wk 10, lec 1 Flashcards
renal corpuscle (glomerulus + bowmans capsule)
location and function
cortex
filtratio
general features of glomerular diseases
proteinuria (foaming urine, edema)
hematuria
vascular injury
pyuria (pus)
nephritic vs nephrotic syndromes
–>Nephritic syndromes (Acute)
* Post infectious glomerulonephritis
* Membranoproliferative glomerulonephritis
* IgA nephropathy
–> Nephrotic syndrome
* Minimal change disease
* Focal segmental glomerular sclerosis (FSGS)
* Membranous glomerulonephritis
* Diabetic nephropathy
nephritic syndrome
causes
change in GFR
presentation
Main sx
infalmmation in glomerulus –> decrease GFR –> salt and water retention, edema, hypertesnion
hypertesnion, hematuria, RBC casts, pyuria, proteinuria (mild)
hematuria
Post streptococcal (infectious)
Glomerulonephrhitis
1-3 wk after pharyngitis infxn
babies, elders
skin and throat affected before kidneys
not better with antibiotics
Post streptococcal (infectious)
Glomerulonephrhitis
nephritic or nephrotic
clinical features and sx
nephritic
hematuria, pyuria, RBC cast, edema, hypertesnion, oliguria, renal failure
sx: anorexia, headache, lethargy, flank pain, adults get proteinuria
Post streptococcal (infectious)
Glomeruloneprhitis
diagnostic findings
renal biopsy (rare)
positive culture for streptococcal infection
low C3, normal C4
antibodies (anti-DNAse, antihyaluronidase)
Post streptococcal (infectious)
Glomeruloneprhitis
treatment
manage BP and edema
dialysis
antibiotics
prognosis good in kids
Membranoproliferative
glomerulonephritis
what is the pathophysio
thicken basement membrane
lower complement in blood
mesagnioproliferative changes
types of Membranoproliferative
glomerulonephritis
- Type I- immune complex-mediated
- Type II and III- majority- non-immunoglobulin-
mediated; alternate complement pathway
pathogenesis of Membranoproliferative
glomerulonephritis
type 1= most proliferative
type II= low C2, thicken glomerular basement membrane
type III= least proliferative, disrupt basement membrane
features of Membranoproliferative
glomerulonephritis
proteinuria, hematuria, pyuria
sx of Membranoproliferative
glomerulonephritis
fatigue and malaise (type I)
acute nephritic picture, decreased renal function
diagnostic findings in Membranoproliferative
glomerulonephritis
renal biopsy, end stage renal disease, low C3
treat Membranoproliferative
glomerulonephritis
steroids (primary), immunosuppressive, treat secondary (autoimmune, infection, neoplasm)
poor prognosis
IgA nephropathy
who most common in
males, 20s-30s
possible genetics
main sx in IgA nephropathy
hematuria
features in IgA nephropathy
bending, go into remission, renal function possibly in tact even with hematuria
sx of IgA nephropathy
URTI –> macroscopic hematuria and proteinuria
or
chronic asympathomatic/microscopic hematuria
dx of IgA nephropathy
elevated IgA, IgA deposits in skin, renal biopsy
treat IgA nephropathy
ACE inhibitors for proteinuria, or steroids or immunosuppressives
…etc
nephrotic syndrome (4)
*Minimal Change Disease
*Focal segmental glomerulosclerosis
*Membranous glomerulonephritis
*Diabetic nephropathy
nephritic syndromes (3)
postscriptococcal glomerulonephritis
IgA nephropathy
- Membranoproliferative glomerulonephritis
presentation of nephrotic syndrome
+++ proteinuria
+ hematuria
hypoalbuminemia
hyperholesterolemia, edema, hypertesntion
fall in GFR –> renal failure
minimal change disease (nephrotic)
who most common in
80% kids, spontaneous remission, atopic and allergic sx
adults- acute renal failure
dx of minimal change disease
renal biopsy, microscopy;; nothing seen?
sx of minimal change disease
- Abrupt onset of edema
- Nephrotic syndrome
- Acellular urinary sediment
- Hypoalbuminemia (severe)
possible: hypertension, allergic, hematuria
treat minimal change disease
steroids
Focal Segmental Glomerular
Sclerosis (FSGS)
who most in
adults, africans
sx of Focal Segmental Glomerular
Sclerosis (FSGS)
- Proteinuria
- Some hematuria
- Hypertension
- Renal insufficiency
dx of Focal Segmental Glomerular
Sclerosis (FSGS)
renal biopsy
deep lesion in cortex
Focal Segmental Glomerular
Sclerosis (FSGS) treatment
RAAS inhibtiors, steroids…
Membranous Glomerulonephritis
who in
males, elders
Membranous Glomerulonephritis pathogeniss
thicken basement membrane
some have normal renal function and some fail
PE, DVT, thrombosis
Membranous Glomerulonephritis features
proteinuria
microscopic hematuria
sx of membranous glomeruloneprhtiis
- Hypertension
- Proteinuria
- Dyslipidemia
- Edema
dx of membranous glomerulonephritis
renal biopsy, immunofloresence deposits of IgG and c3
treat Membranous Glomerulonephritis
steroids, RAAS inhibitors, immunosuppresants
most common cause of renal failure
diabetic nephropathy
Diabetic Nephropathy
Thickening of the GBM secondary to the long-
standing effects of hyperglycemia, advanced
glycosylation end products, and reactive
oxygen species
risk factors for Diabetic Nephropathy
- hyperglycemia,
- hypertension,
- dyslipidemia,
- smoking,
- a family history of diabetic nephropathy,
- genetics
diabetic nephropathy pathogenesis
increase glomerular capillary pressure
increase GFR
glomerular hypertension
hyperglycemia: activates RAAS, up regulates SGLT1 and SGLT2, decrease Na+ in macula densa, hyper filtration increased more
dx of diabetic nephropathy
renal biopsy
IgG deposits (immunofluoresncen)
tx of diabetic nephropathy
blood sugar and BP management
RAAS inhibitors
SGLT2 inhibitors
nephrotic vs nephritic
nephrotic:
severe proteinuria >3.5, minimal hemturatia
severe edema
normal BP
nephritic:
mild proteinuria
severe hematuira
mild edema
hypertension
decrease GFR
