XIV - The Kidneys and Its Collecting System (with pics) Flashcards
(154 cards)
1
Q
A glomerular syndrome dominated by the acute onset of usually grossly visible hematuria, mildly moderate proteinuria, azotemia, edema and hypertension.
A
Acute nephritic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
2
Q
A glomerular syndrome characterized by heavy proteinuria, hypoalbunemia, severe edema, hyperlipidemia and lipiduria.
A
Nephrotic syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
3
Q
Characterized by bacteriuria and pyuria, which may be asymptomatic.
A
Urinary tract infection(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 542
4
Q
Most common type of collagen found in glomerular basement membrane.
A
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 543
5
Q
Most frequent cause nephrotic syndrome in children. Under light microscope, the glomerular basement membrane appears normal, but on electron microscopy, GBM shows uniform and diffuse effacement of foot processes of the podocytes. SEE SLIDE 14.1. Good response to corticosteroid therapy.
A
Minimal change disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550
6
Q
A lesion characterized histologically by sclerosis affecting some but not all glomeruli and involving only segments of each affected glomerulus. SEE SLIDE 14.2.
A
Focal segmental glomerulosclerosis (FSGS)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550
7
Q
Slowly progressive disease characterized by the presence of subepithelial immunoglobulin-containing deposits along the glomerular basement membrane. Histologically, there is diffuse thickening of the BM. (+) spike and dome pattern on electron microscopy. SEE SLIDE 14.3. Often resistant to steroid therapy.
A
Membranous glomerulonephritis (Membranous Nephropathy)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 551
8
Q
Characterized by discrete SUBENDOTHELIAL electron-dense deposits in irregular granular pattern. SEE SLIDE 14.4.
A
Type I MPGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 553
9
Q
GBM is thickened, showing a “tram-track” appearance on PAS stains. There is proliferation of mesangial and endothelial cells as well as infiltrating leukocytes. SEE SLIDE 14.5.
A
MPGN(Membranoproliferative Glomerulonephritis)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 553
10
Q
MPGN wherein the lamina densa and the SUBENDOTHELIAL space of the GBM are transformed into an irregular, ribbon-like extremely electron dense structure. SEE SLIDE 14.6.
A
Type II MPGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 554
11
Q
Caused by glomerular deposition of immune complexes resulting in diffuse proliferation and swelling of resident glomerular cells. There is uniformly increased cellularity of glomerular tufts. Electron microscopy show subepithelial “humps” against the GBM, with granular deposits of IgG and complement. SEE SLIDE 14.7.
A
Acute postinfectious (poststreptococcal) Glomerulonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 555
12
Q
Most common cause of recurrent microscopic or gross hematuria and is the most common glomerular disease revealed by renal biopsies.
A
IgA Nephropathy (Berger disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 555
13
Q
Pathologic hallmark of this disease is the deposition of IgA in the mesangium. SEE SLIDE 14.8.
A
IgA nephropathy (Berger Disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 556
14
Q
Nephritis accompanied by nerve deafness, lens dislocation, posterior cataracts and corneal dystrophy. Pathogenesis is due to a mutation of one of the alpha chains of Type IV collagen, leading to these manifestations.
A
Alport syndrome(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 531
15
Q
Caused by mutations in genes encoding GBM collagen, manifest as hematuria and slowly progressing proteinuria and declining renal function. GBM has “basket-weave” appearance due to splitting and lamination of the lamina densa. Interstitial cells also show foamy appearance.
A
Hereditay nephritis (Such as Alport Syndrome) (TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 531
16
Q
A clinical syndrome characterized by rapid and progressive lossof renal function with features of nephritic syndrome,often with severe oliguria. Histologic feature is the presence of crescents. SEE SLIDE 14.9.
A
Rapidly Progressive Glomerulonephritis (Crescentic GN)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557
17
Q
CrGN characterized by linear deposits of IgG and C3 on the GBM. anti-GBM Ab also bind to pulmonary alveolar capillary basement membranes to produce pulmonary hemorrhages associated with renal failure. SEE SLIDE 14.9.
A
Anti-Glomerular Basement Membrance Antibody (Type I) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557
18
Q
CrGN which are immune complex-mediated disorders, as a complication of any of the IC nephritides including PSGN, IgA Nephropathy and HSP. There is segmental necrosis and characteristic granular pattern of the underlying immune complex disease.
