Nephrology Flashcards
Define Autosomal Dominant Polycystic Kidney Disease
An A. dominant renal condition characterised by the growth of numerous cysts on the kidneys
Leads to progressive kidney damage and CKD
Autosomal Dominant Polycystic Kidney Disease features
Renal:
- Cyst rupture = flank pain and haematuria
- Cyst infection = flank pain, haematuria and urinary symptoms
- HTN
- Slowly progressing CKD
Extrarenal:
- Cysts in other organs = liver, pancreas, spleen
- Intracranial berry aneurysms
- Mitral valve prolapse and aortic regurgitation
- Diverticular disease
Autosomal Dominant Polycystic Kidney Disease investigations
US is primary modality:
- Ages 15-39 = at least 2 renal cysts (uni/bilaterally)
- Ages 40-59 = more than 2 renal cysts bilaterally
- Ages > 60 = more than 4 renal cysts bilaterally
CT/MRI can be used to determine extent of disease
Autosomal Dominant Polycystic Kidney Disease management
- Support of CKD
- Manage HTN
- Tolvaptan has been shown to slow the formation of cysts and decline in renal function
Define Acute Tubular Necrosis
Acute injury to the tubular epithelial cells of the kidneys due to ischaemic events or direct toxicity
Most common cause of renal AKI
What are the causes of Acute Tubular Necrosis?
Ischaemic:
- Hypotension
- Shock
- Direct vascular injury = trauma, surgery
Nephrotoxic:
- Aminoglycosides
- Amphotericin
- Chemo (e.g. cisplatin)
- Antivirals (e.g. tenofovir)
- NSAIDs
- Contrast
- Myoglobin - in rhabdomyolysis
- Haemoglobin - in haemolysis
- Uric acid - tumour lysis syndrome
Acute Tubular Necrosis features
- AKI
- Oliguria
- Uraemia
- Electrolyte imbalances
Acute Tubular Necrosis investigation
- U&Es
- Renal USS to rule out post-renal causes
- Identify nephrotoxic drugs
Acute Tubular Necrosis management
- Correct underlying cause
- Remove nephrotoxic drugs
- Supportive care - may require hemofiltration or haemodialysis
Define Acute Interstitial Nephritis
An interstitial hypersensitivity reaction to certain medications which are not directly toxic, or chronic inflammation
This causes an intrinsic kidney injury and a renal AKI
What are the causes of Acute Interstitial Nephritis?
Drugs:
- Beta lactams
- Cephalosporins
- Fluoroquinolones
- NSAIDs
- Diuretics
- Rifampicin
- Allopurinol
- PPIs
Chronic inflammation:
- Sjogrens syndrome
- SLE
Acute Interstitial Nephritis features
- Rash
- Fever
- Eosinophilia (<10% of cases)
- Progressive AKI, esp following initiation of a new drug
Acute Interstitial Nephritis management
- Discontinuation of causative drug - most AKIs resolve after this
- Glucocorticoids if no improvement after stopping drug
Define Acute kidney injury
Decline in renal function that happens over hours to days.
KDIGO criteria, one of:
- Increase in serum creatinine by >= 26.5 w/in 48 hrs
- Increase in serum creatinine by >= 1.5x the baseline w/in the last 7 days
- Urine output < 0.5 ml/kg/h for 6 hours
What are the causes of pre-renal AKIs?
Most common, occur due to decreased renal perfusion;
- Hypovolaemia (dehydration, haemorrhage, GI loss, burns)
- Renovascular disease (renal artery stenosis)
- Medications to reduce blood pressure or renal blood flow (NSAIDs, ACEi, ARBs, diuretics)
- Hypotension due to reduced CO
What are the causes of renal AKIs?
Occur due to structural damage to the kidneys:
- Glomeruli = glomerulonephritis, nephrotic syndrome
- Tubules = ATN, rhabdomyolysis
- Interstitium = Acute interstitial nephritis
- Renal vessels = renal vein thrombosis, vasculitis
What are the causes of post-renal AKIs?
Occur due to obstruction to urinary flow anywhere along the urinary tract:
- Luminal = ureteric stones or blocked catheter
- Intramural = ureteral/ureteric stricture, ureteric carcinomas
- External compression = abdo/pelvic tumour, BPH)
What are the stages of AKI?
