B&B Renal: Other Flashcards
Cystitis
UTIs
Bladder infection
* Lower urinary tract
Pyelonephritis
UTIs
Kidney infection
* Upper urinary tract
UTI
Etiology
- E. coli: 75-90% of cases
- Proteus mirabilis
* Urease-producing –> struvite kidney stones - Klebsiella pneumoniae
- Staphylococcus saprophyticus
- Enterococcus faecalis
Typically enteric bacteria
- Dysuria
- Frequnecy
- Urgency
- Suprapubic pain
- No systemic symptoms
- Usually normal plasma WBC count
Signs & Symptoms
Cystitis
- Systemic symptoms: fever, chills
- Flank pain
- CVA tenderness
- Urine: hematuria; WBC casts
Signs & Symptoms
Pyelonephritis
Ascending infection –> will also have cystitis symptoms
UTI
Diagnosis
- Urinalysis
- Cloudy urine
- Leukocyte esterase –> produced by WBCs in urine
- Nitrites –> 90% of UTI bugs convert nitrates to nitrites
- > 10 WBC/hpf
- Urine culture
- > 100,000 CFUs
UTI
Risk Factors
- Women: 10x more likely than men
* Shorter urethra, closer to fecal flora - Sexual activity
- Urinary catheterization
- Diabetes
- Pregnancy
- Infants with vesicoureteral reflux
- Abnormal insertion of ureters into bladder
- Chronic backflow of urine back into ureters
- Urinary obstruction
- Anatomic abnormalities in children
- Bladder tumors in adults
- Enlarged prostate in older mens
UTI
Treatment
Fluoroquinolones: ciprofloxacin, levofloxacin, ofloxacin
* Nitrofurantoin: used in pregnancy
Chronic Pyelonephritis
UTIs
- Consequence of recurrent pyelonephritis
- Children w/ vesicoureteral reflux
- Adults w/ recurrent kidney stones
- Results in kidney injury
- Corticomedullary scarring
- Blunted calyces
- Renal thyroidization: tubules contain eosinophilic material, look like thyroid on LM
Cystic Kidney Diseases
- Multicystic Dysplastic Kidney
- Autosomal Recessive PKD
- Autosomal Dominant PKD
- Medullary Cystic Kidney Disease
PKD = Polycystic Kidney Disease
Multicystic Dysplastic Kidney
Cystic kidney Diseases
Abnormal ureteric bud-mesenchyme interaction in gestation
* Kidney replaced with cysts
* No / little functioning renal tissue
* Absent ureter
* Unilateral –> remaining kidney hypertrophies
* Bilateral –> Potter’s syndrome
* Oligohydramnios
* Failure of lung maturation
* Compression of face / limbs
* Not compatible with life
* Spontaneous congenital abnormality
* Not-inherited, unlike other cystic kidney diseases
Autosomal Recessive PKD
PKD
- Occurs in infants; rare
- Bilateral –> Potter’s syndrome
- Renal failure
- High BP
- Key associations:
* Liver disease: fibrosis, cysts
* Portal hypertension: ascites
Autosomal Dominant PKD
PKD
- Occurs in adults; more common
- Microscopic cysts present at birth
- Cysts are too small to visualize with U/S
- Kidneys appear normal at birth
- Cysts develop over many years
- Inherited mutation: APKD1 or APKD2 gene
- Key assocation
- Berry aneurysm –> subarachnoid hemorrhage
- Liver cysts
- Mitral valve prolapse
- Young adult
- High BP
- Hematuria
- Renal failure
- Fx of sudden death (aneurysm)
Presentation
Autosomal Dominant PKD
Medullary Cystic Kidney Disease
Cystic Kidney Diseases
- Autosomal dominant disorder
- Cysts develop in medullary collecting ducts
- Most patients do not have cysts
- Fibrosis of kidneys –> small, shrunken kidneys
- Kidneys are enlarged in other cystic diseases
- Often associated with early-onset gout
- Due to inability to properly filter uric acid
- Renal failure
Types of Kidney Stones
Kidney Stones
- Calcium
- Struvite
- Urate
- Cystine
- Flank pain (between ribs & hip)
- Colicky pain (waxes & wanes in severity)
- Hematuria
Signs & Symptoms
Kidney Stones
Kidney Stones
Risk Factors
- High amount of stone substance in blood
- Hypercalcemia
- Hyperuricemia
- Low urine volume
- Usually from dehydration
- Increases concentration of urine substances
Calcium Stones
Kidney Stones
- Most common type of kidney stone (80%)
- Calcium oxalate: most common
- Calcium phosphate
- Key risk factors:
- Hypercalcemia
- High oxalate levels in blood
- Radiopaque –> visible on X-Ray, CT
Calcium Stones
Risk Factors
Most common etiology: idiopathic hypercalciuria
* Hypercalcemia (hyperparathyroidism)
* High oxalate levels
* Crohn’s disease
* Gastric bypass patients
* Ethylene glycol –> produces oxalate
* Vitamin C abuse –> produces oxalate
Calcium Stones
Treatment
- Most stones pass on their own
- Larger stones that do not pass require surgery
- Recurrent stone formers may take prophylactics
* TZ diuretics: decrease Ca2+ in urine
* Citrate: binds Ca2+, inhibits stone formation
Dietary Sodium
Calcium Stones
- Sodium balance
- Sodium intake increases ECV –> turns off RAAS
- Inactive RAAS decreases Na+ resorption in PCT
- Decreased Na+ resorption reduces Ca2+ resorption in PCT
- More serum [Na] = more urine [Ca]
- High Na diet –> increased risk of stone
- Low Na diet –> prevents stone formation