patient with acute, rapidly progressive or chronic kidney disease
primarily involves establishing the correct diagnosis and estimating the degree of renal
dysfunc tion. The causes of ac ute or chronic kidney disease are traditionally classified by
that portion of the renal anatomy most affected by the disorder. These include prerenal,
vasc ular, glomerular, tubulointerstitial, and obstruc tive disease. (See 'Introduc tion' above
and 'Major c auses of kidney disease' above.)
Patients with renal disease may present in a variety of ways. These include signs and
symptoms resulting direc tly from alterations in kidney function, asymptomatic elevations in
the plasma creatinine c onc entration or abnormalities on urinalysis, symptoms and/or signs
of renal failure, systemic symptoms and findings, and/or incidental findings on radiographic
testing performed for some other reason. (See 'Presenting manifestations' above.)
Once renal disease is discovered, the degree of renal dysfunction is assessed. The most
common methods utilized to estimate the GFR in adults are the serum creatinine
concentration, the c reatinine clearance, and estimation equations based upon the serum
creatinine c onc entration: the Cockcroft-Gault equation and Modification of Diet in Renal
Disease (MDRD) study equation. Serum creatinine and GFR estimation equations can only
be used in patients with STABLE kidney function. With acute renal failure, the GFR is
initially markedly reduced but there has not yet been time for c reatinine to accumulate and
for the serum c reatinine conc entration to reflect the degree of renal dysfunction.
However, in most c linical settings (other than dose adjustment for medications), exact
knowledge of the GFR is not required. (See 'Glomerular filtration rate' above.)
The urinalysis is the most important noninvasive test in the diagnostic evaluation, sinc e
characteristic findings on microscopic examination of the urine sediment strongly suggest
certain diagnoses. (See 'Urinalysis' above.)
In ac ute renal failure, the fractional excretion of sodium (FeNa) is the most accurate
screening test to differentiate between prerenal disease and ac ute tubular necrosis. A
value below 1 percent suggests prerenal disease; in comparison, a value between 1 and 2
percent may be seen with either disorder, while a value above 2 percent usually indicates
ATN. (See 'Ac ute renal failure' above.) By comparison, among patients with chronic kidney
disease, the addition of a prerenal process may not result in a low urine sodium
concentration or FENa. (See 'Chronic kidney disease' above.)
An important aspect of the initial evaluation is the determination of disease duration.
Although the distinction between ac ute, rapidly progressive, and chronic kidney disease is
arbitrary, the differential diagnosis c an frequently be narrowed if the disease duration is
known. This assessment is best performed by c omparing the current urinalysis or plasma
creatinine c onc entration with previous results, if available.
Because of safety, ease of use, and the information provided, the most c ommonly used
radiographic technique in patients presenting with renal disease is renal ultrasonography.
Sinc e obstruction is a readily reversible disorder, all patients presenting with acute or
chronic renal failure of unknown etiology should undergo ultrasonography, the modality of
choice to assess possible obstruc tive disease. (See 'Radiologic studies' above.)
A renal biopsy is most c ommonly obtained in patients with suspec ted glomerulonephritis or
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vasc ulitis and in those with otherwise unexplained ac ute or subacute renal failure. (See
'Renal biopsy' above.)

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REFERENCES
1. Rose, BD. Pathophysiology of Renal Disease, 2d ed, Mc Graw-Hill, New York, 1987, p. 41.
2. Esson, ML, Schrier, RW. Diagnosis and treatment of acute tubular necrosis. Ann Intern Med
2002; 137:744.
3. Lameire, N, Van Biesen, W, Vanholder, R. Acute renal failure. Lancet 2005; 365:417.
4. Liao, F, Pascual, J. Epidemiology of acute renal failure: a prospec tive, multic enter,
community-based study. Madrid Ac ute Renal Failure Study Group. Kidney Int 1996; 50:811.
5. Mehta, RL, Pasc ual, MT, Soroko, S, et al. Spectrum of ac ute renal failure in the intensive
care unit: the PICARD experienc e. Kidney Int 2004; 66:1613.
6. Presc ott, GJ, Metcalfe, W, Baharani, J, et al. A prospective national study of acute renal
failure treated with RRT: inc idenc e, aetiology and outc omes. Nephrol Dial Transplant 2007;
22:2513.
7. Zhang, L, Wang, M, Wang, H. Ac ute renal failure in c hronic kidney disease--c linical and
pathologic al analysis of 104 cases. Clin Nephrol 2005; 63:346.
8. Madaio, MP. Renal biopsy. Kidney Int 1990; 38:529.
9. Appel, GB. Renal biopsy: How effective, what technique, and how safe. J Nephrol 1993;
6:4.
10. Mendelssohn, DC, Cole, EH. Outc omes of perc utaneous kidney biopsy, including those of
solitary native kidneys. Am J Kidney Dis 1995; 26:580.
11. Schow, DA, Vinson, RK, Morrisseau, PM. Perc utaneous renal biopsy of the solitary kidney: a
contraindication? J Urol 1992; 147:1235.

