G69 Renal Insufficiency and Acute Renal Failure

C^ n Principal signs and symptoms: decrease or absence of urinary excretion,

"O increased solute retention in the blood, possible edema

§ n Classification: Renal failure is classified as prerenal, due to diminished renal blood

I* flow; intrinsic (renal), caused by renal parenchymal damage; and postrenal, due to jj blockage of urine flow.

• Prerenal: fluid deficit

"5 • Renal: glomerulonephritis (Tables 21 and 22) or interstitial nephritis (Table 23)

• Postrenal: Can be positively confirmed or excluded by sonography C • Acquired

Table 21 • Classification of glomerulonephritis

Acute glomerulonephritis

Rapidly progressive glomerulonephritis

Chronic glomerulonephritis (membranous, membranoproliferative, mesangioproliferative) Thrombotic microangiopathy Minimal-change nephritis

Table 22 . Occurrence of glomerulonephritis

In systemic diseases

Wegener granulomatosis

Panarteritis Lupus erythematosus

Antiglomerular basement membrane disease

In metabolic diseases

Diabetes mellitus

(Kimmelstiel-Wilson glomerulosclerosis) Amyloidosis

Table 23 • Classification of interstitial nephritis

Form of nephritis Causes

Bacterial nephritis Bacterial infection Abacterial nephritis Drug-induced Metabolic Obstruction Autoimmune

Other causes: polycystic kidneys, multiple myeloma, sickle cell anemia, Balkan nephritis, radiation nephritis n Differential diagnoses: Listed in Table 24 according to their frequency in the general hospital setting.

Table 24 • Differential diagnosis of renal insufficiency ^

Diagnosis Sonographic signs


Fluid deficit (p. 126) Collapsed vena cava, empty bladder, normal-appearing kidneys Kimmelstiel-Wilson Kidneys initially enlarged; signs of chronic glomerulonephritis o glomerulosclerosis appear as the disease progresses (see below), followed by signs of (p. 128) chronic pyelonephritis (see below) C

Heart failure (p. 127) Hypoechoic kidney with a thickened parenchymal rim, congested CL renal vein

Less common

Chronic pyelonephritis Small kidney with contour irregularities due to scarring; thin, (p. 130) echogenic parenchyma; calyces are cystic or ectatic

Chronic glomerulone- Diffusely increased echogenicity, loss of corticomedullary differen-phritis (p. 128) tiation, prominent hypoechoic medullary pyramids

Hydronephrosis Full bladder, obstructed ureter, dilated pyelocalyceal system,

(p. 131) displaced renal sinus, loss of renal parenchyma

Ureteral obstruction Dilated ureter, possible dilatation of the pyelocalyceal system (p. 131)

Pyonephrosis (p. 132) Dilated renal collecting system, occasional high-level internal echoes

Analgesic nephropathy Poor delineation, irregular increase in parenchymal sonodensity,

(p. 133) papillary tip calcification

Atrophic kidney Disproportionately small kidney, parenchymal thinning, increased

(p. 134) parenchymal echogenicity


Bladder tamponade Full bladder, often with high-level internal echoes (blood, debris, (p. 134) stone)

Acute glomerulone- Thickened renal cortex, hyperechoic to the prominent medullary phritis (p. 135) pyramids

Hepatorenal syndrome Normal-appearing kidneys, ascites, signs of hepatic cirrhosis or (p. 135) injury

Shock kidney (p. 136) Enlarged kidneys, markedly hypoechoic parenchyma, swollen medullary pyramids, narrow renal sinus Renal lithiasis (p. 137) Features vary depending on the location of the stone and duration of the disease:

- echogenic renal pelvis with an acoustic shadow

- obstructed renal pelvis, shadowing ureteral stone

Antiglomerular Enlarged, rounded kidney; ill-defined medullary pyramids;

basement membrane nonhomogeneous echogenic parenchyma disease (p. 129)

g Table 24 • Differential diagnosis of renal insufficiency - continued o

Diagnosis Sonographic signs

^ Renal artery embolism Wedge-shaped echogenic area in the renal parenchyma due to loss

