Renal Flashcards
What are the functions of the kidneys?
Endocrine release - epo, renin, prostaglandins
Removal of waste products - urea, drugs
Metabolism - proteins, vit D
Fluid regulation
What are the 3U’s that must always be remembered in investigation for renal disease?
U&E, urinalysis, USS
How is proteinuria measured?
Albumin:creatinine ratio (<2.5 men, <3.5 women)
24 hr collection albumin
If they have proteinuria do culture of urine
What is the main cause of haematuria? What are some other causes?
- Glomerular disease (>1g)
- Transient causes - orthostatic, exercise, fever (<1g)
- Tubulointerstitial disease (<1g)
- Upper/lower UTI (<1g)
- Diabetes (30-300mg)
- Minimal change disease (30-300mg)
In terms of proteinuria, what are the indications for biopsy?
Persisent (>3g) or alongside haematuria
How much blood is usually lost in the urine?
<1uL/day
What is the main cause of proteinuria? What are some other causes?
- Glomerular disease (IgA nephropathy, thin basement membrane disease)
- Transient causes (UTI, exercise, menstruation)
- Neoplasia (painless, bladder/renal)
- Drugs
Which drugs may cause haematuria?
Cephalosporins
Ciprofloxacin
Furosemide
NSAIDS
What is the 2WW criteria for haematuria?
Visible >45 yers
Non-visible >60yrs
Do renal USS and cystography
What are the normal values for glucose in the urine?
0-0.8mmol/L
What causes glycosuria?
DM
Pregnancy
Sepsis
Renal tubular damage
What causes nitrites/leucocytes in the urine?
UTI, high protein meal
What causes ketones in the urine?
Starvation, ketoacidosis
What does urine microscopy look for? What do they show?
CASTS
white cell casts - UTI, acute interstitial nephritis
red cell casts - glomerular bleeding, vasculitis, nephritis
epithelial casts - acute tubular necrosis
What factors influence creatinine levels?
Muscle mass
Muscle catabolism
Liver function
What causes high creatinine levels?
- Kidney dysfunction
- Hypertension
- Drugs (statins)
- Rhabdomyolysis
- Large muscle mass
What are the problems associated with measuring creatinine levels?
- Muscle mass
- Log relationship to GFR ( as GFR decreases lots, creatinine only increases a little)
- Tubular and gut secretion
- Variability of assay
How is eGFR calculated?
Takes into account creatinine, age, gender and ethnicity
What is the definition of AKI?
A rapid reduction in kidney function over hours to days, as measured by serum urea and creatinine and leading to a failure to maintain fluid, electrolyte and acid-base homeostasis
How is AKI diagnosed?
- Rise in creatinine >26umol/L in 48hours
- Rise in creatinine >1.5 x the baseline
- Urine output <0.5ml/kg/h for 6 consecutive hours
1st line investigations - U&Es and creatinine
What are the symptoms of AKI?
Urinary - dysuria, oliguria, anuria, haematuria,
Systemic - fever, vomiting, myalgia, diarrhoea
Kidney dysfunction - oedema, bruising
What are the risk factors for AKI?
- Age>75
- CKD
- Cardiac failure
- Sepsis/infection
- PVD
- Chronic liver disease
- Diabetes
- Drugs
- Poor fluid intake
Which investigations results would raise your index of suspicion for AKI secondary to CKD?
- Small kidneys
- Anaemia
- Low calcium
- High phosphate
- Previous bloods
What investigations should be done in AKI?
BEDSIDE - urinalysis, BP, ECG
BLOODS - FBC, U&E, CRP, LFTs, bone profile, CK, clotting, ESR, cultures, immunoglobulins, complement, autoantibodies
IMAGING - renal USS, CXR
SPECIAL - kidney biopsy
What are the indications for kidney biopsy for AKI?
Intrinsic cause other than ATN is suspected, such as glomerulonephritis
How can you tell it is a pre-renal cause of AKI?
Restoration of blood flow will resolve the problem with no cell injury
What are some pre-renal causes of AKI?
Volume depletion - GI bleed, diarrhoea, vomiting, burns
Low CO - tamponade, massive PE, MI
Distributive - sepsis, anaphylaxis, hepatorenal, pancreatitis
Drugs - NSAIDS, contrast, antihypertensives
How do NSAIDs cause kidney injury?
Vasoconstriction of the afferent arteriole (supplying the kidney) and therefore decreased GFR
How do antihypertensives cause kidney injury?
Cause vasodilation of efferent arteriole, causing a decrease in filtration pressure, causing decreased GFR
What are some renal causes of AKI?
