urinary Flashcards
how many nephrons
2 million
what are the 2 developmental abnormailities
: Renal agenesis (only 1 kidney)or solitary horse shoe kidney:- both kidneys are fused together
Polycystic Kidney disease:
adult polysystic
Adult Polycystic
1. 8-10% of all ESRD
2. Mode of Inheritance
Autosomal dominant
3. Pathology: Gross (huge 2-3 Kg): Bilateral Markedly enlarged Numerous cysts Associated With: liver cysts (full of whole- tubules) Berry aneurysm of circle of willis (10-30%) Clinical: 4th decade sense of heaviness bilateral flank masses hematuria Azotemia CRF gene is called polysystic (senses that cell is damage and keeps repairing (proliferating) where there is no damage- dont need to know) Rx: Dialysis and Transplant
glomerulus deseases affect
filtration
immune mediated
antibodies get deposited or antibody complexes get deposited and interfere with filtration and attract inflamatory cells :
acute renal failure, nephritic(i for inflamation) syndrome, nephrotic (o for edema fluid leaks out ) syndrom, isolated hematuria (blood in urine)
metabolic mediated
diabetes (so much sugar in blood), amyloidosis (abnormal protein get deposited )
circulatory mediated
hypertension, atherosclorosis DIC (not enough blood or nutrients so starts to die)
Acute Renal Failure
Sudden onset – renal failure (anuria or oliguria) when urine output is less then 300 ml
#Pre-Renal
Shock or heart failure
#Renal
Glomerular or tubular disease
#Post-Renal
Urinary obstruction (due to stones, prostatic enlargement)
mesured by mesuring createnin tells us its not functioning
Nephrotic Syndrome
Dx by clinical findings Edema more than3g/day Proteinuria Hypoalbuminemia Hyperlipidemia (when losing so much protein so the liver starts making lots of proteins and lipids at the same time) more creatinin means not filtering properly
Nephritic syndrome
Dx by clinical findings Edema (not as much) Hypertension (increase BP)(na and cl are retained so pulls more water in) Hematuria Proteinuria Hypoalbuminemia
Lipoid Nephrosis
Also known “Minimal change disease” “Nil lesion disease” Unknown etiology Most common cause of Nephrotic syndrome in children
filtratrion barrier
1: endothelial cell (
2: glomerular basement membrane
3: podocytes and slit diafragms
what is the ultimate filtration barrier
SD outside the gbm- in nephrotic this is where the damage is
in nephritic what is damaged
damage the GBM AND BLOOD GOES OUT (HEMATURIA)
nephrotic syndrome
Minimal Change disease most common in children( under microscope we dont see any lesions or abnormality becasue too small witha tiny slit )
Focal segmental glomerulosclerosis
Membranous nephropathy
lipoid nephrosis
Histology Light – nil (cant see any change) Immuno – nil EM – fusion of foot processes (cytoscleton cannot maintain erectile stature because of slit) of podocytes Clinical Responds to steroids
Membranous nephropathy (changes in the membrane)
Immune mediated glomerulopathy
Diffuse thickening of glomerular basement membrane
Massive deposition of immune complexes (gbm tries to eat all the imunoglobulin so grows and grows to sufficates
Nephrotic syndrome
of membranous nephropathy
Nephrotic syndrome
No signs of inflammation
Most common cause of nephrotic syndrome in adults
Etiology unknown in 85%
what is the histology of Membranous Nephropathy
Histology Thickened basement membrane No cellular changes Immuno-fluorescence Granular immune complexes
Nephritic Syndrome
Dx by clinical findings Edema Hypertension ( BP) Hematuria Proteinuria Increased serum creatinine
Acute Post-Infectious Glomerulonephritis
Immune mediated inflammatory glomerulopathy
1 – 2 weeks after acute infection (strep throat
Anti-strep antibodies are formed
Ag-Ab complexes are trapped in glomerular basement membrane
Complexes activate complement
Attract inflammatory cells to glomerulus
- blodd cannot go through
what is th histology of Acute Post-Infectious Glomerulonephritis
Histology
Glomeruli are hypercellular
increase Inflammatory cells within capillary lumen- block blood flow
clinical Acute Post-infectious Glomerulonephritis
Clinical
Damaged basement membranes “leak”
Proteinuria & hematuria
Urine is murky brown
Decreased blood flow and retention of sodium—Hypertension
decrease Blood flow in glomeruli —increase Renin= High blood pressure
Loss of albumin :decrease serum albumin = edema
prognosis of Acute Glomerulonephritis
Prognosis
Short lived illness
Most recover completely 1 – 2% lead acute renal failure <10 % end stage renal failure
Crescentic Glomerulonephritis
Exudate in glomerular space (mainly macrophages)
Occurs after focal necrosis of capillaries from Goodpasture’s Syndrome (renal and lung disease)- (ANCA (neutrophase cytoplasmic antibodies) associated vasculitis)
Antibodies to basement membrane collagen
Crescents compress capillary loops
decrease Blood flow decrease glomerular filtration increase Anuria
Recovery rare dialysis
anti gbm anti body vs anca anti body
anti- agaisnt one of the types of collagen in the gbm goes stright for it and destroys it and going to make a whole and can see it blood leaks out the body sees this and cleans up and send all the macrophages to eat all the blood and this compresses to glomerulus- acute renal failure
2 ANCA: not agasint gbm, are agaisnt cytoplasmic proteins in the neutrophils some antibody get attached to endothelial - make whole in capilary loop, macrophages come in and crescent is formed again-acute reanl failure
what is the most common cause of adult nephrotic syndrome
Membranous Nephropathy
