Term
| congenital anomaly, bladder develops outside of pelvis. Twice as frequent in males. Defect in lower abdominal wall allows exposure of bladder to outside world → risk of infection, ulceration, adenocarcinoma (10%), squamous cell carcinoma (7%). The risks persist after surgical repair. |
|
Definition
|
|
Term
| infection and inflammation of the bladder causing short term increased urinary frequency, lower abdominal pain, dysuria. More common in young women and older men. Most often caused by E. coli (or other bugs), chemo, or trauma. Obstruction increases risk. May progress to pyelonephritis. |
|
Definition
|
|
Term
| the leading cause of hematuria and bladder cancer (SCC), parasite that lays eggs in vein muscularis propria. The inflammatory response begins as eosinophilia, necrosis → ulceration → fibrosis, granulomas, dystrophic calcification |
|
Definition
|
|
Term
| irritative voiding, gross hematuria. NOT pre-neoplastic. Caused by cyclophosphamide, radiation therapy, adenovirus, HSV, CMV irritating the bladder. Severe cases may require cystectomy |
|
Definition
|
|
Term
| Chronic edematous inflammation of the bladder (stubby finger-like/polypoid protrusions on histology) usually due to trauma (catheterization, fistula) |
|
Definition
|
|
Term
| Usually women. An inflammatory plaque in the bladder from dysfunctional histiocytes leading to gram negative bacteria invasion (E coli, Proteus). Michaelis-Gutmann bodies on histology (giant histiocytes with calculosperules in the center) |
|
Definition
|
|
Term
A squamous metaplasia not tied to SCC
Common in women, trigone area |
|
Definition
Non-keratinizing (glycogenated) squamous metaplasia
vs. Keratinizing metaplasia which IS tied to SCC |
|
|
Term
| a benign growth (fibrous core, normal urothelium) in the bladder lining especially in young people |
|
Definition
|
|
Term
| What are the risk factors for Papillary Cancer? |
|
Definition
| Tobacco smoke, arylamines, phenacetin, cyclophosphamide |
|
|
Term
| What are the risk factors for SCC in the urinary bladder? |
|
Definition
|
|
Term
Which Bladder pathologies are pre-cancerous / carry increased cancer risk?
Which do not?
Bladder extrophy
Schistosomiasis
Hamorrhagic cystitis
Squamous metaplasia (keratinizing and non)
Glandular metaplasia |
|
Definition
SCC risk
-Bladder extrophy
-Schistosomiasis #1!!
-Keratinizing Squamous metaplasia
adenocarcinoma risk
-Bladder extrophy
-Glandular metaplasia
no risk
- Hemorrhagic cystitis
- Non-keratinizing Squamous metaplasia |
|
|
Term
| What are Michaelis-Gutmann bodies and what do they indicate? |
|
Definition
giant histiocytes with calculosperules in the center on histology
--> malakoplakia |
|
|
Term
What are the gender prevalences of
Bladder extrophy
Acute cystitis
Malakoplakia
Non-keratinizing squamous metaplasia |
|
Definition
Women:
Malakoplakia
Non-keratinizing Squamous metaplasia
Male:
Bladder extrophy
Young women, old men:
Acute cystitis |
|
|
Term
| Benign. Increasingly common as we age, linked to long term hemodialysis. Cortical lesion, well circumscribed, of less than 5mm. Papillary morphology (finger-like projections) that look glandular. |
|
Definition
|
|
Term
| Benign. usually one large unilateral mass, but can be multifocal in tuberous sclerosis. Large tumors over 4cm tend to bleed and need to be removed surgically. On histology there are thick walled blood vessels, smooth muscle, and fat molecules. |
|
Definition
|
|
Term
| Benign. Men over 50, asymptomatic. Brown lesion with a central scar. Histology – uniform pink cells in loose fibrous stroma (islands). These make up 4-7% of adult renal epithelial tumors. |
|
Definition
|
|
Term
Malignant (therefore usually men over 50). Metastasize to the lungs before the lymph nodes!
