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
Membranoproliferative glomerulonephritis investigations
- Urinalysis = +ve for blood and protein
- MC&S = dysmorphic RBC which suggest bleeding from the glomerular
- Acute renal screen
- Renal biopsy (gold standard) = double contour of the BM
Membranoproliferative glomerulonephritis management
- No cure
- Aim to reduce CVD risk = reduce salt intake, treat HTN
- Treat proteinuria w/ ACEi/ARBs
- Treat underlying cause
50% of pts progress to ESKD by 10 years
Define End-stage kidney disease (ESKD)
eGFR < 15, or pt on dialysis
What are the causative agents in Infection-associated glomerulonephritis?
Bacterial:
- Streps
- Staphs
- Pneumococcal
Viral:
- Hep B
- EBV
- CMV
- Influenza
- Mumps
- Rubella
Fungal:
- Candidiasis
Parasitic:
- Malaria
- Toxoplasmosis
- Schistosomiasis
What are the causes of Glomerulonephritis?
Nephritic:
- IgA nephropathy
- Rapidly progressive = vasculitis/GMB disease
- Membranoproliferative
- Infective-associated
- IgA vasculitis (Henoch-Schonlein)
- SLE
Nephrotic:
- Minimal change disease
- Membranous
- Focal segmental glomerulosclerosis
- Membranoproliferative
- IgA nephropathy
- SLE
- DM
- Amyloidosis
What’s the difference between membranous glomerulonephritis vs membranoproliferative?
The part of the kidney affected
Membranous = BM and capillary walls, causes them to thicken
Membranoproliferative = BM and mesangium, causes them to split
Define Haemolytic uraemic syndrome
The triad of microangiopathic haemolytic anaemia, thrombocytopenia and AKI
What are the causes of Haemolytic uraemic syndrome?
Typical:
- E.coli
- Shigella
- Salmonella
- Yersinia
- Campylobacter
Atypical:
- Inherited
- AI complement deficiencies
Haemolytic uraemic syndrome investigations
- Urinalysis = blood and protein
- FBC = normocytic anaemia due to haemolysis, thrombocytopenia and raised neutrophils
- U&Es = raised urea and creatinine
- Blood film = reticulocytes and schistocytes due to MAHA
- Low haptoglobin due to haemolysis
- Stool culture to identify causative organism
Haemolytic uraemic syndrome management
Typical = supportive, including renal support if necessary
Atypical = refer to specialist centre for eculizumab treatment
Define IgA nephropathy
A type of glomerulonephritis due to the deposition of IgA in the mesangium of the glomerulus
Generally occurs 12-72 hours after an URTI or GI infection
Most common cause of GN
IgA nephropathy features
- Gross or microscopic haematuria
- Mild proteinuria
- HTN
- Less commonly presents w/ nephrotic syndrome or rapidly progressive GN
IgA nephropathy investigations
- Urinalysis and MC&S = blood/protein, dysmorphic RBC
- Renal biopsy (gold standard) = diffuse mesangial IgA deposition
- Serum IgA elevated in 50% of pts
IgA nephropathy management
Reduction of CVD risk:
- Reduced salt intake
- Proteinuria management w/ ACEi/ARBs
- HTN management
Pts stratified into low/high risk of progression to CKD:
- High = corticosteroid treatment
- Immunosuppression for those in rapidly progressive GN
Define Nephritic syndrome
A combo of:
- Haematuria
- Non-nephrotic range proteinuria (+/++ on dipstick)
- HTN
- Mild oedema
This symptoms are topically due to glomerular inflammation and damage to the tiny blood vessels w/in the kidneys
Nephritic syndrome management
- Treat the underlying cause
- Treat the symptoms = antihypertensives, diuretics, ACEi
- Monitor renal function
- Low sodium diet
- Renal replacement therapy if ESKD
Define Nephrotic syndrome
A clinical syndrome that arises secondary to increased permeability of serum proteins through a damaged glomerular BM
Nephrotic syndrome features
- Proteinuria (> 3-3.5 g/day)
- Oedema (esp periorbital and peripheral)
- Hypoalbuminaemia
- Hyperlipidaemia
- Lipiduria
Nephrotic syndrome investigations
- Dipstick = proteinuria +++
- Urinalysis = raised ACR
- Renal biopsy - indicated in all adults and children w/ atypical presentation (steroid unresponsiveness, haematuria, under 1 years or over 12 years old)
Nephrotic syndrome management
High dose corticosteroids
What are the complications of Nephrotic syndrome?
