Nephrology Flashcards
What is AKI?
A syndrome of decreased renal function
Rise in creatinine >26 umol/L within 48h
Or rise in creatinine >1.5x baseline within 7 days
Urine output <0.5mL/kg/hr for >6h
Staging of AKI
1- 1.5 x baseline creatinine within 1 week
2 x baseline
3 x baseline
Pre-renal causes of AKI
Reduced renal perfusion Hypovolaemia Sepsis HF renal artery disease Dehydration
Renal causes of AKI
Intrinsic renal disease
Glomerulonephritis
Vasculitis
Interstitial nephritis - secondary to medications (NSAIDs)
Post-renal causes of AKI
Obstruction to urinary outflow tract
Tumors
Clots
Calculi
Features of AKI
Oliguria Fluid overload - peripherl oedema, SOB Acidosis - kussmaul breathing Uraemia - malaise, lethargy, pruritis Hyperkalaemia - chest pain, palpitations
Management of AKI
General - supportive, monitor fluid - avoid over-load and hypovolaemia. Abx if sepsis
Review medications - stop nephrotoxins
Refer to nephrology if intrinsic cause, urology if post-renal. In put and output managing
Manage complications
Causes of CJD
Diabetes
HTN
Renovascular disease
Glomerulonephritis
Investigations of CKD
Blood - u+e, urea, Hb, glucose, calcium, PTH
Urine - distick, MC&S, albumin and protein to creatinine ratio
Imaging - USS, CT - obstruction
Histology
Management of CKD
Referral to nephro
Treatment to slow progression and treat complications
Renal replacement therapy
Slow progression - target BP <140, offer ACEi
Glycaemic control
Bone protection - bisphospanates
Other - stations, CVD protection (lifestyle) urology input for obstruction, iron if anaemia
Caution drugs - NSAIDs
Renal transplant
Renal replacement therapy
Classification of CKD
G1 - eGFR (>90) G2 - eGFR (60-89) G3 - eGFR (30-59) G4 - eGFR (15-29) G5 - eGFR (<15)
Signs and symptoms of CKD
Early stages - asymptomatic. Signs of cause - diabetes, HTN, proteinuria (glomerulonephritis)
Later stages - BROKEN PIDDLE BAGS
BP - HTN RBCs - anaemia Oedema K+ - raised Neurological symptoms Pericarditis Itch Dermal darkening Diuresis Lipid elevation Bone osease GI - nausea vomiting Skinny - weight loss
What is nephritic syndrome?
Presence of haematuria, variable proteinuria, renal impairment, and HTN
Known as glomerulonephritis
Describes the presence of an inflammatory process within the glomeruli
Causes of nephritic syndrome
Due to inflammation.
Can be due to inflammation of the small vessels within the capillary tuft or formation of anti-glomerular basement membrane autoantibodies
Immune complex deposition - deposition of immunoglobulin and complement. Typical of a systemi disease (SLE, post-strept. Glomerulonephritis, IgA nephropathy)
Small vessel vasculitis - limited or no immune deposition in the glomeruli. Instead patients have circulating ANCA (targets self-antigens leading to inflammation) - broadly 3 diseases- microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis
Anti-GBM - formation of GBM antibodies that target IV collagen in the basement membrane.
What is IgA nepropathy, what type of disease is it?
Immune complex deposition causing nephritis-type condition
Galactose deficient IgA recognised by IgG and a different IgA type - forms an immune complex that deposits in the renal mesangium
What is presentation of IgA nephropathy?
Asymptomatic non-visible haematuria or visible haematuria following an infection (typically a URTI)
Increased BP
Think of in young males, with episodic haematuria following an acute URTI
Diagnosis of IgA nephropathy
Urinalysis - haematuria and rarely proteinuria
FBC, renal function, LFTs, bone profile
Imaging - USS / CT - exclude structural symptoms
Renal biopsy is definitive
Treatment of IgA nephroapthy
Optimal supportive care, control of BP, reduction of proteinuria
Lifestyle modifications - weight loss, smoking cessation, dietary sodium restriction has shown benefits
ACEi / ARB
What are the 3 ANCA-associated vasculitis conditions?
