Nephrology Flashcards
complications of peritoneal dialysis ?
Peritonitis - coagulase-negative staphylococci such as Staphylococcus epidermidis is the most common cause.
Abx given should cover both gram negative and gram positive organisms - he BNF recommends vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid OR vancomycin added to dialysis fluid + ciprofloxacin by mouth
Sclerosis peritonitis
which patients are at risk of contrast induced nephropathy?
Risk factors include
known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs
what is contrast induced nephropathy?
Contrast media nephrotoxicity may be defined as a 25% increase in creatinine occurring within 3 days of the intravascular administration of contrast media. Contrast-induced nephropathy occurs 2 -5 days after administration.
how to prevent contrast induced nephropathy?
the evidence base currently supports the use of intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure. There is also evidence to support the use of isotonic sodium bicarbonate
N-acetylcysteine has been given in the past but recent evidence suggests it is not effective*
Patients who are high-risk for contrast-induced nephropathy should have metformin withheld for a minimum of 48 hours and until the renal function has been shown to be normal. This is due to the risk of lactic acidosis.
how to work out anion gap?
(Na+ + K+) - (Cl- + HCO-3).
what is a normal anion gap?
The normal range = 10-18 mmol/L
What causes metabolic acidosis with normal anion gap?
Normal anion gap ( = hyperchloraemic metabolic acidosis)
gastrointestinal bicarbonate loss:
prolonged diarrhoea: may also result in hypokalaemia
ureterosigmoidostomy
fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease
what causes metabolic acidosis with a raised anion gap?
Raised anion gap
lactate:
shock
sepsis
hypoxia
ketones:
diabetic ketoacidosis
alcohol
urate: renal failure
acid poisoning: salicylates, methanol
what are the causes of metabolic acidosis due to raised lactate?
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
what may happed to eGFR in body builders?
The eGFR is often inaccurate in people with extremes of muscle mass. Body builders often have an inappropriately low eGFR.
what are the stages of CKD?
1 Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)
2 60-90 ml/min with some sign of kidney damage (if kidney tests* are normal, there is no CKD)
3a 45-59 ml/min, a moderate reduction in kidney function
3b 30-44 ml/min, a moderate reduction in kidney function
4 15-29 ml/min, a severe reduction in kidney function
5 Less than 15 ml/min, established kidney failure - dialysis or a kidney transplant may be needed
Initial management of renal colic?
NSAIDs are the treatment of choice
the NICE guidelines suggest for patients who require admission: ‘Administer a parenteral analgesic (such as intramuscular diclofenac) for rapid relief of severe pain’
Alpha blockers - promote smooth muscle relaxation and dilatation of the ureter potentially easing stone assuage - consider if stone less than 10mm
Investigations for renal stone?
urine dipstick and culture
serum creatinine and electrolytes: check renal function
FBC / CRP: look for associated infection
calcium/urate: look for underlying causes
stone analysis should be considered once the stone has passed
also: clotting if percutaneous intervention planned and blood cultures if pyrexial or other signs of sepsis
Non-contrasr CT KUB - within 24 hours of admission
USS for pregnant woman and children
management of renal stones?
Simplified first-line NICE guidance (please see guidelines for more details) NICE
Renal stones
watchful waiting if < 5mm and asymptomatic
5-10mm shockwave lithotripsy
10-20 mm shockwave lithotripsy OR ureteroscopy
> 20 mm percutaneous nephrolithotomy
Uretic stones
shockwave lithotripsy +/- alpha blockers>< 10mm shockwave lithotripsy +/- alpha blockers
10-20 mm ureteroscopy
Stones < 5 mm will usually pass spontaneously. Lithotripsy and nephrolithotomy may be for severe cases.
what is shockwave lithotripsy?
A shock wave is generated external to the patient, internally cavitation bubbles and mechanical stress lead to stone fragmentation
The passage of shock waves can result in the development of solid organ injury
Fragmentation of larger stones may result in the development of ureteric obstruction
The procedure is uncomfortable for patients and analgesia is required during the procedure and afterwards.
What is ureteroscopy?
A ureteroscope is passed retrograde through the ureter and into the renal pelvis
It is indicated in individuals (e.g. pregnant females) where lithotripsy is contraindicated and in complex stone disease
In most cases a stent is left in situ for 4 weeks after the procedure.
what is percutaneous nephrolithotomy?
In this procedure, access is gained to the renal collecting system
Once access is achieved, intra corporeal lithotripsy or stone fragmentation is performed and stone fragments removed.
How are renal stones prevented?
Calcium stones may be due to hypercalciuria, which is found in up to 5-10% of the general population.
high fluid intake
add lemon juice to drinking water
avoid carbonated drinks
limit salt intake
potassium citrate may be beneficial NICE
thiazides diuretics (increase distal tubular calcium resorption)
Oxalate stones
cholestyramine reduces urinary oxalate secretion
pyridoxine reduces urinary oxalate secretion
Uric acid stones
allopurinol
urinary alkalinization e.g. oral bicarbonate
what conditions typically present with a nephritic syndrome?
Rapidly progressive glomerulonephritis - aka crescentic glomerulonephritis
rapid onset, often presenting as acute kidney injury
causes include Goodpasture’s, ANCA positive vasculitis
IgA nephropathy - aka Berger’s disease, mesangioproliferative GN
typically young adult with haematuria following an URTI
there is considerable pathological overlap with Henoch-Schonlein purpura (HSP)
What conditions may present with mixed nephritic/nephrotic presentation?