A
Immune Complex-Mediated (Type II) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 558
19
Q
CrGN defined by the lack of anti-GBM Ab and immune complex deposition. Glomeruli show segmental necrosis, negative immunofluorescence.
A
Pauci-immune (Type III) CrGN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 558
20
Q
An important cause of end-stage renal disease presenting as chronic renal failure. Kidneys are symmetrically contracted, surfaces are red-brown and diffusely granular. Glomeruli are obliterated with marked interstitial fibrosis.
A
Chronic glomerulonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 559
21
Q
A common suppurative inflammation of the kidney and renal pelvis caused by bacterial infection, either by hematogenous spread or through ascending infection.
A
Pyelonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 560
22
Q
Hallmark of this disease is scarring involving the pelvis or calyces, or both, leading to papillary blunting and marked calyceal deformities.
A
Chronic pyelonephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 562
23
Q
Nephritis with prominent eosinophilic and mononuclear inflitrate, with pronounced edema in the INTERSTITIUM. SEE SLIDE 14.10
A
Acute Drug-Induced Interstitial Nephritis(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 536
24
Q
A clinicopatholigic entity characterized by damaged tubular epithelial cells and clinically by acute suppression of renal function.Most common cause of acute renal failure. SEE SLIDE 14.11.
A
Acute tubular necrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564
25
Characterized by necrosis of short segments of the tubules, seen in the straight portions of the PCT and TALOH. There is a variety of tubular injuries, associated with proteinaceous casts (consisting of Tamm-Horsfall protein) in the distal tubules and collecting ducts.
Ischemic ATN(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 538
26
ATN characterized by necrosis and injury of the PCT with sparing of the tubular membranes.
Toxic ATN(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
27
Phase of ATN lasting about 36 hrs, dominated by the inciting medical, surgical or obstetric event. Slight decline in renal output and a rise in serum creatinine.
Initiation phase(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
28
Phase of ATN where urine output falls markedly, between 50-400mL/day. Dominated by signs and symptoms of uremia and fluid overload.
Maintenance phase(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
29
Phase of ATN characterized by a steady increase in urine volume, electrolyte imbalance and increased vulnerability to infection.
Recovery(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
30
Chronic interstitial nephritis associated with renal papillary necrosis. The necrotic papillae appear yellowish-brown, showing coagulative necrosis associated with loss of cellular detail with preservation of tubular outlines. SEE SLIDE 14.12.
Analgesic nephropathy(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564
31
T-cell mediated immune reaction of the kidneys to an offending agent, characterized by interstitial inflammation, with abundant eosinophils and edema.
Drug-induced interstitial nephritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 564
32
Renal changes in benign hypertension, associated with hyaline arteriolosclerosis, appearing as homogenous, pink hyaline thickening of arterial walls. Larger blood vessels show fibroelastc hyperplasia.
Benign nephrosclerosis. SEE SLIDE 14.13. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 566
33
The kidneys show small, pinpoint petechial hemorrhages, "flea-bitten" appearance. Concentric arrangement of cells, described as "onion-skin" lesions cause marked narrowing of arterioles and small arteries (hyperplastic arteriolosclerosis).
Malignant hypertension. SEE SLIDE 14.14. (TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 540
34
Characterized by widespread thrombosis and presence of fibrin thrombi in glomeruli and small vessels resulting in acute renal failure. Consequence of childhood HUS and TTP.
Thrombotic microangiopathies(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 568
35
One of the main causes of acute renal failure in children.
Hemolytic Uremic Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 568
36
Innocuous lesions of the kidney, 1-5cm in diameter, translucent, lined by a gray, glistening, smooth membrane, filled with clear fluid. Composed of a single layer of cuboidal or flattened cuboidal epithelium, usually confined to the cortex.
Simple renal cyst(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
37
Autosomal dominant. Kidneys are enlarged, composed solely of cysts without intervening parenchyma. Cysts are filled with clear or turbid fluid. Cysts may arise at any level of the nephron, with variable, often atrophic lining.
Adult polycystic kidney disease (APKD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
38
What is the pathology behind APKD?
