Applied Physiology of Renal Disease Flashcards
What are the 4 lab results that Nephrotic Syndrome is characterized by
- > 4g/24 hours proteinuria (normal is 0.3)
- Low serum albumin
- Hyperlipidemia (elevated cholesterol, LDL, triglyc)
- Urine microscopy - OVAL FAT BODIES (maltese crosses) = foamy urine
What are some symptoms are Nephrotic Syndrome?
Edema
Hypercoagulability
Immunocompromised state
What is the dysfunctional part of the glomerulus that causes Nephrotic syndrome
something wrong with the foot processes of podocytes (can be seen as missing foot processes in microscopy)
What are some causes of Nephrotic syndrome?
- membranous nephropathy
- Focal segmental glomerulosclerosis (FSGS)
- Amyloidosis
- MPGN, IgA, lupus (usually present as nephritic though)
- rare - diabetes
Why does Nephrotic syndrome cause edema?
lowered albumin in the blood = lowered oncotic pressure to draw fluid back into the capillaries
Why does Nephotic syndrome cause Hyperlipidemia?
The liver reacts to hypoalbuminemia and starts craning out a bunch of lipids = increased LDL, triglycerides, cholesterol
What is Hyperlipidemia associated with and what 2 things does it cause a signficant increase in risk in?
Nephrotic syndrome
increases risk in: atherogenesis + cardiac risk
What rare dermatological symptom can be seen with nephrotic syndrome
Xanthelasmas (from hyperlipidemia)
What are two nephrotic complications
- Hypercoagulability (DVT, PE) increased liver prod of coagulable factors
- Increased risk of infection (loss of IgG through urine, fragile skin, loss of ZINC + TRANSFERRIN)
What are symptoms of Nephritic Syndrome?
headache, Hx of cough, rash, DARK BROWN URINE, HTN (from sodium retention)
What are some lab signs of Nephritic Syndrome?
Acute kidney failure GFR ~10
Urine: RBCs and small proteinuria
Red cell casts + dysmorphic RBCs (mickey mouse ears)
What part of the glomerulus is injured in Nephritic Syndrome
injury to GBM or endothelial cells
What are causes of nephritic syndromes
Most common: SLE, IgA nephropathy
ANCA related, MPGN, Anti-GBM disease, Post streptococcal GN
How do you differentiate between Nephrotic and Nephritis syndrome?
Nephrotic: insidious, edema, high proteinuria
Nephritic: Abrupt, HTN, increase Jugular venous pressure
What are presenting Sx of End Stage Renal Disease
Altered Mental Status Emaciated/Lethargic Rash Volume Overload Muscle Wasting
What are lab signs of End Stage Renal Disease
Renal failure Acidosis Anemia low Vit D high PTH high Phosphate UREMIC FROST!!!!! - rare in US (chronic kidney disease)
What are the two general functions of the kidney?
- Clearance (toxins, meds, electrolytes)
2. Hormonal (activation of 1,25 hydroxy Vit D, ERYTHROPOIETIN)
What are 3 indications of ESRD
- Uremia
- Bone metabolism problems (hyperparathyroidism)
- Anemia
What are Sx of Uremia
Lethargy Anorexia/weight loss (meats have metallic taste) ASTERIXIS pericarditis itching increased bleeding ***UREMIA IS NOT CAUSED BY UREA
Why does dialysis not work very well with Uremia?
Uremic toxins produced by gut bacteria (p-cresyl, indole) are bound to albumin = not excreted very well
What lab result indicated Uremia
BUN approached ~100mg/dL
What can cause falsely low/high BUN?
falsely low - poor diet
falsely high - steroids, GI bleeding
What are signs of Uremic pericarditis, and what is this a hard indication for?
pericardial pain, rub
unexplained cardiomegaly, hemodynamic instability
Tx: Aggressive Hemodialysis
What 3 things are Uremic Pericarditis associated with
- Underdialysis
- Concurrent viral infections
- systemic disease (Lupus)
What is the treatment for Uremic Pericarditis
Aggressive hemodialysis
pericardial drainage
What are 4 bone metabolism findings in ESRD?
- Elevated phosphorus
- Elevated PTH
- Low Calcium
- Low Vit D
What fx do 1,25(OH)2D3 have on the parathyroid gland and the GI tract? What happens in ESRD?
normally:
parathyroid gland - decreases activity
GI - increases absorption of calcium phosphate (increase bone mineralization)
ESRD - Vit is not activated by kidneys
What is the most common disease of bone metabolism in ESDR patients and what are the Sx
Secondary hyperparathyroidism:
elevated PTH, phosphorus, and low calcium
How do you distinguish Secondary hyperparathyroidism from primary and tertiary hyperparathyrodism?
secondary - low calcium
What is the pathophysiology of Secondary parathyroidism
initial insult = low clearance of phosphate (low GFR)
Increased FGF23, reduced Vit D - factors that increase parathyroid activity
What is the Tx for high parathyroid hormone? (prone to fractures)
Vit D, Calcimimetics, parathyroidectomy
What is the Tx for high phosphorus
dietary control, PHOSPHATE BINDERS,
reduce parathyroid hormone (Vit, Calcimimetics)
What are the side fx of Tx for high parathyroid hormone
- hypocalcemia (parathyroid gland thinks Ca levels are fine)
- parathyroidectomy - “hungry bone syndrome” - bone sucks up all Ca (hypocalcemia)
What causes Tertiary Hyperparathyroidism and what are the Sx
seen in pt with chronic secondary hyperparathyroidism
lab: high phosphorus, high PTH, HYPERCALCEMIA
Sx: hyperplasia of thyroid gland
What is the treatment for tertiary hyperparathyroidism
parathyroidectomy, calcimimetic
How does ESRD cause Anemia?
Low erythropoietin (kidney exposed to HIF-2)
Chronic Inflammation
Iron deficiency - poor diet
increased bleeding
What two things must be corrected before treating anemia with EPO in ESRD
chronic inflammation, iron deficiency
What are Sx of Pre-renal Kidney Injury
- Low Urine sodium (increased RAAS)
–Fractional excretion of Sodium <1% - Hyaline Casts - clear, hard to see
caused by precipitation of Tamm Horsefall Proteins - Orthostatic hypotension
Treatment - give more fluids
What are symptoms of Acute Tubular Necrosis
- high urine sodium
2. Urine shows MUDDY BROWN CASTS (degraded tubular cells)
What is the pathophysiology of Acute Tubular Necrosis
Acute kidney injury by: hypotension, sepsis, meds
two mechanism:
1. tubule obstruction by sloughing tubular cells
–tubular cells are sensitive to ischemia
2. very high sodium loss
Tx: supportive
