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,
Nephrotic management
Diuretics, fluid management, ACEi, anticoagulation, Tx cause
Nephritic basics
Endothelial or mesanglial damage. Proliferative plus GBM thickening.
HTN, haematuria, casts in urine, proteinuria, oliguria, oedema, C3/C4 reduction (overuse)
May have ANA, anti-dsDNA, ANCA, antiGBM
Often abrupt onset
Acute post infectious
Most common nephritic globally.
Group A beta haemolytic streptococcus
IgA disease
Often macroscopic haematuria (often cola coloured). Can occur post URTI or HVB
Most common nephritic.
IgA/C3 deposits
Henoch scholein purpura
Systemic IgA vasculitis.
Typically get cola urine, widespread rash (esp extensors), arthalgia, abdominal pain, haematochezia
Rapidly progressing glomerulonephritis
Crescents, rapid loss of renal function.
Can be anti GBM (goodpastures if lung too)
Immune complex disease (IgA, post strep, SLE)
Pauci immune (very few Igs on staining)
Polyangitis
Churg strauss vasculitis
Poor prognostic indicators in nephritic
Sequalae
Severe renal impairment at presentation, persistent heavy proteinuria, HTN.
Adults often has long term complications
(can be HTN encephalopathy, HF, uraemia (dialysis))
PRGN nephritic screen
ANCA/anti GBM
SLE nephritic screen
ana, DS-dna, COMPLEMENT
myeloma nephritic screen
Igs, serum electrophoresis
RA associated GN screen
Rheumatoid factor
membranoproliferative glomerulonephritis (MCGN)
HBV/HBC screen
Post streptococcal nephritic screen
ASA
SLE associated diseases
Can be mix of nephrotic and nephritis. May see membranous, membranoproliferative and FSFN
CKD
Irreversible progressive renal function decline. Can be diagnosed if EGFR decreases over 3 months
CKD S+S
HTN, proteinuria, anaemia, nocturia (loss of concentrating), fatigue, dyspnoea, ED, oedema (peripheral/pulmonary)
Late shows pruritus, anorexia, N&V
Very late: hiccups, Kussmaul’s resp (met acid), muscle twitch, drowsiness, coma, fits
May have pericardial rub
CKD investigation
- Bloods (U&E - can show hyperkalaemia, increased urea, creatinine)
- FBC (?haemanitinics)
- Calcium, phosphate, PTH
- Lipid profile
- Glucose, HBa1C
- Albumin
- Bicarb
- Myeloma screen
- HIV/HEP serology if transplant needed
- ECG
- Urinalysis (can quantify protein with PCR
Renal US to exclude obstruction ans assess kidney size and any asymmetry (small kidney in CKD, asymmetry suggests renovascular/developmental disease. Polycystic kidney?)
CKD stagings
1 is mild with normal eGFR
2) 60-90
3a) 45-60
3b) 30-45 (anaemia present)
4) 15-30 (electrolytes)
5) <15 (dialysis once <10)
Management of CKD`
ACEi/ARB are key for BP control. Diabetes control.
Referral to nephrologist if young, CK4, rapid deterioration), significant proteinuria/haematuria
CKD complications
anaemia (Target 100-120 with EPO to avoid HTN and thrombosis)
Renal osteodystrophy (lack of 1 alpha hydroxylase, hyperphosphataemia cause lack of calcium) - can get tertiary hyperparathyroidism
Fluid overload (needs water/salt restriction)
Electrolyte disturbances (often hyperkalaemia, acidosis)
Myopathy (poor nutrition, hyperparathyroidism, vit D deficiency, electrolyte derangement)
Peripheral neuropathy
Anorexia
Immunocompromise
N&V
Peptic ulcer disease
Depression
CV issues (pericarditis, atherosclerosis, HTN, hyperlipidaemia)
Dialysis needed if
intractable acidosis, intoxicants (methanol, ethylene glycol, lithium), too much fluid and anuric), uraemic symptoms (N&V, pericarditis, seizures, bleeding, encephalopathy), severe electrolyte derangement
CKD causes
Most common diabetes, then interstitial disease, idiopathic, HTN, systemic inflammation, renal artery stenosis, congenital and drug induced
Diabetic nephropathy
Causes and management
Mediated by HTN, hyperglycaemia (extent and duration) as well as glomerular hyperfiltration, smoking, obesity, physical inactivity, dyslipidaemia, proteinuria, dietary factors, genetic susceptibility
Managed as per CKD (reduce proteinuria, control BP, modify CV risk, BM control)
PCKD
S+S
Investigation
ADPKD more common (autosomal dominant)
ARPKD is recessive and less common - earlier renal failure
Renal cyst, extra renal cyst, IC aneurysm, dolichoectasias, aortic root dilatation/aneurysm, mitral valve prolapse, abdominal wall herniae
HTN, CKD, abdo swelling +/- ruptured IC aneurysm
FHx is key. echo and MRI brain if suspected