Case 23- Glomerulonephritis Flashcards
Normal urine output
<0.5ml/kg/hour
NB- less than this for 6-12 hours is an AKI
NSAIDS and ACE-I
Can both cause an AKI
ACE-I dilate the efferent arterioles
NSAIDS block prostaglandins causing construction of the afferent arteriole
Complications of an AKI
Fluid overload
Metabolic acidosis
Hyponatraemia
Hyperkalaemia
Hyperuraemia
Hypocalcaemia
Hyperphosphataemia
Nephrotic syndrome
Podocyte damage- protein leaking out
Features of nephrotic syndrome
Proteinuria- urine is frothy
Oedema- starts as periorbital and then develops into pitting
Hypoalbuminaemia
Hyperlipidaemia- hypoalbuminaemia causes liver to increase protein production to compensate and this causes lipid production to increase
Hypercoaguable state due to urinary loss of antithrombin 3
Increased risk of infection- immunoglobulin loss
HHH PIO- hypercoaguable, hypoalbuminaemia, hyperlipidaemia, proteinuria, infection, oedema
NB- can rarely get protein casts also, and reduced T4
Causes of nephrotic syndrome
Minimal change disease
FSG
Membranous nephropathy
Membranoprolifertiave glomerulonephritis
Secondary causes- SLE, Hep B, Hep C, HIV, DM (nephropathy)
Management of nephrotic syndrome
Input from renal team
Low sodium and low protein diet
Fluid restriction- 1-1.5L/ hour
Loop diuretic
ACE/ ARB to reduce proteinuria (controversial as ACE can damage the kidney)
VTE prophylaxis
Statins for hypercholesterolaemia
Renal biopsy
Nephritic syndrome
Inflammation causes breakdown that allows RBC/ WCC/ protein to leak
Features of nephritic syndrome
Haematuria- intermittent gross haematuria (cola coloured urine)
Hypertension- low EGFR causes fluid retention
Oliguria- low EGFR
Uraemia- anorexia, n and v, pruritis, pericarditis, CNS abnormalities (confusion)
RBC casts- acanthocytes (dystrophic RBC)
Sterile puris
Mild proteinuria
Mild to moderate oedema
Causes of nephritic syndrome
IgA nephropathy
Post strep glomerulonephritis
GOODPASTURES (GBM)
Membranoprolifertiave glomerulonephritis (also nephrotic)
HSP- henloch-schenlein purpura
Management of nephritic syndrome
Input from renal team
Low sodium diet and water restriction
ACE ARB for proteinuria/ HTN
May need immunosuppressive theory (depends on cause)
If severe may need RRT
Glomerulonephritis
Renal disease characterised by inflammation and damage of the glomeruli- allows protein and or blood to leak into the urine. Immune response causes glomerular injury
May present with;
Isolated haematuria and or proteinuria
Nephrotic syndrome
Nephritic syndrome
AKI
CKD
Non proliferative causes- nephrotic syndrome
Proliferative causes- nephritic syndrome
Non proliferative glomerulonephritis
Lack of proliferation of cells in the glomeruli
Typically causes nephrotic syndrome
Minimal change glomerulonephritis
Focal segmental glomerulosclerosis
Membranous glomerulonephritis
Proliferative glomerulonephritis
Increased cells in the glomerulus
Usually presents with nephritic syndrome. Dangerous- can progress to ESRD over weeks to years
IgA nephropathy
Post infectious glomerulonephritis
Membranous glomerulonephritis- BOTH
Rapidly progressive glomerulonephritis
GOODPASTURES
Vasculitic disorders eg. Wegeners granulomatosis/ microscopic polyangitis
Minimal change glomerulonephritis
Presents as nephrotic syndrome
Often children affected
Supportive care and steroids (cyclophosphamide if non-responsive to steroids)
Focal segmental glomerulosclerosis (FSGS)
Nephrotic syndrome and CKD
Causes- idiopathic, renal pathology eg. IgA, HIV, heroin, Alport, sickle cell
Biopsy- sclerosis and hyalinosis, effacement of foot processes
Salt restriction and diuretics
Statins
Transplant required (High recurrence rate in renal transplant);
Membranous glomerulonephritis
Nephrotic syndrome
Slowly progressive
30-50 years commonly affected
Idiopathic but can be associated with Hep B/ malaria/ SLE/ malignancy/ drugs eg. NSAID
Histology;
-basement membrane thickening
-subepithelial spikes on silver stain
-PLA2
IgA nephropathy
Most common type in adults
