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Renal 2 Test 1 > Renal Pathology Part 7 > Flashcards

Renal Pathology Part 7 Flashcards

1
Q

Urinary Tract Obstruction (Obstructive Uropathy)

A
  • obstructive lesions of the urinary tract increase susceptibility to infection and to stone formation, and unrelieved obstruction almost always leads to permanent renal atrophy, termed hydronephrosis or obstructive uropathy
  • obstruction may be sudden or insidious, partial or complete, unilateral or bilateral; it may occur at any level of the urinary tract from the urethra to the renal pelvis
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2
Q

Common causes of urinary tract obstruction

A
  • Congenital anomalies: posterior urethral valves and urethral strictures, meatal stenosis, bladder neck obstruction; ureteropelvic junction narrowing or obstruction; severe vesicoureteral reflux
  • Urinary calculi
  • BPH
  • Tumors: carcinoma of the prostate, bladder tumors, contiguous malignant disease (retroperitoneal lymphoma), carcinoma of the cervix or uterus
  • inflammation: prostatis, ureteritis, urethritis, retroperitoneal fibrosis
  • sloughed papillae or blood clots
  • pregnancy
  • uterine prolapse and systole
  • functional disorders: neurogenic (spinal cord damage or diabetic nephropathy) and other functional abnormalities of the ureter or bladder (often termed dysfunctional obstruction)
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3
Q

Hydronephrosis

A
  • dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney due to obstruction to the outflow of urine
  • even with complete obstruction, glomerular filtration persists fro some time because the filtrate subsequently diffuse back into the renal interstitium and peritoneal spaces, from where it ultimately returns to the lymphatic and venous systems
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4
Q

When urinary obstruction is sudden and complete, it leads to

A

-mild dilation of the pelvis and calyces and sometimes to atrophy of the renal parenchyma

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5
Q

When urinary obstruction is subtotal or intermittent,

A

-progressive dilation ensues, giving rise to hydronephrosis

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6
Q

Depending on the level of the urinary block,

A
  • the dilation may affect the bladder first, or the ureter and then the kidney
  • kidney may be slightly to massively enlarged, depending on the degree and the duration of the obstruction
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7
Q

Urinary obstruction morphology

A

-earliest features are those of simple dilation of the pelvis and calyces, but in addition there is often significant interstitial inflammation, even in the absence of infection

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8
Q

In chronic cases of urinary obstruction, there is

A

cortical tubular atrophy with marked diffuse interstitial fibrosis
-progressive blunting of the apices of the pyramids occurs, and these eventually become cupped

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9
Q

Acute urinary obstruction may provoke

A
  • pain attributed to distention of the collecting system or renal capsule
  • most of the early symptoms are produced by the underlying cause of the hydronephrosis
  • calculi lodged in the ureters may give rise to renal colic, and prostatic enlargement may give rise to bladder symptoms
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10
Q

Unilateral complete or partial hydronephrosis may

A

-remain silent for long periods, since the unaffected kidney can maintain adequate renal function

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11
Q

In early stages of urinary obstruction,

A

-relief of obstruction leads to reversion to normal function

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12
Q

In bilateral partial obstruction,

A
  • the earliest manifestation is inability to concentrate urine, reflected by polyuria and nocturne
  • some patients develop distal tubular acidosis, renal salt wasting, secondary renal calculi, and chronic tubulointerstitial nephritis with scarring and atrophy of the papilla and medulla
  • hypertension common
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13
Q

Complete bilateral obstruction of rapid onset result in

A

-oliguria or anuria and is incompatible with survival unless the obstruction is relieved

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14
Q

After relief of complete urinary tract obstruction,

A
  • postobstructive diuresis occurs

- this can often be massive, with the kidney excreting large amounts of urine that is rich in sodium chloride

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15
Q

Urolithiasis

A
  • affects 5-10% of Americans in their lifetime and the stones may form anywhere in the urinary tract
  • men affected more than women, peak age at onset is between 20 and 30 years
  • familial and hereditary predisposition to stone formation
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16
Q

4 main types of calculi

A
  • calcium stones (about 70%) composed largely of calcium oxalate or calcium oxalate mixed with calcium phosphate
  • another 15% of triple stones or struvite stones, composed of magnesium ammonium phosphate
  • 5-10% are uric acid stones
  • 1-2% are made up of cysteine
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17
Q

Calcium oxalate stones

A
  • associated in about 5% of patients with hypercalcemia and hypercalciuria, such as occurs with hyperparathyroidism, diffuse bone disease, sarcoidosis, and other hypercalcemic states
  • about 55% have hypercalciuria without hypercalcemia
  • caused by several factors, including hyper absorption of calcium from intestine, an intrinsic impairment in renal tubular reabsorption of calcium, or idiopathic fasting hypercalciuria with normal parathyroid function
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18
Q

Magnesium ammonium phosphate stones

A
  • formed largely after infections by urea-splitting bacteria (proteus and some staphylococci) that convert urea to ammonia
  • resultant alkaline urine causes precipitation of magnesium ammonium phosphate salts
  • form some of the largest stones, as the amount of urea excreted is large
  • staghorn calculi occupying large portions of renal pelvis are frequently consequence of infection
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19
Q

