Deck 7 Flashcards
Renal corpuscle info
Bowman’s capsule, inner (visceral) podyctres), outer (parietal) simple squamous
DCT absorption
Na/K/Ca
AKI
Rapid decline in kidney function (hours/days) as measured by urea and creatinine
AKI RF
65+, hypovolaemia, sepsis, diabetes, chronic liver disease, HF, chronic kidney disease
Pre-renal AKI
Reduced perfusion.
Hypovolaemia, hypotension, fluid overload, reduced CO, vascular causes (renal artery stenosis/occlusion, NSAIDs, ACEi, renal vein thrombosis, AAA)
Gives ATN
Initially get high urine osmolarity (>500), then isotonic urine with high sodium as concentrating power lost
Intrinsic renal damage causes
Glomerular problems (glomerulonephritis, HUS, IgA)
AIN (drug induced, infection, autoimmune or lymphoma)
ATN (most common, ischaemia, rhabdomyolysis, radiocontrast agent)
Vascular (vasculitis, thrombosis/embolii)
HUS (post elcoli or URTI)
Post renal aki causes
luminal (stones, clots, sloughed papillae)
Mural (malignancy, BPH, stricture)
Extrinsic compression (pelvic malignancy, retroperitoneal fibrosis)
AKI S+S
Can be asymptomatic Oliguria, N&V, dehydration, thirst, confusion, fatigue Signs of fluid imbalance. May have vasculitis features. May have palpable abdominal mass
AKI diagnosis
RIFLE (risk, injury, failure, loss, ESRD)
AKIN is like rifle but uses time as well
KDIGO uses serum creatinine and/or urine output
KDIGO 1
1.5-1.9x baseline or >0.3mg/dl increase in sCR
OR <0.5mL/kg/h urine over 6-12 hours (~35mL/ hour)
KDIGO2
2.0-2.9x baseline,
OR <0.5kg/kg/h over 12+h (~35mL/h)
KDIGO3
3+x baseline, or 4mg/dl increase
OR
<0.3mL/kg/h (~21mL/h) for 24h or anuria for over 12 hours
Can also be RRT start or below 18 years with eGFR <35
AKI investigations
FBC (?eosinophilia in acute interstitial nephritis or vasculitis)
Creatinine kinase if ?rhabdomyolysis
Immunology (myeloma screen, lupus screen, vasculitis screen)
Imaging (renal USS to rule out obstruction), CXR is pulmonary oedema), CY KUB in obstruction)
Metformin in AKI
caution. High renal excretion, can lead to lactic acidosis.
AKI complications
Hyperkalaemia Hyperphosphataemia Hyponatraemia Hypermagnesaemia hypocalcaemia Metabolic acidosis Fluid overload Uraemia CKD
Secondary causes of glomerunephritis
N: neoplasm S: SLE A: amyloid I: infection D: diabetes HSP: henoch Schonlein purpura
Features of glomerulonephritis
Immunological attack by Ab or T cell attacking antigen.
Capillary -endothelial proliferation (bigger fenestra) with capillary wall necrosis and mesangial scaring (glomerulosclerosis), thickened BM (more permeable) and cell deposition in Bowman’s space)
Nephrotic basics
BM damaged, allows protein through. Protein loss >3.5g/day Ig loss, hyprecholesterolaemia, oedema (oncotic pressure loss and sodium retention via RAAS), thombosis due to clotting imbalance. May have haematuria Non proliferative histologically.
Nephrotic signs and symptoms
xanthalasma, xanthoma, fatigue, leukonychia, oedema, dyspnoea (can be pleural effusion or pulmonary oedema), may have frothy urine
Nephrotic investigation
MSU, dipstick, FBC, LFT, calcium, U&E, CRP, glucose, Ig (serum, urine), autoimmune screen, hepatitis screen, HIV screen, CXR, renal biopsy
Minimal change
Most common childhood nephrotic
No LM, but podocyte effacement on EM. IF shows IgM in mesangium.
NSAID, allergy and hodgkin lymphoma associations
Membranous glomerulonephritis
30% of adult nephrotic. LM: mesangium expansion and capillary thickening IF shows IgG and C3 EM shows GBM thickening PLA2R antibodies
Penicillin, NSAIDs, malignancy (lung, colon melanoma), SLE, HBV, HVC, syphilis, scistomiasis, malaria
FSGS
Most common adult nephrotic
Often has azotaemia and haematuria
IgM and C3 can be present in sclerotic areas/mesangium
Can be secondary to HIV, heroin, sickle cell
Other nephrotics
Diabetes (most common cause), amyloidosis, HBV,HCV,