MTB Nephro Flashcards
The “best initial test” in nephrology is
a urinalysis and the blood urea nitrogen (BUN) and creatinine.
Severe proteinuria means
glomerular damage.
White blood cells in UA
inflammation, infection, or allergic interstitial nephritis. You cannot distinguish neutrophils from eosinophils on a UA. Neutrophils indicate infection. Eosinophils indicate allergic or acute inter- stitial nephritis.
Hematuria is indicative of:
- Stonesinbladder,ureter,orkidney
- Hematologic disorders that cause bleeding (coagulopathy) • Infection (cystitis, pyelonephritis)
- Cancerofbladder,ureters,orkidney
- Treatments (cyclophosphamide gives hemorrhagic cystitis)
- Trauma; simply “banging” the kidney or bladder makes them shedred cells
- Glomerulonephritis
When “dysmorphic” red cells are described, the correct answer is
glomerulonephritis.
The answer is cystoscopy when there is
hematuria without infection or prior trauma and:
• The renal ultrasound or CT does not show anetiology.
• Bladder sonography shows a mass for possible biopsy.
White cell cast
pylonephritis
red cell cast
Glomerulonephritis
AKI is categorized into 3 types:
- Prerenal azotemia (decreasedperfusion)
- Postrenal azotemia (obstruction)
- Intrinsic renal disease (ischemia and toxins)
prerenal azotemia
BUN rising more than the creatinine.
AKI presentation
AKI may present with only an asymptomatic rise in BUN and creatinine. When symptomatic, the patient feels: • Nauseated and vomiting • Tired/malaise • Weak • Shortofbreathandedemafromfluidoverload
Very severe disease presents with:
• Confusion
• Arrhythmia from hyperkalemia and acidosis
• Sharp, pleuritic chest pain from pericarditis
Urine osmolality in ATN is inappropriately .
low
nephrotoxic antibiotics
Vancomycin, gentamicin, and amphotericin
Urine dipstick cannot tell the difference between:
- Hemoglobin
- Myoglobin
- Red blood cells
Acute (allergic) interstitial nephritis (AIN) is
a form of acute renal failure that damages the tubules occurring on an idiosyncratic (idiopathic) basis. Antibodies and eosinophils attack the cells lining the tubules as a reaction to drugs (70%), infection, and autoimmune disorders.
Tubular disease doesnt cause
nephrotic syndrome ie no proteinuria
Tubular Diseases
- Acute
- Toxins
- None nephrotic
- No biopsy usually
- No steroids
- Never additional immunosuppressive agents
Glomerular Diseases
- Chronic
- Not from toxins/drugs
- All potentially nephrotic
- Biopsy sample
- Steroids often
• UA with hematuria
• “Dysmorphic” red cells (deformed as they “squeeze” through an abnormal
glomerulus)
• Red cell casts
• Urine sodium and FENa are low • Proteinuria
Cancer (solid organ): Children: Injection NSAIDs: SLE:
Cancer (solid organ): membranous
Children: minimal change disease
Injection drug use and AIDS: focal-segmental NSAIDs: minimal change disease and membranous SLE: Any of them
Both TTP and HUS are associated with:
- Intravascularhemolysis • Renalinsufficiency
* Thrombocytopenia
Polycystic kidney disease (PCKD) presents with:
Pain Hematuria Stones Infection Hypertension
The most common causes of hyponatremia with a hypervolemic state are:
- CHF
- Nephroticsyndrome
- Cirrhosis
The most common causes of hyponatremia with euvolemia (normal volume status) are:
- Pseudohyponatremia (hyperglycemia)
- Psychogenic polydipsia
- Hypothyroidism
- Syndrome of inappropriate ADH release (SIADH)
The EKG in severe hyperkalemia shows:
- Peaked T waves
- Wide QRS
- PR interval prolongation
Distal RTA (Type I)
The distal tubule is responsible for generating new bicarbonate under the influence of aldosterone.
Proximal RTA (Type II)
Normally 85% to 90% of filtered bicarbonate is reabsorbed at the proximal tubule.
The most common cause of kidney stones (nephrolithiasis) is calcium
oxalate, which forms more frequently in an alkaline urine. The most common risk factor is the overexcretion of calcium in the urine.
Crohn disease causes kidney stones because of
increased oxalate absorption.
Uric acid stones are not detectable on
x-ray but are visualized on CT.
NSAID-induced renal disease does not show
eosinophils.
Furosemide causes
ototoxicity by damaging the hair cells of the cochlea, resulting in sensorineural hearing loss
