Week 1 (Path Stuff) Flashcards
Diabetes Mellitus is a ___ disease (microvasculature) manifestations
Systemic hypertension is a vascular disease (arteriolar) manifestations (aka ____ disease)
Glomerular
Tubulointerstitial
Increased BUN and creatinine levels related to DECREASED GFR is _____ and can be classified as
1) ____ azotemia which occurs after hypoperfusion of the kidneys that impairs renal function in the absence of renal parenchymal damage
2) ____ azotemia which is when urine flow is obstructed distal to the calyces and renal pelvis
____ is azotemia PLUS a constellation of clincal findings and biochemical abnormalities resulting from renal damage
Azotemia
Prerenal azotemia
Postrenal azotemia
Uremia
AKI (Acute kidney injury aka Acute renal failure) is often associated with acute ____ necrosis aka acute tubular injury (ATI) (BUT NOT ALL OF THEM) and is characterized by a rapid ___ in GFR and CAN be reversible, or progress to ____
** So just to clear up some terms, there is AKI (Acute kidney injury, sometimes called ARF), ATI (Acute tubular injury, sometimes called ATN)
AKI is when there is a loss of renal function that develops within 7 days and therefore associated with decreased GFR, increased BUN and Creatinine (azootemia)
ATI is when the epithelial cells in the renal tubules necrosis and this can present WITH AKI, or it can turn INTO AKI and the necrosis is either due to ischemia or toxins
CKD (Aka chronic renal failure) is mild to clinically silent at first and overtime it progresses with azotemia, and then to the clinical signs and symptoms which then are called UREMIA and the GFR is extremely ___ (Less than 60ml/min for at least 3 months) and/or persistent albuminuria is seen
^** Also this is generally irreversible
ESRD (End stage renal disease) is when the GFR is less than ____ of normal and is the end stage of uremia
Tubular, decline, CKD (Chronic kidney disease)
^**CKD is also referred to as CRF (Chronic renal failure)
Decreased
5%
____ syndrome is glomerular disease characterized by SEVERE proteinuria aka MORE than ____gms per day
^** The protein lost is mainly ____, so you get HYPOalbuminemia, severe generalized edema, hyperlipidemia, and lipiduria
^** Manifestations of lipids is due to the fact that the liver is stressed and goes into compensatory mode that produces lipoproteins
*** SO NEPHROTIC SYNDROME IS LARGELY ASSOCIATED WITH ____
Nephrotic syndrome, 3.5
Albumin
PROTEINURIA
____ syndrome is glomerular disease dominated by acute onset of visible HEMATURIA, mild/moderate proteinuria, and hypertension…. Proteinuria and edema is common, but not as severe as nephrotic syndrome
*** SO NEPHRITIC SYNDROME IS LARGELY ASSOCIATED WITH ____
Nephritic
HEMATURIA
____ has signs of nephritic syndrome (hematuria) AND rapid decline in GFR (aka acute renal failure) and implies very severe glomerular injury
Isolated urinary abnormalities present with subnephrotic range proteinuria (aka protein in the urine, but less than 3.5 gm/day) and possibly some degree of hematuria
RPGN (Rapidly progressive glomerulonephritis)
Prototypical localizations of immune complexes in the glomerulus include
1) ____ seen in acute post-infectious glomerulonephritis
2) ____ deposits seen in Membranous nephropathy or Heymann Glomerulonephritis
3) ___ deposits seen in Lupus nephritis or Membranoproliferative Glomerulonephritis
4) ___ deposits seen in IgA nephropathy
5) Basement membranes
1) Subepithelial humps
2) Epimembranous
3) Subendothelial
4) Mesangial
The glomerulus can be injured via Humoral-mediated immune injury (aka Abs), Cell mediated immune injury, and activation of alternative complement pathway
The humoral (antibody) immunity can have:
1) ___ immune complex deposition with Fixed or Planted Ags
2) ____ immune complex deposition with Endogenous (native to body) or Exogenous Ags