Microscopic polyangiitis
Granulomatosis with polyangiitis (wegener’s)
Eosinophilic granulomatosis with polyangitis
What is granulomatosis with polyangiitis?
Also known as wegeners granulomatosis
Small vessel vasculitis - ANCA associated
Usually develops from an initiating event in a genetically predisposed individual
Can affect any organ system
Features of granulomatosis with polyangiitis
ELK (ENT nose throat)
ENT - sensioneural hearing loss, epistaxis, otitis, sinusitis, saddle shaped nose deformity
Lung - haemostasis
Kidney - asymptomatic haematuria, proteinuria, nephritic syndrome
Also eye symptoms- conjunctivitis, episcleritis
Also - fever, lethargy, weight loss anorexia
Investigations of granulomatosis with polyangiitis
Biopsy - of affected organ (kidney, nose)
ANCA positivity
Also - urinalysis- blood/protein
Red cell casts - suggestive of glomerulonephritis
Routine bloods - FBC, coag, u+e, crp, LFT, bone profile
Vasculitis screen - ana, complement, anti-GBM
Imaging - CXR (effusions), CT sinuses
Management of granulomatosis with polyangiitis
Immunosuppression
Induce - steroids in combination with retuximab in life-threatening
Maintenance - multiple agents - rituximab, azathioprine, methotrexate
Post-streptococcal glomerulonephritis presentation and management
1-2 weeks after infection
Myalgia, headache, haematuria, proteinuria
Supportive management
What is nephrotic syndrome?
Proteinuria >3.5 g/day
Hypoalbuminaemia <25g/L
Oedema
Hyperlipidaemia
Causes of nephrotic syndrome
Primary:
Minimal change disease
Focal segmental glomerulosclerosis
Membranous nephropathy
Secondary:
DM
Amyloidosis
HIV
Presentation of nephrotic syndrome
Features of fluid overload Fatigue Poor appetite Peripheral and periorbital oedema SoB - Pleural effusions Foamy urine - protein
Diagnosis of nephrotic syndrome
Proteinuria >3.5 g/day
Hypoalbuminaeamia <35 g/L
Oedema
Complications of nephrotic syndrome
Thromboembolism Infection Hyperlipidaemia Hypocalcaemia Acute renal failure
What is minimal change disease?
Common childhood cause of nephrotic syndrome
Characterised by podocyte fusion under electron microscopy
Cause is often idiopathic but some due to drugs and malignancy and infections
Symptoms of minimal change disease
Nephrotix syndrome
Oedema
Proteinuria
Diagnosis of minimal change disease
Children - assumption
Adults - renal biopsy
Managemet of minimal change disease
Prednisolone - most recover 6-8 weeks
If dont respond - more steroids or more intensive immunosuppressives
What is focal segmental glomerulosclerosis?
Describes a histological lesion - focal (particular glomeruli involved) segmental (only part of glomeruli involved)
Sclerosis = scarring
Causes of Focal segmental glomerulosclerosis
Primary secondary or genetic
Primary - circulating factor that damages podocytes (spreads out which reduces effectiveness of filtration barrier)
Secondary - adaptive response to injury. Cause e.g. obesity
Diagnosis of focal segmental glomerulonephritis
Renal biopsy
IgM deposition scarring certain segments
Management of focal segmental glomerulonephritis
Differentiate between primary and secondary
Primary = more like minimal change disease = immunosuppressives
Secondary = treat cause e.g. weight loss
What is Membranous nephropathy?
Most common cause of neprotic syndrome in adults
Characterised by glomerular basement membrane thickening. Formation of immune deposits and subsequent thickening of the membrane
Secondary causes - malignancy, autoimmune diseases, infection, gold, drugs (penicillamine)
Diagnosis of membranous nephropathy
Histological - renal biopsy Serological antibodies (anti-PLA2R)
Management of membranous nephropathy
Depends on natural history
Some people may recover spontaneously
Steroids / immunosuppressive for those with not irreversible disease
What bone problems occur in CKD?
