GU + Renal Flashcards
what are the causes of acute nephritis?
- post-infectious (e.g. strep).
- Vasculitis - HSP, SLE, Wegner’s Granulomatosis (ie ANCA +ve),
- IgA nephropathy
- Alport Syndrome- fhx deafness/ renal failure
what are the clinical features of acute nephritis?
decreased urine output + volume overload
HT (which may result in seizures)
oedema - first: periorbital
haematuria (brown urine) + proteinuria
what is the pathophysiology of acute nephritis?
increased glomerular cellularity, reduces blood flow and therefore filtration rate.
what is HSP? How does it present?
Henoch-Schonlein Purpura is characterized by:
symmetrically distrib skin rash- palpable purpura (non-blanching) on extensor surfaces (partic lower limbs). PRESENT IN 100% cases
arthralgia/ arthritis
periarticular oedema
abdo pain
Glomerulonephritis- ie haematuria, proteinuria, red cell casts. (mild- severe forms)
often follows URTI; male > female; 3-15 years old
IgA deposition in small vessels of affected organs with similar histopath of IgA nephropathy. IgA nephropathy as the name suggests is ISOLATED to the kidney unlike HSP.
What is the management including long-term of HSP? What are the possible long term complications of HSP?
Depending on the effect of HSP on their kidneys, the management changes.
- Joint pain + mild/mod abdo pain- analgesics (paracetamol)
- severe oedema- oral pred 1-2mg/kg/day
- severe abdo pain- oral pred 1mg/kg/day
- if proteinuria + reduced GFR: refer to renal + methyprednisolone sodium succinate + prednisolone
- If rapidly progressive nephritis:
methylprednisolone sodium succinate + pred + azathioprine.
followed up for 1 year to detect any ongoing haematuria/ proteinuria.
Due to HSP Nephritis, long term consequences are HT and CKD.
what is the management for acute nephritis?
if post-strep and no HT, no oedema, no electrolyte imbalance just supportive care + phenoxymethyl penicillin, managed OP.
Fluids: no added salt diet, careful input/output monitoring. If oligouric restrict intake to replace insensible losses + previous day’s urine output.
if overloaded w/ HT/oedema furosemide 1-2mg/kg up to BD.
if euvolaemic w/ HT: nifedipine/ amlodipine NO ACEI
if hyperK+: furosemide (if not dehyd), check Ca + bicarb (replace if low), cont Cardiac monitor + K+ check.
what are the initial investigations for a child presenting with acute glomerulonephritis?
URINE Urine Dip, culture, microscopy for casts, protein: creatinine ratio
BLOOD U+E, Creatinine, Ca, P, Cl, Bicarb, Albumin
FBC, antistreptococcal antibody titres (ASOT), C3 + C4 levels (reduced post-strep), ANA antibodies (anti-nuclear)
what are the initial investigations for a child presenting with acute glomerulonephritis?
URINE Urine Dip, culture, microscopy for casts, protein: creatinine ratio
BLOOD U+E, Creatinine, Ca, P, Cl, Bicarb, Albumin
FBC, antistreptococcal antibody titres (ASOT), C3 + C4 levels (reduced post-strep), ANA antibodies (anti-nuclear)
Consider: Renal US, Anti-GBM/ ANCA Ab, other specific to SLE etc if suspected.
What are the causes of nephrotic syndrome? what is its incidence?
minimal change disease (90%)
others: focal segmental glomerulosclerosis, membranous glomerulonephritis
2/100,000
associated atopy + south asian descent
what are the clinical features of nephrotic syndrome? What is the definition of nephrotic syndrome?
Heavy proteinuria –> hypoalbuminaemia + oedema
periorbital oedema partic on waking (early)
scrotal, vulval, leg, ankle oedema
ascites
breathlessness due to pleural effusion + abdo distension
infections e.g. peritonitis, septic arthritis, sepsis due to loss of Ig in urine.
Definition: heavy proteinuria (+++/+ dipstick) or urinary protein:creatinine >250mg/mmol; hypoalbuminaemia <20g/l, oedema.
what are the indicators of fluid overload in kids?
HT, Tachy
oedema, raised JVP, hepatomegaly
respiratory distress due to pulmonary oedema
warm peripheries
what are the indicators of hypovolaemia in kids?
increased cap refill time cool peripheries tachy, HT abdominal pain elevated Urea + Hb
what are the atypical features of nephrotic syndrome that would prompt considering 2nd line therapy?
atypical features indicating unlikely to respond to steroids.
- raised creatinine
- <1 year old >11years old
- macroscopic haematuria
- HT
- fhx nephrotic syndrome
- steroid resistance
- frequent relapsing nephrotic syndrome
how is nephrotic syndrome managed?
- admit
- prednisolone to induce remission + diuresis: 28 day oral course of 60mg/m2/day then tapering course for next 28d to stop.
- ranitidine/ omeprazole if symptoms of gastritis from steroids
- if oedematous/ ascitic slight fluid restriction; if severe + not hypovolaemic, give furosemide
- IV albumin if hypovolaemic +/or severe resistant oedema
- encourage mobilisation to reduce thrombosis risk
- if HT and euvolaemic atenolol/ nifedipine
- if oedematous/ ascitic oral penicilin prophylaxis to prevent pneumococcal infection.
- all kids- pneumococcal immunization
what are the common causes of childhood UTI? what is the incidence of UTI in children?
e.coli, klebsiella, proteus, pseudomonas, strep faecalis
3-7% girls and 1-2% boys will have at least 1 symptomatic UTI before the age of 6 and about 20% will have a recurrence.