Defective gene PKD1,which codes for polycystin-1.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
39
Function of policystin-1?
Protein that is involved in cell-cell or cell-matrix adhesion.(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 569
40
Autosomal recessive. There are numerous small cysts in the cortex and medulla, giving the kidney a "sponge-like" appearance. Cysts have uniform cuboidal epithelium. Associated with multiple cysts in the liver.
Childhood Polycystic Kidney Disease (CPKD)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 570
41
An under-recognized cause of chronic kidney disease in children and young adults, associated with mutations in several genes that encode neohrocystins that may be involved in ciliary function. Kidneys are contracted and contain multiple cysts.
Medullary cystic disease(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571
42
Calculus formation at any level of the urinary collecting system.
Urolithiasis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571
43
Most common composition of kidney stones.
Calcium oxalate and/or calcium phosphate(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 571
44
Most important cause of kidney stone formation.
Supersaturation(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
45
Kidney stones occuring in patients with alkaline urine due to UTI, particularly Proteus vulgaris and Staphylococci.
Struvite stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
46
Component of struvite stones.
Magnesium ammonium phosphate(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
47
Kidney stones seen in patients with gout and leukemias. Urine pH is decreased.
Uric acid stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
48
Kidney stones associated with a defect in the renal transportation of certain amino acids. Forms in acidic urine.
Cystine stones(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
49
Branching structures which create a cast of the renal pelvis and calyceal system.
Stagnorn calculi(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
50
Most common composition of staghorn calculi.
Magnesium ammonium phosphate (Struvite)(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
51
Dilation of the renal pelvis and calyces, accompanied by atrophy of the renal parenchyma, caused by obstruction to urine outflow. Histologically, there is tubular dilation followed by atrophy and fibrous replacement of the tubular epithelium.
Hydronephrosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 572
52
Dilation of the ureters secondary to obstruction.
Hydroureter(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573
53
Most common malignant tumor of the kidney.
Renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573
54
Tumors derived from renal tubular epithelium, located primarily at the cortex. With three common forms, clear cell, papillary renal cell and chromophobe renal carcinomas.
Renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573
55
Most common form of renal cell carcinoma and associated with homozygous loss of the VHL tumor suppressor gene.
Clear cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 549
56
Renal carcinoma, usually solitary and large, spherical masses reaching up to 15cms in diameter. Cut surface show yellow orange to gray-white, with prominent areas of cystic softening and hemorrhage. Cells appear vacuolated or may be solid. Often invades the renal vein. SEE SLIDE 14.14.
Clear cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 549
57
Renal carcinoma exhibiting varying degrees of papilla formation with fibrovascular cores. Cells have clear to pink cytoplasm. Associated with increased activity of MET oncogene. Tend to be bilateral.
Papillary renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 549
58
Renal cell carcinoma which tends to be tan-brown, cells have clear, flocculent cytoplasm with very prominent, distinct cell membranes. Nuclei surrounded by halos of cleared cytoplasm.
Chromophobe-type renal cell carcinoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 574
59
Tumor of the urinary bladder, characterized as small, frond-like structures having delicate fibrovascular core covered by multilayered, well-differentiated transitional epithelium.
Benign papilloma(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 575
60
Dominant clinical presentation of bladder carcinoma.
Painless hematuria(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 575
61
Protozoa associated with increased risk of bladder carcinoma.
Schistosoma haematobium(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 576
62
Chemotherapeutic agent associated with development of hemorrhagic cystitis and increased risk of bladder carcinoma.
Cyclophosphamide(TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 576
63
Electron Microscopy: Subepithelial humps
PSGN. SEE SLIDE 14.7. (TOPNOTCH)
64
Light Microscopy: Hyalinized glomeruli
Chronic Glomerulonephritis. SEE SLIDE 14.15. (TOPNOTCH)
65
Electron Microscopy: Subepithelial deposits
Membranous glomerulopathy. SEE SLIDE 14.3.(TOPNOTCH)
66
Electron Microscopy: Loss of foot processes
Minimal Change Disease. SEE SLIDE 14.1 (TOPNOTCH)
67
Electron Microscopy: Subendothelial deposits
MPGN Type 1. SEE SLIDE 14.4. (TOPNOTCH)
68
Flourescence Microscopy: Linear IgG and C3
Goodpasture's disease. SEE SLIDE 14.9. (TOPNOTCH)
69
Light Microscopy: Normal, with lipid in tubules
Minimal Change Disease. SEE SLIDE 14.1 (TOPNOTCH)
70
What are the 3 classic diagnostic features of RCC?