Diffuse proliferative glomerulonephritis
classical post-streptococcal glomerulonephritis in child
presents as nephritic syndrome / acute kidney injury
most common form of renal disease in SLE
Membranoproliferative glomerulonephritis (mesangiocapillary)
type 1: cryoglobulinaemia, hepatitis C
type 2: partial lipodystrophy
what conditions usually present with nephrotic syndrome?
Minimal change disease
typically a child with nephrotic syndrome (accounts for 80%)
causes: Hodgkin’s, NSAIDs
good response to steroids
Membranous glomerulonephritis
presentation: proteinuria / nephrotic syndrome / chronic kidney disease
cause: infections, rheumatoid drugs, malignancy
1/3 resolve, 1/3 respond to cytotoxics, 1/3 develop chronic kidney disease
Focal segmental glomerulosclerosis
may be idiopathic or secondary to HIV, heroin
presentation: proteinuria / nephrotic syndrome / chronic kidney disease
What is the mechanism of action of spironolactone?
Spironolactone is an aldosterone antagonist which acts in the cortical collecting duct.
aldosterone antagonists lead to increased sodium (and water) excretion while conserving potassium
Indications for Spironolactone?
ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used
hypertension: used in some patients as a NICE ‘step 4’ treatment
heart failure (see RALES study below)
nephrotic syndrome
Conn’s syndrome
adverse effects of spironolactone?
hyperkalaemia
gynaecomastia: less common with eplerenone
What is fanconi syndrome?
Fanconi syndrome describes a generalised reabsorptive disorder of renal tubular transport in the proximal convoluted tubule
what does fanconi syndrome lead to?
type 2 (proximal) renal tubular acidosis
polyuria
aminoaciduria
glycosuria
phosphaturia
osteomalacia
Causes of Fanconi syndrome?
cystinosis (most common cause in children)
Sjogren’s syndrome
multiple myeloma
nephrotic syndrome
Wilson’s disease
features of HIV associated nephropathy?
There are five key features of HIVAN:
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
what is Alpert’s syndrome?
Alport’s syndrome is usually inherited in an X-linked dominant pattern*. It is due to a defect in the gene which codes for type IV collagen resulting in an abnormal glomerular-basement membrane (GBM). The disease is more severe in males with females rarely developing renal failure.
what are the features of Alpert’s syndrome?
microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
renal biopsy: splitting of lamina densa seen on electron microscopy
How is Alpert’s syndrome Diagnosed?
Diagnosis
molecular genetic testing
renal biopsy
electron microscopy: characteristic finding is of the longitudinal splitting of the lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance
what causes acute interstitial nephritis?
drugs: the most common cause, particularly antibiotics
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome
infection: Hanta virus , staphylococci
what is the pathophysiology of acute interstitial nephritis?
marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules
what are the features of acute interstitial nephritis?
fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension
what are the investigations for acute interstitial nephritis?
sterile pyuria
white cell casts
what is seen in membranous glomerulonephritis on renal biopsy?
Renal biopsy demonstrates:
electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance
how does membrane glomerulonephritis present?
Membranous glomerulonephritis is the commonest type of glomerulonephritis in adults and is the third most common cause of end-stage renal failure (ESRF). It usually presents with nephrotic syndrome or proteinuria.
causes of membranous glomerulonephitits?
idiopathic: due to anti-phospholipase A2 antibodies
infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
How is membranous glomerulonephritis managed?
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
good prognostic features in membranous glomerulonephritis ?
Good prognostic features include female sex, young age at presentation and asymptomatic proteinuria of a modest degree at the time of presentation.
genetics of autosomal dominant polycystic kidney disease?
Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited cause of kidney disease, affecting 1 in 1,000 Caucasians. Two disease loci have been identified, PKD1 and PKD2, which code for polycystin-1 and polycystin-2 respectively
ADPKD type 1 - chromosome 16
ADPKD type 2 - chromosome 4
management of ADPKD?
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.
Causes of nephrogenic DI
genetic:
more common form affects the vasopression (ADH) receptor
less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes
hypercalcaemia
hypokalaemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
Causes of cranial DI
idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
haemochromatosis
what is diabetes insipidus?
Diabetes insipidus (DI) is a condition characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).
investigation for diabetes insipidus?
high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test
management of diabetes Insipidus?
nephrogenic diabetes insipidus
thiazides
low salt/protein diet
central diabetes insipidus can be treated with desmopressin
pathophysiology of minimal change disease?
T-cell and cytokine-mediated damage to the glomerular basement membrane → polyanion loss
the resultant reduction of electrostatic charge → increased glomerular permeability to serum albumin
features of minimal change disease?
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
management of minimal change disease?
oral corticosteroids: majority of cases (80%) are steroid-responsive
cyclophosphamide is the next step for steroid-resistant cases
how is lupus nephritis classified?
WHO classification
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis
Class IV (diffuse proliferative glomerulonephritis) is the most common and severe form. Renal biopsy characteristically shows the following findings:
glomeruli shows endothelial and mesangial proliferation, ‘wire-loop’ appearance
if severe, the capillary wall may be thickened secondary to immune complex deposition
electron microscopy shows subendothelial immune complex deposits
granular appearance on immunofluorescence
how is lupus nephritis managed?
Management
treat hypertension
initial therapy for focal (class III) or diffuse (class IV) lupus nephritis
glucocorticoids with either mycophenolate or cyclophosphamide
subsequent therapy
mycophenolate is generally preferred to azathioprine to decrease the risk of developing end-stage renal disease
endocrine effets of renal cell cancer?
may secrete erythropoietin (polycythaemia)
parathyroid hormone-related protein (hypercalcaemia), renin
ACTH
features of renal cell cancer?
haematuria
loin pain
abdominal mass
pyrexia
varicocele
majority are left-sided
caused by the tumour compressing veins
what is Stauffer syndrome?
