Renal Flashcards
AKI dx
Serum creatinine.
NICE: rise in Cr >25micromols/L in 48h
>50% in 7 days
Urine output of <0.5ml/kg/h for > 6h.
Risk factors AKI
Acute infection surgery CKD Heart failure DM Liver disease >65 cognitive impairment Nephrotoxic meds: NSAIDs, ACEi. Contrast dyes.
Causes of AKI
Pre renal (most common) - Dehydration, hypotension (shock), e.g. Sepsis, Heart Failure
Renal - glomerulonephritiis, ATN, interstitial nephritis
Post renal - Kidney stones, cancer, ureter/urethral strictures, prostate cancer, BPH
Ix
FBC U+E, glucose, clotting, ca, esr
ABG
if unclear GN screen: ASOT, ANA, dsDNA, complement, ANCA, gbm, serum protein electrophoresis. ig. hep b/c
Urine dip: protein, blood, nitrites, leukocytes. glucose
MC+S, chemistry - U+E, pcr, osmolality , BJP
ECG - hyperkalaemia
CXR
USS: obstruction.
Mx
A-E. GCS
B pul oedema -sit up , high flow o2.
C fluid status.
Tx Hyperkalaemia, pul oedema, consider dialysis need.
Shock/dehydration
- Fluid challenge 500ml over 15mins.
- repeat as necessary
- aim 20ml/hUO
Cardiac monitor
catheterise - UO
cvp
fluid balance chart
evidence of post renal causes.
hx + ix - acute v chrnoic Bloods, abg, urine dip MCS chem ecg CXR, REnal USS
Tx sepsis - blood cultures, empirical abx.
call urology if obstructed depsite atehter.
care with nephrotoxic drugs.
Assess: Hx- acute/chronic.
Fluid status
GU tract obstruction - suprapubic pain, enlarged prostate,
Stop nephrotoxic meds. Stop ACEi, Stop NSAIDs.
Fluids - IV
monitor UO, catheterise. fluid balance, weights. Bp, Fbc,
Prerenal: IV fluids
Post renal: catheter.
Severe: renal specialist
Dialysis.
Complications: Hyperkalaemia Fluid overload metabolic acidosis Uraemia.- encephalopathy, pericarditis.
Causes of haematuria
Renal: Congenital PKD Trauma Infection (pyelonephritis) Glomerulonephritis, tubular interstitial nephritis Neoplasm.
Extrarenal: Trauma (stones, catheter)
Infection (cystitis, prostatitis, urethritis)
Neoplasm (bladder, prostate)
Bleeding diathesis
Drugs (NSAIDs, Frusemide, cipro, cephalosporins).
False + (pophyria, myoglobin)
Glomerulonephritis presentations
asymptomatic haematuria
nephrotic syndrome
nephritic syndrome
Causes of glomerulonephritis
Idiopathic immune (SLE, Goodpastures, vasculitis) infection (HBV, HCV, strep, HIV) Drugs: penicillamine amyloid
Ix glomerulonephritis
Bloods: FBC U+E ESR complement ANA, dsDNA, ANCA, GBM serum protein electrophoresis, Ig Infection (ASOT, HBC, HCV serology).
Urine: Dipstick (protein, blood)
Spot PCR
MCS
bence jones protein
Imaging
CXR (inflitrates: goodpastures, wegeners)
Renal USS +/- Biopsy
General mx
Refer nephrologist
Treat HTN (<130/80)
causes of asymptomatic haematuria
IgA nephropathy
Thin BM disease
Alports syndrome
Features IgA nephropathy
commonest GN developed world young males: episodic haematuria after URTI rapid recovery increased IgA can -> nephritic syndrome.
Ix: Biopsy (IgA in mesangium).
Mx: steroids, Cyclophosphamide (if reduced renal function). Tx HTn w ACEi.
Prognosis: 20% ESRF in 20y.
Thin BM disease
Autosomal dominant
commonest cause asymptomatic haematuria
Alports syndrome
x linked Haematuria , proteinuria -> ESRF. sensoneurinal deafness retinal flecks cataracts female: Haematuria.
Post strep glomerulonephritis (nephritic syndrome)
young child HTN, Haematuria, proteinuria (oedema) oliguria, progressive renal impairment. increased ASOT decreased C3 1-2 w after strep throat/skin Biopsy: IgG and c3 deposition mx: supportive. 95% recover fully.
Crescentic RPGN
can -> ESRF in days.
crescents in BM
Type 1: Anti GBM 5%.
-haematuria, haemoptysis
cxr- infiltrates.
Mx: Plasmapharesis, immunosuppression.
Type 2: Immune complex deposition
-complication of igA, Endocarditis, SLE.
Type 3: Pauci immune
cANCA - GPA (wegeners)
pANCA - eos GPA (churgstrauss), Microscopic PA.
