wk 10, lec 1 Flashcards by Claire Jamieson

renal corpuscle (glomerulus + bowmans capsule)

location and function

cortex

filtratio

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general features of glomerular diseases

proteinuria (foaming urine, edema)

hematuria

vascular injury

pyuria (pus)

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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

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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

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Post streptococcal (infectious)
Glomerulonephrhitis

1-3 wk after pharyngitis infxn

babies, elders

skin and throat affected before kidneys

not better with antibiotics

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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

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Post streptococcal (infectious)
Glomeruloneprhitis

diagnostic findings

renal biopsy (rare)

positive culture for streptococcal infection

low C3, normal C4

antibodies (anti-DNAse, antihyaluronidase)

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Post streptococcal (infectious)
Glomeruloneprhitis

treatment

manage BP and edema

dialysis

antibiotics

prognosis good in kids

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Membranoproliferative
glomerulonephritis

what is the pathophysio

thicken basement membrane

lower complement in blood

mesagnioproliferative changes

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types of Membranoproliferative
glomerulonephritis

Type I- immune complex-mediated
Type II and III- majority- non-immunoglobulin-
mediated; alternate complement pathway

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pathogenesis of Membranoproliferative
glomerulonephritis

type 1= most proliferative

type II= low C2, thicken glomerular basement membrane

type III= least proliferative, disrupt basement membrane

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features of Membranoproliferative
glomerulonephritis

proteinuria, hematuria, pyuria

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sx of Membranoproliferative
glomerulonephritis

fatigue and malaise (type I)
acute nephritic picture, decreased renal function

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diagnostic findings in Membranoproliferative
glomerulonephritis

renal biopsy, end stage renal disease, low C3

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treat Membranoproliferative
glomerulonephritis

steroids (primary), immunosuppressive, treat secondary (autoimmune, infection, neoplasm)

poor prognosis

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IgA nephropathy

who most common in

males, 20s-30s

possible genetics

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main sx in IgA nephropathy

hematuria

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features in IgA nephropathy

bending, go into remission, renal function possibly in tact even with hematuria

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sx of IgA nephropathy

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URTI –> macroscopic hematuria and proteinuria

chronic asympathomatic/microscopic hematuria

dx of IgA nephropathy

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elevated IgA, IgA deposits in skin, renal biopsy

treat IgA nephropathy

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ACE inhibitors for proteinuria, or steroids or immunosuppressives
…etc

nephrotic syndrome (4)

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*Minimal Change Disease
*Focal segmental glomerulosclerosis
*Membranous glomerulonephritis
*Diabetic nephropathy

nephritic syndromes (3)

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postscriptococcal glomerulonephritis

IgA nephropathy

Membranoproliferative glomerulonephritis

presentation of nephrotic syndrome

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+++ 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

wk 10, lec 1 Flashcards

(45 cards)