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A. URINALYSIS Urinalysis is one of the basic tests to evaluate the presence

and severity of kidney and urinary tract disease. Physical parameters of importance in the evaluation of a

urine sample are color, turbidity, odor, relative density, pH, glucose, protein, hemoglobin (dipstick for blood), leuko-cyte esterase, nitrites, and ketones.

Urine dipstick testing results are described in Table 2011. Urine microscopy is an integral part of urinalysis, and adds

valuable information to the physicochemical investigation. The various cells of the urine sediment are illustrated in

Figure 2011. They are derived from the circulation (e.g., erythrocytes and leukocytes) and from the epithelia lining

the urinary tract (e.g., renal tubular cells, uroepithelial cells, and squamous cells).

Casts are elements with a cylindrical shape (Fig. 2012) that form in the lumen of distal renal tubules and collecting ducts. Table 2012 describes the clinical signi cance of uri-nary casts.

Urine can also contain crystals; common types are illus-trated in Figure 2013. The nding in the urine of few uric acid, calcium oxalate, or calcium phosphate crystals is not uncommon. Usually, it is a nding without clinical impor-tance because it re ects a transient supersaturation of the urine caused by the ingestion of some foods (e.g., meats [uric acid], spinach or chocolate [calcium oxalate], milk or

201 Section 8: Kidneys

Chapter 201 Diagnostic tests and procedures

TABLE 2011 Urine dipstick testing

Parameter False-negative results False-positive results

Speci c gravity Reduced values in the presence of glucose, urea, alkaline urine

Increased values in the presence of protein 1 g/L, ketoacids

PH Reduced values in the presence of formaldehyde

Hemoglobin Ascorbic acid, high nitrite concentration, delayed examination, high density of urine, formaldehyde (0.5 g/L),

Myoglobin, microbial peroxidases, oxidizing detergents, hydrochloric acid

Glucose Ascorbic acid, urinary tract infection Oxidizing detergents, hydrochloric acid

Albumin Immunoglobulin light chains, hydrochloric acid, tu-bular proteins, globulins, colored urine

Alkaline urine (pH 9), quaternary ammonium detergents, chlorhexidine, polyvinylpyrrol-idone

Leukocyte esterase isotonic urine, vitamin C (intake 1 g/day ), protein 5 g/L, glucose 20 g/L, mucous specimen, cephalosporins, nitrofurantoin; mercuric salts, tryp-sin inhibitor, oxalate, 1% boric acid

Oxidizing detergents, formaldehyde, sodium azidie, colored urine caused by beet inges-tion, or bilirubin

Nitrites No vegetables in diet, short bladder incubation time, vitamin C, gram-positive bacteria

Colored urine

Ketones Improper storage Free sulfhydryl groups (e.g., captopril) L-dopa, colored urine

From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.

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TABLE 2012 Clinical signi cance of urinary casts

Cast Main clinical associations Cast Main clinical associations

Leukocyte Acute pyelonephritis

Acute interstitial nephritis

Proliferative glomerulonephritis

Epithelial Acute tubular necrosis

Acute interstitial nephritis

Glomerulonephritis

Myoglobin Rhabdomyolysis

From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.

Hyaline Normal subject

Renal disease

Granular Renal disease

Waxy Renal insuf ciency

Rapidly progressive

Glomerulonephritis

Fatty Marked proteinuria

Nephrotic syndrome

Erythrocyte Glomerular bleeding

Proliferative, necrotizing glomerulonephritis

Hemoglobin Glomerular bleeding

Proliferative, necrotizing glomerulonephritis

Hemoglobinuria

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Chapter 201: Diagnostic tests and procedures 201

