Renal disease pt 2 Flashcards
How does the liver compensate for loss of albumin? Caveat?
Make lipoproteins/lipids to restore oncotic pressure, but lipids are small and can end up in urine
Nephrotic syndrome UA findings
- Massive proteinuria > 3.5 g/dL
- Low levels of serum albumin
- High levels of serum lipids
- Pronounced edema
- RBC
- Fat droplets
- RTE
- Epithelial casts
- Fatty casts
- Waxy casts
Why is there edema in nephrotic syndrome?
- Loss of albumin reduces oncotic pressure such that water leaves capillaries to the tissues
- Tissues are hypertonic to blood, so water leaves to tissues
Minimal Change Disease aka
Liver nephrosis
What happens in minimal change disease?
Little cellular change, thus allowing some proteins to pass through glomerulus
Minimal change disease typically found in
Children
Minimal change disease clinical findings
- Edema
- Fat droplets
- Marked proteinuria
- Transient hematuria
Focal Segmental Glomerulosclerosis (FSGS)
Affects only certain glomeruli, others can stay normal
FSGS features what kind of deposits?
Immune deposits of IgM and C3 (complement)
FSGS UA findings
- Elevated protein
- RBC
Alport Syndrome
- Inherited disorder affecting glomerular basement membrane (GBM)
- GBM thin, no antibody effect
Alport syndrome symptoms
- Same as nephrotic syndrome
- Massive proteinuria > 3.5 g/dL
- Low levels of serum albumin
- High levels of serum lipids
- Pronounced edema
Most common cause of end-stage renal disease
Diabetic Nephropathy
How does damage occur in diabetic nephropathy?
- Glomerular membrane thickening
- Mesangial cell proliferation
- Increased deposition of cellular material
- Vascular sclerosis
Diabetic nephropathy features what kind of deposits and where?
Glycosylated proteins deposit in capillary tufts
List tubular disorders
- Fanconi Syndrome
- Nephrogenic diabetes insipidus
- Renal glycosuria
- Acute tubular necrosis
Acute tubular necrosis features
RTE cell damage
Causes of acute tubular necrosis
- Ischemia (reduced blood flow/lack of oxygen) due to surgery, trauma, or shock
- Toxic substances (aminoglycosides, anti-fungals, radiographic dye, anti-freeze, heavy metals, Hgb, Mgb
Acute tubular necrosis UA findings
- Hallmark: RTE cells and RTE casts
- Mild proteinuria
- Wide variety of casts (granular, waxy, broad)
Fanconi’s syndrome
Failure of tubular reabsorption in PCT, which means there’s disrupted transport, cellular energy, and membrane permeability
Substances affected in Fanconi’s syndrome
- Glucose
- Amino acids
- Phosphorus
- Sodium
- Potassium
- Bicarb
- Water
List an inherited cause of Fanconi’s syndrome
Wilson’s disease
List an acquired cause of Fanconi’s syndrome
Multiple Myeloma
List an exogenous cause of Fanconi’s syndrome
Heavy metals
Nephrogenic Diabetes Insipidus
Inability of tubules to respond to ADH
Nephrogenic Diabetes Insipidus UA findings
- Low specific gravity
- Frequent urination
Renal glycosuria
- Inherited disorder where glucose receptor on PCT cell won’t work or not enough expressed
- Only glucose reabsorption affected
Serum and urine glucose levels in renal glycosuria
- Serum glucose = normal
- Urine glucose = increased
Most common renal disease
UTI (upper or lower)
Interstitial disease affects
The interstitium and tubules
Most common interstitial disorder
Cystitis (bladder infection)
Cystitis UA findings
- Numerous WBC
- Numerous bacteria
- Mild proteinuria
- RBC (not from glomerulus)
Pyelonephritis
Upper UTI
Acute pyelonephritis result of
Bacteria ascending upwards from lower UTI due to renal calculi, pregnancy, or reflux of urine
Acute pyelonephritis symptoms
- Urination frequency
- Burning
- Lower back pain
- Correlation btwn acute pyelonephritis and bacteremia
Acute pyelonephritis UA findings
- Numerous WBC
- Numerous bacteria
- Proteinuria
- WBC casts (tubule infection)
How to distinguish between upper and lower UTI?
Upper UTI = casts present (WBC) because only nephron makes casts and bladder (lower UTI) can’t
More serious form of pyelonephritis
Chronic
Chronic pyelonephritis often diagnosed in
Children (poorly formed kidneys)
Chronic pyelonephritis congenital urinary structural defect effects
- Bladder reflux to ureters or renal pelvis
- Cannot empty collecting ducts
What can lead to chronic renal failure?
Permanent tubular damage
UA findings in chronic pyelonephritis
- Numerous WBC
- Bacteria
- WBC casts
- Granular casts
- Waxy casts
- Broad casts
Acute interstitial nephritis
- Inflammation of renal interstitium or tubules
- Associated with allergic reaction to meds (penicillin class, sulfonamides, cephalosporin, NSAIDs)
Acute interstitial nephritis UA findings
- No bacteria
- Eosinophils (do Hansel stain)
- RBC
- Proteinuria
- Numerous WBC
- WBC casts
Final progression to end-stage renal failure looks like:
- Marked GFR reduction (<25ml/min)
- Steady increase serum BUN/creatinine
- Electrolyte imbalance
- Lack of renal concentrating ability
- Positive urine protein/glucose
- Increase granular, waxy, and broad casts
Acute vs chronic renal failure
Acute renal failure shows sudden loss of renal function and is frequently reversible
Pre-renal causes of renal failure
Sudden reduction in blood flow
Renal causes of renal failure
Acute glomerular or tubular disease
Post-renal causes of renal failure
Renal calculi or tumor obstructions
Acute renal failure general rule of thumb UA findings
- RTE cells + casts = acute tubular necrosis
- WBC casts = interstitial infection of inflammation
- Abnormal cells = malignancy
Renal lithiasis
- Kidney stones that form in the kidney, ureters, and bladder
- Calculi vary in size
Conditions favoring kidney stone formation
- pH
- Chem concentration
- Urinary stasis
- Presence of certain crystals
75% of kidney stones consist of
Calcium oxalate or phosphates
Other kidney stones may consist of
Mag-ammonium phosphate, uric acid, cystine
Patient management of kidney stones
- Maintaining urine pH to prevent crystallization
- Hydration
- Dietary restrictions
Renal lithiasis UA findings
Microscopic RBC due to irritation of the tissue by kidney stone (aka calculus)