70% of adult renal epithelial tumors, look very yellow from high lipid content. On histology there are large lipid and glycogen inclusions in the cells. Developed from proximal convoluted tubules. No large foamy cells (macrophages) on histology.
Risk factors : smoking, obesity in women, chronic hypertension, tuberous sclerosis, von Hippel Lindau dz |
|
Definition
| Clear Cell Renal Cell Carcinoma |
|
|
Term
Presents with café au lait spots, angiomatosis, hemangioblastomas, pheochromocytoma, clear cell renal cell carcinoma, pancreatic cysts
AD mutation in VHL gene (tumor suppressor gene) linked to Clear Cell Renal Cell Carcinoma. |
|
Definition
|
|
Term
Malignant
10-20% of adult renal cell carcinomas, mostly in men. Develop from PCT or DCT of nephron. Associated with trisomy 7, 17, and loss of Y. Usually quite hemorrhagic and large. On histology – Calcium deposits (more if more malignant), large foamy cells (macrophages) |
|
Definition
| Papillary Renal Cell Carcinoma |
|
|
Term
Men over 70 with hematuria, especially who have smoked cigarettes or abused analgesics (eg. aspirin). More than half have a co-existing bladder tumor. Linked to phenacetin nephropathy, radiologic dye, cyclophosphamide (anti-cancer therapy).
Renal tumor arises from renal pelvis and erodes to expose blood vessels. |
|
Definition
|
|
Term
| kids under 6 with large abdominal mass (grow very fast), often with Denys-Drash syndrome, Beckwith-Wiedemann syndrome, or WAGR syndrome. Triphasic – blastema (glandular), epithelium, and stroma (spindle cells). This is a very aggressive tumor and most children will die. |
|
Definition
Wilm's Tumor
aka. Nephroblastoma |
|
|
Term
| Wilms tumor (child <6), gonadal dysgenesis (underdeveloped), nephrophathy, presenting with failure to thrive, abnormal skeletal development, insomnia, anuria. Mutation in WT1 gene. |
|
Definition
|
|
Term
| Wilms tumor (child <6), exophthalmos (bug eyes), macroglossia (big tongue), gigantism, hemihypertrophy (one side of body more developed than other) |
|
Definition
| Beckwith-Wiedemann syndrome |
|
|
Term
| Wilms tumor (child <6), aniridia (no iris), genitourinary anomalies, mental retardation. Deletion on chromosome 11. |
|
Definition
|
|
Term
| What 3 syndromes are linked to Wilm's tumor? |
|
Definition
Denys-Drash syndrome
Beckwith-Wiedemann syndrome
WAGR syndrome |
|
|
Term
| What renal cancer is associated with trisomy 7, 17, or loss of Y |
|
Definition
| Papillary Renal Cell Carcinoma |
|
|
Term
What renal cancer is Von Hippel Lindau disease associated with?
This disease presents café au lait spots, angiomatosis, hemangioblastomas, pheochromocytoma, pancreatic cysts |
|
Definition
| Clear Cell Renal Cell Carcinoma |
|
|
Term
| What Renal Cancer metastazies to the lungs before the lymph nodes? |
|
Definition
| Clear Cell Renal Cell Carcinoma |
|
|
Term
| What are the risk factors for Clear Cell Renal Cell Carcinoma? |
|
Definition
smoking
obesity in women
chronic hypertension
tuberous sclerosis
Von Hippel Lindau dz |
|
|
Term
A brown lesion on the kidney with a central scar is?
Man over 50, asymptomatic. |
|
Definition
|
|
Term
| What renal lesion is associated with long term hemodialysis? |
|
Definition
|
|
Term
| What makes up tumor staging T1, T2... T4? |
|
Definition
staging is size and spread
T1 - <7cm, in kidney only
T2 - >7cm, in kidney only
T3 – beyond kidney but still within Gerota’s fascia (in major veins, adrenal gland, or perinephritic tissue)
T4 – beyond Gerota’s fascia |
|
|
Term
What makes up Fuhrman nuclear GRADING?