A B

C D

E F

Fig 2011Urinary sediment cells. A, Isomorphic nonglomerular erythrocytes. The ar-rows indicate the so-called crenated erythrocytes, which are a frequent nding in nonglomerular hematuria. B, Dysmorphic glomerular erythro-cytes. The dysmorphism is mainly caused by irregularities of the cell membrane. Inset, Acanthocytes, ring-formed cell bodies with one or more blebs of different sizes and shapes. These cells are the most reli-able marker of glomerular bleeding. C, Neutrophils. Note their typical lob-ulated nucleus and granular cyto-plasm. D, An ovoid renal tubular cell. The nucleus is large and the cyto-plasm is granular. E, Two cells from the deep layers of the uroepithelium. F, Three cells from the super cial lay-ers of the uroepithelium. Note the difference in shape and nucleus-to-cytoplasm ratio between the two types of uroepithelial cells (A-E, phase contrast microscopy, 400).(From Johnson RJ, Feehally J: Compre-hensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

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A B C

D E F

Fig 2012Casts. A, Finely granular cast (arrow). The two other elements shown are hyaline granular casts, which are also frequent in patients with a glomer-ular disease. B, Waxy cast. Note the typical appearance of melted wax and the hard edges. C, Erythrocyte cast. The arrows indicate the erythro-cytes embedded in the matrix of the cast. D, Hemoglobin cast, identi able by its typical brownish hue. E, Leukocyte cast. The polymorphonuclear leukocytes are easily identi able because of their lobulated nucleus. F, Epithelial cast. It contains both large ovoid cells deriving from the proximal tubular segments (bottom) and smaller cells deriving from the distal tubular segments (top) (phase contrast microscopy; A, 160; B-F, 400).(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

cheese [calcium phosphate]), or mild dehydration. How-ever, such crystals may also be associated with pathologic conditions. For example, the presence of uric acid crystallu-ria in repeated samples may re ect hyperuricosuria, and large amounts of uric acid crystals may be associated with acute renal failure caused by uric acid nephropathy. Some crystals are always pathologic; this is the case with choles-terol, which is found in patients with marked proteinuria.

Bacteria is a frequent nding, because urine is usually col-lected and handled under nonsterile conditions and exami-nations are often delayed. Urine infection can be suspected only if bacteria are found in noncontaminated freshly voided midstream urine, especially if numerous leukocytes are also present.

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A B C

D E F

G H I

Fig 2013Crystals. A, Uric acid crystals. This rhomboid shape is the most frequent (phase contrast microscopy, 400). B, Bihydrated calcium oxalate crys-tals. They have the typical appearance of a letter envelope. C, Different types of monohydrated types of monohydrated calcium oxalate crystals (phase contrast microscopy, 400). D, A star-like calcium phosphate crystal. E, Triple phosphate crystal on the background of a massive amount of amorphous phosphate particles (phase contrast microscopy, 400). F, Cholesterol crystal. G, Cystine crystals (phase contrast microscopy, 400). H, Sulfadiazine crystal. This has a typical amber color and radial striations (phase contrast microscopy, 400). I, Intratubular precipitation of monohydrated calcium crystals seen on renal histology. This phenomenon can be caused by drugs such as naftidrofuryl oxalate or vitamin C (polarized light, 250)(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

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201 Section 8: KidneysB. IMAGING Renal failure associated with contrast administration has been

reported as the third most common cause of in-hospital renal failure, after hypotension and surgery. In patients with se-rum creatinine 1.5 mg/dL, iodinated contrast should be used with caution because the risk of contrast-induced renal failure is increased.

Box 2011 describes risk factors for contrast nephrotoxicity. Proper hydration and the correct choice of imaging will minimize the time and cost of effective evaluation.

The rst-choice imaging techniques in common clinical sit-uations are shown in Table 2013.

Plain lms and intravenous urography The typical urogram consists of a large plain lm of the ab-

domen to include the region of the bladder (KUBkidneys, ureter, bladder) and one smaller lm, a tomogram through the renal regions prior to contrast administration (Fig. 2014).

Plain lms are used to assess for soft tissue masses, the bowel gas pattern, calci cations (Fig. 2015), and renal lo-cation. IV urography (IVU; Fig. 2016) is now only rarely

used and has been replaced by computed tomography (CT) and ultrasound.

Retrograde pyelography (Fig. 2017) is performed when the ureters are poorly visualized on other imaging studies or when samples of urine need to be obtained from the kidney for cytology or culture.

