Acute renal failure Flashcards
List some DDx for a presentation of:
- peripheral oedema
- HTN
- tachypnoea
- raised urea and nitrogen
- urinalysis showing RBCs, proteins and casts
• Nephritic syndrome (haematuria, HTN, elevated urea/creatinine, oliguria):
o Acute post-strep glomerulonephritis (strep pyogenes, weeks following UTI)
o Rapidly progressive (crescentic) glomerular nephritis- Good Pastures Syndrome (anti-GBM Ab damage GBM), vasculitic disorder (Wegner’s Granulomatosis, microscopic polynagitis, Churg Strauss disease)
o Diffuse proliferative glomerular nephritis (DPGN)
o IgA nephropathy (<48hrs of UTI/GIT infection)
o Alport syndrome
o Membrano-proliferative glomerulonephritis (MPGN)- primary immune mediated or secondary (SLE, HBV, HCV)
• Nephrotic syndrome (proteinuria, hypoalbuminaemia, nil haematuria)
o Minimal change disease (most common in children)
o Focal segmental glomerulosclerosis
o Membranous nephropathy (most common in adults)
o Amyloidosis
o Diabetic glomerulonephropathy
- AI disease- SLE
- Malignancy- RCC, mets
What imaging would you conduct to investigate nephritic syndrome?
• Imaging
o Renal US- shrunken kidney morphology (atrophy)
o CT abdo/pelvis- visualize pathology (e.g. dilated renal pelvis)
• Core biopsy- confirm diagnosis, investigate cause of nephrotic syndrome
What urine tests would you conduct to investigate nephritic syndrome?
Urine tests:
o Urinalysis- blood, protein, glucose, nitrates, pH, casts
o 24 hr urine collection- confirm nephrotic-range proteinuria (>3.5g/day)
o Urine MCS- casts, proteinuria, haematuria, culture (causative organism)
List some cellular cast types and their causes?
Cellular casts:
- RBC casts: GN, malignant HTN
- WBC casts: tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
- Bacterial casts: bacterial infections
List some acellular cast types and their causes?
Acellular casts:
• Hyaline casts- non-specific, normal or acute tubular necrosis (cellular cast break down)
• Granular casts- acute tubular necrosis (cellular cast break down, plasma protein aggregates, Ig light chain aggregates)
• Waxy casts- chronic kidney disease (end product of cellular breakdown in v low urine output state)
• Fatty casts: nephrotic syndrome (breakdown of lipid-rich epithelial cells, ie hyaline casts w fat globule inclusions)
• Crystal: oxylates, urates, sulphonamides
What blood tests would you conduct to investigate nephritic syndrome?
Blood tests:
o FBC- WBC (infection, immunity), Hb (anaemia, bleed), platelets (coag), pancytopenia (BM infiltration)
- Normocytic, normochromic anaemia- reduced EP
- Polycythemia (increased RBC)
o ESR/CRP- inflammatory process
o Comprehensive metabolic panel (CMP)- paraneoplastic syndromes
o LFTs- liver function, paraneoplastic syndromes
o UEC- kidney function (urea, creatinine), dehydration
o Blood culture- sepsis
o ABG- pH, bicarb, lactate
o BSL- diabetic GN (nephrotic)
o AI markers- ANA (SLE), ANCA (vascularities), complement levels (IgA nephropathy)
What is nephritic syndrome?
Nephritic syndrome: an inflammatory disease of the nephron, characterised by a triad of haematuria, hypertension and elevated serum nitrogen waste products (urea and creatinine).
Features:
• Haematuria: inflammation and damage to glomeruli -> podocytes develop large pores -> allowing RBCs and protein to pass from the damaged GBM
• HTN: damaged juxtoglomeruli cells -> impaired RAS system -> unable to regulate BP (through vasodilation)
• Oliguria (<300ml/day): results in build up of nitrogen waste products (azotaemiae)
What is nephrotic syndrome?
