Exam 3: Renal Nephrotic vs Nephritic Diseases Flashcards
Mesangium:
Mesangium are _______ cells that secrete the ____
Can influence GFR by _____
Mesangium:
modified smooth muscle cells that interweave between capillaries
They secrete the ECM, cytokines
Can influence GFR by contracting and relaxing to alter blood flow
Glomerular Transit:
Renal blood flow comprises what?
What is renal plasma flow
Normal GFR (in mL/min and L/day)? Normal filtered fraction?
Renal blood flow is plasma + hematocrit
Because under normal circumstances, RBCs do not filter through, renal plasma flow is just the plasma
GFR is 120 mL/min or 180 L/day
20% is the normal filtered fraction
What are the factors that affect GFR? Think of the equation
GFR equation:
Surface area (can be affected by mesangium)
Hydrostatic pressure in bowman space can be affected by renal stones
oncotic pressure of bowman’s space is normally zero, but can be a factor in renal failure, causing GFR to decrease significantly
Spectrum of Glomerular Diseases:
Explain the mechanisms for nephrotic vs nephritic diseases
Nephrotic:
- injury to podocytes
- changed architecture
- scarring
- deposition of matrix or other elements
Nephritic:
- inflammation
- reactive cell proliferation
- breaks in GBM
- blood cell cresent formation
Presentation of Glomerular Diseases:
Nephritic Vs Nephrotic:
Which is more hypertensive? Which patient has more edema? What does the urine look like and why
Nephritic:
- way more hypertensive
- urine looks angry - coke like with RBCs and RBC casts
- Why? ongoing inflammation in glomeruli and leakage of RBCs from glomeruli
Nephrotic:
- edematous (puffy patient)
- foamy urine due to lots of protein - beer like NO RBCs
- Why? No inflammation in glomeruli, protein no longer passing through cell membranes
Describe the differences in nephrotic and nephritic diseases in the various categories:
Onsent, how much edema, blood pressure, jugular venous pressure, proteinuria, hematuria, RBC casts, serum albumin
Look at the chart:
Nephrotic: slower onset, more edema, normal to slightly raised BP, normal JVP, way more protein, NO RBC casts, low serum albumin (losing it in urine)
Nephritic: sudden onset, less edema but still some, raised BP and JVP, little proteinuria, hematuria present, has RBC casts, normal serum albumin
Picture the visual differences between nephritic and nephrotic (that visual picture)
Studying Glomerular Diseases
What can an immuno stain and an electron microscopy help in diagnosing glomerular disease?
Immuno stains: stain for a particular antibody
Electron Microscopy: can tell where the immune complexes are aggregating
BOTH require a biopsy sample
Presentation of Acute Nephritis:
Reduction in ____
Oliguria, ___, edema (a little)
______ with dysmorphic RBcs and RBC casts, variable _____
WBC and WBC casts
Presentation of Acute Nephritis:
Reduction in GFR
Oliguria, HTN, edema (a little)
Hematuria with dysmorphic casts, RBC casts, variable proteinuria
WBC and WBC casts
Explain the LOCATION of the following syndromes aka where is the problem in the nephron:
Acute Post streptococcal glomerulonephritis
Goodpasture’s Syndrome
Wegner’s Granulomatosis
Meningeal Proliferative Glomurulonephritis
Acute Post Strep: endothelial cell proliferation
Goodpasture Syndrome: GBM issues
Wegener’s granulomatosis: blood vessels
Meningeal Proliferative…: mesangium issues
Post Streptococal GLomerulonephritis (PSGN)
Clinical Presentation:
nephritis 1-3 weeks after ____ or ______
oliguria, edema, and ______
diuresis starts within a weeK
Mechanism?