1. Costovertebral Pain (TOPNOTCH)2. Palpable Mass3. Hematuria
71
Among the 3 classic diagnostic features of RCC, which feature is the most reliable?
Hematuria (TOPNOTCH)
72
RCC morphology: pale eosinophilic cells, often with a perinuclear halo, arranged in solid sheets with a concentration of the largest cells around the blood vessels
Chromophobe RCC (TOPNOTCH)
73
RCC morphology: rounder or polygonal shape and have abundant clear or granular cytoplasm with stains with glycogen and lipid
Clear Cell RCC (TOPNOTCH)
74
RCC morphology: arise from DCT and are typically hemorrhagic and cystic
Papillary RCC (TOPNOTCH)
75
RCC morphology: irregular channels lined by highly atypical epithelium with a hobnail pattern.
Collecting Duct Carcinoma (TOPNOTCH)
76
RCC morphology: Interstitial foam cells and psamomma bodies
Papillary Carcinoma (TOPNOTCH)
77
Urolithiasis: most common type
Calcium Oxalate stones (TOPNOTCH)
78
Urolithiasis: staghorn calculi
Triple stones/ struvite stones/ Magnesium Ammonium Phosphate stones (TOPNOTCH)
79
Urolithiasis: caused by genetic defects in the renal absorption of amino acids
Cystine stones (TOPNOTCH)
80
Urolithiasis: associated with urea-splitting bacteria
Triple stones/ struvite stones/ Magnesium Ammonium Phosphate stones (TOPNOTCH)
81
Urolithiasis: radiolucent
Uric Acid Stones (TOPNOTCH)
82
Urolithiasis: common in patients with leukemia
Uric Acid Stones (TOPNOTCH)
83
What is the most common cause of renal artery stenosis?
Occlusion by an atheromatous plaque at the origin of the renal artery (TOPNOTCH)
84
What is the most common type of Fibromuscular Dysplasia; intimal, medial, or adventitial?
Medial (TOPNOTCH)
85
Gross morphology: flea bitten appearance of the kidneys
Malignant Hypertension (TOPNOTCH)
86
What are the two histological alterations in the blood vessels of patients with malignant hypertension?
1. Fibrinoid Necrosis of arterioles2. Onion-skinning (TOPNOTCH)
87
What are the 3 complications of acute pyelonephritis?
1. Papillary Necrosis2. Pyonephrosis3. Perinephric Abscess (TOPNOTCH)
88
Among the 3 complications of acute pyelonephritis, which one is mainly seen in diabetics and in those with urinary tract obstruction?
Papillary necrosis (TOPNOTCH)
89
Morphology: acute neutrophilic exudate within tubules and the renal substance
Acute pyelonephritis (TOPNOTCH)
90
ATN morphology: focal tubular epithelial necrosis at multiple points along the nephron, with large skip areas in between
Ischemic ATN (TOPNOTCH)
91
ATN morphology: manifested by acute tubular injury with non specific tubular necrosis
Toxic ATN (TOPNOTCH)
92
ATN morphology: Eosinophilic hyaline casts containing Tamm Horsfall protein
Ischemic ATN (TOPNOTCH)
93
ATN morphology: severely injured cells that are not yet dead might contain large acidophilic inclusions
Mercuric Chloride ATN (TOPNOTCH)
94
ATN morphology: accumulation of neutral lipids in injured cells
Carbon Tetrachloride poisoning (TOPNOTCH)
95
ATN morphology: marked ballooning and hydrophic or vacuolar degeneration of proximal convulated tubules and often times calcium oxalate crystals are seen in the lumen
Ethylene Glycol ATN (TOPNOTCH)
96
Morphology: patchy interstitial suppurative inflammation, intratubular aggregates of neutrophils, and tubular necrosis
Acute pyelonephritis (TOPNOTCH)
97
Gross morphology: irregularly scarred; if bilateral, the involvement is asymmetric
Chronic pyelonephritis (TOPNOTCH)
98
Gross morphology: kidneys are diffusely and symmetrically scarred
Chronic glomerulonephritis (TOPNOTCH)
99
Morphology: hallmark is the coarse, discrete, corticomedullary scar overlying a dilated, blunted, or deformed calyx
Chronic pyelonephritis (TOPNOTCH)
100
What is the main cause of renal dysfunction in Multiple Myeloma?
