Nephrology Flashcards
NICE diagnostic criteria AKI
- Rise in creatinine >25um/L in 48 hours
- Rise in creatinine >50% from baseline in 7 days
- Urine output <0.5ml/kg/hr for >6 hours
Nephrotoxic drugs
GOD SAD MAN
Gentamicin / Opiates / Diuretics / Sulfonylureas / ACEi & ARBs / DOACs / Metformin / Aldosterone antagonists / NSAIDs
Pre-renal causes of AKI
Pre-renal = hypoperfusion
1. True hypoperfusion = GI losses, dehydration, burns, haemorrhage
2. Relative hypoperfusion = NSAIDs + ACEi
Renal causes of AKI
Glomerulonephritis
Acute tubular necrosis
Acute interstitial nephritis
Vascular causes e.g HUS or malignant HTN
Post-renal causes of AKI
Bilateral pelvic-ureteric obstruction
Bilateral ureteric obstruction
Bladder outflow obstruction
Urethral obstruction
Complications of AKI
Hyperkalemia
Hyperphosphatemia
Uremia
Fluid overload
Metabolic acidosis
Classification of CKD
Stage 1 = Kidney damage + GFR > 90
Stage 2 = Kidney damage + GFR 60-89
Stage 3 = GFR 45 - 59
Stage 3b = GFR 30 - 44
Stage 4 = GFR 15 - 29
Stage 5 (ESRF) = GFR <15
Which medication can cause rhabdomyolysis
Statins
Staging of AKI
Stage 1 = Creatinine rise of >26 in 48hours or 1.5-1.99 x increase from baseline in 7 days
Stage 2 = Creatinine rise of 2 - 2.9 x baseline in 7 days
Stage 3 = Creatinine rise 3x of baseline in 7 days or >350 within 48 hours
Indications for dialysis
“AEIOU”
Acidosis
Electrolyte derangement resistant to treatment
Intoxication
Pulmonary Oedema
Uremia
What should be prescribed to diabetics with a A:CR of >3
ACE inhibitor
Symptoms of uremia
Pruritus
Loss of appetite
Metallic taste in mouth
N&V
Neuropathy
Encephalopathy
Management of CKD
Optimise risk factors - HTN/diabetes etc
Treat any glomerulonephritis
Reduce CVD risk = Atorvostatin 20mg
Reduce complications risk - Low K+ and phosphate diet, maintain healthy weight, stop smoking etc
Complications of CKD
Hypertension
Anemia
Renal bone disease
Hyperkalemia
Management of CKD induced anemia
EPO
Side effects of EPO
Bone aches
Flu like symptoms
Skin rashes
Hypertension
Iron deficiency anemia
Treatment of renal bone disease
Active Vitamin D (calitrol)
Oral calcium supplementation
Bisphosphonates
Xray findings in renal bone disease
Rugger jersey spine (osteosclerosis at edges of vertebrae with osteomalacia in the center)
Management of hyperkalemia
IV Insulin + Dextrose infusion
Calcium gluconate - to stabilise cardiac membrane
Nebulised salbutamol
IV fluids
Calcium resonium - removal of K+ from the body
Consider sodium bicarb if acidotic or Dialysis if severe
Acute renal transplant failure
Presents <6 months after transplant with Proteinuria + Raised leucocytes + Rising creatinine
Acute interstitial nephritis
Inflammation of the interstitium
Sx = AKI + Hypertension + Hypersensitivity reaction e.g fever, arthralgia, eosinophilia.
Cause = penecillins / NSAIDs usually
Management = Steroids
Acute tubular necrosis
acute necrosis of the epithlium in the renal tubules leading to an AKI. Classically resulting from ischemia or toxins.