Also called BERGERS disease
Presents as nephritic syndrome- macroscopic haematuria
Often appears 24-48 hours after an URTI
Can be benign or lead to ESRD
Renal biopsy
Immunochemistry +ve for IgA deposits in the matrix and glomerular mesangial proliferation
Post infectious/ Post streptocccal glomerulonephritis
Nephritic syndrome
Can occur after any infection (but tends to be strep pyogenes)
Typically presents 2 weeks after the URTI (not like 2 days- IgA nephropathy), or 3-6 weeks after a skin infection
Bloods- low complement (C3), raised ASO
Biopsy- subepithelial humps, starry sky (granular) appearance
Membranoprolifertiave glomerulonephritis
Nephrotic syndrome
IgG and complement deposits on the basement membrane
Majority idiopathic
Can be secondary to malignancy rheumatoid disorders (SLE) and drugs (NSAIDS)
Renal biopsy- tram track appearance
Rapidly progressive glomerulonephritis
Also known as crescenteric glomerulonephritis
Poor prognosis
Any type of GN can progress to this, but some may only ever present as this
Typically after GOODPASTURES
GOODPASTURES syndrome (Anti GBM Disease)
Anti GBM antibodies- attack the glomeruli and the alveoli
Present with renal failure (nephritic syndrome) and haemoptysis
Can have rapid progression to ESRD
Anti GBM antibodies and IgG deposited in the basement membrane of the glomerulus
Raised transfer factor due to pulmonary haemorrhage
IV steroids
Plasmapheresis
Can’t reverse kidney damage caused
Wegeners granulomatosis
Affects lungs, kidneys and other organs
Caused by cANCA (test for this)
IV steroids
Microscopic polyangitis
Renal- glomerulonephritis
Systemic- Fever, lethargy, myalgia, weight loss, rash (palpable purpura)
Resp- cough, dyspnoea, haemoptysis
Mononeuritis multiplex
PANCA (test for this)
Steroids
Plasmapheresis
General investigations for glomerulonephritis
Urine dipstick and microscopy (MSU)- hameaturia, proteinuria, dysmoephic RBC, leukocytes, RBC casts
24 hour urinary collection, urinary ACR
UE (renal failure or normal), LFT (deranged if related to hepatitis), FBC (anaemia), lipid profile (hypercholesterolaemia)
Specialist- RENAL BIOPSY (required to elucidate cause in nephrotic/nephritic syndrome)
General management of GN
Treat underlying cause
Restrict dietary salt and water
Immunosuppression (steroids)
Blood pressure control (ACE or ARB)
Sx of ADPKD
Chronic renal failure, abdominal and flank pain (cyst rupture, UTI, stone), recurrent UTI, renal stones, palpable kidneys, extra renal manifestations;
Cerebral aneurysms
Hepatic (most common), splenic, pancreatic, prostatic cysts
Cardiac valve disease (MR)
Colonic diverticulum
Aortic root dilation
LVH
Arterial HTN (morning headaches)
NB- but, cerebral events are more liekly to occur than liver ones ie. SAH more common than l;iver failure
Investigations for ADPKD
Urine dipstick
Bloods- FBC UE fasting lipid profile (raised)
Renal USS (scan of choice), MRI scan head (aneurysm), abdomen and pelvis (other cysts)
Genetic testing- chromosomal involvement
Management of ADPKD
Manage complications- ace, ABX for infections, dilaysis in ESRD, cysts drainage, avoid NSAID
Tolvaptan (vasopressin receptor antagonist)- slows progression of the cysts
Other steps- genetic counselling, avoid contact sports, avoid NSAIDS and anticoagulants, regular BP and ultrasounds and UE
Genetic testing for immediate family members
Renal transplant- only curative option
Henoch schoenlein purpura
IgA vasculitis (NOT AN IGA NEPHROPATHY- bergers disease, no rash in latter as it affects kidneys, not all the blood vessels) commonly presenting with a purpuric rash affecting the lower limbs or buttocks in children
Often triggered by an URTI (tonsillitis) or a gastroenteritis
Purpura, joint pain, abdominal pain, renal involvement (affects kidneys 50% of the time- IgA nephropathy)
No thrombocytopenia
NB- exclude other pathology and assess for organ damage;
-FBC, UE, albumin (nephrotic), CRP, ESR
-Blood cultures (rash), urine dipstick, urinary albumin:creatinine, BP etc.