Stauffer syndrome
a paraneoplastic disorder associated with renal cell cancer
typically presents as cholestasis/hepatosplenomegaly
it is thought to be secondary to increased levels of IL-6
how is renal cell cancer managed?
for confined disease a partial or total nephrectomy depending on the tumour size
patients with a T1 tumour (i.e. < 7cm in size) are typically offered a partial nephrectomy
alpha-interferon and interleukin-2 have been used to reduce tumour size and also treat patients with metatases
receptor tyrosine kinase inhibitors (e.g. sorafenib, sunitinib) have been shown to have superior efficacy compared to interferon-alpha
tumour markers associated with testicular cancer?
germ cell tumours
seminomas: seminomas: hCG may be elevated in around 20%
non-seminomas: AFP and/or beta-hCG are elevated in 80-85%
LDH is elevated in around 40% of germ cell tumours
what are the types of germ testicular cancers?
Around 95% of cases of testicular cancer are germ-cell tumours. Germ cell tumours may essentially be divided into:
seminomas
non-seminomas: including embryonal, yolk sac, teratoma and choriocarcinoma
Non-germ cell tumours include Leydig cell tumours and sarcomas.
features of testicular cancer?
a painless lump is the most common presenting symptom
pain may also be present in a minority of men
hydrocele
gynaecomastia
this occurs due to an increased oestrogen:androgen ratio
germ-cell tumours → hCG → Leydig cell dysfunction → increases in both oestradiol and testosterone production, but rise in oestradiol is relatively greater than testosterone
leydig cell tumours → directly secrete more oestradiol and convert additional androgen precursors to oestrogens
A mutation in the gene that encodes aquaporin 2 is most likely to result in:
nephrogenic diabetes insipidus
what is calciphylaxis?
Calciphylaxis is a rare complication of end-stage renal failure. The underlying mechanism is not clear, however it results in deposition of calcium within arterioles causing microvascular occlusion and necrosis of the supplied tissue. It most commonly affects the skin and presents with painful necrotic skin lesions.
how is calciphylaxis managed?
Treatment of calciphylaxis focuses on reducing calcium and phosphate levels, controlling hyperparathyroidism and avoiding contributing drugs such as warfarin and calcium containing compounds.
how may renal vascular disease present?
It may present as hypertension, chronic renal failure or ‘flash’ pulmonary oedema.
Another common presentation is a sharp rise in creatinine following the initiation of ACE inhibitor therapy (e.g. hypertension that may itself be linked to the underlying renal artery stenosis).
ACE inhibitors reduce angiotensin II levels, which normally constrict the efferent arterioles in the glomerulus to maintain glomerular filtration pressure, especially in states of decreased renal perfusion
- when an ACE inhibitor is introduced, the reduction in angiotensin II levels leads to dilation of the efferent arterioles
in patients with renal artery stenosis, this change can significantly reduce the glomerular filtration rate (GFR), causing a sharp rise in serum creatinine
investigations for renal vascular disease?
MR angiography is now the investigation of choice
CT angiography
conventional renal angiography is less commonly performed used nowadays, but may still have a role when planning surgery
what is suggestive of falcon syndrome?
a normal anion gap metabolic acidosis, reduced serum bicarbonate and potassium levels, alongside increased urinary excretion of amino acids, glucose, bicarbonate, and phosphate, are indicative of Fanconi syndrome. Fanconi syndrome is characterised by impaired reabsorptive function in the PCT leading to excessive urinary loss of these substances. Consequently, this dysfunction can result in renal tubular acidosis (RTA) type 2 due to diminished bicarbonate reabsorption causing metabolic acidosis.
what are the complications of nephrotic syndrome
increased risk of thromboembolism related to loss of antithrombin III and plasminogen in the urine
deep vein thrombosis, pulmonary embolism
renal vein thrombosis, resulting in a sudden deterioration in renal function
hyperlipidaemia
increasing risk of acute coronary syndrome, stroke etc
chronic kidney disease
increased risk of infection due to urinary immunoglobulin loss
hypocalcaemia (vitamin D and binding protein lost in urine)
stages of diabetic nephropathy?
Stage 1
hyperfiltration: increase in GFR
may be reversible
Stage 2 (silent or latent phase)
most patients do not develop microalbuminuria for 10 years
GFR remains elevated
Stage 3 (incipient nephropathy)
microalbuminuria (albumin excretion of 30 - 300 mg/day, dipstick negative)
Stage 4 (overt nephropathy)
persistent proteinuria (albumin excretion > 300 mg/day, dipstick positive)
hypertension is present in most patients
histology shows diffuse glomerulosclerosis and focal glomerulosclerosis (Kimmelstiel-Wilson nodules)
Stage 5
end-stage renal disease, GFR typically < 10ml/min
renal replacement therapy needed
What is associated with renal cell cancer?
more common in middle-aged men
smoking
von Hippel-Lindau syndrome
tuberous sclerosis
incidence of renal cell cancer is only slightly increased in patients with autosomal dominant polycystic kidney disease
what is a example of a non-steroidal anti-androgen used in treatment on metastastic prostate cancer?
bicalutamide
non-steroidal anti-androgen
blocks the androgen receptor
What is an example of a steroidal anti-androgen used in treatment of metastatic prostate cancer?
cyproterone acetate
steroidal anti-androgen
prevents DHT binding from intracytoplasmic protein complexes
used less commonly since introduction of non-steroidal anti-androgens
What is Abiraterone?
abiraterone
androgen synthesis inhibitor
option for the treatment of hormone-relapsed metastatic prostate cancer in patients who have no or mild symptoms after androgen deprivation therapy has failed, and before chemotherapy is indicated
Why is nephrotic syndrome assoctaed with hypercoaguable state?
