Chronic kidney failure Flashcards
List some DDx for a presentation of:
- 27yo F
- fatigue
- pallor
- nocturnal diuresis
- elevated urea and creatinine
- urine: protein, nil haematuria, glucose, hyaline casts
- hx recurrent pyelonephritis in childhood
PDx. chronic kidney failure secondary to reflux nephropathy
DDx.
Nephrotic syndrome (proteinuria, hypoalbuminaemia)
- minimal change disease (most common children)
- membranous nephropathy (most common adults)
- focal segmental glomerulosclerosis
- amyloidosis
- diabetic glomerulonephropathy
Nephritic syndrome (haematuria, HTN, urea/creatinine, oliguria)
- acute post-strep GN
- rapidly progressive GN
- diffuse proliferative GN
- IgA nephropathy
- Alport syndrome
- membrano-proliferative GN
AI disease- SLE
Malignancy- RCC, mets
Obstructive- renal calculi, prostatic disease
List some causes of polyuria?
1) increased osmotic load (e.g. DM)
2) fluid overload- increased fluid intake, oedematous states (e.g. CCF)
3) Diuretics- dietary (caffeine, ETOH), medical
4) decreased renal concentrating ability
- congenital (e.g. renal tubular acidosis type 1)
- infective (e.g. post-infective interstitial nephritis)
- post-obstructive
- endocrine (DI, DM)
- metabolic (hypercalcaemia, hypokalaemia)
What investigations would you do?
Diagnostic: - renal US (possible biopsy) - voiding cystourethrogram (VCUG) - urinalysis - ABG Labs: - FBC - ESR/CRP - CMP and PTH- renal oesteodystrophy - LFT, Alb - Coag studies - lipid profile - serum and urine protein electrophoresis (MM) - EUC - 24hr protein - 24hr creatinine clearance (GFR) - urine MCS GN screen: - AI markers- ANA, ENA, ANCA - complement levels (IgA nephropathy) - anti-GBM - HBV, HCV
What points to chronic renal failure as the cause?
Renal failure indicators:
- increased nitrogen waste products (due to deficient filtration)
- pallor (due to decreased EPO production) -> normocytic, normochromic anaemia
- nocturnal diuresis (due to increased filtration)
- proteinuria (due to GBM damage)
Chronic picture indicators:
- pallor without haematuria (due to LTM decreased EPO production -> anaemia)
How would you calculate GFR?
GFR: represents the amount of blood that can be filtered by the kidney per unit of time (ie through the glomeruli/min)
Normal GFR= 100mL/min
• Ideally measured with freely filtered solute that is neither reabsorbed nor modified in renal tubules (insulin ideal, but costly)
• Creatinine clearance used as approximate measure of GFR (via 24hr urine collection)
- but slightly overestimates GFR because creatinine is moderately secreted by the PCT
OR Cockcroft-Gault equation- approximates GFR based on serum creatinine
eCCr = ((140-age) x mass (kg) x (constant)) / serum creatinine (umol/L)
(constant: males 1.24, females 1.04)
What might this patients patient’s acid base status be and why?
Metabolic acidosis
1) bicarb loss: kidney failure -> loss of intrinsic ability to produce bicarb (normally buffer)
2) gain strong acid: lack of K+ clearance -> hyperkalaemia -> attempted compensation via H+/K+ pump -> increase serum H+ -> acidosis
Explain the electrolyte disturbances?
1) high urea and creatinine: progressive tubular damage -> poor filtration -> retaining waste products
2) low bicarb:
- reduced production by kidneys
- consumptive decreased to buffer acidosis (combines with hydrogen ions)
3) high chloride: resorbed with Na (as Na unable to combine with bicarb) -> maintain neutrality in PCT
4) low Ca: kidneys cannot convert vit D to active form
- later hypercalcaemia (due to PTH aiding resorption of Ca from bone)
5) high phosphate: excess phosphate not excreted in urine
6) high PTH: low Ca -> stimulates increased Ca absorption from food and bones -> hypercalcaemia (later stage) AND renal osteodystrophy (low bone remodelling/turnover)
Why is glucose in the urine despite normal blood glucose?
Normally: glucose is small molecule freely filtered by kidneys into Bowman’s space -> completely resorbed in PCT by Na+/glucose co-transport
Tubular damage: damaged Na+/glucose co-transporter -> increased glucose filtered into urine
Normal plasma glucose= 60-120mg/dL
What is the role of ammonia?
Ammonia (NH3):
- filters across kidney into lumen (PCT) -> binds H+ ions to form ammonium (NH4+) -> trap H+
-> ammonium trapped in lumen and excreted
Acidosis: increased ammonium excretion -> increasing extracellular pH towards normal
What are the complications of renal failure?
(mnemonic MAD HUNGER): MA- metabolic acidosis D- dyslipidaemia (esp TG) H- hyperkalaemia U- uremia N- Na+/H20 retention (causing HF, APO, HTN) G- growth retardation and developmental delay R- renal osteodystrophy
