Renal Flashcards
what is ORTHOSTATIC PROTEINURIA?
risk groups?
is a condition where an abnormally large amount of protein is excreted in the urine when the patient is in an upright position and normal protein excretion in the supine position
It usually occurs in tall, thin adolescents
How is ORTHOSTATIC PROTEINURIA diagnosed?
the patient has no proteinuria in early morning samples but has low-grade proteinuria (less than 1g/24h) at the end of the day.
diagnosis of orthostatic proteinuria is made by collecting the urine from the first morning void after the patient has been recumbent overnight.
It is associated with good long-term prognosis.
what are the criteria for AKI in a child?
o Increased serum creatinine >28mmol/L/24 hours
o >50% rise in serum creatinine in past 7 days
o Fall in UO to <0.5ml/kg/hr (oliguria)
o 25% fall in eGFR within past 7 days
How would we ivx suspected AKI?
Blood test;
U&E:
- An acutely rising Creatinine may be the only sign.
- compare creatinine to baseline if you can
FBC;
- Hb; anaemia - multiple myeloma, HUS, vasculitis
- platelets - low in TTP
- WCC; high/low in sepsis
US;
- obstruction of the urinary tract
- small kidneys - chronic kidney disease
- large, bright kidneys - loss of cortical medullary differentiation typical of an acute process.
how may AKI present?
what are some signs?
AKI is often asymptomatic so is easily missed
OR:
Suspected or confirmed sepsis
Hypovolaemia (with or without hypotension) - may be related to dehydration or over-diuresis
Hypotension
Oliguria (urine output <0.5ml/kg/hour)
Acute rise in early warning score (e.g., NEWS2 >5)
How do we treat AKI?
Pre-renal; 80% due to hypovolaemia
- Fluid resus - give bolus. wide bore cannula
Renal:
Review meds - eg nephrotoxic ones; NSAIDs
Treat underlying cause and complications - sepsis 6 etc
A. Fluid restriction + challenge with a diuretic
B. High calorie, normal protein diet to reduce uraemia and high K+
C. rapidly progressive glomerulonephritis -steroids/immunosuppression.
D. Treat electrolyte imbalance
Postrenal failure:
1. assessment of the site of obstruction
and relief by nephrostomy or bladder catheterization.
2. surgery once stabilised
Monitoring;
Monitor growth,
anaemia (decreased EPO),
phosphate (causes increased PTH and bone damage),
How do we treat metabolic acidosis in AKI?
sodium bicarbonate
How do we treat hyperphosphataemia in AKI?
calcium carbonate
diet restriction - High calorie, normal protein
How do we treat hyperkalaemia in AKI?
Calcium gluconate if ECG changes
Salbutamol (nebulized or intravenous)
Calcium exchange resin
Glucose and insulin
Dietary restriction - High calorie, normal protein
Dialysis
what are the causes of AKI?
Pre-renal;
• Hypovolaemia:
– gastroenteritis
– burns
Renal;
Vascular: – vasculitis, HUS
HUS - most common cause of AKI in previously healthy child
- Tubular: – acute tubular necrosis
- Glomerular: – glomerulonephritis
- Interstitial: – interstitial nephritis
Post-renal;
Calculi, congenital obstruction, blocked catheter
what is glomerulonephritis?
a term used to refer to several kidney diseases (usually affecting both kidneys). Many of the diseases are characterised by inflammation either of the glomeruli
not all conditions involve inflammation
what are the forms of glomerulonephritis and which conditions are classed as this?
- Primary causes;
(Non-proliferative (no change in cell number)):- cause nephrotic syndrome -
a. Minimal change disease - 90%
b. Focal segmental glomerulosclerosis
c. Membranous glomerulonephritis/nephropathy
- Secondary; diabetes, SLE, post-infectious, Hepatitis, Malaria etc
Proliferative:
- cause nephritic syndrome -(presents -> haematuria)
IgA nephropathy
Post-infectious / Post-streptococcal
Membranoproliferative
Rapidly progressive glomerulonephritis:
- quick detioration in renal function -
Goodpastures
Granulomatosis with polyangiitis
Immune complex mediated
etc
what is the commonest cause of Post-infectious glomerulonephritis ?
Streptoccocus! - Pyogenes
- antistreptolysin O found
Characterise Minimal change disease;
epidemiology, ivx, mx
Children 2-4y,
-> causes 90% of nephrotic syndrome presentations
• Normal renal function / complement / BP
• Associated atopy – usually responds to high dose steroids - prednisolone
no progression to CKD
ivx: A. FBC - U&Es - normal - Hb/haemotocrit high in volume depletion 1. Urinee dip - proteinuria 2. Serum albumin - low 3. serum lipid - high 4. Serum complement - normal 5. GFR - norrmal 6. LFTs - normal
Others:
7. Biopsy
A. light microscopy - no visible changes in the glomerulus
B. electron microscopy - within the glomeruli may show a fusion of the foot processes of the podocytes
what is the definition of nephrotic syndrome in kids?
