141

ULTRASOUND

Hedvig Hricak, M.D.2

Cosme Cruz, M.D.Raymond Romanski, M.D.M. H. Uniewski, R.N.

N. W. Levin, M.D.

Beatrice L. Madrazo, M.D.Michael A. Sandler, M.D.William R. Eyler, M.D.

Renal Parenchymal Disease:

Sonographic-Histologic Correlation1

A retrospective study of 109 patients whounderwent renal biopsy was designed tocorrelate the sonographic appearance ofthe kidney with the histologic changesand clinical and laboratory findings invarious renal parenchymal diseases. Theclinical, pathologic, and sonographic datawere analyzed blindly and independentlyby a team from each corresponding disci-pline. There was no correlation betweenthe specific sonographic appearance andthe type of renal disease. There was a sig-nificant correlation between renal lengthand the prevalence of global sclerosis,focal tubular atrophy, and the number ofhyaline casts per glomerulus. A signifi-cant positive correlation was also foundbetween cortical echogenicity and the se-verity of global sclerosis, focal tubular at-rophy, the number of hyalin#{231} casts perglomerulus, and focal leukocytic infiltra-tion. While there was overall significantcorrelation between the degree of corticalechogenicity and blood urea nitrogen andcreatinine concentrations in each group, awide range of variance was present. It isnot currently feasible to distinguish dif-ferent types of renal medical disordersusing diagnostic ultrasound.

Index terms: Kidney, diseases #{149}Kidney. ultrasound

studies, 8(1)1298

Radiology 144: 141-147, July 1982

1 From the Departments of Diagnostic Radiology(H.H., B.L.M., M.A.S., W.R.E.), Medicine (CC.,M.H.U., N.W.L.), and Pathology (R.R.), Henry FordHospital. Detroit, MI. Presented at the Sixty-sixth Sci-entific Assembly and Annual Meeting of the Radio-

logical Society of North America, Dallas. TX. Nov.16-21, 1980. Received June 22, 1981; revision request-

ed Sep. 18, 1981; revision received and accepted Nov.10, 1981.

2 Present address: University of California, Schoolof Medicine, San Francisco, CA. ht

R EFINEMENTS in ultrasound technology have advanced the use of

this modality beyond the simple display of anatomy, anatomic

relationships, and spatial localization of lesions. Ultrasound yields

gross anatomic information, but by imaging the interfaces between

tissue structures it also reflects the histopathologic characteristics of

an organ.There are reports of the specific sonographic appearance of the

kidney and liver in different parenchymal diseases (1-6). At present,

specific tissue characterization by sonography is a field of active re-search. This retrospective study was designed to correlate the sono-graphic appearance of the kidney with the histologic changes andthe clinical and laboratory findings in patients with various renal

medical diseases.

MATERIALS AND METHODS

Between January 1978 and October 1980, 180 renal biopsies wereperformed at our hospital. In each patient, an ultrasound examination

was attempted prior to biopsy. The gray-scale images were analyzedretrospectively in all 180 patients. Fifty-six patients had technically

inadequate ultrasound images and were therefore excluded from thestudy. When all tissue sections were reviewed, only those that had

at least 10 glomeruli per level were included in the study, eliminatingfifteen additional patients. This investigation therefore is based onthe results of 109 patients, aged from 8-78 (mean 39.8). There were

55 females, aged 11-78 (mean 40.0), and 54 males, aged 8-75 (mean

39.6).The renal diseases included in this study were lupus nephritis

(N = 31), focal segmental glomeruloscierosis (N 12), membranous

glomerulonephritis (N = 12), focal glomenulonephnitis (N 15),

membranoproliferative glomeruionephnitis (N = 5), chronic gb-

merubonephritis (N 5), diabetic gbomerubosclerosis (N 1 1), chronicinterstitial nephritis (N 9), acute tubular necrosis (N 2), amyboi-

dosis (N = 1), myeloma kidney (N = 1), and miscellaneous and un-classified (N 5).

The clinical, pathologic, and sonographic data were analyzedblindly and independently by three different teams of corresponding

specialists.