Uric acid stones

A
  • common individuals with hyperuricemia, such as patients with gout, and diseases involving rapid cell turnover, such as the leukemias
  • more than half of patients have neither hyperuricemia nor increased urinary excretion of uric acid
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20
Q

Cysteine stones

A
  • caused by genetic defects in the renal reabsorption of amino acids, including cysteine, leading to cystinuria
  • form at low urinary pH
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21
Q

Urolithiasis Morphology

A
  • stones are unilateral in about 80% of patients
  • favored sites for formation are within renal calyces and pelves and int he bladder
  • if formed in renal pelvis tend to be small
  • may have smooth contours or may take the form of an irregular, jagged mass of spicules
  • often many stones are found within one kidney
  • on ocasión, progressive secretion of salts leads to development of branching structures known as stag horn calculi, which create a cast of the pelvic and calyceal system
22
Q

Urolithiasis Clinical Features

A
  • may be asymptomatic, produce severe renal colic and abdominal pain, or may cause significant renal damage
  • larger stones often manifest themselves by hematuria
  • stones also predispose to superimposed infection, both by their obstructive nature and by trauma they produce
23
Q

Renal Papillary Adenoma

A
  • small, discrete adenomas arising from renal tubular epithelium
  • most frequently papillary
  • present invariably within the cortex and appear grossly as pale yellow-gray, discrete, well-circumscribed nodules
  • complex, branching, papillomatous structures with numerous complex fronds; or as tubules, glands, cords, or sheets of cells
  • cuboidal to polygonal in shape
  • do not differ from low-grade papillary renal cell carcinoma histologically
24
Q

Angiomyolipoma

A
  • benign neoplasm consisting of vessels, smooth muscle, and fat originating from perivascular epithelioid cells
  • present in 25-50% of patients with tuberous sclerosis (loss of function mutations in TSC1 or TSC2)
25
Q

Tuberous sclerosis characterized by

A
  • lesions of the cerebral cortex that produce epilepsy and mental retardation, a variety of skin abnormalities, and unusual benign tumors at other sites, such as the heart
  • susceptibility to spontaneous hemorrhage
26
Q

Oncocytoma

A
  • epithelial neoplasm composed of large eosinophilic cells having small, round, benign-appearing nuclei that have large nucleoli
  • thought to arise form intercalated cells of CDs
  • eosinophilic cells have numerous mitochondria
  • tumors are tan or mahogany brown,r relatively homogeneous and usually well encapsulated with a central scar in 1/3 of cases
  • may achieve a large size
27
Q

Renal Cell Carcinoma

A
  • represent about 3% of all newly diagnosed cancers in U.S. and accounts for 85% of renal cancers in adults
  • occur most often in older individuals in their 60s and 70s and 2:1 male preponderance
28
Q

Renal Cell carcinoma risk factors

A
  • tobacco
  • obesity
  • hypertension
  • unopposed estrogen therapy
  • exposure to asbestos, petroleum products, and heavy metals
  • ESRD, chronic kidney disease, acquired cystic disease and tuberous sclerosis
29
Q

Von Hippel-Lindaue (VHL) Syndrome

A
  • half to 2/3s of individuals with VHL develop renal cysts and bilateral, often multiple, renal cell carcinomas
  • studies implicate VHL gene in development of both familial and sporadic clear cell carcinomas
30
Q

Hereditary leiomyomatosis and renal cell cancer sydnrome

A
  • autosomal dominant disease
  • caused by mutations of the FH gene, which expresses fumarate hydratase
  • characterized by cutaneous and uterine leiomyomata and an aggressive type of papillary carcinoma with increased propensity for metastatic spread
31
Q

Hereditary papillary carcinoma

A
  • autosomal dominant form
  • multiple bilateral tumors with papillary histology
  • series of cytogenetic abnormalities and mutations in the MET porto-oncogene
32
Q

Birth-Hogg-Dubs Syndrome

A
  • autosomal dominant
  • mutations involving the BHD gene, which expresses folliculin
  • constellation of skin (fibrofolliculomas, trichodiscomas, and acrochordons), pulmonary (cysts or blebs), and renal tumors with a wide range of histologic subtypes
33
Q

Clear Cell carcinoma

A
  • most common type, accounting for 70-80% of renal cell cancers
  • tumors made up of cells with clear or granular cytoplasm and non papillary
  • Can be familial but most cases are sporadic
  • In 98%, associated with VHL syndrome, there is loss of sequences on short arm of chromosome 3
  • VHL gene acts as a tumor suppressor and encodes a protein that is part of a ubiquitin ligase complex involved in targeting other proteins for degradation
  • important among targets of VHL is transcription factor HIF-1
34
Q

When VHL is inactive,

A
  • HIF-1 levels remain high,e even under normoxic conditions, causing inappropriate expression of a number of genes that are turned on by HIF
  • these include genes that promote angiogenesis, such as VEGF, and genes that stimulate cell growth, such as insulin-like growth factor-1
35
Q

