Hematuria Flashcards
90% of uncomplicated UTIs are caused by ____.
90% of uncomplicated UTIs are caused by E. coli.
The diagnosis of a UTI in a young, otherwise healthy, non-pregnant woman with symptoms of acute uncomplicated cystitis may be made. . .
. . . clinically.
All other forms of UTI require testing.
Findings of glomerular biopsy antibody staining in ANCA-associated nephropathy
No antibodies! Antibodies and immune complex deposition are not a part of the pathology of ANCA-associated nephropathies.
For this reason this is also sometimes called “pauci-immune glomerulonephritis”
Transient hematuria is seen in
- Vigorous exercise
- Sexual intercourse
- Menstruation
- Mild trauma
- UTI
Pathotypes of E. coli
Pathogenesis of UPEC infection
In men, a UTI may spread to the . . .
. . . prostate and epididymis
Questions to ask when evaluating hematuria
- Is it really blood?
- Is it microscopic or macroscopic?
- Is it transient or sustained?
- Is it painful or painless?
- Is it glomerular or non-glomerular?
Patient presents via telemedicine with what you believe to be glomerulonephritis. You are only able to followup several months later, but decide to biopsy. This is what you see. What was the likely etiology?
Post-infectious glomerulonephritis
The very sparse deposition suggests subepithelial ICs that formed in tandem with subendothelial ICs, but the subendothelial portion has been clearned up by invading neutrophils during the patient’s glomerulonephritic episode.
This may present with mild hematuria.
Organisms that commonly cause uncomplicated UTIs
- E. coli
- Proteus mirabilis
- Klebsiella pneumoniae
- Staphylococcus saprophyticus (in young, sexually active women)
- Enterococcus
- Note that most of these are fecal flora
Mechanisms of glomerular damage in glomerulonephritis
- In-situ immune complex formation in the sub-epithelial space due to direct IgG against glomerular basement membrane antigens
- Ectopic immune complex formation and deposition in the sub-endothelial space (may be IgG, IgA, or poly-Ig as seen in Lupus), sometimes with sparse accompanying subepithelial deposits
- ANCA-associated disease. Exact mechanism is not known, but neutrophil hyperactivation is suspected.
Diagnosing ADPKD
- Ultrasound or CT showing unusually large # of cysts given individual’s age
- PKD1 or PKD2 genotyping
What is the likely disease process in this biopsy?
IgA nephropathy
Note the loss of capillary loops and expanded mesangium
Acute uncomplicated pyelonephritis
Renal infection in a woman with a normal GU tract that presents with evidence of a UTI, as well as evidence for upper tract disease including costovertebral angle tenderness, fever, nausea, or vomiting.
Looking for bacteriuria
- Dipstick for nitrate
- Urine culture (~1-2 days)
- Urine gram stain (only 50% sensitive)
Patient presents with nephritic syndrome two weeks following streptococcal infection. Biopsy is performed yielding the below. What is the likely etiology?
Post-infectious glomerulonephritis
Note the spotty, “starry night” pattern of the IgG and C3
Virulence factors of UPEC
Red flags that your hematuria is probably glomerular in origin
- Proteinuria
- Renal dysfunction (elevated creatinine and BUN, reduced GFR)
- Acanthocytic red cells
- NOT crenated red cells
- Red cell cast
Which is a faster onset: Acute nephritic syndrome, or rapidly progressive nephritic syndrome?
Acute.
Go figure. Terrible nomenclature.
Treating acute uncomplicated pyelonephritis
Treating anti-GBM disease and Goodpasture’s syndrome
- Plasmaphoresis to remove anti-basement membrane antibody
- Immunosuppression
Hematuria – Is it really blood? What else can cause red urine?
Cyclophosphamide
Chemotheraueptic that may cause kidney damage, resulting in hemorrhage in the renal tubules and hematuria
Proliferation of parietal epithelial cells in Bowman’s capsule during glomerulonephritis
If the glomerular basement membrane is damaged by infiltrating neutrophils (as it often is in GM), then neutrophils and macrophages may enter the urinary space and induce proliferation of parietal epithelial cells.
This may lead to massive proliferation and a “fibrocellular crescent” which encircle the glomerular channels and compresses them to one wall of Bowman’s capsule.