Grades 1-4 |
|
Definition
Grading = histologic appearance
Fuhrman is mostly for Clear cell renal cell carcinoma.
Grade 1 – nucleus is small, round, uniform, < 10 microns. Similar to lymphocyte size.
Grade 2 – slightly irregular nucleus, can see nucleoli at 40x magnification, > 15 microns
Grade 3 – very irregular nucleus, nucleoli visible, > 20 microns
Grade 4 – very irregular cells, sometime macronucleoli, multinucleated, irregular mitotic figures, spindle cell differentiation |
|
|
Term
effect the kidneys, joints, serous membranes, blood and skin. Diagnosis requires positive ANA (sensitive but not specific) and anti-dsDNA or anti-Sm (specific not sensitive).
Key symptoms = SOAP BRAIN MD.
o Serositis, Oral ulcers, Arthiritis, Photosensitivity/pulmonary fibrosis, Blood cells, Renal/raynauds, ANA, Immunologic (anti-Sm, anti-dsDNA), Neuropsych, Malar rash, Discoid rash |
|
Definition
|
|
Term
SLE with
Very limited clinical activity, normal everywhere except elevated ANA
Mesangial hypercellularity and increased matrix
IgG Dense deposits in the mesangium |
|
Definition
| Mesangio-proliferative lupus nephritis |
|
|
Term
SLE with
Severe Clinical activity. More than half of glomeruli show histology as below. Urinalysis positive for everything, massive proteinuria, low GFR, hypocomplementemia, both ANA and anti-dsDNA elevated.
Endocapillary proliferation (occluded vessels)
Extracapillary proliferation (cellular crescents) * negative prognostic indicator.
Karyorrhexis (fragmented dying nuclei) * negative prognostic indicator
Fibrinoid necrosis (from glomerular rupture and fibrin deposition)
Wire loops (very pink eosinophilic capillary loops)
Tram-tracking from new GBM formation
Pseudothrombi (immune complex clumps occluding blood vessel) |
|
Definition
|
|
Term
SLE with
Thickened capillary loops without proliferation
Granular IF on loops
Subepithelial dense deposits → spike and dome formation |
|
Definition
| Membranous lupus nephritis |
|
|
Term
Presents as 50 year old man with the triad of acute necrotizing granulomas in respiratory tract with hemoptysis, necrotizing or granulomatous vasculitis in small-medium vessels, acute nectrotizing and/or crescentic GN. On histology you see crescent formation in glomerulus from fibrin deposits.
c-ANCA (against proteinase 3), granulomas, medium sized vessels attacked after triggering event (infection) that causes cytokine activation |
|
Definition
|
|
Term
Presents as palpable purpura with hemoptysis, arthralgia, abdominal pain, hematuria, proteinuria, hemorrhage, muscle pain/weakness. On histology you see crescent formation in glomerulus from fibrin deposits
p-ANCA (against myeloperoxidase), small vessels attacked after triggering event (infection) that causes cytokine activation |
|
Definition
|
|
Term
Presents as child/young adult with palpable cutaneous purpura. On histology you see numerous dense deposits of IgA in the mesangium, and mesangial proliferation.
No ANCA. IgA1 deposited within arterioles which activates alternative complement pathway causing vasculitis in arterioles. |
|
Definition
|
|
Term
What kind of ANCA is each of the following related to:
Wegener's granulomatosis
Microscopic polyangiitis
Henoch-Schonlein Purpura |
|
Definition
Wegener's granulomatosis
-- c-ANCA (against proteinase 3)
Microscopic polyangiitis
-- p-ANCA (against myeloperoxidase)
Henoch-Schonlein Purpura
-- no ANCA, it's IgA1 |
|
|
Term
Where are the deposits in each of the following:
Mesangio-proliferative lupus nephritis
Diffuse lupus nephritis
Membranous lupus nephritis |
|
Definition
Mesangio-proliferative lupus nephritis
--mesangium
Diffuse lupus nephritis
--everywhere
Membranous lupus nephritis
--subepithelial |
|
|
Term
Presents as a 55 year old patient with bone pain/fracture (esp in the spine), hypercalcemia, prone to infection, and anemia/thrombocytopenia
Neoplasms of antibody secreting B cells. These neoplastic B cells require IL-6 and other cytokines to proliferate, therefore high IL-6 is a poor prognostic indicator. The antibody they secrete is homogenous, so although they are hypergammaglobunemic the Ig is nonfunctional. The plasma cells live in the bone marrow and cause osteoclastic disease leading to fracture and hypercalcemia.