Bence Jones protein (TOPNOTCH)
101
Morphology: bence jones tubular casts appear as pink to blue amorphous masses, sometimes concentrically laminated, often with fractured and angulated appearance, filling and distending the lumens
Multiple Myeloma (TOPNOTCH)
102
Morphology: classic diagnostic finding is enlarged hypercellular glomeruli
PSGN (TOPNOTCH)
103
Gross morphology: wedge-shaped lesions, with base against the cortical surface and the apex pointing toward the medulla
Renal infarcts (TOPNOTCH)
104
What is the first step in the pathogenesis of ascending infection that leads to pyelonephritis?
Colonization of the distal urethra and introits by coliform bacteria (TOPNOTCH)
105
Morphology: "fibrin caps" and "capsular drops"
Diabetic kidney (TOPNOTCH)
106
Morphology: diffuse increase in mesangial matrix and characteristic PAS positive nodules
Diabetic glomerulosclerosis (TOPNOTCH)
107
Flourescence microscopy: deposition of IgA, sometimes with IgG and C3, in the mesangial region
Henoch Schonlein Purpura (TOPNOTCH)
108
Gross morphology: wedge-shaped lesions, with base against the cortical surface and the apex pointing toward the medulla
Renal infarcts (TOPNOTCH)
109
What is the most common cause of clinical pyelonephritis?
Ascending infection (TOPNOTCH)
110
Morphology: collapsed glomerular tufts and the crescent shaped mass of proliferating cells and leukocytes internal to Bowman capsule
Rapidly Progressive Glomerulonephritis (TOPNOTCH)
111
Morphology: glomeruli show thickening and sometimes splitting of capillary walls, due largely to endothelial and subendothelial swelling, and deposits of fibrin-related materials in the capillary lumens, subendothelially, and in the mesangium.
Childhood Hemolytic Uremic Syndrome(TOPNOTCH)
112
Gross morphology: fine, leathery granularity of the surface of the kidney
Nephrosclerosis(TOPNOTCH)
113
What is the emerging viral pathogen that causes pyelonephritis in kidney allografts?
Polyoma virus(TOPNOTCH)
114
Morphology: enlarged tubular epithelial cells with nuclear inclusions
Polyoma kidney (TOPNOTCH)
115
Electron microscopy: irregular thickening of the BM of the glomerulus, lamination of the lamina densa, and foci of rarefaction
Alport Syndrome (TOPNOTCH)
116
Morphology: lamina densa of the GBM is transformed into an irregular, ribbon like, extremely electron dense structure
Dense Deposit Disease or Type II MPGN. SEE SLIDE 14.6. (TOPNOTCH)
117
ESRD is defined as GFR less than how many percent of normal?
5%(TOPNOTCH)
118
Renal failure is defined as GFR less than how many percent of normal?
20%-25%(TOPNOTCH)
119
In renal insufficiency is defined as GFR less than how many percent of normal?
20%-50%(TOPNOTCH)
120
Diminished renal reserve is define as GFR less than how many percent of normal?
50%(TOPNOTCH)
121
An 18 y/o female presented with decreased in urine volume and edema. BP = 150/100. RBC cast was present in the urine. What is the most likely light microscopy pattern of this condition?
Acute glomerulonephritis (TOPNOTCH)
122
An 18 y/o female presented with decreased in urine volume and edema. BP = 150/100. RBC cast was present in the urine. Two weeks prior, patient had sore throat and tonsillar swelling. What is the clinical impression?