Glomerulonephritis
Conditions that cause inflammation of or around the glomerulus. A cause of intrinsic AKI
Small vessel vasculitides
HSP
Eosinophilic granulomatosis with polyangitis (CS)
Microscopic polyangitis
Granulomatosis with polyangitis (wegeners)
Medium vessel vasculitides
Poly arteritis nodosa
Eosinophilic granulomatosis with polyangitis (CS)
Kawasaki
Large vessel vasculitides
GCA
Takayasu
Non specific features of vasculitides
Fatigue
Fever
Weight loss
Anorexia
Anaemia
Arthralgia
Vasculitides investigations
MSU dipstick and microscopy and analysis, OBS (BP in each arm), BM
Bloods- FBC UE LFT TFT CRP ESR blood viscosity (inflammation) ANA ANCA HBA1c glucose
Imaging- CT angiography, biopsy of affected vessel, CXR (lung manifestations) and XRay of affected joints
Other potential features of vasculitides
Purpura
Joint and muscle pain
Peripheral neuropathy
Renal impairment
GI disturbance
Anterior uveitis and scleritis
HTN
pANCA
Microscopic polyangitis
CS (eosinophilic granulomatosis with polyangitis)
cANCA
Wegners (granulomatosis with polyangitis)
Eosinophilic granulomatosis with polyangitis (CS)
Paranasal sinusitis
Mononeuritis multiplex ;wrist drop, foot drop etc.)
Presents with severe asthma
Elevated Eosinophils
Joint pain
NB- LTRA may precipitate the disease
Microscopic polyangitis
Renal failure
Also affects lungs- SOB and haemopytiss
Granulomatosis with polyangitis (Wegner)
URT- Nosebleeds, crusty secretions, hearing loss, sinusitis, saddle shaped septum
LRT- Cough wheeze and haemoptysis with consolidation on CXR
Renal- Rapidly progressing glomerulonephritis (pauci immune)
Other- Proptosis, cranial nerve lesions etc.
Poly arteritis nodosa
Associated with Hep B C and HIV
Renal impairment, stroke, MI, skin etc.
libido reticularis
Takayasu
Aorta and it’s branches (and pulmonary arteries)
Aneurysms and pulselessness
Arm claudication or syncope
Kawasaki
Young children under 5
Renal failure and haemoptysis
GOODPASTURES syndrome (anti-GBM disease)
Granulomatosis with polyangitis (Wegner)
(Microscopic polyangitis)- less so.