^** Bacterial endocarditis is an example of an exogenous circulating Ag
In situe deposition on FOOT processes is seen in ____
In situ complex nephritis (Heymann) AND Circulating immune complex has a ___ pattern and Anti-GBM has a ___ pattern
1) In-situ
2) Circulating
Heymann
Granular, linear
Acute Diffuse Proliferative Glomerulonephritis (which can be post-streptococcal or Postinfectious)
Is an immune complex injury triggered by exogenous bacterial, viral, or fungal Ags
More importantly, we think of this Post-infectious glomerulonephritis is due to ____
This is characterized by marked _____ (involves everything in the glomerulus) AND leukocyte infiltration (aka inflammatory cell infiltration) with exudation within the glomerular tuft
Electron microscopy will show ____ immune complexes and these deposits fluoresce (IgG, IgM, and C3 in the mesangium and along the GBM which correspond to these humps)
This is generally seen in ___ (adults or children?) following pharyngitis or skin infections and associated with the strep pyogenic exotoxin ___ elaborated by Group A Beta-hemolytic strep
Also these patients present like ___ syndrome with hematuria, fever, malaise, nausea, and oliguria and also dysmorphic red cells or RBC ___ are seen
**Children tend to get ____, and adults tend to ____
^** You ____ (should or should not?) do a renal biopsy on a child since they tend to clear in 6-8 weeks… So just maintain sodium and water balance
Group A Beta-hemolytic strep
Hypercellularity, exudation (aka interstitial edema)
Subepithelial hump
Children, B (Strepotococcal pyogenic exotoxin B aka SpeB)
Nephritic, Casts
Better, NOT get better
Should NOT
Rapidly Progressing Glomerulonephritis (RPGN) aka Crescentic Glomerulonephritis
Characterized by ____/compacted glomerular tufts, ____ shaped mass of proliferating visceral and parietal epithelial cells, rapid obliteration of the urinary space, and infiltration of macrophages and leukocytes
RPGN also presents with nephritic syndrome and rapid decrease in GFR (if untreated)
^** Realize that this is NOT a single disease, but rather a feature of various diseases with the common denominator in ALL types being SEVERE glomerular injury
******* So once again, lets say a patient has goodpastures syndrome. Ok, so they have that disease. Now lets say that during the course of Goodpastures syndrome, the GFR declines 50% within 3 months and nephritic syndrome is seen along with crescent formation and linear anti-GBM Abs…. Now the patient’s disease would be called _____
Collapsed, Crescent
RPGN Type 1
RPGN can be classified as Type 1, Type 2, or Type 3
1) Type 1 is also called ____ and is associated with pulmonary or renal hemorrhage such as in ____ syndrome
^** IgG deposits in the GBM can be seen and ______ can be used to treat the patients aka Type 1 DOES respond to plasmapheresis, but type 2 and 3 DO NOT!!!
** So if you see Anti-IgG localized to the GBM with diffuse ____ staining deposits, think goodpasture syndrome
2) Type 2 is also called ____ and biopsy shows IgG and C3 deposits in the GBM
^** ___ pattern of staining, which is characteristic of immune complex deposition
Name the 4 important Type 2 associated diseases
3) Type 3 is also called ____ and associated with ____ antibodies, skin rash, upper respiratory granulomas, etc.
^** There is NO anti-GBM antibodies or immune complexes seen (pauci = few)
Name if these diseases can become Type 2 or Type 3
A) Lupus nephritis B) IgA nephropathy C) Granulomatosis with poluangiitis (Wegners) D) Henoch-Schonlein purpura E) Microscopic polyangiitis F) Post infectious glomerulonephritis
*****Dont be confused, realize the Acute Diffuse Post-infectious glomerulonephritis does not present with cresents… It simply means that OVER TIME, it can progress to CRESENTIC Glomerular disease
Same idea with the other shit….