Nephrotic syndrome is defined as the presence of proteinuria (>3.5 g/24 hours - changes in kids! -> 40mg/sqm/hr per)
hypoalbuminaemia (<30 g/L adult) <2.5g/dL?
and peripheral oedema
tests/ivx for nephrotic syndrome?
tests for glom; urine dip, serum albumin, cholesterol, creatinine clearance test
light and electron microscopy
renal biopsy - for confirming histology
- Urine protein dipsticks and quantification (24h sample or protein:creatinine ratio)
- GFR
- FBC, ESR, U&Es, creatinine, albumin
- Complement
- Antistreptolysin I or anti-DNAase B titres, throat swab (often precipitated by respiratory infections)
- Urine MCS
- Urinary Na conc
- Hep B or C
- Malaria screen if travel
Characterise focal segmental glom;
epidemiology, ivx, mx
Segmental scarring and foot process fusion,
common in older children
Presentation;
• Haematuria, HTN, impaired renal function
MX – 50% respond to steroids
ivx:
microscopy - areas of mesangial collapse and sclerosis
tests for glom; urine dip, serum albumin, cholesterol, creatinine clearance test
RENAL BIOPSY - confirms
Characterise membranous nephropathy;
basement membrane thickening without associated cellular proliferation or infiltration
has primary and secondary causes
IVX
- diffuse, granular IgG deposition throughout the capillary walls
- electron microscopy - electron dense deposits in the subepithelial space.
- New basement membrane growth - classic ‘spike and dome’ appearance.
how do we mx Nephrotic syndrome?
First line: Corticosteroid - Prednisolone
2nd line drug (if no response to prednisolone):
- Cyclosporin (immunosuppresant)
- then consider doing Renal biopsy
Also:
Prophylactic trimethoprim – for early phases of treatment due to immunosuppression
Others:
• Correct the water and electrolyte balance
- Albumin infusion
• Treat oedema - diuretics and potassium supplement
• BP management, dietary advice, lipid lowering therapy
• Antithrombotics
• IVIG
• Dialysis If haematuria or proteinuria with no obvious cause → think acute nephritis and refer to nephrology team
haemo - home
peritoneal - centre
list some clinical signs of nephrotic syndrome?
- Periorbital oedema – earliest sign
- Scrotal or vulval, leg, ankle oedema
- Ascites
- Breathlessness due to pleural effusions and abdo distension
what is the efficacy of steroids in the mx of nephrotic syndrome?
- 90% resolves with corticosteroid (oral prednisolone)
- 4 weeks, high dose, 4 weeks, reduced dose
Steroid sensitive nephrotic syndrome
• Most commonly 1-10yo
• No haematuria, normal BP/complement/renal function
• If unresponsive after 8 weeks, renal biopsy may be indicated
• Complications → hypovolaemia, thrombosis, infection, hypercholesterolaemia
10% - Steroid resistant nephrotic syndrome
• Refer to paediatric nephrologist
• Require diuretics, salt restriction, ACEI (BP control), NSAIDS - reduce rate of renal decline
what are the causes of Steroid resistant nephrotic syndrome ?
focal segmental glomerulosclerosis FGS (most common);
mesangiocapillary glomerulonephritis (older children and haematuria,
decreased complement,
membranous nephropathy (associated with hep B or SLE
what is the cause of CKD in kids?
Most common causes are those that are congenital
- congenital dysplasia
- inherited renal disease (e.g., autosomal recessive polycystic kidney disease and Alport syndrome)
- reflux nephropathy (when VUR leads to scarring of kidneys)
- chronic glomerulonephritis (e.g., IgA nephropathy)
how does renal failure typically present in kids?
o Oliguria or anuria
o Discoloured urine – brown
o Oedema – feet, legs, abdo, weight gain
o Fatigue, lethargy, N&V
What is WILMS TUMOUR / NEPHROBLASTOMA ?
Wilms tumour originates from embryonal renal tissue
and is the most common renal tumour of childhood.
what is the epidemiology of WILMS TUMOUR
Over 80% of patients present before 5 years of age and
it is very rarely seen after 10 years of age.
how does a WILMS TUMOUR present?
Haematuria - BRIGHT RED BLOOD
-> usually only presenting sx (so initially they thinks it’s UTI)
Abdominal mass - incindental find usually
Uncommon: Abdominal / Flank pain Anaemia (haemorrhage into mass) Hypertension Anorexia
5% bilateral
how do we ivx a WILMS TUMOUR?
Initially (what I saw on wards):
• Urinalysis - rule out UTI, gross or microscopic haematouria
•US kidney or IV pyelogram +/- renal angiography
• CT or MRI :
- (staging)
- shows an intrinsic renal mass distorting the normal structure.
• renal biopsy as it may worsen condition? (Was done when I saw it)
-confirms the diagnosis with characteristic pathological appearances
• Renal function - normal or elevated creatinine if very abnormal - bilateral
• FBC - normal or Anaemia - normocytic n chromic
——————
• Genetic studies - WT1 tumour suppressor inactive
