Renal + urology Flashcards
(83 cards)
Gitelman syndrome
Mutations in the thiazide-sensitive Na/Cl symporter
Autosomal recessive
Features:
- Normotensive
- Low Cl-, K+, Mg2+, Ca2+
- Metabolic alkalosis
- Raised urinary Na+ and K+
Investigations:
- Bloods
- 24h urinary Na+ and K+
Management:
- K+ and Mg 2+ supplementation
- Trial of aldosterone antagonists
Conn syndrome
Primary hyperaldosteronism
- Usually due to adrenal adenoma
Features:
- Hypertension
- Normal/raised Na+, low K+
Management:
- Aldosterone antagonists
- Adrenalectomy
Liddle syndrome
Pseudo-hyperaldosteronism due to mutations in the ENaC
- Autosomal dominant
- Increase ENaC activity = increased Na+ reabsorption
Features:
- HTN
- Hypokalaemia
- Metabolic alkalosis
- Low renin + aldosterone
Management:
- Potassium-sparing diuretics e.g. amiloride
Acute interstitial nephritis
Inflammation of the renal tubulointerstitium
Aetiology:
- Drug hypersensitivity
- Rifampicin, allopurinol, antibiotics, NSAIDs
- Autoimmune
- SLE, Sjogrens
- Idiopathic (rare)
- Viral
- Hantavirus
- Bacterial
- Leptospirosis, mycobacteria
Features:
- AKI
- Fever
- Eosinophilia
- Sterile pyuria
- Nephrotic syndrome if NSAID-induced
Management:
- Treat cause
- Steroids
Renal tubular acidosis
Type I - distal
- Failure of distal and collecting tubular cells to secrete H+ and reabsorb K+
- Features:
- Renal stones - due to urinary alkalosis +
increased secretion of Ca2+ in serum
acidosis
- Diabetes insipidus
- Salt wasting
- Severe metabolic acidosis + hypokalaemia
Type II - proximal
- Failure of proximal tubule cells to reabsorb HCO3
- Features:
- Mild metabolic acidosis +/- hypokalaemia
- Osteomalacia
- Rickets
Type III
- Combined type I and type II
Type IV
- Either low serum aldosterone or renal resistance to aldosterone activity
- Features:
- Hyperkalaemia
- CKD
Type 1 renal tubular acidosis
Failure of distal and collecting tubular cells to secrete H+ and reabsorb K+
Aetiology:
- Idiopathic or genetic
- Autoimmune disease
- Nephrocalcinosis
- Drugs incl. lithium
Features:
- Renal stones
- due to urinary alkalosis + increased secretion
of Ca2+ in serum acidosis
- Diabetes insipidus
- Salt wasting
- Severe metabolic acidosis + hypokalaemia
Type 2 renal tubular acidosis
Failure of proximal tubule cells to reabsorb HCO3
Aetiology:
- Idiopathic
- Fanconi syndrome
- Drugs incl. NSAIDs, heavy metals
Features:
- Mild metabolic acidosis +/- hypokalaemia
- Osteomalacia
- Rickets
Fluid requirements
Adult:
25-30 ml/kg/day
50-100g glucose
Child:
- 100ml/kg/day for first 10kg, then 50ml/kg/day for next 10kg, then 20ml/kg/day for the remainder
Central pontine myelinolysis (osmotic demyelination syndrome)
A disorder in which myelin +/- neuronal cells are damaged by rapid correction of hyponatraemia
- A rise of > 1 mmol/hr or >10 mmol/day
- Symptoms start 2-3 days after hyponatraemia
Features:
- Reduced GCS
- Confusion
- Limb weakness, paralysis, paraesthesia
- Dysphagia
- Dysphasia
- Impaired coordination
- Can progress to coma/death
Management:
- Supportive
- May recover over months or be left with permanent disability
Functional parts of kidney
Glomerulus
- Receives 600ml/min
- Filters (GFR) 120ml/min
- Filtration depends on molecular weight and charge of molecule
- Foot processes and BM are -ve charge
- Molecules > 4nm are completely blocked (e.g. cells, protein), 2-4nm partially blocked.