Nephrotic syndrome is associated with a hypercoagulable state due to loss of antithrombin III via the kidneys
What is the most common cause of peritonitis secondary to peritoneal dialysis?
Coagulase-negative staphylococcus (staph epidermidis) is the most frequently identified organism followed by Staphylococcus aureus, Streptococcus and Enterococcus.
What drug is most important to co-prescribe for the first three weeks of goserelin treatment for prostate cancer?
Anti-androgen treatment such as cyproterone acetate should be co-prescribed when starting gonadorelin analogues due to the risk of tumour flare. This phenomenon is secondary to initial stimulation of luteinising hormone release by the pituitary gland resulting in increased testosterone levels.
what antibodies are seen in granulomatosis with polyangitis?
cANCA
What antibodies are seen in Good pasture’s?
Anti-GBM
what are eamples of rapidly progressive glomerulonephritis and what are the features?
Rapidly progressive glomerulonephritis is a term used to describe a rapid loss of renal function associated with the 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)
What antibody is associated with eosinophilic granulomatosis with polyangitis?
pANCA
what is granulomatosis with polyangitis?
Granulomatosis with polyangiitis is now the preferred term for Wegener’s granulomatosis. It is an autoimmune condition associated with a necrotizing granulomatous vasculitis, affecting both the upper and lower respiratory tract as well as the kidneys.
Features of granulomatosis with polyangitis?
upper respiratory tract: epistaxis, sinusitis, nasal crusting
lower respiratory tract: dyspnoea, haemoptysis
rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)
saddle-shape nose deformity
also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions
Investigations and treatment for granulomatosis with polyangitits?
Investigations
cANCA positive in > 90%, pANCA positive in 25%
chest x-ray: wide variety of presentations, including cavitating lesions
renal biopsy: epithelial crescents in Bowman’s capsule
Management
steroids
cyclophosphamide (90% response)
plasma exchange
median survival = 8-9 years
What is EGPA?
Eosinophilic granulomatosis with polyangiitis (EGPA) is now the preferred term for Churg-Strauss syndrome. It is an ANCA associated small-medium vessel vasculitis.
Features
asthma
blood eosinophilia (e.g. > 10%)
paranasal sinusitis
mononeuritis multiplex
renal involvement occurs in around 20%
pANCA positive in 60%
Anti GBM disease - what is it?
Anti-glomerular basement membrane (GBM) disease (previously known as Goodpasture’s syndrome) is a rare type of small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis.** It is caused by anti-glomerular basement membrane (anti-GBM) antibodies against type IV collagen. **
what HLA is anti GBM disease associated with?
It is associated with HLA DR2.
Features of anti-GBM disease?
pulmonary haemorrhage
rapidly progressive glomerulonephritis
this typically results in a rapid onset acute kidney injury
nephritis → proteinuria + haematuria
Investigations and management of anti-GBM disease?
Investigations
renal biopsy: linear IgG deposits along the basement membrane
raised transfer factor secondary to pulmonary haemorrhages
Management
plasma exchange (plasmapheresis)
steroids
cyclophosphamide
What drugs are used for renal transplant in immunosupression?
Example regime
initial: ciclosporin/tacrolimus with a monoclonal antibody
maintenance: ciclosporin/tacrolimus with MMF or sirolimus
add steroids if more than one steroid responsive acute rejection episode
Ciclosporin
inhibits calcineurin, a phosphotase involved in T cell activation
Tacrolimus
lower incidence of acute rejection compared to ciclosporin
also less hypertension and hyperlipidaemia
however, high incidence of impaired glucose tolerance and diabetes
Mycophenolate mofetil (MMF)
blocks purine synthesis by inhibition of IMPDH
therefore inhibits proliferation of B and T cells
side-effects: GI and marrow suppression
Sirolimus (rapamycin)
blocks T cell proliferation by blocking the IL-2 receptor
can cause hyperlipidaemia
Monoclonal antibodies
selective inhibitors of IL-2 receptor
daclizumab
basilximab
What monitoring do patients on long-term immunosuppression for organ transplantation require?
Cardiovascular disease - tacrolimus and ciclosporin can cause hypertension and hyperglycaemia. Tacrolimus can also cause hyperlipidaemia. Patients must be monitored for accelerated cardiovascular disease.
Renal failure - due to nephrotoxic effects of tacrolimus and ciclosporin/graft rejection/recurrence of original disease in transplanted kidney
Malignancy - patients should be educated about minimising sun exposure to reduce the risk of squamous cell carcinomas and basal cell carcinomas
what is HIV associated nephropathy ?
HIV-associated nephropathy (HIVAN) accounts for up to 10% of end-stage renal failure cases in the United States. Antiretroviral therapy is the treatment of choice for the disease. If a patient is already taking antiretroviral therapy (which should be all HIV-diagnosed patients) adherence should be checked.
what do investigations show in HIV associated nephropathy?
Ultrasound shows large echogenic kidneys. Light microscopy most commonly shows a pattern of collapsing focal segmental glomerulosclerosis (FSGS) which often shows marked focal or global collapse of the basement membrane associated with hypertrophy and hyperplasia of the overlying podocytes. Therefore, podocyte proliferation with marked focal collapse of the glomerular basement membrane is correct.
How does alcohol lead to polyuria?
Alcohol bingeing can lead to ADH suppression in the posterior pituitary gland subsequently leading to polyuria
mechanism of action of abiraterone?
