Renal quickfire Flashcards
Urinary sodium concentration - what value indicates normal renal tubular function?
Urinary sodium concentration < 10 mmol/L
(ATN will generally cause urine Na >40)
Drugs that cause inhibition of creatinine secretion, so cause a rise in serum creatinine without actually affecting renal function (pseudo-AKI)
Trimethoprim, co-trimoxazole (note - this can also cause type 4 RTA)
Cimetidine
Renal tubular acidosis
- 4 types, causes and features
- Tests to confirm RTA
- Which one causes hypercalciuria and stones?
Type 1 (distal)
- Failure of H+/K+ co-transporter (inability to acidify the urine, retain too much H+)
- Causes: SLE, Sjogren’s, RA, Sickle cell, renal transplant rejection, chronic pyelonephritis, lithium, amphotericin
- Features: low K+, NAGMA, calcium stone formation (does not occur in the other RTAs) and bone demineralisation (hypercalciuria and calcium loss), high urinary pH (>5.5)
Type 2 (proximal)
- Failure of HCO3- reabsorption (lose too much bicarb)
- Causes: Fanconi syndrome, amyloidosis, myeloma, Wilson’s (all cause loss of protein), acetazolamide
- Features: hypoK+ (due to secondary hyperaldosteronism), NAGMA, bone demineralisation (hypophosphataemia, vit D deficiency), appropriately acidic pH (<5.5)
Type 3 (combined proximal + distal)
Type 4 (hyperkalaemic)
- Aldosterone antagonism
- Low aldosterone, low renin (hyporeninaemic hypoaldosteronism)
- Causes: diabetes*, obstructive uropathy, Addisons, trimethoprim, NSAIDs, ACE/ARB, spironolactone, LMWH, ciclosporin/tacrolimus
*reduces conversion of prorenin to renin
To confirm RTA:
1. Confirm normal anion gap metabolic acidosis
2. Take urinary sample:
- If pH >5.5 –> type 1 (distal) RTA
- If low/absent urine ammonium –> type 4 (hyperkalaemic)
3. Bicarbonate infusion test
- If fractional bicarbonate excretion exceeds 15% –> type 2 (proximal) RTA
Renal papillary necrosis
a) What is it?
b) Causes (POSTCARDS)
c) Features
d) Treatment
a) Necrosis of the renal papillae due to ischaemia
b) Pyelonephritis, obstruction of the urogenital tract, sickle cell disease, tuberculosis, cirrhosis of the liver, analgesia/alcohol use disorder, renal vein thrombosis, diabetes mellitus, and systemic vasculitis.
c) Back/loin pain, dysuria, fever, passing debris, haematuria, oliguria
d) Supportive
Stenting if any obstruction
HAGMA vs NAGMA
(MUDPILES vs ABCD)
HAGMA
- Exogenous acid excess
Methanol (alcohol)/metformin
Uraemia
DKA (or other ketoacidosis)
Paracetamol/propylene glycol/paraldehyde
Iron/Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates (aspirin)
NAGMA
- Bicarb loss/chloride excess
Addisons/acetazolamide
Bicarb loss (RTA)
Chloride excess
Diuretics/diarrhoea
ATN
a) Causes
b) Phases
c) Diagnosis (vs. pre-renal AKI)
d) Urine dipstick
e) Complications
a) Acute ischaemic/nephrotoxic event (sepsis, hypotension, rhabdomyolysis, NSAID, contrast, gentamicin, amphotericin B etc.)
b) Initiation phase - acute rise in Cr +/- oliguria
Maintenance phase - sustained rise in Cr (lasts 1-2 weeks)
Recovery phase - tubular function restored, Cr falls, urine volume rises
c) Urine Na >30 (vs pre-renal: urine Na <10*)
Urine osmolality = plasma osmolality (vs pre-renal: high urine osmolality)
*due to low renal perfusion driving aldosterone which reabsorbs Na from the tubules
d) “Bland” urine dipstick - generally no blood/protein/etc.
e) - Infection - gram negative sepsis is most common cause of death
- ESRF
- Fluid overload
AIN
a) What is it?
