General overview Flashcards
Nephritic syndrome requirements
Haematuria Oliguria Fluid retention Proteinuria less than 3mg/l in 24 hours- any more and it becomes nephrotic syndrome HIGH BP
Nephrotic syndrome
Peripheral oedema
Hypoalabuminaemia- less tha 24g/l
Proteinuria- more than 3mg/L
Hypercholesterolaemia
Pre-renal AKI causes
Hypovolaemia:
Renal loss from diuretic overuse, osmotic diuresis- DKA
Extrarenal loss from vomiting, diarrhoea, burns, sweating, blood loss
Systemic vasodilation- sepsis- neurogenic shock
Decreased cardiac output: HF and MI
Renal , cellular damage/intrinsic
Tubular: acute tubular necrosis- ischaemia, drugs, toxins, paracetamol, NSAIDs ACE-I contrast, myoglobinuria in rhabdomyolysis
GLOMERULONEPHRITIS, interstitial nephritis- TUMOUR LYSIS SYNDROME
VASCULAR vessel obstruction
Post-renal=obstruction
Luminal: stones, clots
Mural: malignancy- uretic, prostate, bladder, BPH, strictures
Retroperitoneal fibrosis
4 Places in the renal system where you can have damage
Tubular, glomerular, interstitial, vascular
Vascular causes of renal disease
Large vessel occlusion: renal artery/vein thrombus
Emboli
Small vessel- microangiopathy
Haemolytic uraemic syndrome (HUS)
Thrombotic Thrombocytopenic Purpura (TTP)
Disseminated Intravascular Coagulation (DIC)
Haemolytic Uraemic Syndrome
characterisations
1) Progressive renal failure- kidneys
Microangiopathic haemolytic anaemia (MAHA)
Decreased Platelet - blood
Most common cause of HUS?
E.coli
Toxin- endothelial damage- thrombosis- decreased platelets- destruction of RBCs, shistocytes- decreased HB
Presentation of patient with HUS?
Abdo pain, bloody diarrhoea, fever, seizures, lethargy
TREATMENT: Supportive- dialysis and plasmapheresis
Thrombotic Thrombocytopenic Purpura (TTP)
Presentation and pathophysiology
Overlap with MAHA,
PENTAD of haemolytic uraemia, thrombocytopenia, uraemia, Fever, neurogenic symptoms
Seizures-, hemiparesis, decreased consciousness and decreased vision
Deficiency of protease- ADAMTS13 that cleaves vWF- multiform of vWF- platelet aggregation and fibrin deposition, microthrombi
Glomerulonephritis meaning
Inflammation of the glomeruli and nephrons
Glomerular inflammation:
Loss of barrier function presentation
Loss of filtering capacity presentation
Loss of barrier function Proteinuria- mild to nephrotic syndrome
Haematuria- mild to macrocytic
Filtering capacity- reduced excretion> accumulation of waste products- AKI
Causes of glomerulonephritis
IgA nephropathy- (days after UTI- increased IgA immune complex- episodic haematuria
Henoch-Shonlein Purpura (HSP)- systemic variant IgA nephropathy- purpuric rash -
Anti-GBM- Goodpastures- Auto Ab to Type IV collage (GBM and lung)- haemoptsis and haematuria
Post Streptoccocal GN- 1-12w after throat infection- nephritic syndrome
Pauci-immune - ANCA associated antibodies- bound to neutrophils- activation within glomerular capillary loops- vasculitis or limited to kidney
Link of oedema with nephrotic syndrome
Hypoalbuminaemia- liver tries to compensate and increases production of lipids- hyperlipidaemia > 10mmol/L
Underlying causes of Nephrotic syndrome
Minimal change glomerulonephritis- children (90%)<5 years
Membranous glomerulonephritis/DM- adults
What is berger’s disease
IgA nephropathy- most common cause of primary glomerulonephritis
NEPHRITIC SYNDROME
Common primary causes of nephrotic syndrome
Membranous glomerulonephritis (ICM) Minimal change disease (Non-ICM) Focal segmental glomerulosclerosis (Non-ICM) Mesangiocapillary glomperulonephritis (ICM/Non-ICM)