Abiraterone acetate is a selective androgen synthesis inhibitor that works by blocking cytochrome P450 17 alpha-hydroxylase. It blocks androgen production in the testes and adrenal glands, and in prostatic tumour tissue.
What is xanthogranulomatous pyelonephritis?
Xanthogranulomatous pyelonephritis is a rare chronic granulomatous disease resulting in a non-functioning kidney. Chronic/subacute infection by organisms such as Proteus mirabilis predispose to renal stones including staghorn calculi. Foamy (lipid laden) macrophages are typically seen.
What kind of kidney stones are associated with proteus mirabilis infection?
Stuvite kidney stones
With regards to uric acid calculi, one of its remarkable characteristic is:
Uric acid nephrolithiasis are radiolucent, requiring ultrasonography or CT KUB (without contrast)
With ultrasonography can demonstrate a calculi by an echogenic foci with distal acoustic shadowing regardless of its nature
Why do patients with chronic kidney disease have a raised phosphate level?
Decreased renal excretion.
Chronic kidney disease (CKD) often leads to a decreased ability of the kidneys to excrete phosphate, which results in elevated serum phosphate levels. This is due to a decline in glomerular filtration rate, impairing the removal of phosphate from the body. The kidneys are the primary regulators of phosphate homeostasis and any impairment in their function can lead to disruptions in this balance.
Basic problems seen in CKD?
Basic problems in chronic kidney disease
* low vitamin D (1-alpha hydroxylation normally occurs in the kidneys)
* high phosphate
* low calcium: due to lack of vitamin
D, high phosphate
* secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D
what are the clinical manifestations of bone disease associated with CKD?
Several clinical manifestations may result:
Osteitis fibrosa cystica
aka hyperparathyroid bone disease
Adynamic
reduction in cellular activity (both osteoblasts and osteoclasts) in bone
may be due to over treatment with vitamin D
Osteomalacia
due to low vitamin D
Osteosclerosis
Osteoporosis
what is membraniproliferative glomerulonephritis?
Overview
also known as mesangiocapillary glomerulonephritis
may present as nephrotic syndrome, haematuria or proteinuria
poor prognosis
What is type 1 membranoproliferatiive glomerulonephritis?
Type 1
accounts for 90% of cases
cause: cryoglobulinaemia, hepatitis C
renal biopsy
electron microscopy: subendothelial and mesangium immune deposits of electron-dense material resulting in a ‘tram-track’ appearance
What is type 2 and type 3 membranoproliferative glomerulonephritis?
Type 2 - ‘dense deposit disease’
causes: partial lipodystrophy (patients classically have a loss of subcutaneous tissue from their face), factor H deficiency
caused by persistent activation of the alternative complement pathway
low circulating levels of C3
C3b nephritic factor is found in 70%
an antibody to alternative-pathway C3 convertase (C3bBb)
stabilizes C3 convertase
renal biopsy
electron microscopy: intramembranous immune complex deposits with ‘dense deposits’
Type 3
causes: hepatitis B and C
AKPKD - what are the two types and what chromosome has the disease loci been found on?
Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited cause of kidney disease, affecting 1 in 1,000 Caucasians. Two disease loci have been identified, PKD1 and PKD2, which code for polycystin-1 and polycystin-2 respectively
Management of ADPKD?
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.
What causes ARPKD?
A defect in a gene located on chromosome 6 which encodes fibrocystin
What is the role of fibrocystin?
It is important for normal renal tubule development
How can ARPKD be diagnosed?
Diagnosis may be made on prenatal ultrasound or in early infancy with abdominal masses and renal failure
What features may newborns with ARPKD exhibit?
Features consistent with Potter’s syndrome secondary to oligohydramnios
When does end-stage renal failure typically develop in ARPKD patients?
In childhood
What other organ involvement is typical in ARPKD?
Liver involvement, for example portal and interlobular fibrosis
What does a renal biopsy typically show in ARPKD?
Multiple cylindrical lesions at right angles to the cortical surface
pathophysiology of mineral bone disease in CKD?
Basic problems in chronic kidney disease (CKD):
1-alpha hydroxylation normally occurs in the kidneys → CKD leads to low vitamin D
the kidneys normally excrete phosphate → CKD leads to high phosphate
This, in turn, causes other problems:
the high phosphate level ‘drags’ calcium from the bones, resulting in osteomalacia
low calcium: due to lack of vitamin D, high phosphate
secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D
management of mineral bone disease in CKD?
Overview
reduced dietary intake of phosphate is the first-line management
phosphate binders
vitamin D: alfacalcidol, calcitriol
parathyroidectomy may be needed in some cases
Alfacalcidol is used as a vitamin D supplement in end-stage renal disease because it does not require activation in the kidneys
How should you collect a urine ACR sample?
Collecting an ACR sample
by collecting a ‘spot’ sample it avoids the need to collect urine over a 24 hour period in order to detect or quantify proteinuria
should be a first-pass morning urine specimen
if the initial ACR is between 3 mg/mmol and 70 mg/mmol, this should be confirmed by a subsequent early morning sample. If the initial ACR is 70 mg/mmol or more, a repeat sample need not be tested.
How to interpret a urine ACR?
the NICE guidelines state ‘regard a confirmed ACR of 3 mg/mmol or more as clinically important proteinuria’
NICE recommendations for referral to a nephrologist:
a urinary albumin:creatinine ratio (ACR) of 70 mg/mmol or more, unless known to be caused by diabetes and already appropriately treated
a urinary ACR of 30 mg/mmol or more, together with persistent haematuria (two out of three dipstick tests show 1+ or more of blood) after exclusion of a urinary tract infection
consider referral to a nephrologist for people with an ACR between 3-29 mg/mmol who have persistent haematuria and other risk factors such as a declining eGFR, or cardiovascular disease
How is proteinuria managed?