- Infection = due to loss of urinary Ig
- VTE = due to urinary loss of antithrombin III
- Hyperlipidaemia = due to increased hepatic production of lipids to restore serum oncotic pressures
Define Post-streptococcal glomerulonephritis
An immune-complex mediated GN that occurs 1-3 weeks after a strep URTI
More commonly occurs in children
Post-streptococcal glomerulonephritis features
- Sudden onset haematuria, oliguria, HTN and/or oedema 1-3 weeks post infection
- Some pts are asymptomatic w/ microscopic haematuria
Post-streptococcal glomerulonephritis investigations
- Urinalyis and MC&S = blood, dysmorphic RBCs
- FBC = raised WCC
- U&Es = AKI
- Ig, complement and autoantibodies (anti-steptolysin) to confirm diagnosis
- Renal biopsy (gold standard in adults) = subepithelial humps
Post-streptococcal glomerulonephritis management
- Treat AKI
- Usually self-limiting
Define Proteinuria
Abnormal protein in the urine - can cause the urine to be foamy/frothy
1+ on dipstick = 30mg/dL
3+ = 300mg/dL
Proteinuria management
- ACEi/ARBs to control HTN and to directly reduce proteinuria
- Treat underlying cause
- Renal replacement therapy in ESKD
Define Rapidly progressive glomerulonephritis
A range of conditions associated w/ severe glomerular damage (glomerular cresenteric formation)
It is characterised by nephritic syndrome liked w/ rapid and progressive loss of renal function
What are the subtypes of Rapidly progressive glomerulonephritis?
Type 1:
- Anti-GMB antibody disease
- Linear pattern of IgG deposits on immunofluorescence
Type 2:
- Immune complex deposition disease
- This is secondary to any immune complex nephritic disease = PSGN, lupus nephritis, IgA nephropathy, IgA vasculitis
- Usually has a granular pattern of staining on immunofluorescence
Type 3:
- Pauci-immune disease
- Defined by the absence of anti-GBM abs or immune complexes as shown by immunofluorescence and electron microscopy
- Primarily mediated by ANCAs
Rapidly progressive glomerulonephritis features
- Oliguria
- Nephritic syndrome
- Fatigue/weakness
- Anorexia
- N&V
- Persistent hiccups
Rapidly progressive glomerulonephritis management
- supportive care for AKI
- Corticosteroids and cyclophosphamide to induce immunosupression and remission
- Treat underlying cause
Summaries Haemodialysis
- Pts blood flows in a counter-current against the dialysate on opposite sides of a semi-permeable membrane
- Solutes transfer via diffusion and water leaves via ultrafiltration
- Treatments is scheduled for 4 hours 3x a week
- Requires an arterio-venous fistula, tunnelled haemodialysis catheter or temporary vascath for access
Summaries Haemofiltration
- Uses convection to remove solutes and fluids
- Doesn’t require dialysate, but a replacement fluid is needed
- This is a continuous treatment usually done on ICU
- A temporary vascath is required for access
What are the complications of Haemodialysis?