PSGN (TOPNOTCH)
123
Patient presented with fever, nausea, and flank pain. Urinalysis showed gross hematuria, increased pus cells, and presence of WBC cast. The most likely diagnosis is:
Acute pyelonephritis (TOPNOTCH)
124
A 10 y/o male presents with generalized edema. BP is 90/60. Urinalysis showed Protein 3+, and presence of fatty cast. The most likely diagnosis is:
Nephrotic syndrome (TOPNOTCH)
125
A 50 y/o patient with long standing hypertension and diabetes presented with complaints of pruritus, lower extremity edema, nausea and vomiting. Urinalysis showed presence of protein and waxy casts. Presence of waxy casts may indicate:
Chronic kidney disease (TOPNOTCH)
126
A 5 y/o child presents with short history of facial edema that has now progressed to swelling of the feet and abdomen. Other symptoms include nausea, vomiting and abdominal pain. High levels of protein was noted in the urine. The parents reported that the child had fever few days before the development of the swelling. Biopsy was done. On light microscopy, no significant structural changes were noted except for the few lipids in the tubules. What can be expected on electron microscopy?
Loss of foot processes (TOPNOTCH)
127
Characterized by rapid decline in GFR, with concurrent dysreglation of fluid and electrolyte balance, and retention of metabolic waste products.
Acute kidney injury(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 898
128
Most frequent clinical presentation of this disease is rapidly progressive glomerulonephritis (with crescent formation). The anti-GBM antibodies cross react with pulmonary alveolar basement membranes to produce pulmonary hemorrhage, associated also with renal failure.
Goodpasture syndrome. SEE SLIDE 14.9. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 912
129
The most common cause/mechanism of acut nephritic syndrome
immune-mediated glomerular injury(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 914
130
Its presence in the urine represents lipoprotein resorbed by tubular epithelial cells and then shed along with injured tubular cells.Present in Nephrotic syndrome
Oval fat bodies(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 914
131
Most frequent systemic causes of nephrotic syndrome
Diabetes, amyloidosis, SLE(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 914
132
Most common cause of nephrotic syndrome in older adults
FSGS 35%, Membranous glomerulopathy 30% (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 524
133
A 6 y/o male presented with massive proteinuria and edema. There is no hypertension or hematuria noted. Patient responded well to corticosteroid. The principal lesion in this condition:
Uniform and diffuse effacement of foot processes(Minimal change disease) (TOPNOTCH)
134
Most common type of glomerulonephritis worldwide
IgA Nephropathy/Berger Disease(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 923
135
Presents with gross hematuria after an infection of the respiratory, GIT or urinary tract, microscopic hematuria, with or without proteinuria. Hematuria last for several days, only to return every few months. These are the clinical features of what renal pathology?
IgA Nephropathy/Berger Disease(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 923
136
This childhood syndrome consists of purpuric skin lesions, abdominal pain, intestinal bleeding, and arthralgia along with renal abnormalities.
Henoch Schonlein Purpura (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 926
137
Most common renal manifestation of multiple myeloma
Chronic kidney disease (TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 938
138
True or False. Patients with malignant hypertension have markedly elevated levels of plasma renin.
True (TOPNOTCH)
139
Most common cause of renal artery stenosis
Narrowing by an atheromatous plaque (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 940
140
Following a prodrome of influenza-like or diarrheal symptoms, this syndrome presents with sudden onset of bleeding manifestation, severe oliguria, hematuria, associated with microangiopathic hemolytic anemia, thrombocytopenia and prominent neurologic changes.
Hemolytic Uremic Syndrome(TOPNOTCH)Robbins Basic Pathology, 9th Ed. p. 942
141
Earliest manifestation in bilateral partial obstruction of the ureter
Polyuria and nocturia(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 951
142
Patient presents with flank pain, hematuria, and flank mass. Abdominal CT revealed a mass on the upper pole of the left kidney. CT guided biopsy showed a tumor that are made up of cell with basophilic cytoplasm and are non-papillary. The most likely histologic type of renal carcinoma described is:
Clear cell carcinoma(TOPNOTCH)
143
Most common site of metastasis of renal cell carcinoma
Lungs(TOPNOTCH) Robbins Basic Pathology, 9th ed. P. 955
144
A 32 year old woman develops tea-colored urine, periorbital edema, and decreasing urine output. A renal biopsy shows glomeruli with collapsed glomerular tufts and crescent-shaped masses of proliferating cells and leukocytes internal to the Bowman's capsule. Which immunofluorescence pattern indicates that she is amenable to plasmapheresis? (A) linear staining of IgG and C3 along the GBM (B) granular "lumpy bumpy" deposits of Ig and/or complement in the GBM and/or mesangium (C) no distinct Ig or complement deposition (D) none of the above
linear staining of IgG and C3 (Anti-GBM antibody CrGN/Type I) (B - Type II - immune complex mediated; C - Type III - pauci immune; neither are helped by plasmapharesis). SEE SLIDE 14.9. (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 557-558.