So as another example: Only SOME IgA nephropathys progress overtime to where they become a cresentic glomerulonephritis and at this point, are classified as a TYPE ___ RPGN
Also 50% of PRIMARY renal diseases associated with RPGN have type ___ patterns
1) Anti-GBM Antibody, Goodpasture syndrome
Plasmapheresis
Linear
2) Immune complex
Granular
Post-infectious, IgA nephropathy, Lupus, and Henoch-Schonlein Pupura
3) Pauci-immune, ANCA
A) 2 B) 2 C) 3 D) 2 E) 3 F) 2
2
3
Nephrotic syndrome
Remember, this is where Proteinuria is seen (Proteinuria > 3.5gm in 24 hour period)
^** Occurs due to the GMB becoming diffusely leaky or porous to proteins, especially albumin… And remember we also usually don’t see hematuria
The serum albumin, which is the main protein being excreted, is therefore ____ aka hypOalbuminemia (usually less than 3gm)
Also severe generalized ____ is commonly seen along with hyperlipidemia and lipiduria
In children younger than 17 that exhibit Nephrotic Syndrome, 95% of these cases are ascribable to ___ glomerular disease caused by ____
In adults, Nephrotic Syndrome is more associated with ____ diseases in contrast to children (specifically, ___ or ___ diseases), but realize still 60% of the adult cases are still Primary glomerular disease
^** so just to recap, BOTH adults and kids more often have nephrotic syndrome due to a primary disease. However, compared to kids, adults have a greater likelihood of getting it from a systemic disease
^** In adults, the primary forms are caused by ____ or ____
Decreased
Edema
PRIMARY, Minimal-change disease (aka nill disease)
Systemic (aka secondary), Diabetes Mellitus or Systemic Lupus Erhthematosus
FSGS (Focal segmental glomerulosclerosis) or Membranous glomerulopathy
So once again, there are usually 3 PURE protein disorders aka Primary renal diseases for nephrotic syndromes which are
1) Minimal change disease (nil disease)
2) Membranous glomerulopathy
^** Realize this is the SAME thing as membranous nephropathy
3) FSGS (Focal segmental glomerulosclerosis)
^** Of the 3 however, ___ is the most likely to have some degree of hematuria
** Realize the # 2 and 3 can be either a pattern OR a diagnosis, but Minimal change disease is ALWAYS a diagnosis
FSGS
Membranous Glomerulopathy (aka nephropathy)
75% of the cases are primary are characterized by Abs to the renal autoantigen _____ receptor with involvement of complement (MAC) and IgG4
Often secondary causes of Membranous Glomerulopathy (describing the pattern, not diagnosis) include ___ like malaria, syphilis, hep B and C, or HIV along with malignant diseases like carcinomas/lymphomas and others, or drugs
85% of Membranous Glomerulopathy cases have ____ syndrome (proteinuria) and one way to contrast Membranous Glomerulopathy with Minimal change disease, is that MG has _____ proteinuria (which means large serum proteins are equally part of the exhibited proteinuria as well as smaller proteins like albumin)
**Another way to contrast MG with MCD is that in MCD, children respond ____ to steroids, and in MG they respond ____*
^** So if a patient has MCD, they ALWAYS respond well to steroids… And if they don’t do well, they probably have some other glomerular pattern like GM or FSGS
** Also patients with Mg do not have kidney transplants because this problem often re-accurs
Upon microscopy, the diffuse ___ of the capillary walls with NO increased cellularity and ___ are often seen projecting from the basement membrane towards the urinary space
** So if you see the word SPIKE and DOME, the answer it ____****
*****There patients are at highest risk for ____
**Also realize you can tell the difference between MN and MPGN due to the fact that MN involves ONLY the basement membrane and MPGN involves BOTH the basement membrane AND mesangial cells***
PLA2
Infections
Nephrotic syndrome, non-selective
Well, poorly
Thickening, spikes
Membranous Glomerulopathy
Renal vein thrombosis
In membranous glomerulopathy 3 things occur:
1) The foot processes of the epithelial cells will be ___
2) The basement membrane will be ___ (5-20x)
3) ____ deposits of dense IgG aggregates will be seen
^** Realize you see foot processes fusion in ANY disorder with nephrotic syndrome, but the only disorder where you see ONLY foot process fusion is ____*****
Immunofluorescences will show granular ____ IgG deposits along the GBM (But realize Lumpy-Bumpy is NOT chracterisitc of this, it is seen in other problems)
1) Effaced (aka removed/fused/simplified),
2) Thickened
3) Sub-epithelial
Minimal change disease (MCD)
Lumpy-Bumpy