PCT
- 70% of reabsorption - esp. glucose, amino acids
- Completely permeable to water and glucose
- Secretes HCO3 to allow H+ reabsorption
- Can vary amount of isotonic reabsorption to modulate the ECF
- Contains a number of organic ion transporters which affect excretion of hormones, drugs, etc.
Loop of Henle
- Establishes the medullary concentration gradient to allow for later reabsorption
DCT
- Contains K+/H+ antiporters which help to maintain plasma K+ and pH
Collecting duct
- Site of ADH action -> aquaporin insertion allowing for reabsorption down the medullary concentration gradient
Afferent and efferent arterioles
Can be modulated by systemic NA/Adr or by local mechanisms to maintain GFR across a range of cardiac outputs
Afferent
- Constriction -> reduced rate filtration, same amount of filtrate
- Myogenic response
- Constricts when stretched due to stretch-
activated calcium channels
Efferent
- Constriction -> increased rate of filtration
- Dilation -> reduced rate of filtration
Renin-aldosterone-angiotensin system
Renin:
- Proteolytic enzyme
- Secreted by juxtaglomerular cells in the afferent arteriole in response to:
- NA action on beta-1 adrenoceptors
- Fall in afferent arteriole stretch
- Decreased Na+ load at the macula densa
- Catalyses cleavage of angiotensinogen to angiotensin - 1
Angiotensin:
- 2 step production:
- Angiotensinogen + renin -> angiotensin -1
- angiotensin-1 + ACE -> angiotensin-2
- AT1 stimulation
- Vasoconstriction - raises BP and GFR
- Increased Na+ reabsorption
- AT2 stimulation
- Increases thirst + Na+ appetite
- Stimulates aldosterone synthesis
Aldosterone:
- Acts on thick ascending limb + collecting ducts to promote Na+ reabsorption, H+ and K+ secretion
- Slowly increases expression of ENAC
Atrial and brain natriuretic peptides (ANP, BNP)
ANP
- Stored in atrial myocytes
- Released in response to atrial stretch (aka high BP)
- Stimulates Na+ and water loss, inhibits ADH and renin
BNP
- Cleaved from NT-proBNP
- Binds to ANP receptors although with reduced efficacy
- Found in brain and heart
ADH/vasopressin
Synthesised in the SON and PVN, stored in nerve terminals in the posterior pituitary
- Release dependent on osmoreceptors
Effects:
- V1
- Vasoconstriction
- V2
- Aquaporin insertion -> increased water
reabsorption
Hereditary angioedema
Mutation/deficiency in C1INH (C1 esterase inhibitor) leading to excessive bradykinin levels and episodes of painful swelling
- Similar mechanism can lead to angioedema
with ACEi use
Management
- Ecallantide - synthetic C1INH
Hypernatraemia
Aetiology:
- Diabetes insipidus
- HHS
- Dehydration
- ATN - early polyuric phase
- Diuretics
- Steroid excess - Cushing, Conn
- Salt poisoning - iatrogenic (NaCl, sodium bicarb), drowning in salt water, high sodium feed
Features:
- Mild (140-180)
- Can be asymptomatic
- Excessive thirst, confusion
- Severe (> 180)
- Ataxia, tremor, coma, seizures
- Raised ICP
Management:
- Aim reduction no greater than 10 mmol/day otherwise risk cerebral oedema
- Hypovolaemic
- Fluid resus + 5% dex
- Euvolaemic
- 5% dex
- Hypervolaemic
- 5% dex + loop diuretic
Hyponatraemia
Hypertonic
- Serum osmolality > 285
- Hyperglycaemia
- Mannitol infusion
Isotonic
- Serum osmolality 280-285
- Hyperlipidaemia or paraproteinaemia
Hypotonic
