Renal Learning Points CSV Flashcards
(125 cards)
Renal differences in the neonate (6)
(1) nephron number multiplies until 36/40 (increased risk hypertension in preterm)
(2) decreased GFR in preterm
(3) oliguria then polyuria (K wasting in polyuric phase)
(4) ADH increases at birth and can be very high in HIE
(5) renal wasting of bicarb - can be acidotic
(6) renal wasting Calcium
what are nephropathies have low C3
5 S’s: 1. post Strep, 2. MeSangioProliferative/Membranous GN, 3. SLE, 4 Septic (SBE, HBV, HCV) 5. Shunt nephritis
Normal complement nephropathies
4 A’s and H: 1. Alport 2. Anti-GBM (Goodpastures) 3. IgA, 4. ANCA associated (Wegeners) & HSP
When will children with HSP develop nephritis by?
by 6-8 weeks but need to be monitored for 6 months
renal biopsy indications
nephritic/nephrotic at presentation,
persistently impaired/deteriorating renal function,
C3 low at 3 months
IgA nephropathy characteristics
Not inherited
gross haematuria with illness, recurrent,
flank pain,
persistent microscopic haematuria
benign in childhood but HTN in adult - treat with ACEi
Alport syndrome characteristics
hearing loss (age 10),
EYE abnormalities (macular flecks)
recurrent gross haematuria post viral ilness persistent microscopic haematuria,
ESRD late teens
With nephropathies are rapidly progressive?
crescents >50% glomeruli ANCA associated (pauciimmune) Anti-GBM (Goodpastures - pulm-renal syndrome) SLE (systemic symptoms) Membranoproliferative (low complement) HSP (IgA)
Definition nephrotic syndrome & most common cause
Oedema,
Proteinuria (uPCR >200, 3+ protein),
Low Alb <25 .
Most common cause = minimal change disease
what explains oedema in minimal change disease
reduced oncotic pressure and increased sodium reabsorption
Complications of nephrotic syndrome
hypothyroidism, rickets, thrombosis, short stature, anaemia
best way to calculate GFR in clinical setting
plasma disappearance of radio-isotope
**inulin gold standard but only in research setting
when does GFR reach adult values
age 2
Triad of HUS
Thrombocytopenia,
Haemolytic anaemia,
Acute kidney injury
Typical HUS - causes
diarrhoea related - E.Coli 0157:H7 - verotoxin/shiga toxin
Shigella – shiga toxin
HUS Atypical causes
Pneumococcal
*Complement (C3, CD46, factor B, H inhibitors) , *ADAMTS13,
Cobalamin deficiency
*lead to activation of alternative complement
what does ADAMTS13 do
acts to cleave vWF multimers and prevent thrombus formation
Long term sequelae HUS
“Microangiopathy” diabetes,
Hypertension,
Proteinuria
CKD
What is the most predictive risk factor for long term sequelae in HUS
duration anuria >10 days,
prolonged dialysis >7 days
Duration follow-up of HUS? ** need to know
at least 5 years as long term sequelae can occur up to 5 years post apparent recovery
Clues to chronic glomerular causes to CKD
Oligouria,
Haematuria/proteinuria,
Hypertension
Clues to tubular disease for CKD
Polyuria, Polydipsia
Sodium loss,
Enuresis
Progression of CKD can be slowed by?
Control HTN,
Control proteinuria,
Treatment anaemia,
Treatment hyperlipidaemia
Complications CKD
- Growth failure
- Osteopenia
- Anaemia,
- Acidosis (impairs GH release),
- Water and electrolyte imbalance,
- Delayed puberty,
- Social and cognitive.