- Cramps
- N&V
- CVD
- Dialyser reactions = accidental disconnection, air embolus, hypotension
- Fistula-related = bleeding, stenosis, thrombosis, aneurysm, infection, steal syndrome, HOHF
- Line-related = infection, malfunctions
- Amyloidosis
- Dialysis disequilibrium syndrome = acute cerebral oedema due to rapid extraction of osmotically active substances)
- Vascular calcification
- malnutrition
- Psychosocial implications
Summarise Peritoneal dialysis
- The diffusion of solutes and water from the blood into the peritoneum across the peritoneal membrane through a PD catheter
- The fluid is then exchanged and replaced
What are the complications of Peritoneal dialysis?
- Peritonitis
- Exit-site and tunnel infections
- Peritoneal leaks
- catheter malfunctions
- Hernias
- Long term use = sclerosing encapsulated peritonitis (thickening and calcification of the peritoneal cavity leading to bowel obstruction)
What are the different types of renal stones?
- Calcium oxalate stones = 85% of stones, radiopaque, linked to hypercalcaemia
- Calcium phosphate stones = radiopaque, linked to renal tubular acidosis types 1&3
- Cystine = semi-opaque, ground glass appearance., due to inborn errors of metabolism
- Uric acid = radiolucent, liked to diseases causing extensive tissue breakdown
- Struvite =, radiopaque, formed from magnesium, ammonium and phosphate, associated w/ chronic UTIs
- Indinavir = associated w/ the antiretroviral protease inhibitor indinavir used in HIV treatment , radiolucent stones of the drug
Renal stones management
Analgesia = diclofenac (preferred rectally) or codeine
Stones < 5mm:
- If no signs of obstruction = watchful waiting for pt to pass the stone
Stones < 2cm:
- Extracorporeal shockwave lithotripsy
- Ureteroscopy = treatment for distal or mid ureteric stones and for pregnant women - can place a stent to prevent obstruction
Stones > 2cm:
- Percutaneous nephrolithotomy
Prophylaxis = thiazides for hypercalcaemia, allopurinol
What are the types of kidney transplant rejection?
Hyperacute:
- Within minutes
- Due to ABO/HLA incompatibility
- Prevents w/ graft thrombosis and systemic inflammatory response syndrome
- Managed by immediate graft removal
Acute:
- W/in first 6 months
- May be T cell or ab mediated
- Presents w/ an acute decline in graft function +/- fever, malaise and tenderness
Chronic:
- After 6 months
- Usually characterised by interstitial fibrosis and tubular atrophy
Define Renal tubular acidosis
A group of disorders marked by an impairment in the renal tubules ability to handle acids
This dysfunction leads to a state of normal anion gap metabolic acidosis while renal function remains w/in the normal parameters
What are the 3 main types of Renal tubular acidosis, and what causes them?
Type 1:
- Characterised by the distal renal collecting duct’s inability to excrete hydrogen ion
- This leads to a persistent state of hypokalaemic, hyperchloremic metabolic acidosis
Type 2:
- Due to a defect in bicarb reabsorption in the proximal collecting tubule
- This causes bicarb wasting and a normal anion gap metabolic acidosis
- Often linked to Fanconi syndrome
Type 4:
- Due to hyporeninaemic hypoaldosteronism
- Low levels of aldosterone result in hyperkalaemia
- This impairs ammonium secretion leading to acidosis
What are the causes of Type 1 Renal tubular acidosis?
- AI = Sjogren’s, SLE, RA
- Drugs = Analgesia, lithium
- Nephrocalcinosis
- Chronic tubulointerstitial nephritis
What are the causes of Type 2 Renal tubular acidosis?
- Myeloma
- Cystinosis
- Lead or cadmium toxicity
- Drugs = acetazolamide, aminoglycosides
What are the causes of Type 4 Renal tubular acidosis?