The clinical and laboratory examinations included serum creati-nine, blood urea nitrogen (BUN), serum albumin, and total serumprotein levels, 24-hour urine protein excretion, and urinary sedimentanalysis with enumeration of red cells, white cells, and cellular casts

per high-power field.The paraffiii-embedded sections of the biopsy specimens, including

multiple hematoxylin and eosin, periodic acid Schiff, tnichnome, and

silver stained slides, were reviewed. The examinations were confined

to the renal cortex, and the following observations and estimations

Figure 1

142 July 1982 Volume 144, Number 1 Hnicak and Others

a. b.

Acute tubular necrosis in a 25-year-old man.a. Parasagittal scan of the right kidney. The echo intensity of the renal cortex is less than that of the adjacent liver. The

cortical echogenicity is classified normal-Grade 0.

b. Photomicrograph (periodic acid-silver methenamine, X158). Mild tubular epithelial changes. uneven tubular dilatation,cellular debris within the lumen of a few tubules, and mild interstitial edema are seen.

were recorded: the maximum numberof gbomeruli in one level; the percent-age of gbomeruli showing global scle-rosis; presence and degree of tubularatrophy, expressed either as percentageof tubules showing overt atrophywhen changes were focal or on a scaleof 0 to 4+ when tubular atrophy wasdiffuse; the number of hyaline castswithin cortex, per level, expressed asthe number of casts per glomerulus.The degree of diffuse interstitial fi-brosis was expressed on a scale of 0 to4+. Focal interstitial fibrosis associated

Figure 2

with focal tubular atrophy was not re-corded. Interstitial leukocytic infiltra-tion, when present, was recorded asmainly focal or mainly diffuse, and thedegree of such infiltration was ex-pressed on a scale of 0 to 4+. Interstitialedema and arteriosclerosis were ex-pressed on a scale of 0 to 4+. The pres-ence of microcalcifications and of in-tratubular crystals was recorded asnumber of such structures per level. Tofacilitate the computer analysis, the 0to 4+ recordings were converted topercentage figures (TABLE I).

The sonograms were obtained using

commercially available units with3.5-MHz transducers. The variablesincluded in the evaluation of the ul-

trasound images were: renal length

(normal 10 cm); appearance of the renalsinus; detectability and size of renal

pyramids; distinctness of the cortico-

medullary boundary; cortical echoge-

nicity. The cortical echogenicity was

analyzed on longitudinal supine scans

by comparing the image echo strength

of the renal cortex with image echostrength of the adjacent liver. None of

a. b.

Interstitial nephnitis in a 75-year-old man.

a. Parasagittal scan of the right kidney. The echogenicity of the renal cortex is equal to that of the liver and is classified

Grade I.b. Photomicrograph (periodic acid-Schiff, X158). A 10% global sclerosis, diffuse interstitial fibrosis, and moderate diffuse

tubular atrophy are seen. There are atheroma emboli in rare vessels.

Figure 3

Renal Parenchymal Disease ULTRASOUND 143

b.

Renal myeboma in a 56-year-old man.a. Parasagittal scan of the right kidney. The echogenicity of the renal cortex is greater than that of the liver, but less than

the renal sinus. Classified Grade II.b. Photomicrograph (periodic acid-silver methenamine, X158). There are multiple casts within the cortex, most of which

have features of myeboma casts. Diffuse tubular atrophy of an uneven degree and overt diffuse interstitial fibrosis

were present.

the patients had clinical or laboratory

evidence of liven disease; liver functiontests were always performed before

biopsy and only patients with normal

liver function tests underwent biopsy.

In grading the renal and liver echoge-nicity, the comparison scans were al-

ways obtained at the same depth to

avoid difficulties due to the transducer

beam pattern (7). Grading the echoge-

nicity of the kidney echoes by com-

paring the adjacent normal liver echoes

also avoided difficulties associated

with changing equipment output (the

Figure 4

ratio is always equal). Scans in which

the gallbladder was anterior to the

kidney were avoided in order to elim-

mate the distal sound enhancementthat would be reflected within the

kidney. The cortical echogenicity wasclassified into four groups:

Grade 0: Normal. The echo intensityof the cortex of the right kidney was

less than that of the liver (Fig. 1).