(p. 129) of perfusion q Urethral obstruction Full bladder; extrinsic compression is usually seen

Polycystic kidney Multiple anechoic masses displacing the renal parenchyma

Renal amyloidosis Both kidneys enlarged with decreased parenchymal echogenicity U (p. 137) ,C

£ Medullary nephro- Markedly echogenic medullary pyramids, possible acoustic shad-calcinosis (p. 138) owing

Gouty nephropathy Small, bulging surface with parenchymal thinning, calculi (p. 136)

Conditions that cannot be diagnosed with ultrasound

Rare: Calcium oxalate nephritis, Fanconi syndrome (congenital defect of tubular transport), amino acid diabetes, renal hypochloremic acidosis, renal hypercalcemia (Fanconi syndrome), potassium loss syndrome (of Albright-Hadorn), salt-losing nephritis (Thorn syndrome), and many others n Classification: prerenal renal failure, due eitherto a decrease in total fluid volume or to decreased fluid delivery to the kidneys (perfusion deficit) n Clinical manifestations: decrease or absence of urinary excretion, possible somnolence, possible fever; signs of low-output syndrome due to heart failure n Diagnosis:

• History: Pay particular attention to the cause of the fluid deficit (decreased intake, increased losses)

• Laboratory tests: simple blood count with hematocrit

• Sonography

• Echocardiography to investigate a cardiac etiology

• A central venous catheter may be used to measure CVP for assessing the fluid deficit. The CVP measurement should be interpreted within the context of the echocardiography findings. Usually there is no need for right heart catheter-ization to measure the left ventricular filling pressure.

n Sonographic findings:

n Note: Scanning conditions are usually poor because of tissue dryness.

• Collapsed vena cava with decreased filling of other veins

• Empty urinary bladder

• Renal morphology appears normal on ultrasound.

• Echocardiography: empty, hyperactive cardiac ventricle due to volume deficit. Pumping action may be impaired even with a dilated ventricle (forward failure; in this case the veins are generally congested and the renal parenchyma is swollen).

n Accuracy of sonographic diagnosis: The sonographic signs of the fluid deficit are unmistakable. The resumption of diuresis after fluid loading is confirmatory.

n See also Shock Kidney, p. 136; Ascites, Right Heart Failure, p. 160; Edema, Left

Heart Failure, p. 119; Hepatosplenomegaly, Cardiac Inflow Stasis, p. 149. ► Note: The effects of cardiac failure are twofold: a decreased arterial supply to the organs (with a potential for anuria) and reflux leading to the venous engorgement of organs (resulting in pleural effusion and eventual ascites). The organic changes can be detected sonographically.

Kidney With Aki Sonographic

Fig. 169a, b Sonographic renal changes in low-output syndrome. a Hypoechoic right kidney with a thickened parenchymal rim. The patient presented clinically with acute anuria, an empty bladder, and mildly elevated creatinine. b The renal vein (RV) is congested. Renal vein thrombosis was excluded by duplex sonography

Fig. 169a, b Sonographic renal changes in low-output syndrome. a Hypoechoic right kidney with a thickened parenchymal rim. The patient presented clinically with acute anuria, an empty bladder, and mildly elevated creatinine. b The renal vein (RV) is congested. Renal vein thrombosis was excluded by duplex sonography

Fig. 170a, b Sonographic liver changes in low-output syndrome. a Diffusely hypoechoic liver with obstructed hepatic veins. The patient presented clinically with extremely high transaminase levels. L = right lobe of liver, RHV = right hepatic vein. b Posterior to the liver (L) is the strongly congested vena cava (cursors), which is dilated to 2.6 cm

■¡j Fig. 171a, b Pericardial effusion (PE) impairs ventricular filling, causing a global reduction of cardiac output. a Echogenic bolus-like mass in the pericardial sac (cursors) is consistent with hemopericardium. The heart shows very little ventri-ricular filling with prominent atria and tricuspid valve regurgitation. LA = left atrium, RA = right atrium, LV = left ventricle, RV = right ventricle. b Echogenic pericardial effusion (cursors: 2.76 cm). The patient presented clinically with impending ventricular tamponade in a setting of myocardial infarction with pericarditis

