Renal Flashcards
Nephrotic syndrome causes
Primary glomerulonepbritis
Systemic disease - DM, SLE, amyloidosis
Drugs - gold, penicillamine
Congenital
Neoplasia
Infection - endocarditis, hepatitis B, malaria
Nephrotic syndrome complications
Increased risk of VTE due to loss of antithrombin III and plasminogen in urine
Hyperlipidaemia
CKD
Increased risk of infection
Hypocalcaemia
What is amyloidosis
Term to describe the extra cellular deposition of amyloid from precursor proteins
Accumulation of amyloid leads to tissue/organ dysfunction
Diagnosis of amyloidosis
Congo red staining : apple green birefringance
Serum amyloid precursor scan
Biopsy of skin- rectal mucosa- abdo fat
ADPKD treatment
Tolvaptan - vasopressin receptor 2 antagonist only if -
- ckd 2/3
- rapidly progressive disease
- needs discount from company
Hyperkalaemia management
Stabilise cardiac membrane - IV calcium gluconate (doesn’t remove K)
Short term shift - insulin/dextrose infusion & salbutamol Neb
Removal of potassium from body - calcium resonium, loop diuretics, dialysis
What causes focal segmental glomerulosclerosis?
Idiopathic
Other renal pathology
HIV
Heroin
Alport’s
Sickle-cell
Investigation of focal segmental glomerulosclerosis
Renal biopsy - focal and segmental sclerosis and hyalinosis on light microscopy
Effacement of foot processes on electron microscopy
What’s the management of focal segmental glomerulosclerosis
Steroids +/- immunosuppressants
Spironolactone - when to use
Ascites- patients with cirrhosis develop secondary hyperaldosteronism
HTN
HF
Nephrotic syndrome
Conn’s
Adverse effects of spironolactone
Hyperkalaemia
Gynaecomastia
Features of autosomal dominant PKD
HTN
Recurrent UTI’s
Flank pain
Haematuria
Palpable kidneys
Renal impairment
Renal stones
Extra renal manifestations of ADPKD
Liver cysts - may cause hepatomegaly
Berry aneurysm
Cardiovascular - mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
Cysts in other organs - pancreas, spleen
Conditions associated with Bergers
Alcoholic cirrhosis
Coeliac/dermatitis herpetiformis
Henoch-Schonlein purpura
Pathophysiology of Bergers
Deposition of IgA immune complexes
Positive immunofluorescence for IgA & C3
Presentations of Berger’s
Young male, recurrent macroscopic haematuria
Recurrent chest infections
Renal failure is unusual
Post-strep glomerulonephritis features
Develops 1-2 weeks after URTI
Proteinuria
Low complement
Can have haematuria but not as common
Management of Berger’s
Nothing needed unless persistent proteinuria (>500mg) - first line is ACE
Active disease or not responding to ACE - steroids
Investigations for renal stones
Urine dip and culture
Serum creat and electrolytes
FBC/CRP - look for infection
Calcium/urate - look for underlying cause
Cultures if Pyrexic
Clotting
Management of renal stones
Watch and wait if <5mm and asymptomatic
5-10mm shockwave lithotripsy
10-20mm shockwave or ureteroscopy
>20mm percutaneous nephrolithotomy
Uretic stones management
Shockwave lithotripsy +/- alpha blockers
10-20mm ureteroscopy
Prevention of calcium stones
High fluid intake
Add lemon juice to water
Avoid carbonated drinks
Limit salt
Potassium citrate
Thiazide diuretics
Prevention of oxalate stones
Cholestyramine reduces urinary oxalate secretion
Pyridoxine reduces urinary oxalate secretion
Prevention of uric acid stones
Allopurinol
Urinary alkalinization (oral bicarbonate)
What’s calciphylaxis
Rare complication of end-stage renal failure
Deposition of calcium in arterioles causing occlusion and necrosis
Presents as painful necrotic skin lesions
Causes of minimal change disease
Idiopathic
Drugs - NSAID’s, rifampicin
Hodgkin’s lymphoma, thymoma
Infectious mono
Pathophysiology of minimal change disease
T-Cell and cytokine-mediated damage to glomerular basement membrane leads to polyanion loss
