Renal Flashcards
Name kidney functions
RAAS => regulates blood volume + BP Acid-base balance Electrolyte balance Excretion of water-soluble waste products via filtration Vit D synthesis => 1-alpha-hydroxylase RBC synthetsis => EPO
AKI vs CKI definition
AKI - rapid decline in renal function over hours or days - measured bye urea and creatinine - failure to maintain homeostasis: = oliguria, vol. overload (fluid) = hyperkalaemia (electrolyte) = metabolic acidosis (acid-base) - potentially reversible
CKI
- impaired renal function for >3 months based on:
= abnormal structure/function or
= GFR <60 ml/min for >3 months
= +/- evidence of kidney damage
- usually progressive and irreversible, leads to end-stage renal failure
AKI staging classifications
Stage I
- creatinine increase x1.5
- UO < 0.5ml/kg/hr for 6 hrs
Stage II
- creatinine increase x2
- UO < 0.5ml/kg/hr for 12 hrs
Stage III
- creatinine increase x3
AKI signs
Hypertension
Distended bladder
Dehydration; postural hypotension
Pallor, rash, bruising (vascular disease)
Fluid overload (heart failure, cirrhosis, nephrotic syndrome)
- increased JVP, pulmonary and peripheral oedema
AKI sx
Confusion, dehydration, underlying cause, N&V, oliguria/anuria***
Pre-renal causes of AKI
*due to inadequate perfusion (55% cases)
Hypovolaemia
- renal loss: diuretic overdose, osmotic diuresis (DKA)
- extrarenal: D&V, burns, sweating, blood loss
Systemic vasodilation
- sepsis, neurogenic shock
Decreased cardiac output
- heart failure, MI
Intrarenal vasoconstriction
- cardiorenal syndrome
- hepatorenal syndrome
Renal causes of AKI
*due to cellular damage (35% cases)
Acute tubular necrosis
- ischaemia, drugs, toxins (i.e. paracetamol, NSAIDs, ACEi, contrast, myoglobinuria in rhabdomyloysis)
Glomerulonephritis
- post-infection
Interstitial nephritis
- drugs, immune disorders (SLE), lymphoma, infections, tumour lysis syndrome following chemo, eosinophilia and haematuria
Vessel obstruction
- thrombosis, vasculitis, haemolytic microangiopathy
Post-renal causes of AKI
*due to obstruction (20% causes)
Luminal
- clots, stones
Mural
- strictures, BPH, malignancy
Extrinsic compressions
- retroperitoneal fibrosis
What types of microangopathy may cause AKI?
1) Haemolytic uraemic syndrome (HUS)
2) Thrombotic thrombocytopenic purpura (TTP)
3) Disseminated intravascular coagulation (DIC)
Compare HUS and TTP
HUS
- occurs mainly in children after a bout of gastroenteritis caused by E.Coli 0157:H7
- poor kidney function, haematuria/proteinuria, pain and bloody diarrhoea, low Hb, low plts
TTP
- mainly occurs in women aged 10-50yo that are deficient in protease that weaves vWF (ADAMTS13)
- haemolytic anaemia, thrombocytopenia, ureaemia, fever, neurologic sx (seizures, hemiparesis, decreased consciousness, blurred vision)
Causes of glomerulonephritis
IgA neuropathy
- after URTI, IgA complexes form
Henoch Schonlein Purpura
- purpuric rash, systemic variant of IgA
Goodpasture’s; anti-GBM antibodies
- also bind to alveolar basement membranes => lung haemorrhage
Post-strep GN
- previously healthy person presents post-throat infection
Pauci-immune
- +ANCA bond to neutrophils, activated within glomerular capillaries loops
Nephrotic syndrome summary card
Proteinuria > 3.5g/24hrs
Oedema
Low serum albumin <25g/L
- also see hyperlipidaemia as liver tries to compensate for low albumin by increasing lipids thus in hypercoaguable state
- children: minimal change glomerulonephritis
- adults: membranous glomerulonephritis
- other causes include focal segmental glomerulosclerosis, mesangiocapillary glomerulonephritis, DM, SLE, amyloid, HBV/HCV
Nephritic syndrome summary card
Hypertension, haematuria, oedema, oliguria (<400ml/day)
- Primary causes: IgA nephropathy, mesangiocapillary glomeulonephritis
- Secondary causes: post-strep, vasculitis, SLE, anti-GBM disease, cryoglobulinemia
Ix and mx for glomerulonephritis
Ix: bloods (FBC, U&Es, CRP, complement, autoantibodies), urine, imaging (renal USS +/- renal biopsy)
Mx: treat underlying cause, steroids/immunosuppression, refer to specialist, BP mx <130/80, ACEi/ARB (decrease proteinuria and pressure on renal function as decreases intraglomerular pressure by inhibiting AGII efferent vasoconstriction)
Which nephrotoxic agents cause renal AKIs?