Grade I: The echo intensity of thecortex of the right kidney equaled thatof the liver (Fig. 2).

Grade II: The echo intensity of the

cortex of the right kidney was greaterthan that of the liver, but less than that

of the renal sinus (Fig. 3).Grade III: The echo intensity of the

renal cortex was equal to that of the

renal sinus (Fig. 4).

After all the data were obtained fromthe clinical, pathological, and ultra-sound teams, statistical analysis of theindependent results from the three

teams was performed using MIDAS(Michigan Interactive Data AnalysisSystem). The variables studied were:

I. Renal Length: The renal length was

b.

Advanced focal segmental glomerubosclerosis in a 35-year-old man.a. Parasagittal scan of the right kidney. The echo intensity of the renal cortex is markedly increased and equal to that

of the renal sinus. The renal cortical echogenicity was classified as Grade III.

b. Photomicrograph (periodic acid-Schiff, X140). Advanced focal segmental gbomerubosclerosis is seen, with an estimated

75(4 obsolescent glomeruli and 80’� global sclerosis. There is moderate leukocytic infiltration.

144 July 1982 Volume 144, Number 1 Hnicak and Others

TABLE I: Pathological Examination

Factors Analyzed

Number of gbomeruli per levelGlobal sclerosis (%)Tubular atrophy (%)

FocalDiffuse

Hyaline casts per gbomerulusDiffuse interstitial fibrosis (%)Leukocytic infiltration (%)

FocalDiffuse

Edema(%)Calcifications per levelCrystals per levelArteriosclerosis (%)

ArteryA rt�rinl�

TABLE II: Renal Length and Disease

Type of Renal Disease

No. of Patients

Renal Length*

TotalNormal Small

Lupus nephritisFocal segmental glomerubosclerosisMembranous gbomerubonephritisFocal glomerubonephritisMembranoproliferative gbomerubonephritisChronic glomerulonephritis

23 810 21 1 1

7 85 0

1 4

31121215

5

5Diabetic gbomerulosclerosisChronic interstitial nephritisAcute tubular necrosis

9 24 52 0

1192

AmyloidosisMyeboma kidneyMiscellaneous and unclassified

1 01 04 1

115

Total 78 31 109

* Normal � lOcm;Small < 10cm

correlated with (A ) the type of renal

disease, by each type separately andalso by diseases grouped into two majorgroups (gbomerular and nongbomeru-bar); in both instances, the statistical testused was a two-way cross-tabulationmethod, (B) each histopathologicfinding, using a two-sample test, and(C) each laboratory finding, using thetwo-way cross-tabulation method.

II. Renal Sinus: The appearance of therenal sinus was correlated with (A ) the

type of renal disease, (B) the histo-

pathologic findings, and (C) the labo-

ratony findings. The statistical test used

was the two-way cross-tabulationmethod.

Ill. Medullary Pyramids: The detect-

ability and the size of the renal pyra-mids were correlated with (A ) the type

of renal disease, (B) the histopathologic

findings, and (C) the laboratory find-

ings. The statistical test used was thetwo-way cross-tabulation method.

1V. Corticomedullari� Boundarii: The

distinctness of the conticomedullany

boundary was correlated with (A ) the

type of renal disease, (B) the histo-

pathologic findings, and (C) the labo-

ratony findings. The statistical test used

was the two-way cross-tabulationmethod.

V. Cortical Ecliogenicity: The corticalechogenicity was correlated with (A)

the type of renal disease, using thetwo-way cross-tabulation method; (B)

each histopathobogic finding sepa-nately, using the rank-order correlation

method with calculation of both SIC

and RHO (the coefficient of rank cor-relation [Spearman rho] was correlated

to show a positive or negative rela-

tionship between two variables); (C)

the laboratory findings, using analysis

of variance (ANOVA test).

