Systemic Diseases (Brozna) Flashcards
Nephrosclerosis
process, not diagnosis
Sclerosis of renal arterioles from age, hypertension, or diabetes–> focal ischemia–> tubuloinsterstitial injury–> reduced renal function
Nephrosclerosis (benign)
Associated with mild to moderate hypertension
Associated with aging
uncommonly leads to renal insufficiency
Longstanding Hypertensive Nephrosclerosis
Arteriolar sclerosis Tubular atrophy Interstitial fibrosis Glomerulosclerosis Interstitial inflammation
Accelerated Nephrosclerosis
Associated with severe hypertension (>200/120 mm)
Petechial hemorrhages are frequently present
Relatively uncommon
Associated with marked elevation of plasma renin
can be associated with encephalopathy, retinal papilledema, acute and subacute kidney injury– elevated creatinine and proteinuria **
Important to exclude acute, ongoing target-organ damage (hypertensive EMERGENCY)
Hypertensive intracerebral hemorrhage
associated w/ basal ganglia hemorrhagic infarct, small arteriole fibrinoid necrosis
Malignant HypertensionPathogenesis
fibrinoid necrosis –> hyperplastic arteriolitis (onion skin change)
typical presentation: blurry vision, elevated BP 245/125, wavy vision, decreased color vision,
papilledema etc. from malignant hypertension
renal pathalogical findings w/ injury from severe hypertension
fibrinoid necrosis of small arterioles and hyperplastic arteriolitis (onion skinning) of small renal arteries.
hypertension and diabetes mellitus
vascular changes are more severe –> systemic small vessel arteriolar sclerosis involving multiple organs.
–> nephropathy
Diabetic Nephropathy
Diabetic nephropathy is a clinical syndrome characterized by:
Persistent albuminuria (> 300 mg/day for at least 3 months)
Progressive decline in the glomerular filtration rate
Elevated arterial blood pressure
*** Urine dipstick becomes positive when protein excretion exceeds ~300-500 mg/day
Clinical stages of diabetic nephropathy
- hyperfiltration
- microalbuminuria 5-15 years
Overt proteinuria 10-20 years
Progressive nephropathy 15-25 years
End-stage renal disease 20-30 years
Glomerulonephritis can be superimposed on diabetic nephropathy
A glomerulus showing a cellular crescent with rupture of Bowman capsule superimposed on nodular DN.
The patient, known to have DN, presented with rapidly deteriorating renal function and red cell casts in the urine
biopsy of diabetic nephropathy
Nodular glomerulosclerosis with mesangial proliferation and diffuse thickening of capillary basement membranes.
Immunofluorescence shows mild linear staining for IgG
Electron microscopy shows diffuse thickening of the tubular and capillary basement membranes.
There are decreased numbers of podocytes and diffuse foot process effacement
Hyaline arteriolosclerosis
Thickening and hyalinization lead to decrease in smooth muscle and collagen and in and more rigid vascular wall
Arteriolar hyalinosis (nonspecific) Much worse systemically when associated with hypertension and responsible for many of the signs/symptoms of diabetes
what might be an early initiating factor for microalbuminuria in early diabetes nephropathy?
disruption of the glycocalyx by glycosylated proteins
Thickening of the glomerular basement membrane, podocyte detachment and damage to the endothelial glycocalyx leads to disruption of the glomerular filtration barrier in diabetes.
Pathogenesis of Microalbuminuria
Glomerular Filtration Barrier is anionic (strong negative charge)
Podocyte membrane coated with sialoglycoproteins
Glomerular basement membrane heparin sulfate
Glycocalyx membrane-bound negatively charged proteoglycans and glycoproteins with integrated soluble plasma proteins
Systemic Lupus Erythematosus: common symptoms
Fatigue Fever Myalgia/arthralgias Weight loss Skin and mucous membrane involvement Vasculitis Raynaud’s phenomenon Renal disease photosensitivity oral ulcers non erosive arthritis pleural pericarditis positive ANA
Constellation of presenting clinical features can make the diagnosis of SLE relatively straightforward or presenting with 1 or 2 isolated complaints can make the diagnosis difficult
Laboratory tests that can support the diagnosis of SLE
Antinuclear antibody
Antiphospholipid antibodies (lupus anticoagulant)
C3, C4 and CH50 complement levels
Erythrocyte sedimentation rate
C-reactive protein
Urine protein to your and creatinine ratio
Systemic Lupus Erythematosus Nephritis
Approximately 60% of patients with SLE have renal disease within five years of diagnosis
Elevated serum creatinine
Urine red blood cells, white blood cells, red blood cell casts
Proteinuria
10-30% the progress to end-stage renal disease
*** Control of blood pressure is critical to delay progression of chronic kidney disease
Clinical manifestations of lupus nephritis can include
Recurrent microscopic or gross hematuria Nephritic syndrome Rapidly progressive glomerulonephritis Nephrotic syndrome Acute and chronic renal failure Hypertension
Urine dipstick becomes positive when protein excretion exceeds
300-500 mg/day
