Haematuria Flashcards
Features of glomerular haematuria
- brown urine
- presence of deformed red cells
- accompanied by proteinuria
Features of lower urinary tract haematuria
- usually red
- occurs at beginning or end of stream
- not accompanied by proteinuria
- unusual children
Causes of haematuria:
Nonglomerular
- infection (bacterial, viral, TB, schistomiasis)
- trauma to genitalia, urinary tract or kidneys
- stones
- tumours
- sickle cell disease
- bleeding disorders
- renal vein thrombosis
- hypercalciuria
Glomerular
- acute/chronic glomerulonephritis (both usually with proteinuria)
- IgA nephropathy
- familial nephritis e.g. Alport syndrome
- thin basement membrane disease
Investigation of haematuria
- urine microscopy (with phase contrast) and culture
- protein and calcium excretion
- kidney and urinary tract ultrasound
- plasma U&E, creatinine, calcium, phosphate, albumin
- FBC, platelets, coagulation screen, sickle cell screen
Investigations if suggestive of glomerular haematuria
- ESR, complement levels and anti-DNA antibodies
- thoat swab and antistreptolysin O/anti-DNAse B titres
- hep B and C screen
- renal biopsy if indicated
- test mother’s urine for blood (if Alport syndrome suspected)
- hearing test (if Alport syndrome suspectec)
Indications of renal biopsy in haematuria:
- significant persistent proteinuria
- recurrent macroscopic heamturia
- renal function is abnormal
- complement levels are persistently abnormal
What is acute nephritis?
Increased glomerular cellularity restricts glomerular blood flow, and therefore glomerular filtration is decreased. This leads to:
- decreased urine output and volume overload
- HTN which may cause seizures
- oedema, characteristically initially periorbital
- haematuria and proteinuria
Causes of acute nephritis?
- post infectious (inc streptococcus)
- vasculitis (HSP or SLE (rare)), Wegener granulomatosis, microscopic polyarteritis, polyarteritis nodosa
- IgA nephropathy and mesangiocapillary glomerulonephritis
- antiglomerular basement membrane disease (Goodpasture syndrome) v rare
Management of acute nephritis
- attention to water and electrolyte balance and use of diuretics when necessary
- Irreversible CKD may occur if left untreated
What is post-streptococcal nephritis?
usually follows a streptococcal sore throat or skin infection and is diagnosed by evidence of a recent streptococcal infection and low complement C3 levels that return to normal after 3/4 weeks
What is Henoch-Schonlein purpura
Combination of:
- characteristic skin rash on extensor surfaces
- arthralgia
- periarticular oedema
- abdominal pain
- glomerulonephritis
Epidemiology of HSP
- usually occurs between 3-10 years
- M:F = 2:1
- peaks during winter months
- often preceded by an URTI
Cause of HSP
unknown
- ? genetic disposition and antigen exposure increase circulating IgA levels and disrupt IgG synthesis, which interact to produce complexes that activate complement and are deposited in affected organs, precipitating an inflammatory response with vasculitis
Clinical presentation of HSP
- fever
- rash symmetrically distributed over the buttocks, extensor surfaces of the arms and legs and the ankles. Urticarial, rapidly becoming maculopapular and purpuric and is palpable.
- joint pain (2/3 pts), particularly knees and ankles with periarticular oedema
- colicky abdominal pain
- over 80% have microscopic or macroscopic haematuria or mild proteinuria.
Risk factors for progressive CKD?
- heavy proteinuria
- oedema
- hypertension
- deteriorating renal function
biopsy to determine if treatment is necessary