In addition, each clinical variablewas separately correlated with eachpathologic finding, using the rank-order correlation test with calculationof both SIC and RHO.

RESULTS

Statistical Analysis

I. Renal Length: 78/109 kidneys had

a length of 10 cm or greaten and there-fore were considered normal. 31/109patients had small kidneys, with a

renal length of less than 10 cm. (A) No

statistically significant correlation was

present between renal length and the

type of renal disease when compared

separately (TABLE II) or when the dis-

eases were grouped into gbomerularand nongbomerubar categories. (B)

There was a significant correlationbetween renal length and the preva-lence of global sclerosis, focal tubularatrophy, and the number of hyalinecasts per gbomerulus (TABLE III). (C) No

statistically significant correlation was

found between the renal length andany laboratory findings.

II. Renal Sinus: A normal-appearingrenal sinus was present in 93/ 109 pa-tients. In 7/109 patients, it appeared

distorted, and in 9/ 109 patients, therenal sinus could not be identified, and

its echogenicity was equal to the sur-

rounding renal parenchyma. No sta-tistically significant correlation was

found between the appearance of therenal sinus and (A ) the type of renaldisease, (B) the histopathobogic find-ings, or (C) the laboratory findings.

III. Medullary Pyramids: The medul-lary pyramids were identified in 66/

109 patients. In 5/66 patients, theywere prominent. The medullary pyra-mids were not seen in 43/109 patients.

No statistically significant correlation

was found between the detectabilityand the size of the medullary pyramidsand (A) the type of renal disease, (B)

the histopathobogic findings (there was

TABLE III: Renal Len gth and Histop athobogic Findings

Median(Renal

GlobalSclerosis

TubularAtrophy.

Focal

TubularAtrophy.

DiffuseHyaline

CastsInterstitial

Fibrosis

LeukocyticInfiltration,

Focal

LeukocyticInfiltration,

Diffuse Edema

Length) Normal Small Normal Small Normal Small Normal Small Normal Small Normal Small Normal Small Normal Small

N< 42 11 36 9 0 0 39 8 0 0 27 11 0 0 0 0

N> 31 20 30 20 18 4 20 13 29 5 11 6 5 4 10 5

N= 5 0 12 2 60 27 19 10 49 26 40 14 73 27 68 26p*

.0041 .0085 .0727 .0471 .0888 .9192 .7573 .5239

* p <.05 is significant

Renal Parenchymal Disease ULTRASOUND 145

a tendency toward correlation betweenthe number of hyaline casts per gb-

merulus and nonvisualization of themedullary pyramids, but this did not

reach statistical significance), or (C) thelaboratory findings.

IV. Corticomedullary Boundary: Adistinct corticomedullary junction wasidentified in 66/ 109 patients. No sta-Listically significant correlation was

found between the distinctness of thecorticomedullary boundary and (A) thetype of renal disease, (B) the histo-pathologic findings, or (C) the labora-

tory findings.V. Cortical Echogenicity: Cortical

echogenicity was considered normal(Grade 0) in 66/ 109 patients, Grade I in19/109 patients, Grade II in 15/109patients, and Grade III in 9/ 109 pa-tients. (A ) No statistically significant

correlation was found between the

type of renal disease and the cortical

echogenicity (TABLE IV). (B) A signifi-cant positive correlation (p �.05) wasfound between cortical echogenicity

and the following histopathologicfindings: global sclerosis, focal tubular

atrophy, hyaline casts, and focal leu-

kocytic infiltration. There was a ten-

dency toward negative correlation be-tween cortical echogenicity and edema,

but it did not reach statistical signifi-cance (TABLE V). (C) There was a sta-tistically significant correlation be-

tween the cortical echogenicity and theBUN and serum creatinine levels

(TABLE VI). However, while there was

an overall significant correlation, there

was a wide range of variance present in

each group (TABLE VII). There was anegative correlation between cortical

echogenicity and serum albumin level

but the correlation was not statistically

significant (TABLE VIII).