ACE inhibitors (or angiotensin II receptor blockers) are key in the management of proteinuria
they should be used first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol
if the ACR > 70 mg/mmol they are indicated regardless of the patient’s blood pressure
SGLT-2 inhibitors
patients who have proteinuric CKD (with or without diabetes) may benefit from treatment with SGLT2 inhibitors
they primarily act by blocking reabsorption of glucose in the proximal tubule → lowers the renal glucose threshold → glycosuria
by blocking the cotransporter, they also reduce sodium reabsorption → natriuresis reduces intravascular volume and blood pressure, but it also increases the delivery of sodium to the macula densa → normalizes tubuloglomerular feedback and thereby reduces intraglomerular pressure
USS Diagnostic criteria for ADPKD?
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
What would Sterile pyuria and white cell casts in the setting of rash and fever raise suspicion of|?
acute interstitial nephritis
Causes of non-visible haematuria?
Causes of transient or spurious non-visible haematuria
urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse
Causes of persistent non-visible haematuria
cancer (bladder, renal, prostate)
stones
benign prostatic hyperplasia
prostatitis
urethritis e.g. Chlamydia
renal causes: IgA nephropathy, thin basement membrane disease
how should you monitor non visible haematuria?
persistent non-visible haematuria is often defined as blood being present in 2 out of 3 samples tested 2-3 weeks apart
renal function, albumin:creatinine (ACR) or protein:creatinine ratio (PCR) and blood pressure should also be checked
urine microscopy may be used but time to analysis significantly affects the number of red blood cells detected
when should you refer a patient with non visible haematuria?
2WW referral
Aged >= 45 years AND:
unexplained visible haematuria without urinary tract infection, or
visible haematuria that persists or recurs after successful treatment of urinary tract infection
Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test
Non-urgent referral
Aged 60 >= 60 years with recurrent or persistent unexplained urinary tract infection
Since the investigation (or not) of non-visible haematuria is such as a common dilemma a number of guidelines have been published. They generally agree with NICE guidance, of note:
patients under the age of 40 years with normal renal function, no proteinuria and who are normotensive do not need to be referred and may be managed in primary care
when does contrast induced nephropathy occur?
Contrast-induced nephropathy occurs 2 -5 days after administration
Risk factors for contrast induced nephropathy?
known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs
Prevention of contrast induced nephropathy?
the evidence base currently supports the use of intravenous 0.9% sodium chloride at a rate of 1 mL/kg/hour for 12 hours pre- and post- procedure. There is also evidence to support the use of isotonic sodium bicarbonate
N-acetylcysteine has been given in the past but recent evidence suggests it is not effective*
Patients who are high-risk for contrast-induced nephropathy should have metformin withheld for a minimum of 48 hours and until the renal function has been shown to be normal. This is due to the risk of lactic acidosis.
Risk factors for renal stones?
dehydration
hypercalciuria, hyperparathyroidism, hypercalcaemia
cystinuria
high dietary oxalate
renal tubular acidosis
medullary sponge kidney, polycystic kidney disease
beryllium or cadmium exposure
drug causes of renal stones?
drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline
thiazides can prevent calcium stones (increase distal tubular calcium resorption)
risk factos for urate stones?
gout
ileostomy: loss of bicarbonate and fluid results in acidic urine, causing the precipitation of uric acid
how do NSAIDS cause AKI?
Non-steroidal anti-inflammatory drugs (NSAIDs), such as Naproxen are prostaglandin inhibitors therefore they constrict the afferent arterioles causing prerenal acute kidney injury by decreasing the glomerular filtration.
extra renal manifestations of ADPKD?
liver cysts (70% - the commonest extra-renal manifestation): may cause hepatomegaly
berry aneurysms (8%): rupture can cause subarachnoid haemorrhage
cardiovascular system: mitral valve prolapse, mitral/tricuspid incompetence, aortic root dilation, aortic dissection
cysts in other organs: pancreas, spleen; very rarely: thyroid, oesophagus, ovary
what is the most common cause of renal disease in patients with SLE?
Diffuse proliferative glomerulonephritis is the most common and severe form of renal disease in SLE patients
WHO classification of lupus nephritis?
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis
what does renal biosy show in SL diffues proliferative glomerulonephritis?
Class IV (diffuse proliferative glomerulonephritis) is the most common and severe form. Renal biopsy characteristically shows the following findings:
glomeruli shows endothelial and mesangial proliferation, ‘wire-loop’ appearance
if severe, the capillary wall may be thickened secondary to immune complex deposition
electron microscopy shows subendothelial immune complex deposits
granular appearance on immunofluorescence
Management of lupus nephritis?
treat hypertension
initial therapy for focal (class III) or diffuse (class IV) lupus nephritis
glucocorticoids with either mycophenolate or cyclophosphamide
subsequent therapy
mycophenolate is generally preferred to azathioprine to decrease the risk of developing end-stage renal disease
causes of rhabdo?
Causes
seizure
collapse/coma (e.g. elderly patient collapses at home, found 8 hours later)
ecstasy
crush injury
McArdle’s syndrome
drugs: statins (especially if co-prescribed with clarithromycin)
features of rhabdo?
acute kidney injury with disproportionately raised creatinine
elevated creatine kinase (CK)
the CK is significantly elevated, at least 5 times the upper limit of normal
elevations of CK that are ‘only’ 2-4 times that of normal are not supportive of a diagnosis and suggest another underlying pathophysiology
myoglobinuria: dark or reddish-brown colour
hypocalcaemia (myoglobin binds calcium)
elevated phosphate (released from myocytes)
hyperkalaemia (may develop before renal failure)
metabolic acidosis
Management of Rhabdo?