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GRAPHICS
Correlation between urinary patterns and renal disease
Urinary
pattern

Renal disease

Hematuria with
red cell casts,
dysmorphic red
cells, heavy
proteinuria, or
lipiduria

Virtually diagnostic of glomerular disease or vasculitis

Multiple
granular and
epithelial cell
casts with free
epithelial cells

Strongly suggestive of acute tubular necrosis in a patient with acute


renal failure

Pyuria with
white cell and
granular or
waxy casts and
no or mild
proteinuria

Suggestive of tubular or interstitial disease or urinary tract obstruction

Hematuria and
pyuria with no
or variable
casts (excluding
red cell casts)

May be observed in acute interstitial nephritis, glomerular disease,


vasculitis, obstruction, and renal infarction

Hematuria
alone

Varies with the clinical setting

Pyuria alone

Usually infection; sterile pyuria suggests urinary tract tuberculosis or


tubulointerstitial disease

Few cells w ith


little or no casts
or proteinuria
(normal or
near-normal)

In acute renal failure, prerenal disease, urinary tract obstruction,


hypercalcemia, myeloma kidney, some cases of acute tubular necrosis,
or a vascular disease with glomerular ischemia but not infarction
(scleroderma, atheroemboli); in chronic renal failure, nephrosclerosis,
urinary tract obstruction, and tubulointerstitial disease

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Classification of glomerular disease according to clinical features


Focal glomerulonephritis
Active urine sediment without renal insufficiency or nephrotic syndrome
Less than 15 years - Mild postinfectious glomerulonephritis, IgA nephropathy, thin basement
membrane disease, hereditary nephritis, Henoch-Schnlein purpura, mesangial proliferative
glomerulonephritis
15 to 40 years - IgA nephropathy, thin basement membrane disease, lupus, hereditary nephritis,
mesangial proliferative glomerulonephritis
Greater than 40 years - IgA nephropathy

Diffuse glomerulonephritis
Active urine sediment with renal insufficiency and variable proteinuria, which can include
nephrotic syndrome
Less than 15 years - Postinfectious glomerulonephritis, membranoproliferative
glomerulonephritis
15 to 40 years - Postinfectious glomerulonephritis, lupus, rapidly progressive glomerulonephritis,
fibrillary glomerulonephritis, membranoproliferative glomerulonephritis
Greater than 40 years - Rapidly progressive glomerulonephritis, vasculitis (including mixed
cryoglobulinemia), fibrillary glomerulonephritis, postinfectious glomerulonephritis

Nephrotic syndrome
Heavy proteinuria, bland sediment although some hematuria allowed
Less than 15 years - Minimal change disease, focal glomerulosclerosis, mesangial proliferative
glomerulonephritis
15 to 40 years - Focal glomerulosclerosis, minimal change disease, membranous nephropathy
(including lupus), diabetic nephropathy, preeclampsia, postinfectious glomerulonephritis (later
stage)
Greater than 40 years - Focal glomerulosclerosis, membranous nephropathy, diabetic
nephropathy, minimal change disease, IgA nephropathy, primary amyloidosis or the related
disorder light chain deposition disease (which can account for 15 to 20 percent of cases in
patients over the age of 60), benign nephrosclerosis, postinfectious glomerulonephritis (later
stage)

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