Laboratory - HistologicCorrelation (TABLE IX)

I. Proteinuria: A significant positivecorrelation was found between the

degree of proteinunia and global scle-rosis, focal tubular atrophy, and the

number of hyabine casts.

II. BUN, Creatinine: A significantcorrelation was found between levelsof BUN and creatinine and the degreeof global sclerosis, focal and diffusetubular atrophy, interstitial fibrosis,

focal leukocytic infiltration, and thenumber of hyaline casts per gbomer-ulus.

III. Serum Albumin-Total Protein: A

negative correlation was found be-

tween both the serum albumin and the

TABLE IV: Cortical Echogenicity and Disease

Type of Renal Disease Cortical Echogenicity* Total

0 I II III

Lupus nephritis 28 0 2 1 31Focal segmental . 6 3 1 2 12

glomerulosclerosisMembranous glomerubonephritis 10 2 0 0 12Focal glomerulonephritis 7 3 4 1 15Membranoproliferative 2 2 1 0 5

glomerulonephritisChronic gbomerulonephnitis 0 1 2 2 5Diabetic gbomeruboscerlosis 3 5 2 1 11Chronic interstitial nephritis 3 2 2 2 9Acute tubular necrosis 2 0 0 0 2Amyloidosis 0 1 0 0 1Myeboma kidney 0 0 1 0 1Miscellaneous and unclassified 5 0 0 0 5

Total 66 19 15 9 109

* See Materials and Methods section for grading system.

TABLE V: Cortical Echogenicity and TABLE VI: Cortical Echogenicity andHistopathobogic Findings Laboratory Findings

Cortical Echogenicity vs. p Rho Cortical Echogenicity vs. p

Global sclerosis .0001k .6157* 24-hour protein .0990Tubular atrophy, focal .0001k .5099* BUN level .0001kTubularatrophy, diffuse .0975 .1576 Serum creatinine level .0001*Hyaline casts .0O01� 5357* Serum albumin level .087 1Interstitial fibrosis, diffuse .2252 .1095 Total serum protein .6100Leukocytic infiltration, focal .0023* .2888* Red blood count .7450Leukocytic infiltration, diffuse .071 1 .1756 Casts .1449Edema .0611 -.1650 Whitebboodcount .1372

*Statistically significant. Correlation is con- � p �.05 (95’4)

sidered significant when: p <.05 (95%); Rho>.1895 (99%).

TABLE VII: Cortical Echogenicity and Creatinine Level

Cortical Creatinine Level (mg/dl)Echogenicity* Range Mean Variance SD

0 0.6-14 1.8109 5.1937 2.2790I 1.3-23 5.2071 36.404 6.0336II 1.0-16 5.6800 19.580 4.4249III 4.0-23 10.720 64.237 8.0148

F = l2.944;p <.0001* See Materials and Methods section for grading system.

TABLE VIII: Cortical Echogenicity and Serum Albumin Level*

Cortical Echogenicityt Mean Variance SD

0 3.2452 .75366 .86814

I 2.9846 .73474 .85717II 2.5200 .73100 .85349

III 1.8667 .71333 .85049

* As cortical echogenicity increases, the serum albumin decreases; but the correlation was not sta-

tistically significant, p .0871.t See Materials and Methods section for grading system.

TABLE IX: Laboratony-Histopathobogic Correlation (expressed in p values)

146 July 1982 Volume 144, Number 1 Hricak and Others

HistopathologicFinding Proteinuria

BUNlevel

SerumCreatinine Level

Hypo-albuminemia

Hypo-proteinemia

Urinary SedimentRed Blood Cells

Globalsclerosis .0026* .0001* .0001* .7134 .4283 .4486Focaltubularatrophy

Diffuse tubular atrophyHyalinecastsInterstitial fibrosis

.0060*

.2551

.0193*

.0731

.0006*

.0324*

.0001*

.0251*

.0001*

.0845

.0001*

.0226*

.3147

.0208*

.9458

.2604

.5208

.0175*

.9951

.0364*

.8776

.2079

.4598

.4321LeukocyticfocalinfiltrationDiffuseleukocyticinfiltrationInterstitial edema

.1177

.9096

.8946

.0042*

.1194

.2592

.0014*

.1101

.3053

.6760.6091.2590

.8925

.2249

.1748

.3679

.2031

.0987

* p <.05; Significant at 5� level.

total serum protein levels and the de-gree of diffuse tubular atrophy. Anegative correlation was also foundbetween the total serum protein leveland the degree of interstitial fibrosis.