- DM
- NSAIDs
- Obstructive uropathy
- Addison’s disease
- Chronic tubulointerstitial nephritis
Fanconi syndrome features
Type 2 renal tubular acidosis + glycosuria + proteinuria + phosphaturia
Type 1 Renal tubular acidosis features
- Hypokalaemic, hyperchloremic metabolic acidosis
- Rickets/osteomalacia
- Nephrocalcinosis and renal stones
- Increased urinary pH > 5.3
- Hypokalaemia
Type 1 Renal tubular acidosis management
Urine alkalinisation w/ potassium citrate or sodium bicarb
Type 2 Renal tubular acidosis features
- Hypokalaemic, hyperchloremic metabolic acidosis
- Urinary pH < 5.3
- Hypokalaemia
Type 2 Renal tubular acidosis management
- Urinary alkalinisation w/ potassium citrate
- Consider thiazide diuretics
Type 4 Renal tubular acidosis features
- Normal anion gap metabolic acidosis
- Hyperkalaemia
Type 4 Renal tubular acidosis management
Mineralocorticoid replacement
Define Renal artery stenosis
Narrowing of one or both renal arteries, compromising blood flow to the kidneys
Primarily caused by atherosclerosis in pts > 50, or fibromuscular dysplasia in < 50s
Can also be caused by thromboembolisms, or external mass compressions
Renal artery stenosis features
- Worsening renal function following initiation of an ACEi due to their effects on glomerular perfusion
- Refractory HTN
- Acute flash pulmonary oedema w/out evidence of cardiac dysfunction - indicative of server or bilateral disease
Renal artery stenosis investigations
- U&Es before ACEi
- Renal USS = may show small kidneys
- Renal angiography (gold standard)
Renal artery stenosis management
- Manage RF for atherosclerosis
- Definitive = transluminal angioplasty =/- stenting
Define Rhabdomyolysis
A condition characterised by the rapid breakdown of and necrosis of skeletal muscle tissue, leading to the release of harmful intracellular contents - mainly myoglobin and potassium
Rhabdomyolysis features
- Muscle pain and welling = usually severe and disproportionate
- Red/brown urine = myoglobulinaemia
- AKI
Rhabdomyolysis investigations
- Serum CK = 5x rise from the upper limit
- LDH
- U&Es = hyperkalaemia, hyperphosphatemia, and hyperuricaemia
- Hypocalcaemia (as calcium is sequestered into the damaged muscle)
- Urine dipstick +ve for blood w/out evidence of RBC on microscopy = myoglobin
Rhabdomyolysis management
Supportive care w/ fluid resus
Define Chronic urinary retention
Lon-term inability of the bladder to completely evacuate its contents
This leads to a progressive bladder enlargement and may cause complete bladder contraction failure
Pts may retain up to 4-5L
What’s the difference in presentation between acute and chronic urinary retention?
No pain or urge to urinate in chronic
What are the classifications of Chronic urinary retention?
Low pressure:
- Due to detrusor inactivity
- Causes distention of the bladder but no back pressure into the kidneys
High pressure:
- Detrusor muscle is still active
- Urine backs up into the kidneys and can cause hydronephrosis
What are the causes of Chronic urinary retention?
- BPH (most common)
- Prostate cancer
- Antihistamines
- Anticholinergics
- Antispasmodics
Chronic urinary retention features
Can be divided into storage or voiding
Storage:
- Frequency
- Hesitancy
- Lower abdo swelling
Voiding:
- Urgency
- Dribbling
- Poor stream
- Nocturia
- Nocturnal enuresis
- Incontinence
Can be asymptomatic
Pyelonephritis features
- Fever/rigors
- Malaise
- Loin/flank pain/tenderness
- Vomiting
- Urine dip +ve for leucocytes and nitrites
Pyelonephritis management
- Admit to hospital for IV abx
- Start w/ broad spectrum cephalosporins, quinolones or gentamicin
- Then treat based on sensitivity
Hydronephrosis features
- Sudden intense loin/flank pain
- Ballotable kidneys
- N&V
- Signs of UTI (more likely as urine is in stasis)
- Fever
Hydronephrosis management
- Urgent nephrostomy to decompress the kidneys
- Removal of obstruction