Common secondary causes of Nephrotic syndrome
Diabetes
SLE
Amyloid
HBV/HCV
Nephritic syndrome primary causes
IgA nephropathy
Mesangiocapillary Glomerulonephritis
Common secondary causes (systemic)
Post-streptococcal
Vasculitis
SLE
Anti-GMB disease- cryoglobulinaemia
Investigations and management of Glomerulonephritis
Bloods- FBC, U&Es, CRP, Complement, Autoantibodies
Urine
Imaging- renal US +/- renal biopsy
Management - Refer specialist
BP management <130/80
ACE-I or ARB- reduce proteinuria and preserve renal function
Steroids/immunosuppression
Tubular causes of AKI- ATN
ATN- most common cause of AKI
ischaemia, nephrotoxic agents
Exogenous drugs: NSAIDs, aminoglycosides, amphotericin b, contrast media, calcineurin inhibitors, cisplatin
Endogenous : myoglobinaemia (rhabdomyolysis) , haemoglobinuria, crystal, myeloma
Pathophys of Acute, tubular necrosis
Hypovolaemia Low CO- cardiac output Systemic vasodilation-sepsis DIC Renal vasoconstriction
Causes of ATN: ISCHAEMIA
Ischaemia- tubular cell injury, necrosis, obstruction of tubule by debris, reduced GFR
3 phases: Initiation- acute reduced GFR, increased Cr and increased UREA
Maintenance of low GFR- increase in creatinine and urea
Recovery- tubular function regenerates- increased urine volume and gradular decrease in urea and CR
Causes of ATN: myeolma
Malignant disease of bone marrow plasma cells- clonal expansion of plasma cells
CRAB:
Calcium- high
Renal failure- increase Urea and increase Cr
(hypercalcaemia and paraprotein deposition)
Anaemia
Bone- bone osteolytic bone lesions- pain fracture (risk cord compression)
Causes of ATN- nephrotoxic agents
Analgesics: NSAIDS Antibiotics: Aminoglycosides, gentamicin, streptomycin CONTRAST AGENTS Anaesthetic agents Chemotherapeutic agents ACE-I and ARBs Immunosuppressants- ciclosporin
Urine Exam- what to look for
pH Protein Blood Glucose Leucocyte esterases Nitrites Specific gravity Ketones Urobilinogen lab tests: Urine MCS Protein- creatinine 24 hour urine
Haematuria: what it indicates
Renal: Pyelonephritis Glomerulonephritis Carcinoma Trauma
Extrarenal Cystitis/prostitis, urethritis Stones trauma Bladder cancer
Proteinuria indications
Nephrotic syndrome DM Amyloid HTN Multiple myeloma CCF
Glucose in blood
DM
Renal tubular damage
Pregnancy
Sepsis
Urinobilinogen
Pre-hepatic jaundice
Ketones
Starvation
DKA
HMG
General management of AKI
Assess volume status- aim for euvolaemia
Stop nephrotoxic drugs
Monitoring and nutrition
Treat underlying cause
Pre-renal correct volume depletion and abx, inotropes
Post renal - catheterise + imaging CTKUB+urology and reversal
Intrinsic renal- nephrology
CKD symptoms
Anorexia, nausea and vomiting, fatigue, pruritis, peripheral oedema, musce cramps, pulmonary oedema, sexual
dysfunction
CKD signs
Skin pigmenetation- uraemia excoriation marks- uraemia Pallor- anaemia of chronic disease hypertension Peripheral oedema Peripheral vascular disease Renal bone disease
Consequences of CKD
1) Progressive failure of homeostatic function - acidosis
Progressive failure of hormonal function- anaemia
Renal bone disease- osteomalacia
Cardiovascular disease- vascular calcification
Uraemia and death
Usual blood results for CKD
Decreased Hb- normocytic anaemia U&Es ( increased urea and creatinine) Glucose- DM eGFR Decreased calcium Increased phosphate Increased ALP- renal osteodystrophy Increased PTH if Severe CKD
Why do you need a CXR in these investigations?