IV. Urinary Sediment: No correlation

was found between any of the histo-logic findings and the various cellularelements in the urinary sediment (redcells, white cells, and casts).

DISCUSSION

Renal diseases in the main involvethe nephron, vascular, or interstitialtissues; these are all interrelated.

Nephron changes will result fromvascular disease, and in turn, vasculardisease will cause nephron and inter-stitial tissue changes. In a similarfashion, interstitial tissue changes in-evitably accompany and follow vas-cular and nephron disease. The kidneythat has been seriously injured for along period of time will lose the dis-tinguishing features of specific disease

regardless of whether the originaldisease was glomerular, tubular, in-

tenstitial, or vascular. All compartments

of the kidney show atrophy and scar-ring. In end-stage kidney disease rec-

ognition of the primary renal disease

is often not possible.

Percutaneous renal biopsy is the

single most important tool in the di-

agnosis of renal parenchymal disease.

Adequate analysis of the biopsy speci-men requires light microscopic, elec-tron microscopic, and immunofluo-

rescent study. The reported success rateof renal biopsy ranges between 89.8%

and 94.9% (8, 9).The percutaneous renal biopsy has

a definite attendant risk, with the rateof complication ranging from 0.7-8.1%

(9, 10). The complications include oh-gunia, decrease in hematocnit 44% (11),hematuria 10-40% (8), arteniovenous

fistuba, renal abscess, gram-negative

septicemia, and perforation of hollow

viscera (12). Hematomas, either sub-capsular, penirenal, or posterior para-renal, are seen in over 50% of the pa-tients, as documented by computedtomographic monitoring (13, 14).Massive bleeding following renal bi-opsy necessitated the performance of

nephrectomies in five out of 8,000 casesand splenectomies in two out of 8,000cases (8). Reported cases of mortalityrange from 0.7-0.17% (8, 12).

As progression of renal disease mustbe monitored closely, particularly whenthere is a discrepancy between the ap-parent diagnostic features and thecourse of the disease or when the ef-fects of therapy need to be monitoredclosely, as in lupus nephnitis, a nonin-

vasive method reducing or obviatingthe need for serial biopsies would as-sume great importance. The use of di-agnostic ultrasound in monitoring theprogression of the disease in these pa-tients therefore is an important ad-vance.

Sonographic characterization of tis-sue is at present an area of active re-search. Measurements of the degree ofabnormality and the definition ofunique tissue signatures are the goals(15). Only a small part of the availableultrasonic data is currently being used.Analysis of the echo amplitude of agiven organ can be performed usingthree basic techniques: B scans, allow-ing visual interpretation by compari-son of two adjacent organs on the samescan or by comparing the same region

using a study performed on two dif-ferent occasions; A-mode analysis; orcomputerized evaluation. Each of themethods has its limitations but, as inthe initial experience of Rosenfield et

a!. (5), each has produced similar re-suits. The visual interpretation by B-

scan analysis is a subjective method oftissue characterization . However, ifcomparison of the adjacent organs isalways done at the same depth, if the

scans with overlying organs throughwhich an ultrasound beam must pass

are eliminated, and if a control organis not diseased, the method has proved

to be adequate (5).The value of sonography in

displaying size and anatomic featuresof an organ is well accepted. Ideally,renal volume should be calculated (16).Our study was retrospective and serialtransverse scans were not recorded inevery patient. However, display of therenal length was always optimal, andsince this measurement of kidney sizeis well accepted in the radiobogic lit-

erature, we chose to assess the kidneysize on the basis of length. The kidneywas considered small when its lengthwas less than 10 cm. Correlating the

type of renal disease with renal length,there was a tendency toward a normalrenal length with membranous gb-merubonephnitis and membranoprohi-

ferative gbomerulonephritis, and gen-erally a prevalence of small kidneylength in chronic gbomerulonephritis.The number of patients in each of thesethree groups was too small to makecorrelation statistically significant.When renal length was correlated withthe histopathobogic changes, there wasa statistically significant correlationbetween length and prevalence ofglobal sclerosis, focal tubular atrophy,and the number of hyaline casts pergbomerulus, suggesting that renal fi-brosis is associated with this finding.