Buckshot lesions can sometimes be seen on Xray.
Dx by M component in serum (the circulating Ig), Bence jones protein in urine (excess light/heavy chains of IgG), and bone marrow biopsy (atypical B cells) |
|
Definition
|
|
Term
triad of abdominal mass, hematuria, flank pain
Sometimes with
hypercalcemia
elevated liver enzymes (Stauffer's syndrome)
Anemia
Erythrocytosis, thrombocytosis
risk factors:
cigarettes, htn, obesity, meds, renal cystic disease |
|
Definition
|
|
Term
What are each of the following types of kidney stones linked to?
Calcium oxalate
uric acid
struvite
cysteine |
|
Definition
Calcium oxalate - IBD, most common
uric acid - acidic pH, IBD
struvite - chronic UTI (alkaline pH)
cysteine - Cystinuria (genetic dz) |
|
|
Term
| Name some risk factors for developing Nephrolithiasis (kidney stones) |
|
Definition
Urinary stasis,
Dehydration,
Alkaline urine (infection, RTA)
Hypercalciuria/oxalauria/uricosuria,
Hypocitraturia,
Calcium abnormalities (sarcoidosis, hyperparathyroidism),
IBD |
|
|
Term
| What nervous systems control urine storage vs expelling urine? |
|
Definition
Urine storage – sympathetic tone (thoracic/lumbar)
Expelling urine – parasympathetic nerves (sacral), detrusor muscle |
|
|
Term
What type of incontinence does each of the following tend to cause?
laughing
bladder infection
autonomic neuropathy in Diabetes
fistula from traumatic childbirth |
|
Definition
Stress Incontinence (laughing)
Urge incontinence (*bladder infection)
Overflow incontinence (*autonomic neuropathy in Diabetes)
Total incontinence (* fistula from traumatic childbirth or congenital ectopic ureter) |
|
|
Term
| The bladder congenital anomaly where the sphincter between ureter and bladder fails, so reflux back into kidneys. Causes complications of stasis, infection, scarring of the kidneys, chronic pyelonephritis |
|
Definition
|
|
Term
| The bladder congenital anomaly where the median umbilical ligament is patent, urine can drain out of belly button. Causes complications of cysts in urachus or cancer. |
|
Definition
|
|
Term
| The bladder congenital anomaly where spinal cord abnormality like spina bifida that affects sacral nerves, causing autonomic bladder dysfunction. |
|
Definition
|
|
Term
| The bladder congenital anomaly where there is abnormal meatus opening on dorsal surface of urethra. |
|
Definition
Epispadias
(Hyperspadius is ventral) |
|
|
Term
| What kind of hematuria does bladder cancer usually present with? |
|
Definition
|
|
Term
| acquired abnormal curvature of the penis |
|
Definition
|
|
Term
dilation of veins of spermatic cord, usually on left side, though 10% are bilateral. If it is unilateral on right side its not caused by valve dysfunction → kidney tumor, retroperitoneal mass
the most common cause of male infertility |
|
Definition
|
|
Term
| Prognosis for a solid mass in the scrotum - outside vs inside the testis? which is worse? |
|
Definition
| If a solid mass is outside the testis its generally benign, inside the testis is likely malignant |
|
|
Term
African American, over 50, diets high in saturated fats and lacking tomatoes (ie. no lycopene)
Elevated ALP, PSA, and PAP (alkaline phosphatase, prostate specific antigen, prostatic acid phosphatase).