Stage 1 - any of:
- Creatinine rise of 26 or more w/in 48 hrs
- Creatinine rise to 1.5-1.99x baseline w/in 7 days
- Urine output < 0.5 mL/kg/hr for > 6 hours
Stage 2 - any of:
- Creatinine rise to 2-2.99x baseline w/in 7 days
- Urine output < 0.5 mL/kg/hr for > 12 hours
Stage 3 - any of:
- Creatine rise to 3x baseline or higher w/in 7 days
- Creatinine rise to 354 or more, with either an acute rise of 26 or more w/in 48 hrs or 50% rise w/in 7 days
- Urine output < 0.3 mL/kg/hr for 24 hours
- Anuria for 12 hrs
AKI features
Asymptomatic and only seen on blood tests
Most symptoms occur due to uraemia:
- N&V
- fatigue
- Confusion
- Anorexia
- Pruritus
- HTN
- Bladder distention
- Signs of underlying cause
AKI investigations
Bedside:
- Urinalysis
- ECG
- Blood gas
Bloods:
- U&Es
- FBC
- LFTs
- Clotting
- Bone profile
- Creatinine kinase
- CRP
- Renal screen
Imaging:
- Bladder scan
- US KUB
- CT KUB
Renal biopsy if cause still unclear
What is done in a renal screen?
- ANA
- DsDNA
- ANCA
- Anti-GBM antibodies
- ESR
- Serum Ig
- Serum electrophoresis
- Serum free light chains
- C3/4 levels
- HIV screen
- Hep B/C serology
AKI management
- Fluid resus
- Medication review, suspend nephrotoxic drugs
- Catheterisation
Renal replacement therapy in the following pts (AEIOU):
- Acidosis (metabolic) = pH < 7.2
- Electrolyte imbalances = resistant hyperkalaemia
- Intoxication = AKI secondary to drugs or poisons
- Oedema = refractory pulmonary oedema
- Uraemia = uraemia encephalopathy or pericarditis
What are the causes of Acute urinary retention?
- Luminal causes = stones, clots, tumours, UTI
- Mural causes = strictures, neuromuscular dysfunction
- Extra-mural causes = abdo/pelvis tumours, retroperitoneal fibrosis
- Neuro = cauda equina, MS
- Obstructive
- Anticholinergics
- Alpha agonists
- Post Op
- Constipation
- Alcohol
Acute urinary retention investigations
- Bladder scan
- Renal US
- DRE
- Urinalysis, urine MC&S
- Post-residual volume
- ## Bloods = FBC, U&Es, CRP
Define Anti-glomerular basement membrane disease
An AI condition caused by abs directed against type IV collagen, which are found in the glomerular basement membrane and in the alveoli of the lungs
Anti-glomerular basement membrane disease features
- Haemoptysis and pulmonary haemorrhage
- Severe and rapidly progressive AKI, leading to renal failure
Anti-glomerular basement membrane disease investigations
- Urinalysis and MC&S = blood and protein, microscopy shows dysmorphic RBCs suggesting bleeding from the glomerulus
- U&Es
- Blood pH to assess acidosis
- CXR
- Acute renal screen
- Renal biopsy is gold standard = shows focal and segmental necrotising crescents and linear IgG staining along the BM
Anti-glomerular basement membrane disease management
- Removal of the circulating abs = plasma exchange
- Immunosuppression = high-dose oral prednisolone and cyclophosphamide
Define Sterile pyuria
The presence of white cells in the urine w/ a negative urine culture
What are the causes of Sterile pyuria?
- Renal TB
- Partially treated UTI
- Drugs = abx, NSAIDs, PPI, cyclophosphamide
- Urinary tract stones
- Papillary necrosis
Define CKD
Abnormal kidney function or structure for > 3 months
This includes a decreased eGFR (< 60) or markers of kidney damage (albumin, electrolyte abnormalities, structural or histological renal abnormalities)
What are the stages of CKD?