Kimmelstiel-Wilson Glomerulosclerosis n See also Kidney, Diabetic Nephropathy, p. 269, 270.

n Clinical manifestations: long-standing diabetes mellitus, hypertension. The disease eventually progresses to terminal renal failure requiring dialysis. n Diagnosis:

• Laboratory tests: 24 hour urine, measurement of total protein excretion; increased solute retention (creatinine, urea)

• Sonography

• Percutaneous biopsy: rarely necessary (histology: diffuse, exudative and nodular changes; in end-stage glomerulosclerosis, the underlying disease can no longer be determined histologically)

n Sonographic findings: bilateral changes:

• Initially, hyperfiltration with enlarged kidneys

• With progression, signs of chronic glomerulonephritis:

- Echogenic parenchyma

- Prominent hypoechoic medullary pyramids

- Loss of parenchyma

• Possible signs of chronic pyelonephritis:

- Scars (echogenic parenchymal retraction)

- Abscesses

- Papillary necrosis

- Papillary calcifications n Accuracy of sonographic diagnosis: Under favorable scanning conditions, the sonographic signs are conclusive. When the underlying diabetes is known, the diagnosis can be established by ultrasound and no further tests are needed.

Generally there is no need for renal biopsy.

n Clinical manifestations: insidious onset with peripheral edema, followed later by hypertension and impaired renal function n Diagnosis: ¡2

• Urinalysis. 24 hour urine collection: nonselective proteinuria, microhematuria, g possible erythrocyturia, possible red-cell and white-cell casts (which confirm ^ glomerular disease), also hyaline and granular cysts £

• Laboratory findings: dysproteinuria, hyperlipidemia

• Sonography with follow-up -q

• Renal biopsy: histologic detection and differentiation (histology shows leukocy- jj tic infiltration, hyaline deposition, sclerosis, fibrosis, and tubular atrophy). to Renal biopsy is unnecessary when overall findings suggest a minimal lesion (good general health, normal filtration rate, acellular urinary sediment, normal ¡o blood pressure). "2

n Sonographic findings: The sonographic findings are uniform, regardless of the cause of the glomerulonephritis. The end stage cannot be differentiated even by j; histologic examination. Sonographic findings may remain essentially normal for (J-some time (at least with regard to renal size), and sonographic abnormalities are found only with the onset of renal failure and significantly elevated creatinine levels (look for subtle changes).

• Diffuse increase in echogenicity

• Loss of corticomedullary differentiation

• Prominent hypoechoic medullary pyramids

• Bilateral small kidneys with a homogeneous echo pattern n Accuracy of sonographic diagnosis: The sonographic findings in later stages are unequivocal, but the cause cannot be determined.

n Clinical manifestations: hemoptysis in cases with pulmonary involvement and consolidation; microcytic anemia; progressive renal failure n Diagnosis:

• History and physical examination, including inspection of the pharynx

• Urinalysis: erythrocyturia and proteinuria

• Chest radiograph: specific changes

• Antibody detection: detection of antiglomerular basement membrane antibodies in the blood (even in emergency cases); renal biopsy for detection of anti-glomerular basement membrane antibodies by fluorescent microscopy. (In Wegener granulomatosis, by contrast, antineutrophilic cytoplasmic antibodies [C-ANCA] are positive in only 88 % of patients with active disease, and in up to 44 % of patients during the remission phase.)

n Sonographic findings:

• Enlarged, rounded kidney

• Ill-defined medullary pyramids

• Nonhomogeneous, echogenic parenchymal pattern n Accuracy of sonographic diagnosis: The signs of acute renal failure are easily recognized with ultrasound, but their cause cannot be determined. An etiologic diagnosis requires additional tests (so that the patient can be referred as soon as possible for antibody elimination therapy such as plasmapheresis).

n See also Upper Abdominal Pain, Renal Infarction, p. 73; Kidney, Renal atrophy due to vascular occlusive disease, p. 270; Vascular Scars, p. 280.