145
An 18 year old female has sore throat and fever. The next day, she develops tea-colored urine for a week, which spontaneously resolves. Six months later, her hematuria recurs. She is also found to have increased serum IgA. Which of the following renal biopsy findings is consistent with her disease? (A) presence of C1q and C4 deposits in the glomeruli (B) IgA deposits in the mesangium (C) granular deposits of IgG and complement (D) subepthelial "humps" on electron microscopy
IgA deposits in the mesangium (Berger disease) (all other choices are seen in PSGN, which develops 1 to 4 weeks after infection). SEE SLIDE 14.8.
146
A 10 year old male presents with periorbital edema. Urinalysis shows persistent albuminuria. Which renal biopsy finding will indicate that he will respond to short coursse corticosteroid therapy? (A) normal-looking glomerulus by light miscroscopy, with podocyte foot process effacement on electron microscopy (B) some glomeruli with segmental increased mesangial matrix and hyaline deposits (C) diffusely thickened GBM on light microscopy, with subepithelial deposits in a "spike and dome" pattern on electron microscopy (D) a "tram track" appearance of the thickened GBM on PAS stain
normal-looking glomerulus on light microscopy, with podocyte foot process effacement on electron microscopy (minimal change disease) (B - FSGS; C - membranous GN; D - membranoproliferative GN) (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 550-554
147
A 38 year old male presents with gross hematuria. Imaging workup shows three renal masses. He undergoes radical nephrectomy, where gross examination of the kidney specimen showed yellowish masses with foci of hemorrhage. The mass nearest the hilum appears to infiltrate into the renal vein. On histopathology, the masses are composed of sheets of clear, vacuolated cells with round to oval nuclei, and occasional mitoses. The patient also had a history of brain surgery at 14 years old for a cerebellar hemangioblastoma. This association raises the possibility which syndrome? (A) Li Fraumeni (B) Von Hippel-Lindau (C) Tuberous sclerosis (D) Gardner
von Hippel-Lindau (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 573-74
148
Which of the following is the most important prognostic factor in bladder tumors? (A) histologic grade (B) painless hematuria (C) histologic type (D) depth of invasion
depth of invasion (TOPNOTCH)Robbins Basic Pathology, 8th Ed. p. 576
149
One of the most common causes of nephrotic syndrome in adults. Initially presents as increased mesangial matrix, obliterated capillary lumina, with deposition of hyaline masses and lipid droplets. In time, causes global sclerosis.
FSGS (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.526
150
Pathogenesis: Auto-antibodies react to endogenous or planted glomerular antigens, most recognized of which is the phospholipase A2 receptor. Immune complex formation activates membrane attack complex (COMPLEMENT C5 to C9) which damages mesangial cells and podocytes.
Membranous nephropathy (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.526
151
Pathogenesis: Excessive complement activation, with autoantibodies against C3 CONVERTASE, which lead to uncontrolled cleavage of C3 and activation of the pathway.
Dense deposit disease (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.527
152
How do you differentiate the three main causes of crescenteric glomerulonephritis from one another (Anti-GBM-mediated, Immune complex-mediated, and pauci-immune)?
Anti-GBM on IF shows LINEAR IgG and C3 deposits; Immune-complex mediated on IF shows granular pattern; pauci-immune on IF shows NO deposits (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.532-533
153
Pathognomonic gross feature of papillary necrosis.
Gray-white to yellow necrosis of the apical two thirds of the pyramids. Remember also the three predisposing conditions: Diabetes, urinary tract obstruction, and analgesic abuse. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.535
154
Grossly, kidneys are symmetrically atrophic due to ischemia. Histology will reveal hyaline arteriolosclerosis (extensive hyaline thickening) in the small arteries and arterioles and fibroelastic hyperplasia in the larger blood vessels. It's an important renal cause of seconday hypertension.
Arterionephrosclerosis (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.539