Difference between GOODPASTURES and Wegners
Saddle shaped nose, pANCA, no anti GBM
Interstitial nephritis
Inflammation of the space in the kidneys between the cells and the tubules (the interstitium)
NB- glomerulonephritis is where there is inflammation around the glomerulus
2 types- AIN & chronic tubulointerstitial nephritis
Acute interstitial nephritis
Presents with AKI, HTN, and generalised hypersensitivity reaction eg. Rash, fever, eosinophilia
Caused by a hypersensitivity reaction to drugs (NSAID, antibiotics) or an infection
Chronic tubulointerstitial nephritis
Chronic inflammation of the interstitium- presents with CKD
Underlying cause- autoimmune, infectious, iatrogenic, granulomatous disease
ATN
Most common cause of AKI
Reversible in early stages
Cause of ATN
Ischaemia- shock, sepsis
Nephrotoxins- aminoglycosides (streptomycin, gentamicin), myoglobin (secondary to rhabdomyolysis), lead, contrast dye
Features of ATN
AKI features- raised urea, creatinine, potassium
NB- muddy brown casts in the urine
Phases of ATN
Oliguric
Polyuric
Recovery
Histology features
Loss of nuclei and detachment of tubular cells from the basement membrane
Dilated tubules
Necrotic cells obstruct the tubule lumen
Causes of AIN
Drugs eg. Penicillin, rifampicin, NSAID, allopurinol, furosemide
Systemic disease eg. SLE, sarcoidosis, Sjogrens
Infection
AIN investigations
Sterile pyuria
White cell casts
Drugs that can worsen renal function in AKI and must be stopped
NSAID
Aminoglycosides (gentamicin, streptomycin)
ACE and ARB
Diuretics
(DAMN- diuretic, ACE-I/ARB, aMinoglycoside, NSAID (except 75mg aspirin))
Drugs that may have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)
Metformin
Lithium
Digoxin
ADPKD Aneurysm screening
Offered to people with ADPKD and a family history of brain ameurysm
If no or only small aneurysms are found, you’ll be offered further scans at intervals of 1 to 5 years to check for new haemorrhages or an increase in the size of an existing one.
Management of HSP
Analgesia
Supportive management for nephropathy
No indication for steroids or immunosuppressants
Management of IgA nephropathy
Minimal proteinuria- no treatment
Elevated proteinuria and slightly reduced eGFR- ACE-I
Active disease (falling eGFR/ no response to ACE)- immunosuppression with steroids
Management of membranous glomerulonephritis
ACE or ARB
Immunosuppression if not responding eg. Corticosteroid with cyclophosphamide
Minimal change disease
Nephrotic syndrome
Idiopathic (small amount of cases- NSAID, malignancy, infectious mononucleosis)
Management- steroids (cyclophosphamide if steroids don’t work)
Biopsy- fusion of podocytes and effacement of foot processes
Nephrotic syndrome and thyroid function
Low total but not free thyroxine levels
Complications of nephrotic syndrome
VTE
Hyperlipidaemia
CKD
Infection risk
Hypocalcaemia
Nephrotoxicity and contrast media
Rise of creatinine 25% 3 days post procedure
Use saline 12 hours pre and post procedure to avoid in high risk patients (or sodium bicarbonate)
If high risk and on metformin, withhold for 48 hours until renal function is normal
Complications of peritoneal dialysis
Peritonitis (S. epidermidis, then S. aureus)- Vancomycin & ceftazidime (or gentamicin)
Peritoneal sclerosis
Causes of renal papillary necrosis
Pyelonephritis
Diabetic nephropathy
Obstructive nephropathy
Analgesic nephropathy (NSAID)
Sickle cell anaemia
Management of vasculitis
Refer to rheumatologist
Steroids eg, oral Prednisolone and immunosuppression (cyclophosphamide) to stop flare up
Continued immunosuppression eg methotrexate
LTRA (monteleukast) and EGPA
Worsen asthma symptoms in EGPA
What to do after an abnormal ACR reading
Repeat with a first pass morning urine specimen
What is the most important infection to monitor for following solid organ transplant?
CMV- treat with Ganciclovir