Sonographic Finding Pain Abdomen
Fig. 173 Normal flow pattern in the Fig. 174 Proximal stenosis of the left proximal right renal artery renal artery (RA)

n Occurrence: Renal artery embolism is probably not an extremely rare condition. Etiologically, renal artery embolism due to cholesterol crystals should be considered in addition to cardiac arrhythmias (e.g., absolute arrhythmia in atrial fibrillation).

n Sonographic diagnosis: CDS can advance the diagnosis. Ultrasound contrast agents are helpful in defining the renal arteries and delineating the perfusion defect in the renal tissue.

n Clinical manifestations: nycturia and other nonspecific micturition problems; progressive renal insufficiency with lethargy, decreased exercise tolerance, fatigue, anemia, and visual deterioration; hypertension. An acute exacerbation of pyelonephritis is marked by local tenderness to pressure. n Diagnosis:

• History: recurrent episodes of pyelonephritis, history of early childhood diseases, known voiding problems (e.g., previous bedwetting, ureterocele)

Urinalysis: bacteriuria; the causative organism should be identified and tested jfl for antibiotic sensitivity; leukocyturia with white-cell casts, proteinuria; crea- g tinine clearance in 24 hour urine ^

Laboratory tests: CRP, simple blood count, electrolytes, creatinine, uric acid, £ urea, glucose

Sonography -q

High-quality scans obviate the need for further tests such as CT, plain radio- £

n Sonographic findings:

graphs, or intravenous pyelography (IVP). to

• Changes usually limited to one side "2

• Circumscribed thinning and increased echogenicity of the parenchymal rim

• Irregular renal surface with areas of scar retraction (differential diagnosis: j; previous renal infarction, resection and nephrostomy, tuberculosis) (J-

• Calyceal cysts or ectasia

• Frequent calcifications

• End stage: Shrunken, atrophic kidney n Accuracy of sonographic diagnosis: Typical sonographic signs with circumscribed parenchymal changes provide a reasonably high degree of confidence.

Calyceal cysts confirm the diagnosis.

n See also Urogenital Organs, Obstructive pyelocalyceal ectasia, p. 380, 382. n Clinical manifestations: possible flank tenderness, slowly progressive decline in renal function. n Diagnosis:

• History: Ask about underlying diseases that may be associated with outflow obstruction, bladder dysfunction, or bladder atony.

• Sonography n Sonographic findings:

• Full urinary bladder in patients with bladder dysfunction

• Obstructed ureter

• Outflow obstruction may be detectable in the ureter, due to an intraluminal stone or extrinsic compression by a tumor/metastasis or lymph node.

• Dilated pyelocalyceal system

• Displaced renal sinus

• Loss of renal parenchyma n Accuracy of sonographic diagnosis: An obstruction can be detected sonographi-cally with up to 98 % confidence, but the precise cause cannot always be determined.

n See also Upper Abdominal Pain, Renal Colic, p. 65.

n Clinical manifestations: colicky flank pain, oligo- or anuria. With an intermittent obstruction, intermittent polyuria may occur. With a long-standing obstruction and reflux, the loss of renal parenchyma leads to renal insufficiency with increased solute retention. n Diagnosis:

• Laboratory tests: complete blood count, creatinine, electrolytes, urea and uric acid jfl • Urinalysis: bacteriuria, leukocyturia (with infection), hematuria (with stone or g tumor), crystals

• Sonography

£ • The diagnostic workup may include IVP and CT

Caution: IVP should be used with caution in renal insufficiency. ■q n Sonographic findings: jj • Ureteral dilatation or obstruction to • Possible dilatation of the pyelocalyceal system jL • Degree of obstruction can be graded based on the extent of the changes lo (see p. 382)

"¡3 • Intraluminal obstruction by a stone, pus, clot, or tumor

• Extrinsic compression by a tumor, metastasis, retroperitoneal fibrosis (Ormond C disease), or malignant lymphoma

^ • An empty bladder is seen only with bilateral obstruction (rare).

n Accuracy of sonographic diagnosis: The sonographic diagnosis is very accurate (almost 100 %) in cases where the renal collecting system has also become dilated (necessary for renal insufficiency to occur). Frequently the cause of the obstruction cannot be identified. Because the ureter is retroperitoneal, it is often difficult to visualize and its course can be traced only when it is dilated. If a high ureteral obstruction is suspected but the cause is not seen on ultrasound, the condition may be confused with fibrolipomatosis or small peripelvic cysts.