Osteoblastic lesions seen on Xray. |
|
Definition
Prostatic adenocarcinoma.
develops in peripheral zone of prostate. Fueled by androgens. Spreads directly to seminal vsicles/bladder, lymphatically to obturator lymph nodes, or hematogenously to vertebrae/pelvis/proximal femur to form osteoblastic lesions (sclerosis-like). Staged with Gleason grading system.
Treatment
– prostatectomy
- anti-androgen therapy (orchiectomy, estrogen but then hypercoagulable, analogs of GnRH like leuprolide, or flutamide to inhibit the androgen receptor. |
|
|
Term
| List some of the obstructive and irritative symtoms of prostatism |
|
Definition
Obstructive symptoms
- decreased flow/caliber of urinary stream
- straining to void
- hesitancy
- dribbling
- interruption of urinary stream
- urinary retention
Irritative
- urgency
- frequency
- nocturia
- urge incontinence |
|
|
Term
A congenital anomaly generally incompatible with life.
Oligohydramnios (low amniotic fluid volume because can’t pee it out), amnion nodosum (nodular fetal surface of amnion)
Beak nose, skin folds under eyes, flat low set ears, limb deformities, pulmonary hypoplasia |
|
Definition
Potter’s Syndrome
(Bilateral Renal Agenesis) |
|
|
Term
| A congenital anomaly where Sprouty1 fails to inhibit excessive GDNF-RET induction of kidney formation |
|
Definition
|
|
Term
Congenital anomaly where
L and R kidney are fused (usually at the inferior end) and therefore can’t rotate and can’t migrate cranially because they get stuck on the inferior mesenteric artery.
Slightly increased risk of Wilms tumor (renal pelvis tumor) |
|
Definition
|
|
Term
Of the following Glomerular Diseases, which are nephritic and which are nephrotic:
Membranous glomerulonephritis
Membranoproliferative glomerulonephritis
Minimal change disease (Nil lesions)
Acute poststreptococcal glomerulonephritis
Focal segmental glomerulosclerosis
Berger’s disease (IgA nephropathy)
Anti-GBM disease (Goodpasture, Wegener, Microscopic polyangitis)
Diabetic glomerulonephropathy
M glomerulonephritis
Congenital Nephrotic Syndrome (Finnish)
Alport's syndrome |
|
Definition
Nephrotic - massive proteinuria, hyperlipidemia, lipiduria, edema, low serum albumin
Membranous
Membranoproliferative
Minimal change disease (Nil lesions)
Focal segmental glomerulosclerosis
Diabetic
M glomerulonephritis
Congenital Nephrotic Syndrome (Finnish)
Nephritic - hematuria, <3.5g/day proteinuria
Membranoproliferative
Acute poststreptococcal
Anti-GBM disease
Berger’s disease (IgA nephropathy)
Alports |
|
|
Term
Of the following glomerular diseases, which are antibody mediated (type II hypersensitivity reaction)
and which are immune complex mediated (type III hypersensitivity reaction):
Hemolytic anemia
Lupus
Arthus reaction
Goodpasture's
Serum sickness |
|
Definition
Type II hypersensitivity reaction = antibody mediated
• Hemolytic anemia
• Goodpasture’s syndrome
Type III hypersensitivity reaction = immune complex mediated
• Some glomerulonephritises
• Lupus
• Serum sickness
• Arthus reaction |
|
|
Term
Nephrotic Syndrome where
The most common cause of adult nephrotic syndrome. This presents at 30-50, with proteinuria and elevated creatinine, Prognosis is variable, only 10-30% have remission of proteinuria, 40% progress to renal insufficiency.
Histology: GBM and diffuse capillary thickening and increased mesangial matrix (on LM), spike and dome subepithelial deposits (on EM), and granular fluorescence (IF).
Cause: drugs, infections, lupus (SLE), solid tumors, NSAIDs, hepatitis, SLE. 85% are idiopathic.
