acute interstitial nephritis - what is it, causes, histology, presentation, investigation
what is the presentation and ix findings for tubulointerstitial nephritis with uveitis
it is a cause of drug induced kidney injury
causes: allopurinol, furosemide, penecillin, autoimmune stuff like SLE
on histology there is interstitial oedema and infiltrates between renal tubules
presents - allergy like rash and raised eosinophils, fever, deranged kidney function
ix: sterile pyuria, white cell casts
tubulointerstitial nephritis with uveitis typically effects young women, red eyes, fever, weight loss urinalysis is positive for leukocytes and protein.
CKD vs AKI
renal US will show bilateral small kidneys in CKD
in CKD you also see hypocalcaemia due to lack of vitamin D
exceptions to small kidney rules: ADPCKD, diabetic nephropathy, amyloidosis, hiv nephropathy
AKI - causes, rf for aki, signs, definition, ix, mx
pre-renal: renal artery stenosis, hypovolaemia
renal: tumour lysis, tubular necrosis, acute interstitial nephritis, rhabdo, glomerulonephritis
post renal: compression on ureter, kidney stone, prostate
rf: lack of urine, nephrotoxic drugs, ckd
signs: asymptomatic, reduced urine output, fluid overload, arrhythmia from high K, uraemia (encephalopathy, pericarditis)
defined: creat rise of 25 in 48 hours, or 50% in 7 days. <0.5ml/kg/hr urine output for 6 hours
ix: ue’s, US if renal tract for post-renal, urinalysis
stop diuretics, acei, arb, aminoglycosides, nsaids. also digoxin, metformin, lithium.
treat hyperkalaemia - calcium gluconate to stabilise heart, insulin/dextrose/ salbutamol to shift K into cells, calcium resonate and loop diuretics to get RID of it.
renal replacement therapy if all fails.
refer to nephrologist - ckd 4/5, vasc/glomerulonephritis/ myeloma
do acute tubular necrosis vs pre-renal uraemia
what is ADPKD, difference between types, presentations, extra-renal manifestations, ix, diagnostic criteria, management
most common inherited cause of kidney disease, autosomal dominant, Caucasians
type 1: 85%, chromosome 16, presents earlier
type 2: 15%, chromosome 4
features: HTN, recurrent UTI, flank pain and enlargement, haematuria, renal stones
extras: renal cysts, berry aneurysms, heart stuff, cysts can be anywhere
ix: abdominal US for relatives
diagnostic criteria: 2 cysts if < 30, 2 cysts in each kidney if 30- 59, 4 cysts in each kidney if >60
tolvaptan (vasopressin 2 receptor antagonist), may be useful if certain criteria met.
anti-hypertensives, drainage, avoid sports/nsaids/ anticoag due to cyst rupture. mr angiography used to screen for cerebral aneurysms.
alport’s syndrome - pathophysiology, typical q, presentation, ix for diagnosis
normally x-linked recessive pattern, collagen IV for glomerular basement membrane not coded properly
failed transplant. anti GBM antibodies form a goodpastures type picture
presents: microscopic haematuria, bilateral SN hearing loss, vision problems
ix: genetic testing, renal biopsy (splitting of lamina densa seen, basket weave appearance)
anion gap - how to calculate, normal, causes of normal anion gap met acidosis (hyperchloraemic), causes of raised anion gap.
(Na+K)-(chloride+bicarb)
8-14
normal anion gap: acetazolamide, GI loss of bicarb, renal tubukar acidosis
raised anion gap: high lactate, uraemia, chronic paracetamol use (5-oxoprolin), poisoning with salicylates and methanol, ketones
how to diagnose CKD and accelerated progression
eGFR < 60 over 3 months
or urine ACR> 3 over 3 months
accelerated progression: eGFR drop of 25% or 15 within 1 year
causes of CKD
hypertension
diabetes
lithium, nsaids aNd meds
PCKD
glomerulonephritis
complications of CKD
anaemia
renal bone disease
end-stage kidney failure
cardiovascular disease - left ventricular hypertrophy risk as well
anaemia: kidneys make less EPO, less erythropoeisis in bone marrow. so you get normochromic, normocytic anaemia. there’s also a reduced absorption of iron
renal bone disease: kidneys can’t excrete the phosphate so phosphate goes up. kidneys can’t activate vitamin D so calcium goes down. pth increases to counteract, causing a hyperparathyroidism. pth increase causes increase in osteoclasts (to break down bown and release calcium), this just causes osteomalacia. osteoblasts try and match them and build bone, but without enough calcium this just causes osteosclerosis as poor mineralisation. rugger jersey spine.
when to refer CKD patient to renal
eGFR<30
ACR >70
accelerated progression
4 antihypertensives and not controlled
management of CKD
optimise underlying cause - diabetes, hypertension, nephrotoxic meds
general: exercise and atorvastatin 20mg
BP: ACEi and SGLT2i, furosemide at later stages
metabolic acidosis: oral sodium bicarb
anaemia: first iron, then EPO. avoid transfusions to treat anaemia as they can sensitise patient.
renal bone: low phosphate diet, phosphate binders, high calcium, vitamin D
diet: low sodium, low potassium, low protein, low phosphate
diabetes insipidus - what is it, presentation, causes, investigations, tell me more about water deprivation test, management
ADH made is hypothalamus and stored in posterior pituitary. ADH allows water to be reabsorbed in collecting ducts. central is when there is no ADH, nephrogenic is when there is resistance to ADH
presents as excessive urination and thirst.
central causes: tumours, head injury, post-surgery
nephrogenic causes: lithium, high calcium, low K, genetic
ix: water deprivation test, 24 hour urine collection, urine osmolality (low), ue’s, plasma osmolality often high
water deprivation - no water for 8 hours, do urine osmolality, then give desmopressin (synthetic ADH), do urine osmolality
primary polydipsia: high urine osmolality
cranial: low urine osmolality -> high
nephrogenic: low urine osmolality -> low
mx: if central give desmopressin
if nephrogenic: thiazides and low salt/ protein diet
haematuria - causes, when to refer haematuria
uti, vigourous exercse, bladder cancer, sti’s causing urethritis, BPH, kidney stones
> 45 and visible haematuria without infection, 2 ww
> 60 with recurrent UTI, do non-urgent referral.
spironolactone - mechanism of action, indications, adverse effects
aldosterone antagonist, acts in cortical collecting duct
step 4 hypertension, HF, ascites, nephrotic syndrome, conn’s syndrome