Hypoperfusion causes = shock/sepsis/dehydration/haemorrhage
Toxins = Constrast dye / gentamycin / NSAIDs
Invx = muddy brown casts on urinalysis
Low urine osmolality + high urinary sodium
Fully reversible. Poor response to fluid chalanges
Apple-green bifringence on congo red staining
Amyloidosis
HSP
Small vessel vasculitis - has overlap with berger’s disease (IgA nephropathy)
Characteristic rash in HSP
Palpable purpuric rash over buttocks & extensor surfaces of arms and legs
Nephritic syndrome
= inflammation of capillary endothelium + GBM
Features:
Proteinuria
Haematuria
Azotemia
Red cell casts
Oliguria
Anti-streptolysin O titre
Hypertension
Sterile pyuria
Nephrotic syndrome
= Podocyte damage in the GBM
Proteinuria (>3g in 24hours)
Hypoalbuminemia
Oedema
+/- dyslipidemia
‘Nephrotic-like’ Glomerulonephritis’
Minimal change
Membranous
Focal segmental
“Nephritic-like” Glomerulonephritis’
Post-streptococcal
Anti-GBM (Goodpastures syndrome)
IgA nephropathy (& HSP)
Rapidly progressive
Small vessel vasculitis (Microscopic polyangitis = pANCA, Granulomatosis with polyangitis = pANCA)
+ Alpert’s syndrome (hearing problems)
Mixed nephrotic + nephritic type GN
Membranoproliferative
SLE
Minimal Change disease
Most common cause of nephrotic syndrome in children.
Histology normal
LM normal
EM = fusion of podocyte foot processes
Membranous Glomerulonephritis
3rd most common cause of ESRF
Caused by immune deposition in GBM causing damage to podocytes.
Invx = Anti-phospholipase A2 antibodies
LM = mesangial expansion
Immunoflourescnce = IgG and C3 deposition
EM = Subepithelial deposits - silver spikes & domes
Focal segmental glomerulonephritis
Most common cause of nephrotic syndrome in adults. (typically younger adults)
LM = Focal and segmental scarring & hyalinosis
EM = GBM thickening
*ANA levels may be risen if SLE is present (common cause of FSGN)
IgA Nephropathy
Typified by IgA complexes within the mesangium - type 3 hypersensitivty reactions.
Occurs 1-3 days after a sore throat.
Associated with HSP
Biopsy not needed as clinical diagnosis - but immunoflourescence would should IgA deposition
Post-streptococcal GN
Occurs 1-3 weeks after a Group A beta-haemolytic streptoccocus infection (usually pyogenes, e.g tonsillitis)
Raised ASO titre
Low C3
Increased anti-DNAaseB
Membranoproliferative GN
Causes proteinuria +/- Haematuria
T1 = caused by immune complex depositis. EM shows ‘tram-track’ appearance
T2 = C3b nephritic factor
Anti-GBM GN (Goodpasture’s syndrome)
Typically presents with AKI + Haemoptysis (pulmonary haemorrhage)
Caused by antibodies to T4 Collagen (which is found in glomerular and alveolar basement membranes)
Invx;
- Linear IgG deposition in GBM
- Raised Transfer factor
Granulomatosis with Polyangitis (Wegener’s)
Features: Sinusitis + Saddle nose deformity + AKI + Haemoptysis + Malaise + Arthralgia
Invx = Raised cANCA
Biopsy = granulomatous inflammation
Management = Steroids + Cyclophosphamide
Rapidly progressive GN
A term used to describe a rapid decline in renal function + Epithelial crescents in bowmans capsule.
Causes = Goodpastures, Wegeners, Microscopic polyangitis + SLE.
Basically the key finding is Epithelial crescents.
Microscopic polyangitis
Nephritic GN
No granulomatous inflammation seen
Raised pANCA (target = myeloperoxidase 3)
Alport’s syndrome
Usually presents in childhood with Microscopic haemturia (nephritic syndrome) + progressive renal failure + bilateral sensorineural hearing loss + lenticonus
Invx = EM shows splitting on lamina densa