NSAIDs Contrast agents Aminoglycosides (gentamicin, streptomycin) ACEi, ARBs Urate crystals Myoglobin from rhabdomyolysis
How does myeloma cause renal AKI?
Myeloma leads to monoclonal paraprotein production
This is deposited in the distal tubules as casts of free light chains of paraprotein precipitates, causing inflammation
Ix for AKI
Dipstick testing
Microscopic examination = urine MCS, protein CR, 24hr urine
Proteinuria quantification
Electrolyte estimation
What do urine dipstick results suggest?
Haematuria
- renal: pyelonephritis, glomerulonephritis, carcinoma, trauma
- extrarenal: cystitis/prostatitis/utheritis, stones, trauma (catheter), bladder/prostate/urethra cancer
Proteinuria
- nephrotic syndrome, DM
Glucose
- DM
Ketones
- starvation, diabetic ketoacidosis
Urobilinogen
- pre-hepatic jaundice
Complications of AKIs
Uraemia, volume overload, hyperkalaemia, hyperphosphataemia, metabolic acidosis, chronic progressive kidney disease
Mx of AKIs
General
- stop nephrotoxic drugs (incl. metformin if GFF <30)
Underlying cause
- pre-renal: correct volume depletion with appropriate fluids, Abx if sepsis, inotropes if signs of shock
- post-renal: catheretise and imaging of renal tract and urology referral
- renal: refer early to nephrology
Manage complications
- pulmonary oedema, ureaemia, acidaemia (50-100ml of 8.4% IV sodium bicarbonate with central line infusion over 15-30mins)
Renal replacement therapy
- haemodialysis and haemofiltration
Causes and classification of CKD
Diabetes, hypertension, atherosclerosis, chronic glomerulonephritis, infective/obstructive uropathy, adult polycystic kidney disease
Staging: I. damage, normal GFR >/= 90 II. damange, mild GFR 60-89 III. moderate low GFR 30-59 IV. severe low GFR 15-29 V. end-stage renal disease <15 (or dialysis)
Signs and sx of CKD
Peripheral vascular disease, peripheral oedema, HTN, pallor (ACD), excoriation marks (uraemia), skin pigmentation (uraemia), renal bone disease, signs of underlying disease (i.e. SLE)
Often asymptomatic, anorexia, N&V, fatigue, pruritus, peripheral oedema, muscle cramps, pulmonary oedema, sexual dysfunction
Ix for CKD
Bloods
- increased urea + creatinine (U&E), normocytic anaemia, glucose (DM), secondary hyperPTH (if severe), GFR, low calcium, high phosphates, high ALP in renal bone disease
Urine
- dipstick, MCS, protein:Cr ratio
Imaging
- USS (size/anatomy/corticomedullary differentiate + eliminate obstruction)
- CKD small kidneys but can be enlarged in infiltrative disorders
CXR
- pericardial effusion, pulmonary oedema
Mx of CKD
1) Limiting progression/complications
= BP <130/80 or <125/75 if diabetic
= tight glucose control if DM
= diet with help of MDT: low protein, potassium and phosphate food
= smoking cessation, wt loss
= renal osteodystrophy: calcichew (Ca2+ supplement), calcium acetate (phosphate binders), cinacalcet (calcimimetic to decrease PTH)
2) Symptom control
= anaemia; human EPO may be required
= acidosis; sodium bicarbonate supplements
= oedema; loop diuretics, restriction of fluids
3) Preparation for renal replacement therapy
= haemodialysis; vascular access required
= transplantation; gold standard, major surgery with life-long immunosuppression
Pathogens that cause UTIs
Common: E. Coli (gram-negative anaerobic) Staph saprophyticus (gram-positive coccus) Proteus mirabilis Enterococci
Immunocompromised:
Klebsiella
Candida albicans
Pseudonomas aeruginosa
RFs for UTIs
Female >>> male Sexual intercourse Exposure to spermicide Pregnancy Menopause Immunocompormised Catheritisation UT obstructon UT malformation
Ix for UTIs
Urine dipstick: + nitrates
MSU for urine MCS: WBC, provide colony forming unti, sensitivity
Bloods: FBC, CRP, U&Es
Complicated UTI: renal USS/IV urography