Minimal Change Disease (MCD) also presents as nephrotic syndrome with edema (similar to MG), but remember ALL YOU SEE IS ____ and most common incidence is between 2-6 years of age and commonly follows a VIRAL ____ infection or viral immunizations…. Be careful because IgA nephropathy also commonly follows a respiratory infection
^** AKA the principle lesion is in the VISCERAL epithelial cells which shows a uniform and diffuse effacement of foot processes
Remember, unlike MG which is ____ proteinuria, this is highly ____ proteinuria (aka mainly composed of albumin)
Last but not least, remember, they respond well to ____, unlike MG
***** So if you see effacement with NORMAL glomeruli, think MMD
Foot process fusion (FPF), Respiratory
Non-selective, selective
Steroids
FSGS (Focal segmental glomerulosclerosis)
^** Can sometimes be confused with Rapidly Progressing Glomerulonephritis (RPGN) aka Crescentic Glomerulonephritis but it does NOT just involve bowmans capsule, instead it is a sclerosing pattern that extends deep into the glomerular tufts
FSGS presents with Neph___ syndrome and more common in ___ (kids or adults?), but in a child who has nephrotic syndrome and does NOT respond to steroids, they most likely have a childhood manifestation of FSGS
Also remember, this is the one that has a higher incidence of hematuria, decreased GFR, and HT
50% of patients progress to ESRD
^** So realize that FSGS can be a primary diagnosis (idiopathic cause) OR it can be descriptive of other diseases but is important for these other diseases because it implies a ___ prognosis due to the fact that most progress to CKD and ESRD
There is also a collapsing variant of FSGS, aka a secondary FSGS, which is called ____ where proliferation and ____ of the glomerular visceral epithelial cells is seen AND ___ within endothelial cells (which are NOT see in idiopathic/primary FSGS and therefore can be diagnostic… These are seen in SLE though)
^** Common in Black people
In contrast to MCD, proteinuria is ____ (selective or non-selective?), there is ___ response to steroids, and higher incidence of hematuria and decreased GFR and HT
^** Realize these are similar to MG, but the difference is that MGs have basement membrane thickening whereas FSGS has sclerosis and hyalinosis… Also ___ and C3 is often seen on microscopy in FSGS
(All 3 MG, FSGS, and MCD have loss of foot processes)
Nephrotic, adults
Poor
HIV nephropathy, hypertrophy, tubuloreticular inclusions
Non-selective, poor
IgM
MPGN (Membranoproliferative Glomerulonephropathy)
Mostly associated with a PATTERN of immune-mediated injury, rather than a specific diagnosis
Primary MPGN is broken down further into 2 different categories
1) Type 1 MPGN
^** Type 1 has _____ deposits seen on electron microscopy and IgG and C3 (complement); along with and C1q and C4 is seen on immunofluorescence, which is not seen in Type 2
^** Realize this is involved with the classic complement pathway AND alternative complement pathway
2) Type 2 MPGN (aka DDD)
^** Type 2 has ____ deposits seen on electron microscopy and is a _____ glomerulopathy (aka Autoantibody alternative complement) aka the C3 complement is NOT inside the dense deposits, instead it is outside
^** So in Type 2, ____ IgG autoantibodies bind to C3 convertase which leads to continuous and excess activation of the ____ complement pathway and this causes C3 to be deposited as granular or linear foci in the BM on either side, but NOT within and also C3 is often seen in the Mesangium in characteristic ___
BOTH of these present with ___ syndrome, but of these 2, Type ___ MPGN is most likely to present also with PROTEINURIA aka Type 1 presents as MIXED
MPGN 1 and 2 characteristics include alterations in the GBM that include thickening and ____ of the BM aka “tram-trak” appearance, ____ cell proliferation (this is why sometimes MPGN can be called Mesangiocapillary glomerulonephritis), and leukocyte infiltration (like neutrophils)
In Type 1 and Type 2 MPGN, one would see GBM thickening and ___ due to an increased mesangial matrix that dissects (aka interposes) and splits the GBM
Most commonly these occur in ____ (children or adults?) and 50% of patients with MPGN Type ___ develop chronic renal failure over a 10 year span but type 2 is a worse prognosis
1) Subendothelial
2) Dense Deposits, C3
C3NeF (Nephritic factor), alternative, mesangial rings
Nephritic, Type 1
Splitting, Mesangial cell
Splitting
Children, 1
Secondary MPGN Type 1 occurs ONLY in ____ (children or adults?) and is associated with chronic ____ from an infection, autoimmune disease, or neoplasia
MPGN Type 2 can NOT be a secondary disease, it is ONLY primary and presents mainly in children (Type 1 primary also presents mainly in children)
Which type of MPGN has a worse prognosis and generally these patients have severe renal disease?