Pericardial effusion or pulmonary oedema
Limiting progression/complications in CKD
BP target <30/80 (<125/75 if diabetic)
Tight glucose control in DM
Decrease CVS risk - stop smoking, lose wieght Diet- restrict K+, AVOID high phoosphate food
Renal osteodystrophy treatment
Calcichew- Ca supplement
Calcium acetate- phosphate binders
Cinacalecet- calcimimetic- reduce PTH levels
Symptom control of:
Anaemia
Acidosis
Oedema
Sodium bicarbonate supplements for patients with low serum bicarbonate
Oedema- loop diuretics- restriction of fluids
Renal replacement therapy
name 2 types
Haemodyalysis- vascular access requires
Transplanatation- gold standard treatment- major surgery
Most common causative agent of an UTI
E.coli
Others- staphylococcus saprophyticus
Proteus mirabilis
Enterococci
Risk factors for UTI
Female Sex Exposure to spermicide Pregnancy Menopause Immunosuppression Catheterisation Urinary tract obstruction
Cystitis symptoms
Frequency
Urgency
Dysuria
Haematuria
Protatitis symptoms
Suprapubic pain
Flu-like symptoms
Low backache
Few urinary symptoms
Acute pyelonephritis symptoms
High fever Rigors Vomiting Loin pain and tenderness Oliguria- AKI
Investigations and management of UTIs
Urine dipstick
MSU for urine MCS
Microscopy
Culture
Bloods: FBC, Uand E, CRP
Management- uncomplicated- cefalexin- 3/7
Nitrofurantoiin- 7/7
Mae- 7/7 cefalexin or ciprofloaxacin 14/7 if suspicious of prostatitis
Pyelonephritis/urosepsis- co-amoxiclav 1-2/7
Polycystic kidney disease
fluid filled cysts grow on the kidney
History acute loin pain, stones
SAH (berry aneurysms)
Examination- renal enlargement, abdo pain and haematuria, renal enlargement
Investigate: haematuria, raised Hb, derranged Uand E, abdominal USS, MRI angiography, IF +ve 1st degree SAH and ADPKD
Renal cell carcinoma
Von-Grawitz tumour, hypernephroma
arising from parenchyal cortex
TRIAD: haematuria, loin abdom mass
Ix: increased BP (renin) Polycythaemai or IDA, ALP- bone mets, RBCS, cannon ball mets CT/MRI-
Renal artery stenosis
Stenosis of renal artery
Caused by atherosclerosis, fibromuscular dysplasia (10% young,)
Increased BP refractory to Tx
Worsening renal function after ACEi, ARB in bilateral RAS
Flash pulmonary oedema
Carotid or renal bruits
Ix
US measurement of kidney size
CT angiogram- risk of cotrast enphotoxicity
DIgital subtration renal angiography- GOLD STANDARD BUT INVASIVE
Membranous glomerulonephrits
Presents with nephrotic syndrome or proteinuria
Renal biopsy: electron microscopy: the basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance
Causes of Membranous glomerulonephritis
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
Features of Alport’s syndrome
Alport’s syndrome usually presents in childhood. The following features may be seen:
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
Features of Rhabdomyolysis
acute kidney injury with disproportionately raised creatinine
elevated creatine kinase (CK)
myoglobinuria
hypocalcaemia (myoglobin binds calcium)
elevated phosphate (released from myocytes)
hyperkalaemia (may develop before renal failure)
metabolic acidosis
Causes of rhabdomyolysis
seizure
collapse/coma (e.g. elderly patients collapses at home, found 8 hours later)
ecstasy
crush injury
McArdle’s syndrome
drugs: statins (especially if co-prescribed with clarithromycin)
Management of Rhabdomyolysis
IV fluids to maintain good urine output
urinary alkalinization is sometimes used
Causes of anaemia in renal failure
reduced erythropoietin levels - the most significant factor
reduced erythropoiesis due to toxic effects of uraemia on bone marrow
reduced absorption of iron
anorexia/nausea due to uraemia
reduced red cell survival (especially in haemodialysis)
blood loss due to capillary fragility and poor platelet function
stress ulceration leading to chronic blood loss
Features of anaemia in patients with CKD
Happens due to reduced EPO levels
Normochromic, normocytic anaemia- beomes apparent when the GFR is less than 35ml/min
Anaemia in CKD predisposes to LVH