- Tubulointerstitial disease - ATN, cast obstruction, acute allergic interstitial nephritis (no haematuria/proteinuria)
- Glomerular disease - glomerulonephritis (haematuria, proteinuria)
- Microvascular - HUS, MAHA, vasculitis, microemboli
- Infection
What is the main cause of renal AKI?
Acute tubular necrosis - this is when ischaemia to tubular cells or exposure to a toxin causes cell death.
Patients will be oliguric first as a compensatory mechanism, but then become polyuric, as the tubules grow back.
Recovery may take weeks
What causes ATN?
Ischaemia - can progress from pre-renal AKI involving hypo perfusion
Toxins - aminoglycosides, cisplastin, contrast
What kind of casts can obstruct the tubules causing renal AKI?
Paraprotein - myeloma
Myoglobin - rhabdomyolysis
Urate - tumour lysis syndrome
Crystals - drugs, alcohol
What is acute interstitial nephritis?
Abnormal inflammatory response, often accompanied by a fever, painful joints and a rash - can cause renal AKI.
How is acute interstitial nephritis diagnosed?
White cell casts, eosinophils
How is acute tubular necrosis diagnosed?
Epithelial casts
What causes allergic acute interstitial nephritis?
NSAIDS, pencilllins, PPIs
What can cause glomerulonephritis?
Immune, drugs, infection
What can cause microvascular damage in intrinsic AKI?
- Haemolytic uraemia syndrome - post-viral
- MAHA - anaemia, shistocytes
- Vasculitis - ANCA
- Microemboli of cholesterol post angiography, causing distal necrosis
What are the post-renal causes of AKI?
Luminal - stones, clots
Mural - malignancy, BPH, strictures, fibrosis
Extrinsic compression - malignancy, retroperitoneal fibrosis
Retention - UTI, constipation
How is AKI managed?
- IV fluids - give boluses then assess
- Stop nephrotoxic drugs
- Monitor (fluid status, U&E)
- Treat sepsis
- Give inotropes if low BP
- Treat cause
- Manage complications
- Dialysis
Which nephrotoxic drugs need to be stopped in AKI?
NSAIDS, antihypertensives, gentamicin, metformin, morphine
How do you treat a pre-renal cause of AKI?
IV fluids, abx, inotropes
How do you treat an intrinsic cause of AKI?
Refer to nephrology
How do you treat a post-renal cause of AKI?
DO USS, catheterize, CTKUB, relieve obstruction
What complications might arise secondary to AKI, and how can they be managed?
Hyperkalaemia - IV calcium gluconate, salbutamol, dextrose and insulin, sodium bicarb, fluids
Pulmonary oedema secondary to fluid retention - MONA
Uraemia - dialysis
Metabolic acidosis - sodium bicarb, dialysis
NB any of these complications could be an indication for dialysis
What is the pathophysiology of glomerulonephritis, and how does this lead to AKI?
- Damage to the glomerulus restricts blood flow, leading to compensatory rise in BP
- Damage to the filtration mechanisms from rise in BP, allows protein and blood to enter the urine
- Loss of usual filtration capacity, leading to AKI
How do patients with glomerulonephritis present?
- Hypertension
- Proteinuira/haematuria
- AKI or other renal impairment
What is a nephritic picture?
- Inflammatory
- Blood + protein on urine
- Very high BP and low eGFR
- Implies immune pathology
- Rarely pain
What are the primary cause of nephritis?
- IgA nephropathy
- Mesangiocapillary glomerulonephritis
What are the secondary causes of nephritis?
- Goodpastures syndrome
- SLE
- Vasculitis
- Post-strep infection
- HSP
What is a nephrotic picture?
- Disturbance of permeability barrier
- Triad of proteinuria, hypo albumin and oedema
- Protein ++++ on urine
- Rarely pain
What are the primary causes of nephrotic syndrome?
- Minimal change disease
- Focal and segmental glomerulosclerosis
- Membranous
What are the secondary causes of nephrotic syndrome?
- Diabetes
- SLE
- Amyloidosis
- HepB/C
- Drugs
Describe the normal structure of the glomerular filtration barrier
3 layers of filtration, all negatively charged to repel plasma proteins:
- Fenestrated capillary endothelium, made from podocalyxin (50-100nm holes)
- Thick basement membrane, made from heparan sulphate proteoglycans
- Filtration slits in between the interdigitating processes of the podocytes (4-14nm)
These ensure that large molecules are not filtered out
What is the pathophysiology of IgA nephropathy, and how is it diagnosed??
At times of infection, IgA deposits in the kidney and attacks the glomeruli.
Diagnosis
- Increased IgA and C3 on immunofluorescnece
- Mesangial proliferation on renal biopsy