Adults, chronic antigenemia (Ags in the blood)
Type 2
IgA nephropathy
Presents with characteristic deposition of ____ in the mesangium upon immunofluorescence and acute, ____, mesangial cellular proliferation along with an increased mesangial matrix is seen
There are mesangial and paramesangial dense deposits
IgA nephropathy is often a cause of ____ gross or microscopic ____… So if you see recurrent hematuria, consider this in your diff dx
Recurrent episodes of hematuria with NO progression of renal disease occurs in most patients, but the disease progresses to CHRONIC renal failure in 15-40% of patients over a 20 year period
**This disease is more common in whites and asians, male, family histories, and older children/young adults… Often IgA nephropathy follows ____ (respiratory or less common, GU), and the infection occurs at the same time as the hematuria*********
^** Note that MCD also commonly follows a respiratory infection (don’t confuse, should be easy)
IgA, focal
Recurrent, Hematuria
Infections
There are two diseases associated with IgA nephropathy and include
1) ____ disease which is a Renal IgA nephropathy that is NOT systemic
2) ____ disease which is an IgA nephropathy that IS systemic, often exhibiting skin (purpuric) manifestations and involvement of the abdominal viscera other than the kidney
^** So HSP is an IgA mediated systemic vasculitis syndrome but if you are considering IgA nephropathy as the diagnosis, rather than a pattern, than it is a PRIMARY Renal-glomerular disease aka ____ syndrome
1) Berger disease
2) HSP (Henoch-Schonlein purpura)
Berger
Primary glomerular diseases progressing to CGN (Chronic Glomerulonephritis) occurs in 90% of patients with _____, 50-80% of patients with ____, and then various percentages in other diseases
CGN is pretty much end stage glomerular disease and usually arises from a known disease (like we just explained with the primary renal glomerulonephritis), but sometimes it can arise from a patient with NO history of any recognized forms of glomerulonephritis (so either these were asymptomatic forms, unknown/unrecognized/ or uremia)
It presents with a ___ cortex, glomeruli obliteration leading to acellular eosinophilic masses, and due to the HT that occurs with it there is arterial and arteriolar ____ and MOST importantly, there is diffuse ____ scaring
^** The symmetrical scaring is important, because it contrasts that from Chronic Pyelonephritis which presents with IRREGULAR scarring
Crescentic GN, FSGS
Thinned, sclerosis, symmetrical
Hereditary nephritis with glomerular involvement consists of two major diseases ____ or ____ and 80% of patients with a family history of hematuria or recurrent hematuria during childhood have one of these disorders
___ has irregular THICKENING of the basement membrane, lamination of the lamina dense, and foci of rarefaction aka “moth eaten” or “frayed”
___ has irregular THINNING of the basement membrane due to mutations in the Alpha3 or Alpha4 chains of ____
Most patients with TBMD are ___ inheritance and Alport syndrome patients are _____ for an ____ inheritance pattern
^** Alport is usually ___-linked and due to defective ____ from one of it’s ___ chains being mutated so if you stain for antibodies to these alpha chains, it will come up NEGATIVE
So once again, if you see “basket weave” or “moth-eaten” thickened basement membranes, think ____
**** AUDITORY AND EYE PROBLEMS CAN DEVELOP IN ___ SYNDROME
Alport syndrome or TBMD (Thin basement membrane disease aka Benign familial hematuria)
Alport syndrome
TBMD, Type 4 collagen
Heterozygous, homozygotes, autosomal recessive
X-linked, Type 4 collagen, alpha
Alport syndrome
Alports
******______ associated with glomerulonephritis is NOT a septic embolic phenomenon, instead it is an immunological phenomenon *******
Bacterial Endocarditis
Diabetic Nephropathy
First, realize diabetic patients usually have an increased ___ levels in their urine
Two major causes for diabetic glomerular lesions to develop
1) Metabolic defects linked to ____ and advanced ____ of end products, which causes the GBM to thicken and the mesangial matrix to increase (sclerosis)
2) Hemodynamic effects associated with glomerular ____ (aka they are under increased pressure)
In diabetic patients, there is DIFFUSE ___ning of the basement membranes in both the tubules and the glomerulus and DIFFUSE mesangial ____ aka increased mesangial matrix
