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
Struvite Stones
Kidney Stones
- 2nd most common type of kidney stone: 15%
- NH3-Mg-PO4 stones
- Consequence of UTI
- Urease-positive bacteria: Proteus, Staph, Klebsiella
- All hydrolyze urea to ammonia
- Alkaline urine –> promotes stone formation
- Can form staghorn calculi
- Stones form a cast of renal pelvis & calyces
- Cannot pass on their own –> require surgery
- Untreated –> bacterial reservoir
* Results in recurrent infections
- Radiopaque –> visible on X-Ray, CT
- UTI symptoms: dysuria, frequency
- Mild flank pain
- Hematuria
- Large, branching staghorn stone on imaging
Presentation
Staghorn Calculi
Uric Acid Stones
Kidney Stones
- Caused by high uric acid in urine or acidic urine
- H+ + Urate- –> Uric Acid
- Lowest urine pH is in distal tubule / CD
- Radiolucent stones –> not visible on X-Ray
- Can see with CT scan
Uric Acid Stones
Risk Factors
- High uric acid levels
* Gout
* Leukemia
* Myeloproliferative disease - Acidic urine –> precipitates uric acid
- Chronic diarrhea
- More common in hot, arid climates
- Low urine volume & pH more common
Uric Acid Stones
Treatment
Dissolve stone
* Hydration
* Alkalization of urine: HCO3-
Cystine Stone
Kidney Stones
- Seen in children with cystinuria
* Tubular defect –> impaired cystine resorption - Also form staghorn calculi
- Treatment: hydration & alkalinzation of urine
Renal & Bladder Tumors
Urinary Tract Tumors
- Renal Cell Carcinoma (RCC)
- Wilms’ Tumor
- Renal Angiomyolipoma
- Transitional Cell / Urothelial Carcinoma (TCC / UC)
- Squamous Cell Carcinoma (SCC)
- Adenocarcinoma
Most common kidney tumor
* Epithelial tumor
* Commonly arises from proximal tubule cells
Renal Tumors
RCC
- Sex: M > F
- Age: 50-70 years
- Cigarette smoking
- Obesity
Risk Factors
RCC
- Classic triad (< 10% of patient):
* Hematuria
* Palpable abdominal mass
* Flank pain - Many patients have fever, weight loss
- Many pts are asymptomatic until advanced disease
* 25% have mets / advanced disease at presentation
Presentation
RCC
- Invades renal vein
- Can block drainage of spermatic vein on left
- Left varicocele = classic finding
- Not right –> R. spermatic drains directly to IVC
- Spreads through venous system
- Common sites for mets:
- Lungs
- Bone
- Can also spread to retroperitoneal lymph nodes
Spread / Metastases
RCC
- Polycythemia –> increased Hct
- EPO production by tumor
- Hypercalcemia
- Tumor production of PTH-related peptide
- Increased Ca resorption from bone
- Hypertension
- Renin production by tumor
- Cushing’s Syndrome
- ACTH production by tumor
- Look for weight gain, HTN, hyperglycemia
Paraneoplastic Syndromes
RCC
Most common type of RCC
Pathology
Clear cell carcinoma
* Cells filled with glycogen & lipids
RCC
Genetics
Associated with chromosome 3 gene deletion
* Von-Hippel-Lindau (VHL) gene
* Sporadic mutation
* Single tumor
* Older patient, usually smoker
* Inherited mutation
* Younger patient
* Multiple, bilateral tumors
VHL Disease
RCC
Autosomal dominant VHL gene inactivation
* Diffuse tumors:
* RCC
* Cerebellar hemangioblastoma
* Retinal hemangioblastoma
RCC
Treatment
- Surgical resection in early disease
- Poorly responsive to CTX / radiation
- Recombinant cytokine: IL-2
* Side effects: hypotension, fevers, chills
Most common renal malignancy of young children
* Proliferation of metanephric mesenchyme
* Embryonic glomerular structures
Renal Tumors
Wilms’ Tumor
Wilms’ Tumor
Genetics
Associated with loss of function mutation in chromosome 11
* WT1 tumor suppressor gene
* May be sporadic, often part of a syndrome
WAGR Syndrome
Wilms’ Tumor
WT1 gene deletion in chromosome 11
* Wilms’ tumor
* Aniridia = absence of iris
* Visual problems
* Genital anomalies
* Cryptorchidism
* Ambiguous genitalia
* Mental retardation
Benign tumor of blood vessels, smooth muscle, and fat in young children
* Associated with tuberous sclerosis
Renal Tumors
Renal Angiomyolipoma
Most common tumor of urinary tract system
* Most common type of bladder cancer
* Locations:
* Bladder: most common
* Also can occur in renal calyces, pelvis, ureters
* Often multifocal & recurrent
* “Field defect”: damage to entire urothelium
Urinary Tract Tumors
Transitional Cell Carcinoma (TCC)
- Smoking
- Cyclophosphamide
- Phanacetin
- Aniline dyes (hair dyes)
- Workplace exposures:
- Rubber, textiles, leather
- Naphthaline (industrial solvent)
- Painters, machinists, printers
Risk Factors
TCC
TCC
Diagnosis
Cytoscopy & biopsy
TCC
Treatment
- Surgical resection
- Radiation
- CTX: combination Tx with platinum-based regimens
* Cisplatin
* Carboplatin
SCC
Bladder Cancers
- Rare bladder cancer
- Requires chronic inflammation of bladder
- Key risk factors:
* Recurrent kidney stones / cystitis
* UTI with Schistosoma haemotobium
Schistosoma haematobium
SCC
Trematode found in Africa & Middle East (Egypt)
* Acquired from freshwater containing larvae
* Penetrate skin & migrate to liver for maturation
* Adult infect bladder
* Usually causes hematuria
* Chronic bladder infection can result in SCC
Adenocarcinoma
Bladder Cancers
- Very rare bladder cancer
- Glandular prolieration in bladder
- Occurs in special circumstances
* Urachal remnant
* Long history of cystitis
* Bladder exstrophy
- Syndrome caused by muscle necrosis
- Can lead to renal failure & death
Rhabdomyolysis
Causes of Muscle Damage
Rhabdomyolysis
- Intense physical exercise –> especially if dehydrated
- Crush injuries: trauma
- Drugs: statins, fibrates
Muscle Contents
Rhabdomyolysis
- Creatine kinase
- Elevated levels are hallmark of rhabdo
- Aldolase
- LDH
- AST / ALT
Muscle Contents
Rhabdomyolysis
- Creatine kinase
- Elevated levels are hallmark of rhabdo
- Aldolase, LDH, AST / ALT
- Potassium & phosphate
* Hyperkalemia & hyperphosphatemia in rhabdo - Purines –> metabolized to uric acid in liver
* Can lead to hyperuricemia - Myoglobin –> binds oxygen for use by muscle
* Contains heme
Renal Toxicity
Myoglobin
- Obstructs tubules
- Toxic to proximal tubular cells
- Vasoconstriction –> especially in medulla
- Leads to hypoxia
- Muscle pain
- Weakness
- Dark urine
Presentation
Rhabdomyolysis
* Dark urine due to myoglobin
Rhabdomyolysis
Diagnosis
- Creatine kinase
* Normal: <250 IU/L
* Rhabdo: >1,000 IU/L - Urinalysis for heme
- Positive dipstick = hemoglobin or myoglobin
- Microscopy for RBCs
- No evidence of RBCs