- Serum osmolality < 280
- Hypovolaemic
- Urine Na < 20
- Vomiting
- Diarrhoea
- 3rd spacing
- Urine Na > 20
- Diuretics
- Addisons’
- Salt wasting nephropathy
- Euvolaemic
- Urine osmolality > 100
- Primary polydipsia
- Beer potomania
- Ecstasy
- Urine osmolality < 100
- SIADH
- Hypothyroidism
- ACTH deficiency
- Hypervolaemic
- Urine Na < 20
- Heart failure
- Liver failure
- Nephrotic syndrome
- Urine Na > 20
- Kidney failure
Severe hyponatraemia management
aka symptomatic with seizures and drowsiness
Admit to ITU
- Aim initial rise of 1-2 mmol/hr over first 3 hr
- Can raise Na+ > 10mmol/day with care
Calculate sodium deficit:
Fluid [Na] - serum [Na]/1 + total body water
(1L 0.9% NaCl = 154 mmol)
Hypoalbuminaemia
Aetiology:
- Decreased production
- Chronic inflammation
- Severe malnutrition
- Liver cirrhosis
- Increased loss
- Renal - nephrotic syndrome
- GI - erosive (IBD, malignancy, PUD), non-
erosive (coeliac, sprue, SIBO, Whipples),
raised lymphatic pressure (CCF, mesenteric
TB)
- 3rd spacing
- Increased catabolism
- Prolonged severe illness e.g. ITU
Management:
- Mostly supportive + treat underlying cause
- HAS if cirrhosis or haemodynamic instability not responding to crystalloids alone
SIADH
Aetiology:
- Malignancy
- SCLC, pancreatic, prostate
- Infections
- TB
- Neurological
- Stroke, SAH, abscess
- Drugs
- SSRIs, Indomethacin, TCAs, thiazide diuretics,
antipsychotics, cyclophosphamide, vincristine
Investigations:
- Paired urine + serum osmolality
- Paired urine + serum sodium
- Water deprivation testing
Management:
- Fluid restriction
- Demeclocycline
Hyperkalaemia
Aetiology:
- Kidney failure
- Rhabdomyolysis
- Tumour lysis
- Metabolic acidosis
- Hypoglycaemia
Features:
- Muscle weakness
- Paraesthesias
- Palpitations
- Arrhythmia
Investigations:
- Bloods
- ECG - tall tented T waves, broad QRS
Management:
- Calcium gluconate 10ml over 10 mins, repeated
- Insulin/dextrose - 10 units in 250ml 10% dextrose
- Salbutamol nebs 5-10mg
Hypokalaemia
Aetiology
- Vomiting or diarrhoea
- Loop and thiazide diuretics
- Conn’s syndrome
- Laxative abuse
- Metabolic alkalosis
- Insulin therapy
- Refeeding syndrome
Features:
- Muscle weakness + myalgia + cramps
- Tremor
- Palpitations
- Constipation
Investigations:
- Bloods
- ECG - T wave flattening/inversion, U waves, QT prolongation
Management:
- Treat underlying cause
- Sando-K TT TDS
- IV KCl
Hypercalcaemia
Aetiology
- Malignancy
- Hyperparathyroidism
- Multiple myeloma
- Dehydration
- Paget’s disease
- Addison’s disease
- CKD
Features:
- Bone pain
- Fatigue, weight loss
- Constipation
- Kidney stones, kidney impairment
- Depression, psychosis
Investigations
- Routine bloods
- TFTs, PTH level, vitamin D
- ECG - shortened QTc
- Imaging of bones
Management:
- Acute:
- IV fluids
- IV bisphosphonates
Hypocalcaemia
Aetiology:
- Vitamin D deficiency
- Hypoparathyroidism (incl. post-surgical)
Features:
- Muscle cramps, twitching -> tetany
- Paraesthesias
- Carpopedal spasms
- Chvostek’s + Trousseau’s signs
- Risk of laryngeal tetany and asphyxiation
Investigations:
- Routine bloods
- PTH and vitamin D levels
- ECG - prolonged QTc
Management:
- Acute (calcium < 1.9, symptoms)
- IV calcium gluconate
- Chronic:
- Cholecalciferol (if vit D deficient)
- Calcitriol (if PTH deficient)