Clinical Disorders Flashcards
What are the features of glomerulonephritis?
Haematuria
Proteinuria
Hypertension
Renal insufficiency
Differential diagnosis for nephrotic syndrome?
Congestive heart failure
Hepatic disease
Two classifications of glomerulonephritis?
Proliferative
Non-proliferative
Diffuse?
Focal?
Global?
Segmental?
Diffuse >50% of glomeruli
Focal <50% of glomeruli
Global: all the glomerulus
Segmental: part of the glomerulus
Types of proliferative glomerulonephritis?
Post infective
IgA nephropathy
Focal necrotising and crescentic
Anti-GBM disease
Types of non-proliferative glomerulonephritis?
Minimal change disease
Focal and segmental
Membranous nephropathy
How might proliferative glomerulonephritis present?
With nephritic syndrome
Blood on STIX
Variable proteinuria
Can cause rapid decline
Early diagnosis and treatment key
How might non-proliferative glomerulonephritis present?
Present with nephrotic syndrome
Renal biopsy is key investigation
Identify cause if possible
Post-infective glomerulonephritis treatment?
Antibiotics for infection
Loop diuretics for oedema (frusemide)
Vasodilators for hypertension (amlodipine)
What is the commonest cause of glomerulonephritis?
IgA nephropathy
IgA deposition in mesangium
Anti-GBM disease management?
Aggressive immunosuppression:
Steroids
Plasma exchange
Cyclophosphamide (cytotoxic)
Crescentic glomerulonephritis management?
Immunosuppression: Corticosteroids Plasma exchange Cyclophosphamide B-cell therapy Complement inhibitors
Nephrotic syndrome management?
General measures:
Treat oedema, hypertension
Reduce risk of thrombosis, infection
Treat dyslipidemia (statins)
Minimal change disease management?
Prednisolone, taper once remission achieved
Initial relapse treated with further steroids
Subsequent relapses cyclophosphamide, cyclosporin, tacrolimus
Focal and segmental glomerulosclerosis management?
General measures
Trial of steroids
Alternatives: cyclosporin, cyclophosphamide, rituximab
Membranous nephropathy management?
General measures for 6 months
Immunosuppression if symptomatic nephrotic syndrome
Cyclophosphamide and steroids alternate for 6 months
Cyclosporine, rituximab
What crosses the glomerular basement membrane (GBM)?
Water
Electrolytes
Urea
Creatinine
What crosses the GBM but is reabsorbed in the proximal tubule?
Glucose
Low molecular weight proteins (α₂ microglobulin)
What does not cross the GBM?
Cells (RBC, WBC)
High molecular weight proteins (albumin, globulins)
CKD definition?
Either:
eGFR<60 ml/min/1.73m²
or
The presence of kidney damage that is present for >3 months
What is the clinical approach to CKD?
Detection of underlying aetiology
Slowing rate of renal decline
Assessment of complications related to reduced eGFR
Preparation for renal replacement therapy
Investigations in CKD?
Bloods: EUC, FBC, COAG, LFT, CK, IGS, SEP, BIC
Urine: STIX, PCR, ACR, 24hr
Histology: Biopsy
Radiology: Ultrasound
Slowing the rate of renal decline?
BP control
Control proteinuria
Treat underlying cause
Complications related to reduced eGFR? and treatment?
Acidosis - bicarb
Anaemia - EPO and iron
Bone disease - diet and phosphate binders
CV risk - BP, aspirin, etc
Death and dialysis - counsel
Electrolytes - diet, drugs?
Fluid overload - salt, fluid restrictions, diuretics
Gout - optimise meds
Hypertension - weight, diet, fluid balance, drugs
Iatrogenic issues - be aware
Preparation for end stage renal disease and replacement therapy?
Education
Selection of modality e.g. HD/PD/transplant/conservative
AKI definition?
Increase in serum Creatinine by >26.5 within 48hrs or to >1.5x baseline within the last 7 days
or
Urine volume <0.5 ml/kg/h for 6 hours
Dangerous consequences of AKI?
AEIOU Acidosis Electrolyte imbalance Intoxication Overload Uraemic complications
Three types of AKI?
Pre-renal
Intrinsic
Post-renal
Causes of pre-renal AKI?
Volume depletion Hypotension/shock Congestive cardiac failure Arterial occlusion NSAIDs/ACE inhibitors
Causes of renal (intrinsic) AKI?
Acute tubular necrosis Toxin-related Acute interstitial nephritis Acute glomerulonephritis Myeloma Intra renal vascular obstruction
Causes of post-renal AKI?
Obstruction
intraluminal, intramural, extramural
What is radiocontrast nephropathy (RCN)?
AKI following administration of iodinated contrast agent
Usually transient, resolving in 72hrs
Can lead to permanent loss of function
Risk factors for RCN?
Diabetes mellitus Renovascular disease Impaired renal function Paraprotein High volume of radiocontrast
Patients at risk of AKI?
STOP Sepsis Toxins Optimise BP and volume Prevent harm
5 R’s for IV prescribing?
Resuscitation Routine maintenance Replacement Redistribution Reassessment
What is Goodpasture’s syndrome?
Nephritis with lung haemorrhage