Fig. 175a, b Prostatic carcinoma in two planes. The prostate (P) has an irregular shape and a nonhomogeneous internal echo pattern. It has indented the bladder (B), leading to outflow obstruction and the collection of sludge (arrows). The ureter

(U) is compressed and obstructed

n See also Kidney, Chronic pyelonephritis, p. 271; Infected obstruction, p. 286. n Clinical manifestations: long history of lethargy, urinary tract infection, and fever.

The systemic manifestations are usually severe, ranging to sepsis. n Diagnosis:

• Laboratory tests: blood chemistry, ESR; bacteriologic testing of urinary sediment; identify the causal organism and determine its antibiotic sensitivity

• Sonography

• Ultrasound-guided aspiration and drainage of the pus; necessary when outflow obstruction is present

Ultrasound Images Pyonephrosis

Fig. 176a, b Pyonephrosis: relatively hypoechoic renal parenchyma (K). The renal ,C pelvis is splayed open, and the renal collecting system (arrows in right image) is dilated into the proximal ureter (arrows in left image) and filled with high-level echoes (pus). a Transverse scan, b longitudinal scan. Clinical presentation: young male with diabetes mellitus

Fig. 176a, b Pyonephrosis: relatively hypoechoic renal parenchyma (K). The renal ,C pelvis is splayed open, and the renal collecting system (arrows in right image) is dilated into the proximal ureter (arrows in left image) and filled with high-level echoes (pus). a Transverse scan, b longitudinal scan. Clinical presentation: young male with diabetes mellitus n Sonographic findings:

• Dilated renal collecting system

• Occasional high-level internal echoes representing pus or debris n Accuracy of sonographic diagnosis: Ultrasound suggests the correct diagnosis, which can be established by percutaneous aspiration biopsy. The therapeutic response and sonographic follow-ups also confirm the diagnosis.

Analgesic Nephropathy n See also Kidney, p. 271.

n Clinical manifestations: diffuse pattern of complaints with pain, mental abnormalities, possible colicky abdominal pain (due to the passage of necrotic papillary tips), and dysuria. Slowly progressive renal insufficiency usually establishes the diagnosis. Pathogenic mechanism: analgesics compromise the blood supply to the kidneys. n Diagnosis:

• History: Most patients do not give a history of heavy analgesic use, partly because they do not appreciate its significance. Careful questioning is essential

• Urinalysis: mild proteinuria, microhematuria, sterile leukocyturia. Salt loss > 30 mmol/day on a salt-free diet, renal tubular acidosis. Metabolites of phen-acetin (paracetamol, N-acetyl-p-aminophenol) are detectable in the urine.

• Blood chemistry: elevated creatinine level, anemia (due also to gastrointestinal blood loss)

• Sonography: May also be used to direct percutaneous biopsy

• Exclude diabetic nephropathy, sickle cell anemia, renal tuberculosis, and acute pyelonephritis.

n Sonographic findings:

• Poor delineation

• Irregular increase in parenchymal echogenicity

• Ringlike calcifications at the tips of the papillae

• Secondary cysts n Note: The changes begin at the papillary tips and spread toward the cortex. Papillary tip necrosis may also occur in chronic pyelonephritis, diabetes melli-tus, sickle cell anemia, and obstructive uropathy.

jfl n Accuracy of sonographic diagnosis: The sonographic detection of papillary tip g necrosis makes a diagnosis of analgesic nephropathy very likely. A known history of analgesic abuse is considered to establish the diagnosis.

Sy n See also Renal Artery Embolism, p. 129; Kidney, Renal atrophy due to vascular O occlusive disease, p. 270. ¡2 n Classification:

Unilateral: chronic pyelonephritis, renal artery stenosis, long-standing renal vein thrombosis. The differential diagnosis includes hypoplastic kidney.