Tx: ACE inhibitors, steroids, cyclophosphamide if steroids fail. |
|
Definition
| Membranous glomerulonephritis |
|
|
Term
Nephrotic Syndrome where
The most common cause of nephrotic syndrome in kids who are generally otherwise healthy with preserved renal function (ie normal creatinine). It is proteinuria due to damage to podocytes, insidiouos onset, but very good prognosis. Only 5% progress to chronic renal failure, 95% recover completely. A lipoid nephrosis that causes loss of albumin but not globulins because GMB loses anions.
Histology: Foot process effacement/fusion (laying down on BM) (EM). IF doesn’t show any immune complexes, so it is likely not autoimmune.
Cause: recent infection or immune stimulus.
Tx: corticosteroids. |
|
Definition
| Minimal change disease (Nil lesions) |
|
|
Term
Nephrotic Syndrome where
Most common glomerular disease in HIV patient and IV drug users. It is important to differentiate from Minimal Change and Membranous type because it has a much worse prognosis (>50% progress to renal failure within 10 years) and does not respond as well to steroids.
Histology: Segmental sclerosis and hyalinosis (ie. little patch in glomerulus full of hyaline matrix becomes sclerotic and scars over time), increased mesangial matrix(LM). No immunoglobulins/complement on IF. |
|
Definition
Focal segmental glomerulosclerosis
This is a focal process so you need to make sure you look at enough glomeruli to find an abnormal one so you can rule out minimal change disease (because it presents the same except for the abnormal glomeruli). |
|
|
Term
Nephrotic Syndrome where
Glomeruli (BM thickening, mesangial expansion, KW lesions, hyaline sclerosis)
Kidney blood vessels (hyaline deposits in both e and a)
Interstitium (scarring)
This is a progressive disease that takes easily 10 years to show.
Histology: Increased mesangial matrix, mesangial hypercellularity, and GBM thickening initially, later → Kimmelstiel-Wilson lesions (Nodular glomerulosclerosis, in 15-30% of pts, pathoneumonic), glossy smooth hyaline inclusions, and hyaline arteriolosclerosis (pathoneumonic when both afferent and efferent arterioles are effected, htn usually only effects 1)(LM)
Cause by nonenzymatic glycosylation of GBM (due to high circulating glucose levels) causing increased permeability and thickening. |
|
Definition
| Diabetic glomerulonephropathy |
|
|
Term
Nephrotic Syndrome where
Onset in first 3 months of life with typical nephrotic syndrome phenotype, with death by 5 from a complication.
AR mutation in nephrin (the key protein of the nephrin zipper, also found in bones, brain, etc).
Complications:
Infection, sepsis (Ig loss)
Thrombosis, coronary atherosclerosis, stroke (coagulant loss)
Malnutrition (loss of protein)
Premature birth, large placenta, skeletal deformities, poor motor development (extrarenal nephrin). |
|
Definition
| Congenital Nephrotic Syndrome (Finish Type) |
|
|
Term
Nephritic Syndrome where
granular IF of C3
Poor prognosis, with half developing chronic renal failure within 10 years. More common in children.
Histology: Diffuse proliferative GN, mesangial proliferation, thickened capillary loops, sometimes endocapillary proliferation, tram-tracking from duplication of BM, granular IF of C3 |
|
Definition
Membranoproliferative glomerulonephritis
type I |
|
|
Term
Nephritic Syndrome where
Abnormal distribution of fat deposits, usually asymmetrical (lipodystrophy), low serum C3 because 70% of patients have an antibody C3 nephritic factor, low serum factor B and properdin.
Histology: linearized bands, Dense deposits |
|
Definition
Membranoproliferative glomerulonephritis
type II |
|
|
Term
Nephritic Syndrome where
A child presents 1-2 weeks after recovering from a soar throat as abrupt onset fever, nausea, oliguria, hematuria (smoky or coke-colored urine). You see periorbital and peripheral edema, mild htn, mild proteinuria, and red cell casts in the urine, and it resolves spontaneously.