Reduction in electrostatic charge leads to increased glomerular permeability to serum albumin
Features of minimal change disease
Nephrotic syndrome
Normotension
Highly selective proteinuria (albumin & transferrin)
Renal biopsy - normal glomeruli on light microscopy, electron microscopy shows fusion of podocytes and effacement of foot processes
Management of minimal change disease
Oral steroids
Cyclophosphamide
Goodpastures features
Pulmonary haemorrhage
Rapidly progressive glomerulonephritis
Goodpastures investigations
Renal biopsy - linear IgG deposits along basement membrane
Raised transfer factor due to pulmonary haemorrhage
Management of Goodpastures
Plasma exchange - plasmapheresis
Steroids
Cyclophosphamide
Causes of anaemia in renal failure
Reduced erythropoietin levels
Reduced absorption of iron
Reduced erythropoiesis due to toxic effects of uraemia on bone marrow
Anorexia/nausea due to uraemia
Reduced red cell survival
Blood loss due to capillary fragility
Stress ulceration leading to chronic blood loss
Renal transplant post op problems
ATN of graft
Vascular thrombosis
Urine leakage
UTI
Important HLA antigens when matching for renal transplant
DR > B > A
How is Alport’s inherited
X-linked dominant
What is Alport’s due to a defect in?
Type IV collagen
What is the favourite Alport’s question?
Alport patient with failing renal transplant caused by presence of anti-GBM antibodies leading to a Goodpastures type syndrome
Alport’s features
Microscopic haematuria
Progressive renal failure
Bilateral sensorineural deafness
Lenticonus
Retinitis pigmentosa
Renal biopsy - splitting of lamina densa seen on electron microscopy
Diagnosing Alport’s
Molecular genetic testing
Renal biopsy - longitudinal splitting of lamina densa of GBM, basket weave appearance
Types of testicular cancer
95% are germ cell - seminomas & non-seminomas (embryonal, yolk sac, teratoma, choriocarcinoma)
Rest are non-germ cell - Leydig cells and sarcomas
Risk factors for testicular cancer
Infertility
Cryptorchidism
Family history
Klinefelter’s
Mumps
Features of testicular cancer
Painless lump
Hydrocele
Gynaecomastia
Tumour markers in testicular cancer
Seminomas - hcg may be elevated
Non seminomas - AFP
LDH is raised in 40% of germ cell tumours
Management of testicular cancer
Orchidectomy
Chemo/radio
Features of fibromuscuar dysplasia
HTN
CKD
Flash pulmonary oedema
What is Fanconi syndrome
A generalised reabsorptive disorder of renal tubular transport in the proximal convoluted tubule
Features of Fanconi syndrome
type 2 (proximal) renal tubular acidosis
Polyuria
Aminoaciduria
Glycosuria
Phosphaturia
Osteomalacia
Causes of Fanconi
Cystinosis
Sjogren’s
Multiple myeloma
Nephrotic syndrome
Wilson’s
Idiopathic membranous glomerulonephritis is due to what?
Anti-phospholipase A2 antibodies
What triad does haemolytic uraemic syndrome cause
AKI
Microangiopathic haemolytic anaemia
Thrombocytopenia
Causes of secondary haemolytic uraemic syndrome (typical HUS)
Shiga toxin - E Coli
Pneumococcal infection
HIV
Rare - SLE, drugs, cancer
Investigation results for primary HUS (atypical)
FBC - Hb <80, negative Coombs, thrombocytopenia, fragmented blood film - schistocytes, helmet cells
U&E - AKI
Stool culture -STEC infection, pcr for shiga
Causes of normal anion gap
GI bicarbonate loss - prolonged diarrhoea, fistula, ureterosigmoidostomy
Renal tubular acidosis
Drugs - acetazolamide
Ammonium chloride injection
Addisons
Causes of raised anion gap
Lactate - shock, sepsis, hypoxia
Ketones - DKA, alcohol
Urate - renal failure
Acid poisoning - salicylates, methanol
Metformin.
Investigations for Bergers
Urinalysis - erythrocytes, proteinuria
Urine microscopy & culture - erythrocytes
C3 & C4 levels normal
Renal uss - normal
CT - normal
Biopsy - diffuse mesangial IgA deposition