Low vitamin D
As kidneys normally excrete phosphate = high phosphate which drags calcium out of bones - resulting in osteomalacia
Low calcium occurs due to lack of vitamin D
Secondary hyperaparathyroidism - low calcium, high phosphate and low vitamin D
Management of bone disease in CKD
Reduce dietary intake of phosphate in the first line
Phosphate binders
Vitamin D - alfacalcidol
Parathyroidectomy in some cases
What should be given in just about all nephrotic syndrome conditions
ACEi / ARB
Reduces proteinuria and improves prognosis
What is haemoyltic uraemic syndrome? Cause?
Generally seen in children
Classic triad of: AKI, Microangiopathic hemolytic anaemia, thrombocytopenia
Causes - most = e. Coli
What would suggest that symptoms are due to CKD rather than an AKI?
Small, bilateral kidneys
Hypocalcaemia
What is tubulointerstitial nephritis and causes
Injury to the renal tubules and interstitium
Inflammation commonly due to a hypersensitivity reaction to a medication (leads to inflammation with or without AKI)
Can be acute or chronic
Causes - drugs (penicillin, Abx, NSAIDs)
Features of tubulointerstitial nephritis
Classic - fever, rash, eosinophilia Arthralgia Oliguria Malaise Haematuria HTN N+V
Associated with Abx use a lot
Management of tubulointerstitial nephritis
Supportive Stop causative agent Treat underlying cause Stop offending drug Steroids in severe cases Renal replacement - severe AKI
Causes of metabolic acidosis with normal anion gap
ABCDE
Addison
Bicarb loss (diarrhoea)
Chloride
Drugs
Causes of metabolic acidosis with raised anion gap
Lactate (shock, sepsis, hypoxia)
Ketone- DKA
Urate - renal failure
Acid poisoning- salicylate, methanol
How long does post stept glomerulonephritis take after a URTI?
1-2 weeks (IgA nephropathy = 1-2 days
What is alport syndrome? Its presentation
Rare hereditary nephropathy due to mutations in genes for collagen IV
Usually X-linked
Affects glomerular basement membrane = nephritis
Features - classic - microscopic haematuria, progressive renal failure, HTN
Bilateral sensineural hearing loss
Ocular defects
Management of alport syndrome
Kidney transplant for cure Lifelong nephrologist care Regular renal monitoring AcEi therapy for HTN/proteinuria Management of extra-renal disease
Management of anaemia in CKD
Determine and optimise iron status
Erthypoeitin-stimulating agents - eryhtropoetin or darbepoetin
Haemostasis and AKI/haematuria and proteinuria should make you think of what?
Anti-GBM (goodpastures)
Rash, impaired renal function, raised urinary WCC, eosinophil would make u think what?
Acute tubulointerstitial nephritis
Prevention of contrast-induced nephrotoxicity
1L 0.9% saline pre and post procedure
Rhabdomyolysis features and management
Typically a patient who has a fal or prolonged epileptic seizure found to have an acute AKI
Elevated creatine kinase Myoglobinuria Hypocalcaemia Elevatee phosphate Hyperkalaemia Metabolic acidosis
IV fluids and urinary alkalinisation
What is lupus nephritis?
Nephritis caused by SLE.
Antibodies against nuclear components (dsDNA)
Deposition of antibody complexes cause inflammation cause tissue damage
Investigation and management of lupus nephritis
Anti-ANA,
anti-dsDNA (titres corresponds to disease severity)
Clinical diagnosis
Treatment - ACEi, hydroxycholoroquine for extra renal disease
Higher class = immunosuppression
Where does furesomide act?
Ascending loop of henle
On Na/K/2Cl transporter
Where do thiazides act?
Distal tubule
Inhibit Na/Cl co-transporrer
What type of abnormality on a ABG can renal tubular acidosis cause?
Hypercholoraemic metabolic acidosis (normal anion gap)
What medication can help in hyperphosphataemia in patients with CKD mineral bone disease
Sevelamer
Try low phosphate diet first
Common complications of renal transplant
Surgical - bleed, thrombosis, infectionz urinary leaks, hernia Delayed graft function Rejection- acute or chronic Infection - CMV common Malignancy - skin common
Most appropriate fluids for rhabdomyolosis?
Saline (0.9%)
Not heartmanns because of potassium
What causes a hypercoagulable state in nephrotic syndrome?
Antithrombin III
What would you find in urinalysis (MC&S) of interstitial nephritis?
White cell casts
Microscopic haematuria
Sterile pyuria
