Hematuria Flashcards
Glomerular vs extraglomerular hematuria
Glomerular: nephritic, IgA nephropathy
Extra-glomerular: renal carcinoma, BPH, UTI, prostate cancer, kidney stones, exercise
Risk factors for malignancy in pts w/ gross hematuria
Smoking
Renal:
Cystic Disease
Obesity
Toxins: asbestos, cadmium, leather tanning & petroleum products
Bladder: Schistosomiasis Hx radiation treatment to pelvis Cyclophosphamides Exposure to hydrocarbons, tryptophan metabolites, industrial chemicals, aromatic amines, chemicals in rubber
Work up for hematuria
** Always work up gross***
Hx
Physical: abdo and kidney
Investigations: Urinalysis, Urine C & S Urine microscopy to confirm presence of intact RBCs and RBC casts Urine Cytology Bladder scan US Abdo & Pelvis Cystoscopy
Pathophysiology of stone
Solutes in urine precipitate and crystallize
Increased solute or decreased solvent
Most common stone
Calcium stones (calcium oxalate)
Causes of UTI
Stasis and obstruction: (reflux, medication, BPH, urethral stricture, neurogenic bladder, stone)
Foreign body: catheter/other instrumentation
Decreased resistance to organisms: DM, malignancy, low estrogen, immunosuppression, etc.
Other factors: trauma, anatomic abnormalities, female, sexual activity, menopause, fecal incontinence
Most likely bacteria UTI?
Ascending (95%): bacteria colonizes mucosa
Most common: E.coli, Staphylococcus, Klebsiella, Proteus Enterobacter
Pathophysiology of nephritic syndrome
Deposits in sub-endothelial or mesangial cells
ALWAYS inflammatory
++ hematuria
Features of nephrotic
Proteinuria, Edema, hyperlipidemia, Frothy Urine, serum albumin low
Features of nephritic
HTN, hematuria, red blood cell casts, azotemia
Abrupt onset
Features of nephritic
HTN, hematuria, red blood cell casts, oliguria
Abrupt onset
Investigations for renal colic
Ultrasound
CT (non-contrast)- more common
Common Nosocomial
Pseudomonas, Enterococci, Enterobacter, Candida albicans, Staphylococcus epidermidis, Corynebacterium species
IgA nephropathy
Most common nephropathy; mixed nephritic and nephrotic
Immune complex deposition (IgA) in the mesangial cells
Post-infectious glomerulonephritis
Nephritic
Inflammation of glomeruli
Complication of bacterial infection (Group A streptococcus infection, impetigo)
More common in children
Lupus nephritis
Nephrotic and Nephritic
Caused by SLE
Immune cells attack –> antibodies (antinucular ) –>
deposit in kidney –> initiate inflammatory rxn
Henoch-Schönlein purpura
Vasculitis of small vessels (IgA associated)
Exposure to allergen/ antigen (infection, drugs) → stimulation of IgA production →deposition of IgA immune complexes in vascular walls → activation of complement → vascular inflammation and damage
Goodpasture syndrome
Anti-GBM–associated acute glomerulonephritis
Autoimmune disease affecting the lungs and kidneys; Nephritic syndrome
Damaging basement membrane–> causing hemoptysis and hematuria
Wegener’s granulomatosis with polyarteritis
Vasculitis of medium sized cells
Necrotizing granulomatous inflammation, small and medium sized vessel vasculitis
Upper and lower respiratory tract, kidneys are affected
Indications of Dialysis
AEIOU Acidosis Electrolyte abnormalities Intoxication Overload of fluid Uremia
Autosomal Dominant Polycystic Kidney Disease
Hereditary disorder of renal cyst formation causing gradual enlargement of both kidneys
Multisystem disorder - associated with cysts in other organs, such as liver, pancreas, and arachnoid membranes
In response to low flow to the kidney which arterioles constrict?
Efferent
GFR determinants
Hydrostatic pressure - driving force for out of vessels - increases GFR
Oncotic pressure - pulling force into vessels - drops GFR
Basement membrane function
Renal artery blood pressure - not a linear correlation due to the autonomic correction
- myogenic reflex - reflex constriction (like any other arteriole)
- Ang2 reflex - renin - RAAS - EFF - increases GFR
- tubuloglomerular feedback (macula densa feedback either adenosine or NO on the AFF arteriole)
Glomerulotublar balance
In response to tubuloglomerular feedback (macula densa/JGA) there can be an increase in GFR, but if the tubules did not respond then there would be ++ loss of fluid as it transited too fast to the distal tubules
SO
The proximal tubules act intrinsically to proportionally increase resorption. Can also act as an extra layer of protection if there is a sudden change in GFR
In other words - Glomerulotubular balance is the action of the tubules in response to GFR (glomerulus) change
Tubuloglomerular feedback is the sensing from the tubules to change the GFR (glomerulus)
Approach to an AKI
Take out nephrotoxins, US, urine study, volume and acid base study, get a serum Ca/phos/uric acid
(Basically make sure it isn’t pre- or post- renal before sending to a nephrologist)
++Albuminuria?
Indicated glomerulus disease (not filtering well at the start)