Week 14 Renal Flashcards
(100 cards)
3 ways to measure urinary protein excretion
24 hour urine collection
Spot sample (in morning) - protein:creatinine ratio
Albumin:creatinine ratio
3 most important measurements for kidney function
Creatinine
Urea
eGFR
Ideally, substance would be freely filtered at golmerulus, not secreted or absorbed
Creatinine
Muscle breakdown prouduct
More sensitive than urea
However affected by:
Muscle mass (higher with high muscle mass)
Plasma volume (increases when dehydrated)
Diet (increaes in high protein diet)
15% secreted by tubules
Urea
40% reabsorbed
Increased in diet high in protein or if there is GI bleed (as blood is digested to protein to urea)
Increased in dehydration (reabsorbed in proximal tubule)
Increased in tissue breakdown e.g. corticosteroids
Lowers in liver failure (as liver produces urea)
Glomerular filtration rate defintion
Volume of plasma which would be cleared of that substance per unit time
urine conc of substance x urine vol divided by plasma conc of substance
(ml/min)
MDRD4 formula
Estimatation of GFR from plasma creatinine conc (eGFR)
Based on:
Creatinine conc
Age
Sex
Race
(ml/min per 173m2)
Relationship between eGFR and creatinine
As eGFR falls, creatinine increases
However, can lose 50% kidney function before creatinine increases
Why can’t eGFR be used for AKI?
eGFR assumes stable renal function
(so not sutiable for AKI)
Important for drug dosing
Glomerulonephritis
Group of inflammatory diseases involving glomerulus and tubules
Primary: limited to kidney
Secondary: due to underlying cause e.g.
- infections: HIV
- inflammatory conditions: IBD, RA,
- drugs: NSAIDs
- malignancy: lung cancer
Symptoms: Haematuria, oliguria, oedea, HTN
Pathophysiology:
Glomerular injury caused by inflammation due to extrinsic or intrinsic factors:
Extrinsic: antibodies, complement
Intrisnic: cytokines, growth factors
Examples:
IgA Nephropathy
Membranous GN
Minimal change disease
RPGN (rapidly progressing glomerular nephritis)
Clinical presentations of glomerulonephritis
Nephritic: blood and protein in urine, high BP, rising serum creatinine
proliferative/acute inflammation
IgA/lupus nephritis
Nephrotic:
>3.5 proteinuria, low seurum albumin, oedema
Non-proliferative/podocyte damage
Minimal change disease 1, membranous
Rapidly progressing glomerulonephritis
Rapidly increasing serum creatinine, crescentic damage
Vasculitis, lupus nephritis
3 features of nephrotic syndrome
>3.5g proteinuria (per 24hrs)
Low serum albumin <30
Oedema
Also have hyperlipidaemia, risk of venous thromboembolism, hypercoagulable state (due to loss of anti-thrombin III)
IgA nephropathy
Most common primary glomerular disease
Can be precipitated by infection - synpharyngitic (occurs same time as pharyngitis)
May be secondary to ceoliac disease, cirrhosis
Pathophysiology:
Abnormal/overproduction of IgA which deposit in mesangial cells leading to mesangial proliferation
Symptoms:
Haematuria, HTN, proteinuria
1/3 progress to ESRF
Treatment: ACEi
Membranous GN
Presents with nephrotic syndrome
Most common in caucasians
Primary: idiopathic
Secondary: Malignancy (e.g. lung cancer), drugs (e.g. NSAIDs), SLE
Pathophysiology:
Immune complexes deposited into glomerular BM - thickening and damaging BM - increased permeability - proteinuria
70% pts with Anti-phopholipase A2 receptor antibody (PLA2R) (protein on podocytes)
Variable history:
1/3 resolve, 1/3 progress to ESRF, 1/3 persistent proteinuria, maintain GFR
Treatment:
Treat underlying disease if secondary
Non-immunological: ACEi, statins, diuretics, low salk diet
Immunological: Steroids, cyclophosphamide, ciclosporin, rituximab (Anti-CD20 (B cells))
Minimal change disease
Commonest form of GN in children, characterised by minimal histological changes
Causes nephrotic syndrome (proteinuria, oedema, hypoalbuminaemia, hyperlipidaemia)
First presentation: periorbital oedema
GFR normal
Primary: idiopathic
Secondary: malignancy
May occur after URTI
Pathogenesis: T cell mediated. Podocytes fuse/merge together, causes leakiness of protein into urine
Normal glomeruli on H and E stain
Assoc. with Hodgkin’s Lymphoma
Treatment: Prednisolone (as damaged mediated by cytokoines due to T cells)
Rapidly progressing glomerulonephritis
Group of conditions which show golmerular crescents on kidney biopsy
Aggressive - 90% pts progress to ESRF
Causes: ANCA vasculitis (small vessel vasculitis) e.g. granulomatous with polynagiitis, Lupus nephritis, Goodpasture’s syndrome (antibodies to glomerular BM), post-infection, Henoch Schonlein Purpura
Investgiations for Glomerulonephritis
UEs, urine dip, 24- hour urine collection (quantify protein), serum albumin, renal US
Glomerulonephritis screen:
HbA1c/plasma glucose - diabetic nephropathy
ANCA - vasculitis
PLA2R - membranous GN
ANA,complement - lupus
Kidney biopsy: required for clinical diagnosis of glomerulonephritis
- biopsy cortex, examine:
light microscopy: structure
immunofluorescnece: Ig, complement
electron microscopy: BM, deposits
Systemic diseases assoc with renal disease
Diabetes
Atheromatous vascular disease
Amyloidosis
SLE
How do systemic diseases present in kidneys?
AKI (creatinine increases)
CKD
Proteinuria
Nephrotic syndrome (creatinine normal, proteinuria)
Nephritic syndrome (high creatinine, blood/protein in urine)
Risk factors for UTI
Less than 1 yrs old
50% children with UTI have congenital renal tract abnormality (commonly vesico-ureteric reflux)
Females - sex
Men - prostate enlargement
Diabetes
Immunosuppression
UTI in childhood - incidence vs age
Males 50% <1 yrs
Females >80% >1yrs old (more common due to short urethra)
UTI symptoms of upper vs lower
Pyelonephritis (Upper urinary tract infection)
Bacteriuria and fever >38
Bacteriuria and loin pain, fever <38
Symptoms:
Fever, general malaise, loin pain
Cystitis (lower urinary tract infection)
Bacteriuria, symptoms UTI not systemic
Symptoms: Abdo pain, urgency, frequency
Investigations UTI
Urine dip stick
Lecuocyte esterase (LE) - correlates with WBCs
Nitrites (bacteria convert nitrates into nitrites)
Microscopy/flow cytometry
Urine culture - gold standard. Required for all children <3yrs before antibiotics.
> 10^5 CFU (colony forming units)
Most common organisms: E.coli, Klebsiella, proteus (stone former), streptococcus (gram +ve)