b) Causes
c) Presentation and urine dip
d) Biopsy results
e) Clinical course and treatment
f) vs. Chronic interstitial nephritis
a) AIN is a hypersensitivity reaction, characterised by inflammation
b) It is usually drug-induced (e.g. penicillins, fluroquinolones, allopurinol, NSAIDs*) but may be caused by certain infections, sarcoid, Sjogren’s malignancy, TINU syndrome
*may also cause ATN
c) 10% cases are associated with classic triad of fever, rash and eosinophilia. Also commonly have arthralgia
- Mild proteinuria and leukocyturia common
- May also have haematuria
(vs ATN which has a ‘bland urinalysis’)
d) Renal biopsy demonstrates interstitial immune infiltrate, eosinophils, and tubulitis
e) Generally improves once offending agent removed
- if severe, give steroids
f) CIN has gradual increase of creatinine over time, blood and protein on urine dip, often due to chronic NSAID use
Renal stones
- Compositions and risk factors
- Treatment of hypercalciuric stone formers
- Which are not radio-opaque? And how do we test for them?
Calcium oxalate
- Short bowel syndrome, small bowel malabsorption
- High oxalate diet e.g. rhubarb
Calcium phosphate
- Hypercalciuria - hyperPTH, acidosis, positive FHx
Calcium urate
- Hyperuricaemia, gout
- Urinary pH <5.5
Ammonium magnesium phosphate
- “Staghorn” calculi
- Proteus, klebsiella or serratia species - urea splitting bacteria
- Causes raised urine pH
Cystine
- Homocystinuria (autosomal recessive)
- Treat with penicillamine
- Not radio-opaque
- Urine microscopy would reveal hexagon shaped crystals
- Diagnostic test is with cyanide-nitroprusside - reveals cystine
Hypercalciuric stones
- Potassium citrate generally preferred
- If very hypercalciuric, may treat with thiazide diuretics (reabsorb calcium in the tubules)
Von-hippel lindau
a) Clinical features (HIPPEL)
b) Inheritance
c) Test recommended from age 10
Haemangioma (cerebellar), haemangioblastoma (retinal)
Increased risk of RCC
Pancreatic endocrine tumour/cysts
Phaeochromocytomas
Epididymal tumours
Liver, renal and pancreatic cysts
b) VHL gene on chromosome 3
Autosomal dominant inheritance
c) Urinary catecholamines
Dialysis related amyloidosis
a) Protein accumulation
b) Presentation
c) Management
a) beta-2 microglobulin - causes amyloidosis
b) - Usually after around 5 years of dialysis
- Generally affects the bones/tendons, but can also affect GI tract (dysphagia), heart (constrictive pericarditis), lung, etc.
- Causes bilateral shoulder pain/stiffness, carpal tunnel syndrome and tenosynovitis commonly
c) Pain control
- If CTS, refer for surgery - flexor retinaculum release
Medullary sponge kidney
a) What is it?
b) Appearance on imaging
c) Complications
a) Congenital disorder with dilated collecting ducts, where cysts form in the renal tubules/collecting ducts, leading to outflow obstruction and increase risk of stones/infection
b) Papilllary blush or paint brush on early and delayed films during intravenous venography
c) Recurrent stones
Recurrent UTIs
RTA
10% progress to ESRD
No metabolic abnormalities on bloods generally
Wilms tumour
a) Cause
b) Associated condition
a) Deletion on short arm Chromosome 11 (Wilms Tumour has 11 letters)
b) WAGR:
Wilms tumour, aniridia, genitourinary malformation, retardation (low IQ)
Amyloidosis
a) Type of amyloid in AL amyloidosis (myeloma, MGUS, primary)
b) Type of amyloid in AA amyloidosis (secondary)
c) Type of amyloid in haemodialysis patients
a) Amyloid Lambda (light) chain amyloid
b) Amyloid A proteins
c) Beta-2 microglobulin
RTA quickfire
a) Which causes hypercalciuria and kidney stones?
b) Which is related to chronic NSAID use?
c) Which leads to hyporeninaemia, hypoaldosteronaemia and HYPERkalaemia?
d) Which is caused by inability to retain HCO3?
e) Which is caused by inability to acidify the urine and lose H+? (causing inappropriately high pH in presence of acidosis)
a) Type 1 (distal)
*Type one = stone (st-ONE)
b) Type 4
c) Type 4
d) Type 2 (proximal) - they lose everything, including bicarb
e) Type 1 (distal)
Causes of large kidneys
Hydronephrosis
Early diabetic nephropathy
Amyloidosis
ADKPD
Renal vein thrombosis
Acromegaly
Scleroderma renal crisis
a) Presentation
b) Pathogenesis
c) Antibody associated
d) More common in limited cutaneous (CREST) or diffuse Scl?