Histology: “lumpy-bumpy” , endocapillary proliferation that occludes capillary loops with mononuclear inflammatory cells (LM), subepithelial humps (vs. spikes are in chronic conditions) (EM), starry sky for IgG and C3 (IF)
This is generally a self-limited disease following the acute serum sickness model, less that 1% progress to severe oliguria and rapidly progressive GN. |
|
Definition
Acute poststreptococcal glomerulonephritis
began as a streptococcal infection of skin or pharynx, especially group A beta-hemolytic strep
This is the same bug that causes rheumatic fever and necrotizing fasciitis.
After strep infection body clears the infection, it forms immune complexes. These deposit in the glomerulus, and there is cross-reaction of antibodies with the glomerulus. |
|
|
Term
Nephritic Syndrome where
This is a rapidly progressive GN. The body creates antibodies to NC1 domain of collagen type 4 in the GBM → ruptured GBM → deposition of fibrin in urinary space of Bowman’s capsule → parietal cell proliferation in Bowman’s capsule → cellular crescents compress the glomerulus.
Histology: Crescent-moon shape of fibrin and plasma proteins glomerulus. No dense deposits (LM), linear IF of IgG |
|
Definition
Anti-GBM disease
includes
--Goodpastures
lung involvement (hematuria/hemoptysis/ acute respiratory distress) from cross reaction to pulmonary BM --> pulmonary hemorrhage
-- Wegeners
cANCA, granulomas
-- Microscopic polyangitis
pANCA |
|
|
Term
Nephritic Syndrome where
asymptomatic hematuria from IgA deposits in the mesangium caused by overproduced underglycosylated IgA. There is no effective treatment, so patients progress to end stage renal disease over decades.
The IgA deposits drive mesangial proliferation and matrix deposition, as seen on IF. More than 3 mesangial cells in the mesangial matrix is abnormal. They are activated because the immune complexes deposit in the mesangium activating the mesangial cells to proliferate.
Underglycosylated IgA aggregates into polymeric IgA1 and deposits in the mesangium.
Flares with URI or acute gastroenteritis. |
|
Definition
| Berger's disease (IgA nephropathy) |
|
|
Term
Nephritic Syndrome where
a mutation in type 4 collagen causing splitting of the GMB. This comes with nerve disorders, ocular disorders, and deafness that is X-linked dominant. |
|
Definition
|
|
Term
Match the following glomerulonephropathies to their IF findings.
linear
granular
mesangial
no deposits on IF
Membranous
Minimal Change disease
Acute poststreptococcal
Berger's
Membranoproliferative
Focal Segmental
Anti-GBM dz |
|
Definition
linear
-- Anti-GBM disease (Goodpasture, Wegener, Microscopic polyangiitis)
granular
-- Acute poststreptococcal
-- Membranoproliferative
-- Membranous
no IF
-- Minimal Change Dz
-- Focal segmental
mesangial
-- Berger's |
|
|
Term
| Which nephritic Syndrome flares with URI or acute gastroenteritis? |
|
Definition
| Berger's disease (IgA nephropathy) |
|
|
Term
What diseases have immune complex deposits in:
Mesangium
Subendothelium
Intramembranous
Supepithelium |
|
Definition
Mesangium (high avidity, neutral)
-- Berger's (IgA)
Subendothelium
-- Membranoproliferative glomerulonephritis
Intramembranous (in GBM)
--acute serum sickness (they deposit everywhere)
Subepithelium (low avidity, positive charge)
-- acute poststreptococcal
-- membranous |
|
|
Term
| What glomerulopathy has Kimmelstiel-Wilson lesions and hyaline arteriolosclerosis of both afferent and efferent arterioles? |
|
Definition
| Diabetic glomerulonephropathey |
|
|
Term
What is the difference between
membranous glomerulonephritis and membranoproliferative glomerulonephritis? |
|
Definition
Membranous = subepithelial
--> only nephrotic
Membranoproliferative = subendothelial
--> nephrotic or nephritic |
|
|
Term
Hyponatremic patient who is
Not hypovolemic
Normal renal funciton
normal adrenal function
normal thyroid function
Inappropriately concentrated urine
(high levels of ADH) |
|
Definition
| SIADH (syndrome of inappropriate anti-diuretic hormone) |
|
|