***** So you might be thinking, how do you differentiate diabetic nephropathy vs MPGN since they both involve basement membrane thickening and mesangial cell proliferation… Well thats easy, first off MPGN also has basement membrane ____ and MOST IMPORTANTLY OF ALL, if the patient is a DIABETIC, they probably have DIABETIC nephropathy
Albumin (aka albumineria)
1) Hyperglycemia (to much glucose in blood), glycosylation
2) Hypertrophy
Thickening, sclerosis
Splitting
Like we said, in a patient with Diabetic Nephropathy, there can be glomerulosceleoris, which is either ___ OR ____
In diffuse diabetic glomerulosclerosis, there is an increase in the mesangial matrix (aka mesangial sclerosis) and diffuse capillary basement membrane thickening ** This was discussed on previous not card**
In nodular diabetic glomerulosclerosis, there is also thickening of the GMB and characteristic ACELLULAR ____ nodules
Diabetic patients will also have advanced renal _____ (thickened, tortuous vascual portions) similar to the presentation seen in HT in the kidney since remember, most diabetic patients are hypertensive
Diffuse or Nodular
PAS+
Hyaline Arteriolosclerosis
Diabetes often progresses to CKD so in end stage diabetic nephrosclerosis, there is a ___ appearance to the cortical surfaces of the kidneys which signifies that the patient was hypERtensive (not necessarily that they were diabetic)
Also realize that 50% of patients have cysts, that have nothing to do with the case
Also Diabetics can have ___ necrosis (but this is also seen in UTIs/obstructions and Analgesic nephropathy)
Granular
SLE (Systemic Lupus Erythematosus)
Presents with a ___ rash on the face
Characterized by ____ upon light microscopy, _____ dense deposits in the glomerular capillary basement membrane and also in the mesangium
There is FOCAL and DIFFUSE proliferative lupus nephritis
Diffuse has increased cellularity, immunofluorescence will show anti-IgG Abs
^** Remember, if RPGN develops it’s a Type ___ RPGN
Butterfly
Wire-loops, Subendothelial
Type 2
_____ is the most common cause of acute renal failure (AKI) and is characterized by focal tubular epithelial cell ____ which can become detached and sloughed off into the tubular lumen leading to ___s that obstruct flow
^** So if you see RBC casts in the urine, think of this for a differential. Remember, casts are also seen in acute proliferative glomerulonephritis and leukocyte (neutrophil) casts will be seen in acute pyelonephritis
It can be classified as either:
1) ____ due to decreased or interrupted blood flow from hypotension/shock (decreased Effective Circulating Blood Volume) or involvement of intrarenal blood vessels like ____ or microangiopathies like HUS, TTP, or DIC
2) ____ due to toxic injury to the tubules from drugs or other toxins
One way to tell Ischemic vs Toxic apart is ____ has the PST and PCT continuous necrosis and in ____ there is only patchy PST and PCT necrosis (aka SKIP lesions… Just think about the fact that ischemia would cause profusion problems causing skipping wheras toxins fuck the entire thing up)
In ATI, the ____ epithelial cells are susceptible to injury leading to swelling, vacuolization, and destruction
ATI (Acute Tubular Injury old term being Acute Tubular Necrosis), necrosis, Casts
1) Ischemic, malignant hypertension
2) Nephrotoxic
Toxi, Ischemic
PCT (Proximal tubule)
ATI has various phases
1) Initiation
2) Maintenance with oliguria (aka decreased urine output 40 - 400 ml with 800-2000ml being normal) and ____ as the clinical problem
3) Recover phase which has ___ output urine volume (3L), ____ as the clinical problem and susceptibility to ____
2) Hyperkalemia
3) High, Hypokalemia, infection
Azotemia (increased BUN, which can progress to uremia) and the inability to concentrate urine (polyuria) can be seen in Primary ____ (this is simply a form of nephritis aka inflammation of the kidneys, that affects the interstitium of the kidneys that surround the tubules)
It is mainly associated with ____ and these can be either acute or chronic, with chronic most closely associated with ____
One way you can tell Acute Vs Chronic tubulointerstitial nephritis apart is that Acute has a RAPID clinical onset, interstitial ___, and leukocyte infiltration (mainly ____ and ____ Aka granulocytes)
Chronic has infiltration (but mainly ____ leukocytes aka agranulocytes aka macrophages, B cells, T cells, NK cells) ____ and tubular ____
Tubulointerstitial nephritis
INFECTIONS, VUR (Vesicoureteral reflux)
Edema, eosinophils and neutrophils
Mononuclear, Fibrosis, atrophy
Nephritic/nephrotic syndromes, tubular