Ultrasound Sonographic examination of the kidneys is relatively inex-

pensive and provides a rapid way to assess renal location, contour, and size (Fig. 2018).

Box 2011 Risk factors for contrast nephrotoxicityPreexisting renal impairment (serum creatinine 1.5 mg/dL)*Diabetes*Age 75 yrFluid depletionMyelomaConcurrent nephrotoxic drugsUricosuriaIonic contrast media

*The greatest risk is presented by the coincidence of diabetes and preex-isting renal impairment.

TABLE 2013 First-choice imaging techniques in renal disease

Renal failure, unknown cause Ultrasound (US)

Hematuria Intravenous urography (IVU) or US plain radiograph of kidneys, ureter, and bladder (KUB)

Proteinuria, nephrotic syndrome US

Hypertension

with normal renal function CT angiography including imaging of the adrenal glands

with impaired renal function MRA

Renal artery stenosis

with normal renal function MRA

with impaired renal function MRA

Renal infection CT

Hydronephrosis detected by US IVU (if renal function is preserved) or 99Tc-DTPA renography

Retroperitoneal brosis CT

Papillary necrosis IVU

Cortical necrosis Contrast-enhanced CT

Renal vein thrombosis Contrast-enhanced CT

Renal infarction Contrast-enhanced CT

Nephrocalcinosis Noncontrast CT

CT, computed tomography; MRA, magnetic resonance angiography.From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.

Fig 2014Scout tomogram of normal kidneys.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

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A B

Fig 2015A, Plain radiograph (kidneys, ureter, and bladder) taken before contrast medium administration for an intravenous pyelogram shows a small radi-opaque calculus shadow (arrow) at the left ureterovesical junction (UVJ). B, Subsequent delayed lm at 40 minutes shows extravasation of the dye at the calyceal fornices (arrows) and columnization of the dye up to the left UVJ calculus.(From Nseyo U, Weinman E, Lamm DL: Urology for Primary Care Physicians. Philadelphia, WB Saunders, 1999.)

Fig 2016Intravenous urogram (IVU) demonstrating pelviureteric junction obstruc-tion. The IVU was obtained in a previously asymptomatic adult to in-vestigate nonspeci c right-sided abdominal and back pain. There is unilateral (right-sided) dilation of the pelvicalyceal system, with abrupt tapering to a normal-sized ureter.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

Fig 2017Retrograde pyelogram. The arrow indicates a small lling defect, which is a calculus in the renal pelvis. The remainder of the study is normal.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

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Fig 2018Normal sagittal renal ultrasound. The cortex is hypoechoic compared with the echogenic fat containing the renal sinus.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

Renal cysts can be identi ed as anechoic lesions and are a frequent coincidental nding during renal imaging.

Differentiation into simple and complex cysts (Fig. 2019) is required to plan intervention.

Color ow Doppler evaluation in a well-hydrated patient can be used to identify a ureteral jet. The jet is produced when peristalsis propels urine into the bladder, with the incoming urine having a speci c gravity higher relative to the urine al-ready in the bladder (Fig. 20110). Absence of the ureteral jet can indicate total ureteral obstruction. The color Doppler in-vestigation of the kidneys provides a detailed evaluation of the renal vascular anatomy. The main renal arteries can be identi ed in most patients (Fig. 20111).

Computed tomography CT examination of the kidneys is performed to evaluate

suspect renal masses, locate ectopic kidneys to investigate

calculi (Fig. 20112), assess retroperitoneal masses, and evaluate the extent of parenchymal involvement in patients with pyelonephritis (Fig. 20113).

Magnetic resonance imaging Magnetic resonance imaging (MRI) should only rarely be

the rst examination used to evaluate the kidneys, but typi-cally it is an adjunct to another imaging technique. The major advantage of MRI over other imaging modalities is its capability of direct multiplanar imaging (Fig. 20114).

MR angiography (MRA) can be performed with or without IV contrast administration, although contrast is preferred. The aorta and branch vessels are well demonstrated (Fig. 20115). MRA is performed to evaluate the renal arteries for stenosis (Fig. 20116) and is less invasive than angiog-raphy.

