renal disease Flashcards
Origin of majority of glomerular disorders
Immune in origin
Damage to glomerulus may consist of:
cellular proliferation
leukocytic infiltration
thickening of the glomerular basement membrane
Scarring of glomerulus
sclorosis
Non-immune causes of glomerular damage
Chemicals and toxins
disruption of the wall of negativity
deposition of amyloid material
basement membrane thickening
Glomerulonephritis
Sterile, inflam process
blood, proteins, casts in urine
Acute post-strep glomerulonephritis
damage to glomerular membrane
symptoms: oliguria, hematuria
following a group A strep infection (M proteins in the cell wall)
Acute post strep glomerulonephritis findings
Immune complexes deposited at glomerular membranes
Elevated: BUN and ASO titer
Rapidly Progressive Glomerulonephritis (Crescentic)
More serious acute Glomerular disease
Example is SLE
Symptoms started by deposition of immune complexes
Crescentic formations containing macrophages, fibroblasts, polymerized fibrin
RPGN Findings
Markedly elevated protein
GFR decreases as disease progresses
Eventually loss of function (glomerulosclerosis)
Goodpasture’s Syndrome
Follows viral respiratory infections
Cytotoxic autoantibodies
Anti-glomerular basement membrane antibody
detectable in serum
Goodpasture syndrome antibody
Attaches to basement membrane
initiates complement
produces capillary destruction
Goodpasture’s findings
proteinuria, RBCs/RBCs casts
progress to end stage renal failure
Vasculitis
systemic vascular system
Wegener’s Granulomatosis
Henocj-Schonlein purpura
Vasculitis Findings
Similar to acute glomerulonephritis
Kidney dmg due to: immune complex, autoantibodies, immune mediated inflamm
Antineutrophilic cytoplasmic antibody (ANCA)
Henoch-Schonlein purpura
Children following upper respiratory infection
Red patches on skin
Henoch-Schonlein purpura findings
increased protein
RBC/RBC casts
Raised platelets. distinguishes from TTP and ITP
Membranoproliferative GN
Membranous GN
M-GN -> IgG complexes
Mprolif GN -> children
Membranous glomerulonephritis
Thickening of basement membrane
IgG complexs
Proteinuria, RBCs, tend towards thrombosis
Membranoproliferative GN
Type 1: Thickening of Bowman’s capsule wall
Type 2: dense deposits in Glomerular basement membrane
Children
poor prognosis
Membranoproliferative GN findings
decreased serum complement
RBCs
Proteinuria
Berger’s disease
Most common glomerular nephritis
serum increase in IgA
Mucosal infection
Berger’s disease findings
Macroscopic hematuria
follows infection or strenuous exercise
20-40% of people suffer chronic GN
Chronic GN
Accumulation of damage from acute GN
symptoms: fatigue, anemia, hypertension
edema, oliguria
Findings: Hematuria, Proteinuria, Glycosuria, decrease eGFR, increase BUN and creatinine
Nephrotic syndrome
Massive proteinuria
low serum albumin
high serum lipids
pronounced edema (due to low albumin)
Nephrotic syndrome findings
proteinuria
RBC
fat droplets
oval fat bodies
RTE
epi cells
fatty/waxy casts
minimal change disease
lipid nephrosis
some proteins pass through glomerulus
minimal change disease findings
edema
fat droplets
market proteinuria
hematuria
Unknown etiology
Focal segmental glomerulosclerosis (FSGS)
only certain glomeruli
elevated protein/RBCs
IgM and C3
FSGS Associations
Unknown
Genetic
heroin abuse/drug toxicity
HIV
Diabetes
Infection
Alport syndrome
inherited disorder
Basement membrane thins
Diabetic nephropathy
Most common cause of end stage renal disease
monitored via microalbumin testing
Diabetic nephropathy damage
GM thickening
proliferation of mesangial cells
deposition of cellular material
vascular sclerosis
Tubular disorders
damage to tubules (antifreeze)
Metabolic/hereditary disorder
Acute Tubular Necrosis (ATN)
Damage to the RTEs
Ischemia: decrease blood flow -> lack of O2
Toxic Substances: Aminoglycosides, antifungals, antifreeze, etc
ATN findings
Lots of casts of various sorts
RTE cells
Fanconi’s syndrome
Failure of tubular reabsorption (proximal convoluted tubules)
Substances affected: phosphorous, Na, K, Bicarb, H2O
Can acquire from heavy metals and MM
Nephrogenic Diabetes insipidus
Don’t respond to ADH
Low specific gravity
urinate frequency
Renal Glycosuria
Reabsorption of glucose affected
normal serum glucose, increased urine glucose
Interstitial disease
affect the interstitium
infection and inflamm
most common: UTI
Cystitis
Most common UTI
Infection of bladder
Cystitis findings
WBCs
Bacteria
RBCs
Proteinuria
Acute pyelonephritis
upper UTI
Bacteria ascending from lower UTI
conditions: calculi, pregnancy, urine reflux
Acute pyelonephritis findings
WBC casts (tubular infection). Differentiates between upper and lower UTI
Chronic pyelonephritis
Congenital structural defects
Can’t empty collecting ducts
often in children
Chronic pyelonephritis findings
WBC casts
Granular/waxy/broad casts (tell urinary status)
Acute Interstitial Nephritis (AIN)
NO BACTERIA
Inflamm of renal interstitium or tubules
Allergic reaction to medications
AIN WBCs/stains
Eosinophils (Allergic reaction)
Hansel stain
AIN findings
Absence of bacteria
Eosinophils
Renal Failures
Acute and chronic
Final stage: end stage renal failure
Renal failure findings
Marked decreased GFR
Rise in BUN
Electrolyte imbalance
Lack of renal concentrating ability
proteinuria, glucosuria
waxy/granular/broad casts
Acute renal failure
Sudden loss, frequently reversible
Pre -> decrease in blood flow
Renal -> acute glomerular/tubular disease
Post -> stones/tumor obstruction
Acute renal failure
RTE/casts -> acuter tube necrosis
WBC casts -> interstitial infection/inflamm
Abnormal cells -> malignancy
Renal Lithiasis
stones in ureters, kidney,bladder
Lithotripsy
High energy shock waves to break stones
Conditions for kidney stone formation
pH
Chem concentration
Urinary stasis
certain crystals
Renal lithiasis examination
examine chemically/xray crystalography
75% calcium oxalate or phosphates
Renal lithiasis management
maintain urine pH
Hydration
Diet restrictions
