Day 7 5/20/15 Flashcards
BUN Creatinine Ratio
The ratio of serum BUN to creatinine is usually between 10:1 and 20:1. An increased ratio may be due to a condition that causes a decrease in the flow of blood to the kidneys, such as congestive heart failure, early stage post-renal failure or dehydration.
Crockoft Gault Equation for Creatinine Clearance (GFR)
Creatinine Clearance (or GFR) = [(140-age) x weight kg] / [serum creatinine x 72] x0.85 for females -slightly overestimates GFR because creatinine is moderately secreted by renal tubules
Fractional Excretion of Na (FeNa) Equation
FeNa = 100 [(Na urinary x Cr plasma) / (Na plasma x Cr urinary)]
1% = damage to kidney itself
nocturia
-need to urinate waking one from sleep
Urinary loss of albumin results in:
- dec. oncotic pressure leading to edema
- hallmark of nephrotic syndrome
Nephrotic Syndrome
- blood albumin leve
- blood gammaglobulin level
- blood coagulation state
- blood lipid and cholesterol level
- hypoalbuminemia- edema
- hypogammaglobulinemia
- hypercoagulable state- loss of antithrombin III
- hyperlipidemia
- hyperchoesterolemia
Nephrotic Syndromes
- minimal change disease
- focal segmental glomerulosclerosis (FSGS)
- membranous nephropathy
- membranoproliferative glomerulonephritis (MPGN)
- diabetes mellitus
Minimal Change Disease Causes
- nephrotic
- common in children
- idiopathic or Hodgkin lymphoma related
- loss of foot processes due to cytokines
Minimal Change Disease Lab Findings
- normal glomeruli on H&E stain
- effacement of foot processes on EM
- negative IF, no immune complexes
Minimal Change Disease Protein Loss
- selective proteinuria
- loss of albumin
- normal immunoglobluin
Minimal Change Disease Treatment
Excellent Response to Steroids
FSGS Causes
- nephrotic
- usually idiopathic
- HIV
- heroin use
- sickle cell disease
- most common nephrotic syndrome in hispanics and african americans
FSGS Labs
- segmental sclerosis on H&E
- effacement of foot processes on EM
- negative IF; no immune complexes
FSGS Treatment
- minimal response to steroids; progresses to chronic renal failure
- usually doesn’t respond to treatment
Membranous Nephropathy Causes
- nephrotic
- most common cause of nephropathy in caucasians
- usually idiopathic
- HEP B/C
- solid tumors
- SLE
- drugs (NSAIDS, penicillamine)
Membranous Nephropathy Labs
- H&E: thick glomerular basement membrane
- granular IF: due to immune complex deposition
- EM: subepithelial (level of podocyte) deposits with spike and dome appearance
Two Types of MPGN & Causes
- nephrotic
- type 1: subendothelial, associated with HBV and HCV, more often associated with formation of tram-tracks
- type 2: intramembranous, associated with C3 nephritic factor autoantibody
MPGN Labs
- H&E: thick capillary membranes, often tram-track appearance in type 1 most commonly
- IF: granular due to immune complex deposition
- can also sometimes be nephritic
DM Nephrotic Syndrome Causes
- high serum glucose causes basement membrane to become leaky and causes hyaline arteriolosclerosis (thickening of blood vessel wall)
- efferent arteriole is most affected, leading to high glomerular filtration pressure
- hyperfiltration injury results in microalbuminuria and progresses to nephrotic syndrome
DM Treatment for Kidney
-ACE inhibitors prevent additional contraction of efferent arterioles in kidney, preventing further injury
Nephritic Syndrome Hallmarks
-limited proteinuria (
Nephritic Syndromes
- post strep glomerulonephritis (PSGN)
- rapidly progressive glomerulonephritis
- IgA nephropathy
- alport syndrome
- benign familial hematuria (thin basement membrane disease)
- focal/necrotizing/crescentic GN
- lupus GN
Post Strep Glomerulonephritis (PSGN) Causes
- nephritic
- arises after group A beta hemolytic strep infection of skin (impetigo) or pharynx
- occurs with nephritogenic strains that carry M protein virulence factor
Post Strep Glomerulonephritis (PSGN) Presentation
- hematuria (cola colored urine)
- oliguria
- hypertension
- periorbital edema
- usually seen in children but can occur in adults
Post Strep Glomerulonephritis (PSGN) Labs
- H&E: hypercellular, inflamed glomeruli
- IF: granular, mediated by immune complex deposition
- EM: subepithelial humps
Post Strep Glomerulonephritis (PSGN) Treatment
- supportive
- children rarely progress to renal failure
- some adults develop rapidly progressive glomerulonephritis (RPGN)
Rapidly Progressive Glomerulonephritis (RPGN) Lab Differentiation
- H&E: crescents in bowmans space, comprised of fibrin and macrophages
- IF:
- linear: goodpastures
- granular: post strep glomerular nephritis (PSGN), or diffuse proliferative GN
- negative IF: pausi-immune: cANCA means wegners granulomatosis, pANCA means microscopic polyangiitis or churg straus
IgA Nephropathy Causes
- nephritic
- IgA immune complex deposition in mesangium of glomeruli
- most common nephropathy worldwide
Alport Syndrome Causes
- nephritic
- inherited defect in type 4 collagen
- most commonly X linked
- results in thinning and splitting of glomerular basement membrane
Alport Syndrome Presentation
- isolated hematuria
- sensory hearing loss
- ocular disturbances
Renal Clearance Equation
C = (U x V) / P
C- clearance of X (mL/min)
U- urine concentration of X (mg/mL)
P- plasma concentration of X (mg/mL)
V- urine flow rate (mL/min) (1440 min per day)
Glomerular Filtration Rate Equation
-inulin clearance can be used to calculate GFR because it is freely filtered and not reabsorbed or secreted
GFR= Kf [(Pgc - Pbs) - (pgc - pbs)]
- gc- glomerular capillary
- bs- bowman space
- pbs normal equals 0
- normal GFR = 100 mL/min
