what is the normal GFR
120-130 ml/min
take as 100ml/min
decraeses with age
what are the 2 equations used in calculating renal
Cockcroft-gault equaiton
- uses age, weight, sex, serum creatinine levels
- calculates CrCl
CKD-EPI equation
- uses age, weight and serum creatinine
- increasingly used ot categorise CKD
- estimate of GFR –> eFGR
what is the definition of renal failure
it is the deterioration of renal funciton, leading to signs and symptoms
- azotaemia = increased concentration of nitrogenous substances and this reflects a decreased GFR (BIOCHEMICAL PRESENTATION)
- uraemia = toxic effects of the nitrogenous substances (CLINICAL PRESENTATION) plasma urea concentration increase
what can renal failure be classified into
- time of onset (acute - days/weeks vs chronic > 3 months)
- location (pre-renal, renal and post-renal)
criterion for AKI
- serum cr increased 0.3 mg/dL over 24h
- serum cr increased x 1.5 ULN within 1 week
- urine output < 0,5ml/min/kg over past 6h
pre-renal
intrarenal and
post-renal
give some examples that can cause renal failure
pre-renal - decreased circulating volume (volume depletion, e.g. vomiting, diarrhoea) and decreased renal perfusion pressure (e.g. renal artery stenosis)
renal - vascular/glomerular, acute tubular necoris (prolonged tubular hypoperfusion leading to intrinsic renal damage( , acute interstitial necrosis (autoimmune)
post-renal - outflow blockage, urethral or bladder blocks s (BPH, strictures)
complications of AKI
- metabolic acidosis (clinically presenting as increased resp rate)
- hyperkalaemia
- uraemia (can lead to encephalopathy and pericarditis)
- fluid overload (fluid retention signs - oedema), heart failure and pulmonary oedema
what are some causes of chronic kidney disease
diabetic nephropathy
hypertensive nephropathy
glomerulonephritis
presentations of CKD
- fatigue and pallor (anaemia)
- foamy urine (proteinuria) and haematuria
- nausea, loss of appetite, pruritus
- oedema, hypertension (due to fluid retention stimulating the RAAS, renal scarring and subsequent focal renal ischaemia - increased renin and hypertensio further causing glomerular damage, decreased GFR)
- peripheral neuropahty
what are the 2 diagnostics for CKD
- eGFR < 60 ml/min/1,73m2
- urine albumin:creatine ration (ACR) > 3mg/mmol
biochemical abnormalities in CKD (short term)
- hypernatremia (decreased Na clearance, leading to oedema and hypertension)
- urine becomes iso-osmotic (inability to concentrate or dilute the urine)
- hyperkalemia
- acidosis - due to renal tubular acidosis and / or high anion gap (AG)
long-term complications of CKD (5)
- bone disease (renal osteodystsrophy)
- hypocalcaemia: vitamin D activated into calcitriol in the kidney, cannot absorb calcium from diet
- secondayr hyperparathyroidism: decreased Ca level increased PTH, causing increased bone resorption
- hyperphosphataemia: decreased secretion, contributing to hypoCa
- acidosis: due to bone acting as buffer, increased PTH demineralises the bone - anaemia - decreased EPO production
- dyslipidaemia - increasing risk of CVDs
- hypertension - due to renin secretion
- endocrine - hyperPRL and hypergonadism (hyperPRL due to decreased renal excretion of PRL and uremic toxins accumulation, impariing the HPA axis)
bone issues
- bone disease (osteomalacia, osteoporosis, osteitis fibrosa cystica, adynamic bone disease)
- metastatic calcification (deposition of calcium phosphate crystal) on soft tissues, arteries and viscera
what is the presentation of nephrotic syndrome
- proteinuria
- hypoalbuminaemia
- oedema
- hyperlipidaemia and lipiduria
what is the presentation of nephritic syndrome
- haematuria (red cell casts)
- azotemia
- oligouria
- mild to moderate hypternsion
- proteinuria, oedema
what is the difference btwn nephrotic and nephritic syndrome
what are the causes of nephrotic syndrome (got 5)
- minimal change disease
- focal segmental glomerulonephritis
- membranous nephropathy
4.. membranoproliferative GN - systemic - diabetic, HSP, lupus, GPA/MPA
what are the causes of nephritic syndrome (4. 4)
children:
1. IgA nephropathy (Berger’s disase)
2. acute proliferative GN (post-strep),
3. Henoch-Scholein Purpura (HSP)
4. HUS
adults
1. rapidly progressive GN (cresenteric, RAPGN)
- goodpasture (type 1), anti-GBM (type 2)
2. membranoproliferative GN
3. SLE, IE
4. ANCA-mediated vasculitis
obstructive causes of kidney - go
increases risk of stone formtaion and infection, and can lead to permamny renal atrophy if not cleared
congenital or acquired
congenital can be: posterior urethral valves or urethral stricture
acquired can be:
tumours, BPH
renal stones
pregnancy uterine collapse
neutrogenic (e.g. spinal cord issues)
are men or female more likely for renal sontes
arise from naywhere in the urinary tract but mainly from kidney
male, 30-60y
genetics can play a rile
- primary hyperoxaluria or cystinuria