___ is inflammation affecting the tubules, interstitium, and renal pelvis and can be Acute or Chronic, with Acute being caused by a ____ infection that has spread up the urinary tract aka ASCENDING INFECTION (or the infection could have come from the blood stream, but usually UTIs are more often cause it)
UTIs are mostly caused by ___
Bladder inflammation (aka ___) is commonly caused by bacteria
So once again, acute pyelonephritis is an acute bacterial infection of the kidney parenchyma
Chronic pyelonephrtitis is recurrent or long term infection of the kidney, which damaged the pelvis AND ____ system and parenchyma resulting in anatomical distortion and broad based scars on the renal cortex (commonly associated with obstruction or VUR)
^** THIS IS IMPORTANT, ONLY CHRONIC PYELONEPHRITIS and ANALGESIC NEPHROPATHY affects the calyx
Once again, 95% of pyelonephrtitis are ___ infections from the bladder and NOT hematogenous infections
Pyelonephrtitis, bacterial
Enteric bacteria (specifically, Gram - bacilli bacteria like E. coli)
Cystitis
Calcyeal
Ascending
Acute Pyelonephrtitis has ____ interstitial ____ inflammation (such as diffuse abscesses or wedge like areas aka exudative purulent localized inflammation that can cause interstitial abscesses), intratubular aggregates of ____ (since this is an suppurative necrosis that produces pus), and neutrophilic tubulitis and tubular necrosis
3 complications of ACUTE pyelonephritis can occur, which include ___ necrosis (ischemic coagulative necrosis that occurs in the pyramids), Pyogenic abscess formation associated with the kidney itself called ___ (due to complete obstruction HIGH in the urinary tract that causes renal pelvis and ureters to fill with pus), and ___ abscesses which are associated with the capsule and into the perinephric tissue
Commonly can occur during pregnancy and associated with ___
Also seen in patients with indwelling catheters
Acute pyelonephritis is almost ALWAYS associated with an ascending cystitis infection (aka bacterial infection that moves into the bladder) combined with a predisposing ___ defect (aka defective vesicoureteral junction)
*** If you see leukocyte ____ (like a neutrophil cast), then it MUST mean the kidney is involved since those are only formed in the tubules
Patchy interstitial suppurative inflammation, neutrophils
Papillary necrosis, pyonephrosis, perinephric abscess
VUR (Vesicoureteral reflux)
anatomical
Casts
Most children with UTIs have reflux due to a defective ____ (which is partial or complete lack of an oblique entry/angle of the intravesical portion of the ureter)
^** This becomes a problem when urinary stasis (urine sitting around) leads to infections that can involve the ureter and kidney
Adults might have bladder outlet obstruction due to prostatic hypertrophy that can cause the reflux
Vesicoureteral Junction (aka a valve malfunction)
In Acute pyelonephrtitis, there is acute inflammation in the tubules
The cortical surface of the kidney will show multiple foci of ____ areas of acute inflammation and abscess formation
Pyogenic (Pus aka yellow-gray)
Papillary necrosis can be seen in
1) DM
2) Analgesic nephropathy
3) Obstruction (like UTIs)
A) Which one of the 3 is more common in males?
B) Which one of the three is NOT often associated with infections
C) Which one of the three does NOT have calcifications
____ has pale gray necrosis limited to the papilla (aka papillary necrosis)
____ has red-brown necrotic papilla sloughed into the calyx
A) Obstruction
B) Analgesic Nephropathy (this is associated with drugs)
C) DM
DM and obstructive (UTIs)
Analgesic nephropathy
Chronic Pyelonephrtitis (more common than acute)
Associated with renal scarring and tubulointerstitial inflammation
This, along with analgesic nephropathy are the ONLY 2 diseases that damage the ___
^** Remember, AN has red-brown necrotic papilla sloughed into the calyx
VUR in chronic pyelonephritis results in ___ scarring
*** So if you see a pyelonephritic scar (aka inflammation, fibrosis, and deformation of the ____ and pelvis), then think CHRONIC Pyelonephritis
You can tell chronic PYELONEPHRITIS vs chronic GLOMERULONEPHRITIS due to the fact that pyelo has ____ scarring and glomerulo has diffuse and ___ scarring
Calyces (calyx)
Polar
Calyx
Irregular, symmetrical
Xanthogranulomatous pyelonephritis often presents as big shaggy yellowish orange masses and accumulation of foamy (lipid-laden) macrophages and this infection is associated with ___ species
Granulomatous interstitial inflammation can be seen in ___ forms of pyelonephritis like that from Candida
Viral forms can be from polyomavirus
Proteus
Fungal