When the sonognaphic appearanceof the renal sinus, the meduhlary pyr-amids, and the distinctness of the cor-ticomedullany boundary were ana-lyzed, no statistically significant cor-relation was present between thosevariables and the type of renal disease,histopathologic findings, or laboratoryvalues.

There was no statistically significantcorrelation between the specific typeof renal disease and cortical echogeni-city. In our experience, and in reports

in the literature (3, 17, 18), there are a

number of renal medical diseases thatcause increased cortical echogenicity,

Renal Parenchymal Disease ULTRASOUND 147

but the finding is not specific to thedisease; rather it reflects the degree of

histopathobogic change within the

renal parenchyma. As the corticalechogenicity was correlated with eachhistopathobogic finding separately,

there was a direct, statistically signifi-cant correlation between the corticalechogenicity and the degree of global

sclerosis, focal tubular atrophy, num-

ben of hyaline casts pen glomerulus,

and focal leukocytic infiltrate. Thecorrelation of cortical echogenicity andtubular interstitial changes was re-ported by Rosenfield et a!. (17). In

contrast to the observations of Rosen-

field et al. , but in agreement with Le-Quesne (3), we found a significantcorrelation between the degree ofglobal sclerosis and cortical echogeni-city. In the normal kidney, the glom-

eruli occupy only 8.6 ± 1.5% of the

renal cortex (18). However, changeswithin the gbomeruli are not isolated,as tubular and interstitial changes

usually follow the gbomerular changes.

The degree of involvement in the twoanatomic areas is similar. The increasein cortical echogenicity is thereforeprobably the result of changes withinthe gbomeruli, tubules, and intersti-titum. The positive correlation of in-creased leukocytic infiltration and

cortical echogenicity is in accord withthe observations reported by LeQuesne(3) and Rosenfield et al. (5) of change in

the cortical echogenicity in response totherapy in acute poststreptococcal

glomerubonephritis and active inter-

stitial disease (the promiuent feature of

any active disease is leukocytic infil-

tration). There was a negative correla-tion between the degree of interstitial

edema and cortical echogenicity, in-dicating that edema in any given organwill cause increased transonicity.

When the cortical echogenicity wascorrelated with laboratory data, anoverall significant accord was foundbetween cortical echogenicity and thevalue of BUN and serum creatinine

levels. This is in contrast to the report

by Moccia, et al. (19). There was, how-

ever, a wide range of variance presentin each group and a normal corticalechogenicity was seen in patients withserum creatinine levels ranging from0.6 to 14 mg/dl.

Correlation of clinical data withhistopathobogic findings yielded anoverall positive significant correlationbetween the degree of glomerular andtubular interstitial changes and pro-teinuna and BUN and serum creatininelevels.

SUMMARY

Histopathologic analysis of the bi-opsy specimen is indispensable for the

initial diagnosis of medical renal dis-ease. Attempts have been made in thepast to identify specific sonographicappearances for individual renalmedical diseases (1, 2, 4). In our expe-

nience such specificity was not found.The lack of specificity of the sonogramsand the limited responses of the kidneyto various pathological insults maywell remain a limitation to specific so-nographic diagnosis, even when ac-curate quantitative measurements byultrasound become available. How-ever, after the initial diagnosis hasbeen made by biopsy, a good correla-tion between cortical echogenicity andthe severity of histopathologic changesprovides a promising noninvasivemethod of monitoring the progressionof the renal disease.

William R. Eyler, M.D.

Department of Diagnostic RadiologyHenry Ford HospitalDetroit, MI 48202

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