Papillary carcinoma

A
  • accounts for 10-15% of renal cancers
  • characterized by a papillary growth pattern and also occurs in both familial and sporadic forms
  • most common cytogenetic abnormalities are trisomies 7 and 17 and loss of Y in male patients in sporadic form, and trisomy 7 in the familial form
  • gene on chromosome 7 for the familial form has been mapped to MET
  • frequently multifocal in origin
36
Q

Chromophobe carcinoma

A
  • 5% of renal cell cancers and composed of cells with prominent cell membranes and pale eosinophilic cytoplasm, usually with a halo around the nucleus
  • multiple chromosomal losses and extreme hypodiploidy
  • thought to grow from intercalated cells of collecting ducts and have excellent prognosis
37
Q

Xp11 translocation carcinoma

A
  • often occurs in young patients and is defined by translocations of the TFE3 gene
  • clear cytoplasm with a papillary architecture
38
Q

Collecting duct (Bellini duct) carcinoma

A
  • approximately 1% or less of renal epithelial neoplasms
  • arise from CD cells in the medulla
  • characterized by malignant cells forming glands enmeshed within a prominent fibrotic stroma, typically in a medullary location
39
Q

Renal cell carcinomas may arise

A

-in any portion of the kidney, but more commonly affects the poles

40
Q

Clear cell carcinomas most likely arise

A

from proximal tubular epithelium, and usually occur as solitary unilateral lesions

41
Q

Clear cell carcinomas are

A
  • bright yellow-gray-white spherical masses of variable size that distort the renal outline
  • yellow color is a consequence of the prominent lipid accumulations in tumor cells
  • commonly large areas of gray-white necrosis and foci of hemorrhagic discoloration
  • margins are usually sharply defined and confined within the renal capsule
  • growth pattern varies from solid to trabecular or tubular
  • tumor cells have a rounded or polygonal shape and abundant clear or granular cytoplasm, which contains glycogen and lipids
  • tumors have delicate branching vasculature and may show cystic as well as solid areas
42
Q

Clear Cell Carcinoma Morphology

A
  • most tumors are well differentiated, but some show nuclear atypic with bizarre nuclei and giant cells
  • as tumors enlarge they may bulge into the calyces and pelvis and eventually fungal through the walls of the collecting system to extend into the ureters
  • tendency to invade renal vein, in which it may grow as a solid column of cells that extends up the IVC, sometimes as far as the right side of the heart
43
Q

Papillary carcinoma morphology

A
  • thought to arise for distal convoluted tubules, can be multifocal and bilateral
  • typically hemorrhagic and cystic, especially when large
  • composed of cuboidal or low columnar cells arranged in papillary formations
  • interstitial foam cells common in the papillary cores
  • Psammoma bodies may be present
  • stroma is usually scant but highly vascularized
44
Q

Chromophobe renal carcinoma morphology

A

-pale eosinophilic cells, often with a perinuclear halo, arranged in solid sheets with a concentration of the largest cells around blood vessels

45
Q

Collecting duct carcinoma morphology

A

-irregular channels lined by highly atypical epithelium with a hobnail pattern

46
Q

Classic clinical features of renal cell carcinoma

A
  • costovertebral pain, palpable mass, and hematuria, but all 3 are seen in only 10% of cases
  • most reliable clue is hematuria, but usually intermittent and may be microscopic; thus, the tumor may remain silent until it attains a large size, often greater than 10 cm
  • at this time, it is often associated with generalized constitutional symptoms, such as fever, malaise, weakness, and weight loss
  • can also produce syndromes due to abnormal hormone production
47
Q

Renal cell carcinoma has a tendency to

A

metastasize widely before giving rise to any local symptoms or signs
-in 25% of patients with renal cell carcinoma, there is radiologic evidence of metastases at the time of presentation

48
Q

Most common location of renal cell carcinoma metastasis are

A

lungs and bones, followed in frequency by regional lymph nodes, liver, adrenal, and brain

49
Q

Urothelial Carcinoma of the Renal Pelvis

A
  • approximately 5-10% of primary renal tumors originate from the urothelium of renal pelvis
  • these tumors range from apparently benign papillomas to invasive urothelial (transitional cell) carcinomas
  • renal pelvic tumors usually become clinically apparent within a relatively short time, because they lie within he pelvis and, by fragmentation, produce noticeably hematuria
  • tumors may block urinary outflow and lead to palpable hydronephrosis and flank pain
50
Q

On histologic exam, pelvic tumors are

A

the exact counterpart of those found in the urinary bladder

  • urothelial tumors may occasionally be multiple, involving the pelvis, ureters, and bladder
  • in 50% of tumors, there is preexisting or concomitant bladder urothelial tumor
  • foci or atypia or carcinoma in situ in grossly normal urothelium remote from pelvic tumor
  • infiltration fo wal lof pelvis and calyces is common
  • prognosis is not good
51
Q

Increased incidence of urothelial carcinomas of the renal pelvis in individuals with

A

Lynch syndrome and analgesic nephropathy

Renal 2 Test 1 (16 decks)

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