• Bilateral: chronic glomerulonephritis, diabetic nephropathy, nephrosclerosis, ci other systemic diseases; less commonly, bilateral chronic pyelonephritis rinn Clinical manifestations: end stage of chronic nephritis with renal insufficiency; t often rapid fatigability, poor exercise tolerance, dyspnea with pleural effusion and edema, anemia. Dialysis is necessary in bilateral cases. n Diagnosis:

• Laboratory tests: simple blood count; urine culture and urinary sediment, 24 hour urine, creatinine: and creatinine clearance

• Sonography n Sonographic findings:

• Disproportionately small kidneys. (When only one kidney is affected, there is generally compensatory enlargement of the contralateral kidney.)

• Parenchymal thinning

• Increased parenchymal echogenicity

• Poor organ delineation. Occasionally the kidney can be identified only by the presence of cortical cysts (cystic degeneration of medullary pyramids or secondary retention cysts).

n Accuracy of sonographic diagnosis: The diagnosis is considered to be established ifthe kidney can be visualized and is disproportionately small. There is no need for percutaneous biopsy because histologic confirmation is unnecessary in end-stage disease.

n Clinical manifestations: anuria, possible lower abdominal pain and tenderness.

Colicky flank pain occurs in long-standing cases with stasis. n Diagnosis:

• History and examination: palpable lower abdominal mass (distended bladder). Ask about a precipitating event (renal biopsy, bladder aspiration, etc.).

Suprapubic Catheter Blogs

Fig. 177 Bladder tamponade. A layered, hypoechoic mass (clotted blood) is visible within the bladder lumen following the insertion of a suprapubic catheter

• Sonography: May also be used to direct percutaneous aspiration jfl

• Cystoscopy g n Sonographic findings: ^

• Frequent high-level internal echoes from clotted blood (e.g., after bladder aspiration, catheterism), debris, stone, or tumor -q n Accuracy of sonographic diagnosis: Bladder tamponade can be confidently diag- g nosed with ultrasound. Other tests are necessary only to investigate the cause. to

... inc n Clinical manifestations: known hepatic cirrhosis, usually decompensated with ascites and gastrointestinal bleeding; hypertension; progressive renal insufficiency ranging to anuria. May be precipitated by forced diuresis, percutaneous aspiration of ascites, bleeding, sepsis, or potentially nephrotoxic drugs. n Diagnosis:

• History and clinical findings: basic neurological staging examination (flapping tremor, writing test, connect-the-numbers test)

• Laboratory tests

• Sonography

• Esophagogastroduodenoscopy: esophageal varices, fundal varices

• Reasons for impaired renal function are not found: urinalysis normal, IVP normal (and therefore rarely necessary), negative renal biopsy (rarely done)

n Sonographic findings:

• Free fluid in the abdominal cavity (ascites)

• Signs of hepatic cirrhosis (see Ascites, p. 155) or other causes of liver cell destruction

• Both kidneys show normal sonographic features.

h Note: It is important to look for other renal diseases that are independent of the liver disease.

n Accuracy of sonographic diagnosis: The sonographic signs are clear-cut, and the diagnosis is supported by the overall clinical presentation and course. The cause of the syndrome is not precisely known but presumably relates to diminished blood flow.

Fig. 178 Acute renal failure in hepatorenal syndrome: hepatic cirrhosis with echogenic areas of liver necrosis and ascites. CDS shows predominantly large-caliber arteries; hepatic veins are not visualized


lj C

n See also Kidney, Acute Renal Failure, p. 267.

n Classification: Shock kidney is characterized by the development of renal failure due to prerenal causes - traumatic, postoperative, or septic. n Clinical manifestations: oliguria, anemia, peripheral edema, hypertension, pulmonary edema n Diagnosis:

• History: may suggest the precipitating cause - volume deficit, cardiogenic shock, sepsis, medications

• Blood tests and urinalysis

• Sonography n Sonographic findings:

• Enlarged kidneys

• Markedly hypoechoic parenchyma; distal acoustic shadowing enhancement may occur (depending on the extent of edema)

• Swollen medullary pyramids

• Typically, the boundary between the renal pelvis and renal sinus is indistinct.