IV fluids to maintain good urine output
urinary alkalinization is sometimes used
assessent of BPH?
dipstick urine
U&Es: particularly if chronic retention is suspected
PSA: should be done if there are any obstructive symptoms, of if the patient is worried about prostate cancer
urinary frequency-volume chart
should be done for at least 3 days
International Prostate Symptom Score (IPSS)
tool for classifying the severity of lower urinary tract symptoms (LUTS) and assessing the impact of LUTS on quality of life
Score 20-35: severely symptomatic
Score 8-19: moderately symptomatic
Score 0-7: mildly symptomatic
Management of BPH?
alpha-1 antagonists - tamsulosin - decreases mooth muscle tone of the prostate and blader
5 alpha reductase inhibitors - finasteride - blocks conversion of testosterone to DHT which is known to induce BPH, causes reduction in prostate volume and may slow disease proression, can take 6 months to work. May also decrease PSA?
if there is a mixture of storage symptoms and voiding symptoms that persist after treatment with an alpha-blocker alone, then an antimuscarinic (anticholinergic) drug such as tolterodine or darifenacin may be tried
surgery
transurethral resection of prostate (TURP)
adverse effects of alpha 1 antagonists?
dizziness, postural hypotension, dry mouth, depression
Adverse effects of 5 alpha reductase inhibitors?
erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia
Inidcations for plasma exchange?
Indications for plasma exchange (also known as plasmapheresis)
Guillain-Barre syndrome
myasthenia gravis
Goodpasture’s syndrome
ANCA positive vasculitis if rapidly progressive renal failure or pulmonary haemorrhage
TTP/HUS
cryoglobulinaemia
hyperviscosity syndrome e.g. secondary to myeloma
Complications of plasma exchange?
hypocalcaemia: due to the presence of citrate used as an anticoagulant for the extracorporeal system
metabolic alkalosis
removal of systemic medications
coagulation factor depletion
immunoglobulin depletion
What are the different types of amyloidosis?
AL amyloidosis
the most common form of amyloidosis
L for immunoglobulin Light chain fragment
due to myeloma, Waldenstrom’s, MGUS
features include: nephrotic syndrome, cardiac and neurological involvement, macroglossia, periorbital eccymoses
AA amyloid
A for precursor serum amyloid A protein, an acute phase reactant
seen in chronic infection/inflammation
e.g. TB, bronchiectasis, rheumatoid arthritis
features: renal involvement most common feature
Beta-2 microglobulin amyloidosis
precursor protein is beta-2 microglobulin, part of the major histocompatibility complex
associated with patients on renal dialysis
What is vesicoureteric reflux?
Vesicoureteric reflux (VUR) is the abnormal backflow of urine from the bladder into the ureter and kidney. It is a relatively common abnormality of the urinary tract in children and predisposes to urinary tract infection (UTI), being found in around 30% of children who present with a UTI. As around 35% of children develop renal scarring it is important to investigate for VUR in children following a UTI
Pathophysiology of vesicoureteric reflux?
ureters are displaced laterally, entering the bladder in a more perpendicular fashion than at an angle
therefore shortened intramural course of the ureter
vesicoureteric junction cannot, therefore, function adequately
Investigations for vesicoureteric reflux?
VUR is normally diagnosed following a micturating cystourethrogram
a DMSA scan may also be performed to look for renal scarring - this is typically located at the upper and lower pole and is associated with cortical thinning
what is the most common opportunistic infection in patients who recieve renal transplant?
Cytomegalovirus infection is one of the most important opportunist infections in transplant receptors. Usually happens between the first month after transplant and the sixth month. Clinically is characterized by fever, deranged transaminases, leukopenia and thrombocytopenia. It is diagnosed by polymerase chain reaction (pcr) and treated with Ganciclovir.
what are the types of organ rejection?
Hyperacute. This occurs immediately through presence of pre formed antibody (such as ABO incompatibility).
Acute. Occurs during the first 6 months and is usually T cell mediated. Usually tissue infiltrates and vascular lesions.
Chronic. Occurs after the first 6 months. Vascular changes predominate.
technical complications following renal transplant?
What is fibromuscular dysplasia?
Renal artery stenosis secondary to atherosclerosis accounts for around 90% of renal vascular disease, with fibromuscular dysplasia being the most common cause of the remaining 10%.
Epidemiology
90% of patients are female
Features
hypertension
chronic kidney disease or more acute renal failure e.g. secondary to ACE-inhibitor initiation
‘flash’ pulmonary oedema
In young female patients who develop AKI after initiation of an ACE inhibitor, fibromuscular dysplasia should be suspected.
Features of epididymo orchitis?
unilateral testicular pain and swelling
urethral discharge may be present, but urethritis is often asymptomatic
factors suggesting testicular torsion include patients < 20 years, severe pain and an acute onset
*The most important differential diagnosis is testicular torsion. This needs to be excluded urgently to prevent ischaemia of the testicle.
Management of epididymo orchitis?
If an STI is the most likely cause advise urgent referral to a local specialist sexual health clinic
if the organism is unknown BASHH recommend: ceftriaxone 500mg intramuscularly single dose, plus doxycycline 100mg by mouth twice daily for 10-14 days
if enteric organisms are the most likely cause
send an MSU as above
treating empirically with an oral quinolone for 2 weeks (e.g. ofloxacin)
further investigations following treatment may be recommended to exclude any underlying structural abnormalities
causes of focal segmental glomerulosclerosis?
idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport’s syndrome
sickle-cell
causes of nephritic syndrome and nephrotic syndrome?