GFR categories:
- G1 = >90
- G2 = 60 - 89
- G3a = 45 - 59
- G3b = 30 - 44
- G4 = 15 - 29
- G5 = < 15
Albumin (ACR) categories:
- A1 = <3
- A2 = 3 - 30
- A3 = > 30
What are the causes of CKD?
Most common:
- DM
- HTN
- PCKD
Other:
- Glomerular = IgA nephropathy, SLE
- Vascular = vasculitis, RAS
- Tubulointerstitial = amyloidosis, myeloma
- Congenital = PCKD, Alport syndrome
- Developmental = vesico-ureteric reflux causing chronic pyelonephritis
What are the complications of CKD?
CRF HEALS:
- CVD (most common cause of mortality)
- Renal osteodystrophy
- Fluid (oedema)
- HTN
- Electrolyte disturbances (hyperkalaemia, acidosis)
- Anaemia
- Leg restlessness (uraemia)
- Sensory neuropathy (uraemia)
CKD management
Preserving kidney function:
- WL, smoking cessation
- Control HTN = BP < 140/90 if ACR <70, or 130/80 if ACR > 70
- Control underlying cause
- Avoid nephrotoxic meds
- Statin and anti-platelets for CVD prevention
- ACEi/ARBs for renal protection
Management of complications:
- Proteinuria = ACEi/ARBs
- Anaemia = investigate source first, if renal then offer EPO
- CKD-mineral bone disorder = dietary [phosphate restriction, phosphate binders and activated vit D
- Oedema = salt restriction +/- diuretics
- Acid-base balance = oral sodium bicarb
Renal replacement therapy:
- Peritoneal/haemodialysis
- Kidney transplant
When do you refer a pt with CKD to the Nephrologist?
- 5-year risk of needing renal replacement therapy >5% as per kidney failure equation
- uACR > 70
- uACR > 30 w/ haematuria
- A decrease in eGFR of > 25% or change in eGFR category w/in 12 months
- A decrease in eGFR of 15 or more per year
- Uncontrolled HTN on 4 agents of more
- Suspected genetic causes
- Suspected RAS
What happens in CKD-related mineral bone disorder?
- Renal excretion of phosphate in response to PTH is impaired
- This leads to an accumulation of phosphate, which triggers more PTH release = secondary hyperparathyroidism
- There is also less 1-alphahydroxylase, and thus less vit D is activated
- Overall this results in low/normal Ca, low Vit D, high phosphate and high PTH
- Can eventually become tertiary hyperparathyroidism or result in renal osteodystrophy
What type of anaemia is seen in CKD?
Normocytic and normochromic
What are the types of Renal osteodystrophy?
Osteitis fibrosa:
- High PTH causes excessive bone breakdown via osteoclasts
- This results in weakened bones
- Symptoms = bone pain and fractures of the long bones and spine
Osteomalacia:
- Due to activated Vit D deficiency
Adynamic bone disease:
- When the bone doesn’t renew itself properly, usually due to low PTH levels
- Characterised by low bone turnover, decreased bone mineralisation and thin osteoid seems
- Symptoms = fractures and CVD
Mixed renal osteodystrophy:
- Signs of osteitis fibrosa and osteomalacia
Define Fibromuscular dysplasia
A non-atherosclerotic, non-inflammatory arterial disease which primarily involves the renal and carotid arteries, but may effect any vascular bed.
Predominantly affects women 30 - 50
Fibromuscular dysplasia features
Renal artery FMD:
- Reno-vascular HTN
- Multifocal stenosis w/ “string of beads” appearance on angiography
Carotid FMD:
- Symptoms related to cerebral ischaemia or dissection
Fibromuscular dysplasia management
- Anti-hypertensives for renal FMD
- Percutaneous angioplasty for severe stenosis
- Reconstructive surgery for complex cases
Define Membranoproliferative glomerulonephritis
A cause of glomerulonephritis where a build-up of abs in the glomerular BM leads to activation of the complement system
Membranoproliferative glomerulonephritis features
Can cause either nephrotic or nephritic syndrome
Nephritic more common
What are the causes of Membranoproliferative glomerulonephritis?
- Hep C
- Mixed cryoglobulinemia
- Monoclonal gammopathies
- AI diseases