Fig 2019Sagittal renal ultrasound showing a complex cyst (arrows).(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

Fig 20110Bilateral ureteral jets detected with color Doppler ultrasound. This is a normal appearance.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

Fig 20111Transverse color Doppler ultrasound of the kidney. The artery is red and the vein is blue.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

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A B CFig 20112Nephrocalcinosis. A, Plain lm showing bilateral medullary nephrocalcinosis in a patient with distal renal tubular acidosis. B, Noncontrast CT scan in a patient with hereditary oxalosis and dense bilateral renal calci cation. The left kidney is atrophic. C, CT scan showing cortical nephrocalcinosis in the right kidney following cortical necrosis.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

Fig 20113Acute pyelonephritis. Contrast CT scan shows areas of lower density caused by infection and edema (arrows).(Courtesy of W. Bush)

A B CFig 20114Normal MR images through the kidneys. A, T1-weighted image. Note the distinct corticomedullary differentiation. B, Fast spin-echo (FSE) image. The urine in the collecting tubules causes the high signal within the renal pelvis on this sequence. C, FSE for normal sagittal image of the right kidney.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

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Fig 20115MR angiography. This coronal three-dimensional image following con-trast administration shows normal renal arteries.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

Fig 20116MR angiography. This coronal three-dimensional image shows left renal artery stenosis (arrow).(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

A B

Fig 20117Left renal artery stenosis and angioplasty. A, Aortogram demonstrating a tight left renal artery stenosis (arrow). B, Postangio-plasty image with marked improvement of the stenosis (arrow).(Courtesy of Dr. Harold Mitty.)

Angiography Angiography is now most often performed for therapeutic

intervention such as embolotherapy or angioplasty. Diag-nostic angiography is now used most often for evaluation of the renal arteries to assess possible stenosis and, in many situations, correct it with angioplasty (Fig. 20117).

C. RENAL BIOPSY The introduction of renal biopsy in the 1950s transformed

the study of renal disease, particularly glomerular disease, by providing the pathologic information that formed the basis for classi cation of disease that is still in current use and offers many insights into pathogenesis.

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Chapter 201: Diagnostic tests and procedures 201 Four groups of patients bene t most from the ndings of

renal biopsy: those with nephritic syndrome, those with re-nal disease in the setting of a systemic disorder, those with acute renal failure, and those with a renal transplant.

Workup for renal biopsy (Fig. 20118) is required to ex-clude problems that may jeopardize the safety of the proce-dure and to identify contraindications to biopsy (Table 2014).

The biopsy should be performed under ultrasound control using a needle biopsy gun (Fig. 20119). Local anesthetic is in ltrated down to the capsule of the kidney, but not into the kidney itself (Fig. 20120). The needle is advanced un-der ultrasound control (the ultrasound probe should be

Workup for renal biopsy

Assessments

Coagulation statusDrug therapy: stop aspirin/NSAID 5 days before biopsyPlatelet count: > 100 109/LProthrombin time:< 1.2 times controlActivated partial thromboplastintime (APTT): < 1.2 times control(if prolonged exclude lupusanticoagulant)Bleeding time (measure if BUN > 60 mg/dL (urea > 20 mmol/L) and high risk): < 10 min(if prolonged give DDAVP0.4 g/kg 23 h before biopsy)

Urineculture:sterile

Bloodpressure:diastolic BP< 95 mm Hg

Renalimaging:two normalsize, unscarred,unobstructedkidneys

Renal biopsy

Fig 20118Workup for renal biopsy. BP, blood pressure; BUN, blood urea nitro-gen; DDAVP, desmopressin; NSAID, nonsteroidal anti-in ammatory drug.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

TABLE 2014 Contraindications to renal biopsy*

Kidney status Patient status

Multiple cysts Uncontrolled blood pressure

Solitary kidney Uncontrolled bleeding diathesis

Acute pyelonephritis, Uremiaperinephric abscess

Renal neoplasm Obesity

Uncooperative patient

*Most contraindications to renal biopsy are relative rather than absolute; when clinical circumstances necessitate urgent biopsy they may be overridden, apart from uncontrolled bleeding diathesis.From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.