e) Treatment
a) - Malignant hypertension (hyper-reninaemic)
- Rapid progression to ESRF (but NOT glomerulonephritis)
- Microangiopathic haemolytic anaemia
b) Obliterative vasculopathy with thickened vascular endothelium and ‘onion skin’ lesions (think thick layers in scleroderma)
c) Anti-RNA polymerase 3
d) Diffuse scleroderma
(CREST classically has NO renal involvement)
e) ACE inhibitors
Dialysis if no improvement
(do NOT give steroids)
Pregnancy-related renal disease
a) Pre-eclampsia vs HELLP vs HUS vs TTP
a) Pre-eclampsia:
- After 20 weeks, and up to 6 weeks post-partum
- Proteinuria + hypertension
HELLP
- Haemolysis, elevated liver enzymes, low platelets
- Usually preceded by pre-eclampsia
- Presents with headache, nausea and vomiting, abdominal pain, blurred vision, bleeding
- Evidence of DIC (clotting abnormalities)
Post-partum HUS:
- Commonly 4-6 weeks post-partum
- Must consider retained products
- Presents with microangiopathic haemolytic anaemia, HTN and severe irreversible renal disease
- Schistocytes present on blood film, but clotting normal (vs HELLP)
TTP:
- Usually before 24 weeks gestation
- FRANT: fever, renal injury, anaemia (MAHA), neurology, thrombocytopenia
- Relatively mild renal injury
Anaemia, recurrent UTIs as a child and renal impairment
a) Likely diagnosis
b) Investigations and findings
c) Treatment
a) Vesico-ureteric reflux
b) US - likely 1 small kidney
VCUG - evident reflux
c) Intermittent ABx
EPO
a) Incidence of hypertension and mechanism
a) 30%
- Reduction in peripheral hypoxic vasodilatation and rise in plasma viscosity
Retroperitoneal fibrosis
a) Sex preponderance
b) Presentation
c) Causes
d) Diagnosis
e) Management
a) Males 2:1
b) - Lower back/abdo pain
- Compression of ureters causing reduced renal function and hydronephrosis
- Compression of vessels causing peripheral oedema, hydrocele and intermittent claudication
- Associated with HTN and VTE
c) Idiopathic
- Methysergide
- Infections e.g. syphilis, TB
- Malignancy, sarcoid, radiation, surgery
d) Ureter displacement towards the midline on imaging
e) Surgery +/- steroids
Barrter vs Gitelman vs Liddle
Barrter:
- NKCC2 transporter mutation
- Hypokalaemia, hyponatraemia, hypocalcaemia (hypercalciuric)
- High renin, high aldosterone (secondary hyperaldosteronism)
- Metabolic alkalosis
- Hypotension
- High renin, high aldosterone
- JGA hyperplasia on renal biopsy
- Rx: replacement
Gitelman:
- Thiazide sensitive sodium-chloride transporter
- Hypokalaemic, hyponatraemic, alkalosis
- Hypocalciuric (but not hypercalcaemic)
- Hypotension
- High renin, high aldosterone
- Rx: replacement
Liddle:
- ENaC channel
- Hypokalaemic alkalosis
- Normal sodium and calcium levels
- HYPERtension
- Low renin, low aldosterone
- Rx: potassium sparing diuretics (amiloride, not an MRA)
Causes of crystalluria
- Aciclovir - in presence of dehydration, crystalluria develops
- Protease inhibitors for HIV e.g. indinavir
- Sulfonamides
- Penicillins
Young patient with hypertension, commenced on ACE inhibitors, wakes up with sudden SOB. Bilateral creps on examination. Bloods show AKI.
a) Diagnosis?
b) Appearance of renal arteries on imaging
c) Management
a) Flash pulmonary oedema secondary to Fibromuscular dysplasia - causes bilateral RAS and secondary hypertension in younger patients
- note: in older patients you would consider atherosclerosis as more likely cause of bilateral RAS
b) Beaded appearance
c) - Surgical - angioplasty
(generally get worse with medical treatment)
50 year old lady with family history of renal disease, has progressive CKD, nephrotic range proteinuria and hepatosplenomegaly
a) Diagnosis?
a) Familial renal amyloidosis
