Kidneys: UTI and Glomerulonephritides Flashcards
Classification of UTIs
Simple
- female
- 1st presentation
- not pregnant
- no pyelonephritis
Complicated
- male
- recurrent - 3+ in a year
- pregnant
- elderly
- catheters
Lower - bladder and distal
Upper - kidneys (pyelonephritis)
UTI
-risk factors
Past UTI Sexually active Pregnant Low estrogen DM, obesity, IC
Stones
Catheters
Surgery, renal transplant
Causative organisms for UTIs
MOST COMMON - Ecoli followed by staph saprophyticus
Associated with stones - proteus mirabilis
Presentation
Investigations and diagnosis of UTI
FUND
-assess triggers, sexual Hx
-DM, stones, neurology, IC
Red flags - sepsis, pyelonephritis (flank pain, fever, N+V)
Clinical diagnosis with urine dipstick (nitrites, leukocytes)
Culture if complicated, recurrent
Management of UTI
If not pregnant and catheterised, only treat if symptomatic
If pregnant, pre and post op, treat even if asymptomatic
Definitive - nitrofurantoin/trimethoprim (teratogenic)
Supportive
- fluids, perineal hygiene, post coital voiding
- remove catheter if present
- if postmenopausal => HRTs to reduce future risk
Characteristics of nephrotic syndromes
- triad
- examples
Glomerular damage => proteinuria, hypoalbuminuria, peripheral edema
Foot effacement - Minimal change disease, FSGS
AB deposition - Membranous
Complex deposition - Membranoproliferative
Minimal change disease
- epidemiology and most common cause
- presentation, investigations
- management
Children - IDIOPATHIC
Nephrotic
Renal biopsy
- normal LM
- EM podocyte foot effacement
1st line - CS
2nd line - cyclophosphamide
Focal segmental glomerular sclerosis
- epidemiology and most common cause
- investigation
- management
Young adults - IDIOPATHIC
Renal biopsy
-glomerular scarring on LM, EM
1st line - CS
2nd line - cyclophosphamide
Membranous glomerulonephritis
- epidemiology and most common cause
- investigation
- management and prognosis
Adults - IDIOPATHIC
EM - antiPLA2 IgG => BM thickening
Management
Supportive - BP control
Definitive - self limiting but if severe => CS + cyclophosphamide combination
Can lead to ESRF
Nephritic syndrome
- triad
- urinary findings
Examples of nephritic syndromes
Glomerular inflammation => inflammation
- Haematuria
- Oliguria and edema
- HTN
Anti GBM
SLE
IgA nephropathy/post streptococcal
ANCA
What is IgA nephropathy or post streptococcal GN?
- key differences
- investigations
- management
- prognosis
IgA/Bergers - most common GN
- young male, nephritic
- 1-2 days after URTI, visible hematuria
- renal biopsy - mesangial hypercellularity, high IgA, C3
Management
- Haematuria only - self limiting
- Persistent proteinuria - BP control
- Falling GFR - CS
Post strep glomerulonephritis => diffuse proliferative GN
- 1-2wks after URTI, proteinuria => edema
- renal biopsy - low complement
Management - symptom relief
How would you manage nephrotic syndromes
Reduce edema => diuretics Reduce HTN => ACEi Reduce DVT risk => anticoagulation Reduce cholesterol => statin Renal biopsy to establish cause
How would you manage nephritic syndromes
Supportive
-Na, water restriction
Pharmacological
-proteinuria/HTN => ACEi, ARB, diuretics
Lupus nephritis => immunosuppressive therapy
AntiGBM AB => plasmapheresis
What are the rapidly progressing glomerulonephritides
- what are 3 examples of this
- how might this present
- management
Rapid destruction of glomeruli => ESRD
Anti GBM disease
ANCA vasculitis (GPA, MPA)
Lupus with pulmonary haemorrhage
Biopsy - crescent formation around glomerulus
Management - CS, cyclophosphamide, plasmapheresis
What is ANCA positive vasculitis
- main symptoms
- 2 main types and their associated AB
Renal - nephritic symptoms Resp - SOB, haemoptysis Systemic - fatigue, weight loss, fever Vasculitic rash ENT - sinusitis
GPA - cANCA (serine proteinase)
MPA - pANCA (myeloperoxidase)
If suspected => MDT approach
Definitive management - immunosuppression
