Vascular and Interstitial Diseases Flashcards
What are the most common causes of ESRF?
DIABETES
HTN
GLOMERULONEPHRITIS
How does Rapidly Progressive Glomerulonephritis present?
Results in ACUTE RENAL FAILURE in days
Urinary Output BELOW 400 cc/day
HEMATURIA (nephritic!)
Dysmorphic RBCs and RBC casts (nephritic!)
Proteinuria
Oliguria vs. Anuria vs. Azotemia
Urinary output < 400 cc/day (OLIGURIA)
Urinary output < 100 cc/day (ANURIA)
Azotemia is increased BUN/Creatinine due to decreased GFR
How does Chronic Renal Failure Present?
Onset is slooower
Azotemia (increased BUN/creat due to decreased GFR)
Signs and symptoms of uremia along with metabolic and biochemical abnormalities
How do Nephrolithiasis and Urolithiasis present?
Nephrolithiasis –> Stones in kidney
Urolithiasis –> Stones elsewhere in urinary system
Renal colic – FLANK PAIN
Hematuria
Recurrent stone formation
Arteriolar Nephrosclerosis
ALWAYS THINK HYPERTENSION
2 Forms –> Benign Arteriolar Nephrosclerosis and Malignant Arteriolar Nephrosclerosis
Benign Arteriolar Nephrosclerosis
Typically seen in OLDER PATIENTS with MODERATE HTN (SBP > 140)
Second most common cause of ESRD!!!!
Associated with THICKENING OF ARTERIOLES –> concentric hyaline thickening
Presents asymptomatically until A LOT of nephron damage has occurred resulting in RENAL FAILURE
Slow and gradual loss due to chronic HTN results in SMALL AND ATROPHIC KIDNEYS
Can be treated with anti-HTN meds! Treat the underlying cause
Malignant Ateriolar Nephrosclerosis
High SBP AND DBP!!!!! Leads to DAMAGE OF VESSEL WALLS
Histologic findings –> fibrinoid necrosis within the walls of the arterioles and smooth muscle PROLIFERATION –> ONION SKIN APPEARANCE
SURFACE CAPILLARY HEMORRHAGES –> “flea bitten appearance”
Damaged BV can lead to fibrin leaks, which can initiate microangiopathic hemolysis and micro infarcts!
HIGH MORTALITY RATE –> associated with papilledema, CNS symptoms, cardiac decompensation
Vasculitis
Etiology is undefined, but though to involve IMMUNE COMPLEX DEPOSITION
Attack on vessel wall by circulating Abs
Autoimmune component
Polyarteritis Nodosa –> Occurs in MEDIUM SIZED VESSELS –> found in 30% of patients who have HepB antigen; infarcts, hemorrhage
Wegener’s Granulomatous –> Associated with vessels of the UPPER, LOWER AIRWAYS and KIDNEYS –> Positive for ANCA
Churg Strauss –> Small vessels -> glomeruli, arterioles, interlobar arteries; can lead to NEPHRITIS
Large Vessel (Giant Cell) and Takayasu Arteritis –> Both can have some renal involvement due to obstruction of blood flow in the larger arteries, which INHIBITS THE DELIVERY OF BLOOD TO THE KIDNEYS; this can result in decreased GFR and renal insufficiency
Renovascular HTN
Decreased flow through the renal arteries –> main cause
Decreased flow –> activate baroreceptors -> release RENIN from JG cells –> RAAS –> Ang II –> VASOCONSTRICTION, increased SNS, increased fluid retention (aldosterone) –> HYPERTENSION
What causes renal HTN?
Decreased flow
Renal Artery Stenosis –> typically due to ATHEROSCLEROSIS in the renal artery leading to DECREASED BF and INCREASED RENIN SECRETION
Takes time for athero to develop –> older
Correctable if plaque removed (HTN subsides when perfusion is re-established)
FIBROMUSCULAR DYSPLASIA –> rare condition that PRIMARILY AFFECTS REPRODUCTIVE AGED WOMEN –> unknown cause –> increased proliferation of smooth muscle and increased fibrosis –> leads to a NARROWING of artery lumen –> low flow –> increased renin –> HTN
Renal Infarction
Caused by a VASCULAR OCCLUSION of any of the renal arteries –> tissue hypoxia –> cell death and necrosis
What kind of necrosis? COAGULATIVE since kidney only has a single blood supply (no collateral circulation) –> infarcts appear PALE surrounded by a HEMORRHAGIC ZONE
Causes –> Mostly EMBOLISM (a fib, mural thrombosis), THROMBUS formation (hypercoaguable patients), ATHEROSCLEROTIC PLAQUE RUPTURE/OCCLUSION, or SEPTIC EMBOLI (infectious colonies from an infected heart valve)
Thrombotic Microangiopathy
Systemic process characterized by ENDOTHELIAL DAMAGE and exposure of VON WILLEBRAND FACTOR –> leads to PLATELET ADHESION –> activation of coagulation cascade and formation of micro-thrombi –> the micro thrombi cross-link and get lodged within small arterioles and capillaries –> leads to small vessel occlusions and damage to RBC (shistocytes)
HUS
Typically associated with verocytotoxin-producing E. coli infections
Bacteria bind and infiltrate GI epithelium –> then enter into the sub-epithelial layer
Endotheliam damage –> vWF –> coagulation cascade
Micro-thrombi that form travel to the renal arteries –> deposited and then lead to destruction and occlusion –> SHISTOCYTES
Low Hb –> as Hb is released from lysed RBCs, HAPTOGLOBIN binds it and becomes all bound, so therefore its levels are also decreased
Usually follows a GI or flu-like prodrome
Can ultimately lead to renal failure, ischemia and necrosis
TTP
Different than HUS –> acquired or congenital and NOT infectious
Mutation in the ADAMTS13 metalloproteinase, which is an enzyme that cleaves vWF
When there are large multimers around there is a HIGHER TENDENCY FOR COAGULATION to occur –> micro-thrombi throughout the body –> particular prone to accumulate in kidneys
PENTAD for TTP --> THROMBOCYTOPENIA, THROMBOTIC HEMOLYTIC ANEMIA (clogged arterioles --> damage/lyse RBCs), FEVER RENAL FAILURE NEUROLOGIC SYMPTOMS