A

B

Fig 20119Renal biopsy gun. A, A 16-gauge needle is loaded in the gun. B, The loaded gun is cocked. The trigger mechanism is on the right.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

Fig 20120Renal biopsy. The skin has been cleaned with Betadine, the lower pole of the left kidney identi ed, and the skin marked appropriately. A ne needle has been inserted for local anesthetic in ltration.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

placed in a sterile sleeve; Fig. 20121) to just short of the renal capsule. The movement of the kidney relative to the probe should be watched during some deep respiratory cycles and the patient told to hold his or her breath so that the kidney is in the correct position to biopsy the lower pole (Fig. 20122). The biopsy gun is then red and the needle withdrawn. The specimen of renal tissue is recovered (Fig. 20123) and handed to the attending pathologist or technician.

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Fig 20121The ultrasound probe for renal biopsy. The probe is mounted in a sterile stocking for use during the biopsy.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

Fig 20122Renal biopsyultrasound appearance of the lower pole of the left kid-ney with biopsy entering.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

Fig 20123Renal biopsy specimen. Shown are the tip of biopsy the needle and the core of tissue obtained at biopsy. This core is only one half the length of the needle.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

In glomerulonephritis (GN), the pathologist will classify the different patterns of histologic injury seen on renal biopsy by examining the specimen with light microscopy, immu-no uorescence, and electron microscopy. This classi cation is not ideal because it cannot always be assumed that one histologic pattern has a single cause or a single clinical pre-sentation. Furthermore, one cause may produce a variety of histologic patterns (e.g., the varied glomerular disease seen in association with hepatitis B infection or lupus).

When evaluating renal biopsy specimens, it is more helpful to regard the renal biopsy appearance as a pattern rather than a disease. In GN, the dominant histologic lesions are in the glomeruli (Fig. 20124). GN is described as focal (only some glomeruli are involved) or diffuse. In any indi-vidual glomerulus, injury may be segmental (affecting only part of any glomerulus) or global. Indirect immuno uores-cence and immunoperoxidase staining are both used to identify immune reactants (Fig. 20125).

Electron microscopy is valuable for de ning the anatomy of the basement membranes and for localizing the site of im-mune deposits, which are usually homogeneous and electron-dense (Fig. 20126).

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A B C

D E F

Fig 20124Pathology of glomerular disease shown by light microscopy. These characteristic patterns of glomerular disease illustrate the range of histologic appearances and the descriptive terms used. A, Normal glomerulus, minimal change disease. B, Segmental sclerosis, focal segmental glomerulo-sclerosis. C, Diffuse mesangial hypercellularity. D, Diffuse endocapillary hypercellularity, poststreptococcal glomerulonephritis. E, Segmental necro-sis, renal vasculitis. F, Crescent formation, antiglomerular basement membrane disease.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

A B

C DFig 20125Pathology of glomerular disease showing common patterns of glomerular staining found by immuno uorescence microscopy. A, Linear capillary wall IgG, antiglomerular basement membrane disease. B, Fine granular capillary wall IgG, membranous nephropathy. C, Coarse granular capillary wall IgG, membranoproliferative GN type I. D, Granular mesangial IgA, IgA nephropathy.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

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A B

D E

A B C

D E F

CL

BS

Fig 20126Ultrastructural pathology of glomerular disease. Some characteristic patterns of electron-dense deposits (EDD) and glomerular basement mem-brane (GBM) abnormalities seen in glomerular disease are shown. A, Normal. B, Foot process effacement, minimal change disease. C, GBM thickening and splitting, Alports syndrome. D, Subendothelial EDD, membranoproliferative glomerulonephritis (MPGN) type I. E, Subepithelial EDD (arrows), membranous nephropathy. F, Mesangial EDD (arrows), IgA nephropathy.(From Johnson RJ, Feehally J: Comprehensive Clinical Nephrology, 3rd ed. St. Louis, Mosby, 2007.)

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