Renal Flashcards
Adult Polycycstic Kidney Disease
Screening and Mx
The screening investigation for relatives is abdominal ultrasound:
Ultrasound diagnostic criteria (in patients with positive family history)
two cysts, unilateral or bilateral, if aged < 30 years
two cysts in both kidneys if aged 30-59 years
four cysts in both kidneys if aged > 60 years
Management
For select patients, tolvaptan (vasopressin receptor 2 antagonist) may be an option. NICE recommended it as an option for treating ADPKD in adults to slow the progression of cyst development and renal insufficiency only if:
they have chronic kidney disease stage 2 or 3 at the start of treatment
there is evidence of rapidly progressing disease and
the company provides it with the discount agreed in the patient access scheme.
Metabolic acidosis classification
Normal anion gap ( = hyperchloraemic metabolic acidosis)
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease
Raised anion gap lactate: shock, sepsis, hypoxia ketones: diabetic ketoacidosis, alcohol urate: renal failure acid poisoning: salicylates, methanol
Metabolic acidosis secondary to high lactate levels may be subdivided into two types:
lactic acidosis type A: sepsis, shock, hypoxia, burns
lactic acidosis type B: metformin
diagnosis of Amyloid
Congo red staining: apple-green birefringence
serum amyloid precursor (SAP) scan
biopsy of rectal tissue
Stag horn calculi
composed of Struvite (ammonium magnesium phosphate, triple phosphate)
form in alkaline urine (ammonia producing bacteria such as Ureaplasma urealyticum and Proteus therefore predispose)
lithium can cause what kidney disorder
nephrogenic diabetes insipidus
Diabetes insipidus Ix and MX
Investigation
high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test
Management
nephrogenic diabetes insipidus: thiazides, low salt/protein diet
acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia
haemolytic uraemic syndrome E coli 0157
Management
treatment is supportive e.g. Fluids, blood transfusion and dialysis if required
there is no role for antibiotics, despite the preceding diarrhoeal illness in many patients
the indications for plasma exchange in HUS are complicated. As a general rule plasma exchange is reserved for severe cases of HUS not associated with diarrhoea
eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS
Diffuse proliferative glomerulonephritis
classical post-streptococcal glomerulonephritis in child
presents as nephritic syndrome / acute kidney injury
most common form of renal disease in SLE
Rapidly progressive glomerulonephritis
rapid loss of renal function
formation of epithelial crescents in the majority of glomeruli.
Causes
Goodpasture’s syndrome
Wegener’s granulomatosis
others: SLE, microscopic polyarteritis
Features
nephritic syndrome: haematuria with red cell casts, proteinuria, hypertension, oliguria
features specific to underlying cause (e.g. haemoptysis with Goodpasture’s, vasculitic rash or sinusitis with Wegener’s)
Focal segmental glomerulosclerosis
Nephrotic syndrome in young adults
high recurrence rate in renal transplants.
Investigations
renal biopsy
focal and segmental sclerosis and hyalinosis on light microscopy
effacement of foot processes on electron microscopy
Management
steroids +/- immunosuppressants
Prognosis
untreated FSGS has a < 10% chance of spontaneous remission
coeliac assw which kidney condition
IgA nephropathy
thiazides prevent what types of stones
calcium oxalate
sinusitis rash haemoptysis renal failure
granulomatosis with polyangitis (wegener’s)_
Rapidly progressive glomerulonephritis
- crescents
Nephrogenic diabetes insipidus may be caused genetic mutations:
the more common form affects the vasopression (ADH) receptor
the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
minimal change disease features
Features nephrotic syndrome normotension - hypertension is rare highly selective proteinuria only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus renal biopsy normal glomeruli on light microscopy electron microscopy shows fusion of podocytes and effacement of foot processes
IgA nephropathy propgnosis
25% of patients develop ESRF
markers of good prognosis: frank haematuria
markers of poor prognosis: male gender, proteinuria (especially > 2 g/day), hypertension, smoking, hyperlipidaemia, ACE genotype DD
IgA nephropathy presentation
Presentations
young male, recurrent episodes of macroscopic haematuria
typically associated with a recent respiratory tract infection
nephrotic range proteinuria is rare
renal failure is unusual and seen in a minority of patients
Features of HIV associated nephropathy
massive proteinuria resulting in nephrotic syndrome
normal or large kidneys
focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy
elevated urea and creatinine
normotension
Renal biopsy demonstrates:
electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance
membranous glomerulonephritis
membranous glomerulonephritis Rx
all patients should receive an ACE inhibitor or an angiotensin II receptor blocker (ARB):
these have been shown to reduce proteinuria and improve prognosis
immunosuppression
as many patients spontaneously improve only patient with severe or progressive disease require immunosuppression
corticosteroids alone have not been shown to be effective. A combination of corticosteroid + another agent such as cyclophosphamide is often used
consider anticoagulation for high-risk patients