PSGN:
Clinical Presentation:
nephritis 1-3 weeks after throat or skin infection (streptococci)
Oliguria (small amounts of urine being produced), edema, and HTN
diuresis starts within a week
Mechanism: immune complex mediated (endothelial cell proliferation creating subepithelial humps)
PSGN:
Pathological Findings:
- excessive cellular proliferation in _____ and _____ within the glomeruli
- _________ “humps”
Treatment and Prognosis:
- supportive, favorable prognosis
- treat with _____
- repeated episodes are uncommon
PSGN:
Pathological Findings
- excessive endothelial cellular proliferation
- subepithelial “humps”
Treatment and Prognosis:
- supportive, favorable prognosis
- treat with immunosuppressive (treat underlying infection)
- repeated episodes are uncommon
Goodpasture’s Syndrome:
Rare
Pathogenesis:
Antibody directed against _______ within the glomerular capillaries and alveolar wall
Goodpasture’s Syndrome:
rare (more males get it than females)
pathogenesis:
antibody directed against non-collagen domain of alpha 3 chain of type 4 collagen in glomerular capillary and alveolar wall
after exposure to smoke, hydrocarbon, (viral respiratory infection)
Goodpasture’s Syndrome:
Onset is caused by what?
How do diagnose it?
How many treated people recover?
Goodpasture’s Syndrome:
Onset: exposure to smoke, hydrocarbons, viral respiratory infections unmask the antigen in alveoli inducing antibody formation
> 70% of treated recover renal function, relapses are uncommon
Diagnose by staining for the antibody against type 4 collagen
Wegener’s Granulomatosus:
Predominant in _______ aged persons
Presentation: chronic upper and lower respiratory tract disease with necrotizing granulmatous vasculitis (blood vessels are dying)
Pathology: diffuse or segmental necrotixing pacuri immune to GN with cresents
Treatment?
Unreated 2 year mortality rate?
Wegener’s Granulomatosus:
Predominant in middle aged persons
Presentation: chronic upper and lower respiratory tract disease with dying blood vessels
Pathology: diffuse or segmental necrotixing, pauci immune GN with cresents
Treatment: respond to steroids and PO Cytoxan is dramatic
Untreated 2 year mortality rate is 80-90%
Mesangial Proliferative Glomerulonephritis (IgA)
- Most common cause of idiopathic nephritis in young males
- Presentation: asymptomatic microscopic or intermittant gross ____ with or without _____
Pathogenesis?
______ disease
Treatment?
Mesangial Proliferative Glomerulonephritis:
Most common cause of idiopathic nephritis in young males
Presentation: asymptomatic microscopic or intermittant gross hematuria with or without proteinuria
Pathogenesis: mucosal IgA reacts with unknown antigen
Progressive Disease
Treatment: immunosupressants
Minimal Change Disease (nephrotic):
Pathogenesis, unknown, primary disorder of ____
Main cause of nephrotic syndrome in ______
Renal Function and BP are _______, HTN may be present in ____
Can be seen in patients taking which two meds? and those with hodgkin’s, leukemia, and HIV
Minimal Change Disease: (nephrotic)
Pathogenesis: primary disorder of podocytes
Main cause of nephrotic syndrome in children
Renal function and BP usually normal, HTN may be present in adults
Can be seen with patients on NSAIDs and lithium, and those with Hodgkin’s, leukemia, HIV
Membranous Nephropathy (nephrotic)
Commonest cause of idiopathic nephrotic syndrome in _______
Nephrotic proteinuria in > 90% with normal ___ at presentation
High incidence of ____ events
Membranous Nephropathy (nephrotic):
Commonest cause of idipathic nephrotic syndrome in middle aged white adults
Nephrotic proteinuria in > 90% with normal GFR at presentation
High incidence of thrombotic events - blood clots in veins because of loss of proteins that prevent clotting
Focal Segmental Glomerulosclerosis (FSGS):
Familial Mutations in genes for podocyte protines “permeability inducing factor”
________ (is the gene)
Most common form of idiopathic NS in ____
Massive proteinuria, HTN, low GFR in 30-40%
Common secondary causes?
FSGS:
Familial mutation in genes for podocyte proteins “permeability inducing factor”
APOL-1
Most common form of idiopathic NS in African Americans
Massive proteinuria, HTN, low GFR
Common secondary causes: IV drug use, sickle cell, morbid obesity
