Renal Disease 1 Flashcards by Carson Spornhauer

what parts of the kidney can be affected by renal disease

glomeruli, tubules, interstitium and vasculature

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how small does a particle have to be to pass through the glomeruli?

less than 70 Kd

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Azotemia

elevated BUN (blood urea nitrogen) and creatinine (breakdown of skeletal mm.)  due to decreased glomerular filtration rate (GFR)
-problem with glomerular filtration unit

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Uremia

azotemia plus clinical symptoms ( gastroenteritis, peripheral neuropathy, dermatitis, acidosis, pericarditis and hyperkalemia)

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Acute nephritic syndromw

HEMATURIA (blood in urine)

acute onset, maybe protenuria or hypertension
INFLAMMATION that destroys the endothelium that leads to bleeding and destroys the glomeruli so reduced GFR

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Nephrotic syndrome

severe PROTEINURIA (high urine albumin > 3.5 gms per day) which will decrease the oncotic pressure, leading to edema (anasarca even in other body parts)
-hypoalbumenima, hyperlipidemia and lipiduria (urine)
FROTHY PEE

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acute renal failure

Oliguria/anuria with sudden onset of azotemia – small amounts of urine

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autosomal dominant (adult) polycystic kidney disease clinical presentation

1/500-1000 people
multiple expanding cysts in both kidneys, gradual onset of renal failure in adults, urinary tract hemorrhage (hematuria), pain, hypertension and urinary tract infection and flank pain around the 4th decade

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etiology of adult polycystic kidney disease

defective gene is PDK1 (in 90% of families) located on chromosome 16, gene encodes polycycstin-1

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AD polycystic extrarenal pathology

1/3 of patients have cysts in liver, “berry” aneurysms may develop in the circle of willis (intracranial) - 30%

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pathology of AD polycystic kid dis

very large kidneys with numerous cysts that arise in every part of the tubular system
~ will not develop the disease until around 20 years old, but need tx

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AR polycystic kidney disease clinical presentation

1/20,000 births (less common than AD)

develops from infancy to several years of age is rare
defective protein is PKHD1 - fibrocystin (not same at AD)

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AR Polcyc kid dis extrarenal pathology

almost all have liver cysts and progressive liver fibrosis

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AR polycys dis pathology

numerous small uniform size cysts from collecting tubules in the cortex and medulla
they are like sponges thats glomeruli are replaced with cysts

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mechanisms of glomerular disease

immune complex depost in the basement memnrace or mesangium (from circulating complexes, antibodies against the glomerulus or planted antigens)
epi and endothelial cell injury

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pathological evaluation of kidney biopsies

light microscopy is the standard but immunofluorecnse is used as well as electron microscopy
silver and PAS stain for basement membrane, trichrome for collagen)

what does the appearance of each glomerular disease mechanism look like on electron microscopy

circulating immune complexes are “dot” like around the glomeruli –> trapped and deposited in a non-linear fashion
circulating antibodies directed against the glomerulus are smooth, linear Ab deposits –> ab directed against the basement membrane of glomerulus
antibodies against non-glomerular antigens are a mix

what are the 4 major types of nephrotic syndrome

minimal change, focal and segmental glomerulosclerosis. membrane nephropathy and nodular glomerulosclerosis

Minimal change disease affects:

-children mainly(2/3 of casess)

minimal change pathology

"minimal change.."
LM - normal
IF - no deposits
EM - foot process effacement (taken out)- kidney can't hold protein
** good response to corticosteroid tx

focal segmental glomerulosclerosis affects:

mainly adults

may be primary or secondary to other glomerular diseases, some are familial(genetic)
affects some (focal) of the glomeruli and part (segmental) of the tuft

pathology focal segmental glomerulosclerosis

LM - focal (some glomeruli) and segmental (part of involved glomerulus) sclerosis with obliteration of capillary loops
If and EM - no deposits in the idiopathic primary form
-poor response to corticosteroids (can control, but not stop the progression - 50% will have renal failure within 10 years) –> eventually all the glomeruli would be affected

Diabetes Mellitus renal failure frequency

renal failure, 2nd to MI as a cause of death

membranous nephopathy

most common in adults (30-50)

-primary disease or secondary to infection, malignancy, SLE (lupus) or drugs

pathology memb nephropathy

LM: nearly normal (variable) IF: deposits --> uniform electron microscopy and thickening of basement membrane EM: deposits in subepi side of GBM -poor to moderate response to corticosteroids (40% go to end stage renal failure in 2-20 years)

diabetis glomerular pathology

LM - nodular glomeruloscerosis --> scarred down IF - no complex deposits EM - Thick GBM other changes: hyaline ateriosclerosis, atherosclerosis and nephrosclerosis (scaring down the whole kidney, not just the glomeruli)

Kimmelstiel - wilson lesion

Diabetes balls of pink material in the tuft --> daignostic | mesangial nodules that is replacing normal tissue

2 major nephritic syndromes

acute postinfectious (poststreptococcal) and IgA nephropathy

Acure postinfetious glomerulonephritis

-most common in children 1-4 wks after strep, but other infections can cause

APG path

LM - prolif endothelial and mesangail cells, infiltration of neutrophils and monocytes - cellular cresents common IF, EM - immune complexes in GBM and sometimes mesangium b/c cross-reactivity from infection -progression to chronic renal disease is more common in adults -spotty granular deposition from circulating deposits

IgA nephropathy usually occurs in

children and young adults

IgA nephropathy

dramatic hemoturia 1-2 days after upper resp tract infec | -will resolve and then come back

Henoch-Schonlen

when pt. has IgA nephropathy (kidney disease) and clinical symptoms like skin rash, GI pain and arthritis

pathology IgA nephropathy

LM- variable mesangel cell prolif If and Em - immune (iGa) complexes within the mesangium - not as destructive becasue IgA doesnt complement well but destruciton from macrophages)

crescentic or rapidly progressive glomerulonephritis

assoc with antibod directed against glomerular basement membrane antigen, deposition of immune complexes (50 % of cases) or lack of immune complex deposition (we call this pauci-immnue b/c we dont really know whats happening) - clinical cluster of syndromes, not a specific form - death in weeks to months is untreated - little urine produced - crescentic due to prolif epi cells with infiltration of histiocytes

end stage chronic renal disease

due to untreated glomerular disease - loss of tubules and glomeruli leads to fibrosis original renal disease cannot be found normally because by time diagnosed - so much scaring - bell curve onset (middle age is sweet spot for developing) -protenuria, hypertnsion and azotemia can help detect renal disease during routine exam -corticosteroids slow down disease, but dialysis and transplant are needed for survival