• Renal sinus is compressed and narrowed as a result of parenchymal swelling. n Accuracy of sonographic diagnosis: The findings resemble the features of right heart failure and renal congestion. Sonography can establish the diagnosis in conjunction with clinical findings.

Fig. 179a,b a Acute prerenal renal failure in a patient with severe vomiting and alcohol disease. The kidney (K) is markedly enlarged to a longitudinal diameter of 15 cm. The parenchyma is thickened and hypoechoic, with swollen medullary pyramids. b Gouty nephropathy; small kidney with elevated echogenicity, swollen pyramids and a secondary lyst (arrow)

n Occurrence, course:

• Chronic hyperuricemia

• Deposition of sodium urate in the pyelocalyceal system

• Crystalization in the renal tubule and collecting duct

• Inflammatory processes

• Development of medullary fibrosis, with fibrosis of the papillary tips n Clinical manifestations: progressive signs of renal insufficiency, frequent hyper-136 tension, frequent pyelonephritis n Diagnosis: ¡2

• Laboratory findings: frequent hyperlipidemia and bacteriuria g

• Small kidneys

• Increased echogenicity d

• Bulging renal surface an

• Parenchymal thinning s

• Calculi ¡^ n Accuracy of sonographic diagnosis: Ultrasound is very accurate when laboratory Si tests show elevated uric acid and other clinical manifestations of gout are present. "JJ

Renal Lithiasis o

,c n See Upper Abdominal Pain, Renal Colic, p. 65; Kidney, Renal calyceal or pelvic Q.

stone, p. 288; Urogenital Organs, Urinary stone colic, p. 380. □ Note: Renal insufficiency may develop in long-standing cases of lithiasis with recurrent episodes of colic.

n Clinical manifestations: upper and midabdominal pain, hematuria, hypertension. Recurrent renal colic due to intracystic hemorrhage and clotting, with possible discharge of clots into the collecting system. Recurrent urinary tract infections; progressive renal failure until dialysis is required n Diagnosis:

• Examination, history: enlarged, palpable kidneys. Familial occurrence; family members should be screened whenever possible

• Urinalysis

• Sonography n Sonographic findings:

• Multiple anechoic masses (cysts)

• Cysts are flattened and spaced close together. The renal parenchyma may be greatly thinned.

• Bilateral involvement n Accuracy of sonographic diagnosis: The sonographic findings are unequivocal, provided the kidneys can still be identified. If so, there is no need for further testing.

Renal Amyloidosis n See also Kidney, p. 269.

n Clinical manifestations: nonspecific proteinuria; symptoms of the underlying disease leading to amyloidosis are predominant. n Diagnosis:

• Laboratory examination of the blood and urine

• Abdominal sonography

• Ultrasound-guided percutaneous renal biopsy with histologic evaluation n Sonographic findings:

• Bilateral renal enlargement

• Thickened, hypoechoic renal parenchyma

• Frequent enlargement of other parenchymal organs (e.g., spleen)

jfl n Accuracy of sonographic diagnosis: The sonographic findings are nonspecific. g Percutaneous biopsy may confirm the presumptive diagnosis.

See also Kidney, p. 282.

Definition: variable degree of calcification of the renal medulla (= renal pyramids). Occurrence:

• Analgesic abuse (phenacetin, acetaminophen [paracetamol], aspirin, etc.)

• Renal tubular acidosis

• Primary hyperoxaluria

• Treatment for cystinuria

Clinical manifestations: progressive renal insufficiency.

Sonographic findings: markedly echogenic medullary pyramids, which may cast acoustic shadows.

n Clinical manifestations: urinary retention with a full bladder; lower abdominal pain usually present; flank pain due to reflux n Diagnosis:

• History: previous surgery, radiotherapy, etc.

• Sonography

• Endoscopy or CT if required. n Sonographic findings:

• Full urinary bladder

• In most cases the urethra is obstructed by extrinsic compression from an enlarged prostate or tumor.

n Accuracy of sonographic diagnosis: The urethra itself can rarely be visualized with ultrasound, but abnormalities about the urethra can be demonstrated, particularly with a full bladder.

Vein Reflux Ultrasound Protocol

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