Nephrotic syndrome: an inflammatory disease of the nephron characterized by:
- proteinuria (>3.5g/day)
- hypoalbuminaemia,
- hyperlipidaemia
- oedema
Define acute kidney injury?
AKI: the abrupt and sustained (>24hrs) loss of renal function -> resulting in the retention of nitrogen waste products and dysregulation of extracellular volume and electrolytes
List the clinical features of AKI?
o Abrupt loss in renal function -> nitrogenous waste retention, dysregulation of extracellular volume and electrolytes (increased urea, K, hydrogen)
o Peripheral oedema: increased fluid -> raised circulating intravascular vol and proteinuria -> hypoalbuminaemia -> decreased plasma oncotic pressure -> oedema
o HTN: decreased GFR -> decreased perfusion detected by macula densa -> activated RAS -> angiotensin II causes vasoconstriction of smooth muscle -> increased TPR -> raised BP
o Tachypnoea: decreased GFR -> decreased organic acid excretion -> metabolic acidosis -> respiratory compensation -> hyperventilation (Kussmaul breathing)
How is AKI diagnosed?
AKI Diagnostic criteria (Acute Kidney Injury Network (AKIN), 2007):
1) increase in serum creatinine (of ≥0.3 mg/dL) in 48hrs
- or ≥50% in 48hrs
2) OR urine output reduction (of <0.5 mL/kg/hour for >6 hrs)
List the consequences of renal failure?
Primarily: inability to excrete nitrogenous wastes and make urine
(MAD HUNGER acronym):
MA- Metabolic Acidosis
D- Dyslipidaemia (esp increased triglycerides)
H- Hyperkalaemia
U- Uraemia (increased BUN, syndrome of nausea/anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction)
N- Na+/H2O retention (HF, pulmonary oedema, HTN)
G- Growth retardation and developmental delay
E- Erythropoietin failure (anaemia)
R- Renal osteodystrophy
What is the GFR and how is it measured?
GFR- represents amount of blood that can be filtered by kidney per unit time
- the volume of blood passing through the glomeruli each minute
Measured:
• Ideally, using freely filtered solute that is neither reabsorbed nor modified in renal tubules (insulin ideal but costly, so creatinine clearance used)
• Formula:
GFR = urine concentration x urine flow rate / plasma concentration
• Creatinine clearance in 24hr urine collection- freely filtered and not reabsorbed
- overestimates GFR since some creatinine also secreted by the PCT
• Cockcroft-Gault equation: approximated GFR based on serum creatinine
eCCr = ((140-age) x (mass) x (constant)) / serum creatinine
- constant = male 1.24, female 1.04
Where is K stored?
K+ is the major intracellular cation -> thus majority stored intracellularly (muscles and liver)
o Function: maintenance of cell homeostasis
o Reliant on dietary intake and renal/GIT elimination
o Stored: muscles and liver (by actions of insulin and B2 adrenergic receptors)
o Excretion: aldosterone enhances K excretion in kidneys (effects on principal cells)
How does hyperkalaemia occur?
Hyperkalaemia causes:
In AKI:
o Reduced GFR -> reduced K+ excretion -> hyperkalaemia
o Metabolic acidosis: K+ efflux as body tries to compensate by exchanging with H+ via the H+/K+ exchanger -> metabolic acidosis
Other causes:
o Excess production: rhabdomyolysis (rapid breakdown of skeletal muscle), haemolysis, tumour lysis
o Acidosis: shift K outside cells in exchange for cellular uptake of H+ (?attempt to lower pH)
o Impaired secretion: renal tubular injury -> reduced K excretion ability
o Adrenal insufficiency: hyperaldosteronism -> decreased reabsorption of Na and decreased excretion of K
o Insulin deficiency/hyperglycaemia/DM: lesser uptake of K into cells
o Pseudo-hyperkalaemia: intravascular haemolysis or exercise
o Drugs: K-sparring diuretics, ACEI, ARBs, B-blockers