What are antibodies?
AKA immunoglobulins
glycoproteins produced by plasma cells in response to an immunogenic stimulus. They form a critical part of the adaptive immune response by recognising and binding to specific antigens. This antigen-antibody interaction triggers a cascade of events including neutralisation of pathogens, opsonisation facilitating phagocytosis, and activation of the complement system leading to cell lysis.
what type of immunoglobulins are responsible for hyperacute graft rejection?
hyperacute rejection, which occurs within minutes to hours after transplantation and is mediated by preformed IgG antibodies. These antibodies are present in the recipient’s circulation before transplantation, usually due to previous exposure through pregnancy, blood transfusions, or previous transplants. When these preformed antibodies encounter donor antigens (typically HLA or ABO blood group antigens) on the endothelial cells of the transplanted organ, they trigger immediate complement activation, leading to rapid vascular injury, thrombosis, and irreversible graft damage. The only treatment is immediate graft removal, as described in this case.
IgG
The most abundant type of antibody is Immunoglobulin G (IgG), making up around 70-80% of the total circulating antibodies. They are predominantly involved in the secondary immune response and have a longer half-life compared to other antibody types. Clinically, elevated levels of specific IgG antibodies could indicate a past infection or successful vaccination.
IgA
Immunoglobulin A (IgA) antibodies are primarily found in mucosal areas such as the respiratory tract and gastrointestinal system. They play a crucial role in local immunity by preventing pathogens from adhering to epithelial cells. In clinical settings, patients with selective IgA deficiency may present with recurrent sinopulmonary infections.
IgM
Immunoglobulin M (IgM) is typically the first antibody produced during an initial immune response. It has a pentameric structure enabling it to effectively agglutinate pathogens for easier phagocytosis. High levels of specific IgM antibodies often suggest an ongoing or recent infection.
IgD
Immunoglobulin D (IgD) serves mainly as antigen receptors on B cells that have not been exposed to antigens. Its exact function remains relatively unclear; however, it may play a role in allergic reactions and chronic urticaria.
IgE
Immunoglobulin E (IgE) is involved in allergic responses and parasitic infections. It binds to mast cells and basophils, triggering the release of histamine when they encounter an allergen. Clinically, elevated serum IgE levels can be seen in conditions such as atopic dermatitis, allergic asthma and parasitic infections.
What HLA is most important in renal transplant HLA matching?
HLA-DR
when HLA matching for a renal transplant the relative importance of the HLA antigens are as follows DR > B > A
Most common cause of nephrotic syndrome in young adults?
Focal segmental glomerulosclerosis
Management of minimal change disease?
oral corticosteroids: majority of cases (80%) are steroid-responsive
cyclophosphamide is the next step for steroid-resistant cases
Features of minimal change disease?
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
Pathophysiology of minimal change disease?
T-cell and cytokine-mediated damage to the glomerular basement membrane → polyanion loss
the resultant reduction of electrostatic charge → increased glomerular permeability to serum albumin
What is seen on histology of IgA nephropathy?
mesangial hypercellularity, positive immunofluorescence for IgA & C3
What cause of nephrotic syndrome is commonly associated with malignancy?
Membranous nephropathy is frequently associated with malignancy
what are the requirements of fluid maintancne?
25-30 ml/kg/day of water and
Sodium - 1mmol/kg
Potassium - 1 mmol/kg
Water - 30ml/Kg
Glucose - 50-100g
So to meet a 60kg patient’s requirements, they need:
1,800mls of water
60mmol of K+
60mmol of Na+
50-100g glucose
what electrolyte derrangements cause nephrogenic DI?
hypercalcaemia
hypokalaemia
What is the most common cause of glomerulonephritis?
IgA nephropathy
Young female, hypertension and asymmetric kidneys???
fibromuscular dysplasia
Assymmetric kidneys are often first noted on ultrasound; imaging of the vessel is done by duplex and most accurately by contrast catheter angiography of the renal artery.
what are the variable in the modification of diet in the modification of diet in renal disease equeation for eGFR
eGFR variables - CAGE - Creatinine, Age, Gender, Ethnicity
What is the MDRD equation?
The Modification of Diet in Renal Disease (MDRD) equation is a tool used to estimate glomerular filtration rate (eGFR), which assesses kidney function
what is invalidate the use of the Modification of Diet in Renal Disease (MDRD) equation to calculate a patients eGFR?
Pregnancy
muscle mass (e.g. amputees, body-builders)
eating red meat 12 hours prior to the sample being taken
CKD classification?
what is Wilm’s tumour associated with?
Wilms’ nephroblastoma is one of the most common childhood malignancies. It typically presents in children under 5 years of age, with a median age of 3 years old.
Associations
Beckwith-Wiedemann syndrome
as part of WAGR syndrome with Aniridia, Genitourinary malformations, mental Retardation
hemihypertrophy
around one-third of cases are associated with a loss-of-function mutation in the WT1 gene on chromosome 11
Features of Wilms tumour?
abdominal mass (most common presenting feature)
painless haematuria
flank pain
other features: anorexia, fever
unilateral in 95% of cases
metastases are found in 20% of patients (most commonly lung)
What type of glomerulonephritis is most characteristically associated with partial lipodystrophy?
Type 2 mesangiocapillary glomerulonephritis is associated with partial lipodystrophy
Management of HIV associoated nephropathy?
The management of HIVAN involves initiating or optimising highly active antiretroviral therapy (HAART), and a regimen combining bictegravir, emtricitabine, and tenofovir is commonly used
