Medicine - Nephrology Flashcards
What does glucose in urinalysis mean?
• Diabetes
What does blood in urinalysis mean?
• Menstruation
• Nephritis syndrome
• Stones
Infection
What does leukocytes in urinalysis mean?
• Infection/UTI
Nephritic syndrome
What does protein in urinalysis mean?
• Nephrotic/nephritis syndrome
Myeloma
What does nitrites in urinalysis mean?
UTI (nitrites are produced by coliform bacteria)
What does ketones in urinalysis mean?
- DKA
* Pregnancy
What does bilirubin in urinalysis mean?
• Jaundice (hepatic/post-hepatic)
What does SG (specific gravity) in urinalysis mean?
• High solute concentration
Define AKI
Reduction in renal function following an insult to the kidneys
High urea and creatinine and low urine output over hrs/days
95% systemic and both kidneys affected
What are the aetiologies of AKI?
1) Pre-renal (issue with blood supply)
- sepsis
- NSAIDs/ACEi
- dehydration, bleeding, burns, D&V
- MI, cardiogenic shock
- renal artery stenosis
2) Renal (mixed)
- due to GN, vessels or tubular issues
- ATN, vasculitis, DIC, HUS, drugs, rhabdomyolysis, myeloma, sarcoidosis
3) Post-renal (obstructive)
- issue after the kidneys e.g. extrinsic compression, ureteric stone, BPH, hydronephrosis, external kidney compression
What are the three stages of an AKI? and its features
Stage 1 = serum creatinine 1.5-1.9x baseline
Stage 2 = serum creatinine 2-2.9x baseline
Stage 3 = serum creatinine >3x baseline
Features: reduced urine output, pulmonary and peripheral oedema, arrhythmias (electrolyte changes and increased K+ as the kidney are not excreting it!), uraemia (pericarditis, encephalopathies)
Describe the effect of NSAIDs and ACEi on the kidney
NSAID’s:
- Stop COX pathways
- No prostaglandin production
- Prostaglandins are needed to dilate the afferent arteriole
- NSAID’s result in reduced blood supply to the kidney = AKI!
ACEi:
- Stop the production of AT1 -> AT2
- AT2 causes the efferent arteriole to constrict to maintain BP within the kidney
- No AT2 -> kidney hypotension = AKI
What investigations should be carried out in AKI?
RENAL! Rule out sepsis Exclude obstruction Note urinalysis Assess fluid balance Look at drugs
Bloods - FBC, U&E, DH, CK (rhabdo?), GN screen (ANCA/ANA) Urinalysis (infection/rhabdo) Renal USS (?obstruction)
What is the management for AKI?
Stop nephrotoxic drugs and give IV fluids
Depends on cause:
- pre-renal: correct volume depletion
- renal: ?biopsy if intrinsic disease
- post-renal: catheterise/nephrostomy
Correct any: hyperkalaemia, pulmonary oedema or hypoperfusion
What are indications for RRT in AKI?
Acidosis
Fluid overload (e.g. pulmonary oedema)
Uricaemia
Hyperkalaemia
Define CKD and its stages
Abnormal kidney structure/function (GFR <60) which is present for >3 months with implications for health
Stage 1 = eGFR >90 Stage 2 = eGFR >60 Stage 3a = eGFR 45-59 Stage 3b = eGFR 30-44 Stage 4 = eGFR 15-29 Stage 5 = eGFR <15
What are the causes of CKD
Diabetic nephropathy Ischaemia/renovascular disease Glomerulonephritis Pyelonephritis ADPKD Obstructive nephropathy
What are the signs and symptoms of CKD?
Signs: pulmonary oedema, peripheral oedema, pericardial rub, rash (due to toxins), HTN, tachypnoea, cachexia, pallor, yellow skin tinge
Symptoms: when eGFR<15, pruritis, weight loss, anorexia, nausea, fatigue, oedema (leg swelling, breathlessness), nocturia, joint/bone pain, confusion
What investigations should be carried out for CKD?
Bloods: U&E, eGFR, creatinine
Urinalysis: microalbuminaemia
Renal USS
How is CKD managed?
5 principles of management
1) nephro referral
2) slow the disease progression: BP control, good DM and glycaemic control, lifestyle measures (diet, smoking, cholesterol)
3) treat CKD complications (AFUS!)
4) treat non-CKD complications (anaemia, mineral bone disorder = ca and vitamin D replacement)
5) prepare for RRT
What are the complications of CKD?
Think normal kidney functions, then what goes wrong:
Water balance - fluid overload Electrolyte balance - hyperkalaemia Toxin destruction - uricaemia BP - HTN EPO - anaemia vit D production - OP
What are the indications for dialysis?
A-FUH
- acidosis
- fluid overloaded
- uricaemia
- hyperkalaemia
What are the pros and cons of transplantation of kidney?
PROS: more independence fertility improved life expectancy better cost saving long term
CONS: immunosuppression increases malignancy risk infection rejection delayed graft function post-transplant diabetes
What are the types of kidney donation?
1 - Living donor (altruistic (no relation, out of kindness) or allogenic (usually a relation))
2 - Deceased donor
What is the typical trio of drugs for immunosuppression regimens?
tacrolimus
prednisolone
mycophenolate
What is the definition of ‘kidney rejection’?
acute inflammatory state of the kidney, causing dysfunction and leukocyte infiltration
-> can lead to microthrombi formation
What is the definition of glomerulonephritis?
renal disease characterised by inflammation and damage to glomeruli, which allows protein +/- blood to leak into the urine
Rare, but can progress to CKD and ESRF
What are the causes of glomerulonephritis?
Primary - immune mediated, inflammatory, antibody deposition and immune complex deposition
Secondary - lupus, myeloma, infection, drugs, malignancy, amyloidosis, metabolic disorders (HTN, DM, thyroditis)
Describe the 4 main congenital abnormalities of the kidneys:
1) VUR
2) BOU
3) PUJO
4) VUJO
Describe ADPKD
AD PKD1/2 genes involved Polycystin protein over-expressed Progressive renal failure Supportive treatment (BP, diuretics, limit H2O intake), RRT, ?tolvaptan (ADH antagonist)
Describe VHL disease
AD
Multiple benign and malignant neoplasms form
Pts need annual screening: phaeos, renal tumours, brain tumours
Describe tuberous sclerosis
AD
Benign hamartoma formation in various organs
CNS involvement, often co-associated with epilepsy
Describe medullary cystic kidney disease
AD
Cysts form at the cortico-medullary junction
Small/normal sized kidneys
S/Sx of gout and increased uric acid
Describe Alport’s syndrome
X-linked
Collagen mutations mean the GBM does not regenerate properly
Describe Fabry’s disease
X-linked
alpha-galactosidase disorder and accumulation of Gb3 protein in glomeruli
Treatment = enzyme replacement therapy
What are the 4 main systemic kidney diseases and how can they present?
- diabetic nephropathy
- amyloidosis
- renal tubular stenosis
- SLE
Present with: AKI, CKD, ESRF, nephrotic syndrome, nephritis syndrome
Describe diabetic nephropathy
Disease of small kidney blood vessels
Presents w haematuria, proteinuria and renal failure
Eventually scarring, nodule formation, fibrosis and ESRF
Describe amyloidosis
Extracellular protein deposition
AA = systemic amyloidosis
AL = light chain amyloidosis
Protein accumulation causes mesangial expansion
Describe renal artery stenosis
part of systemic atheromatous vascular disease
reduced eGFR
Treatment: BP control, statins, lifestyle, angioplasty
Describe SLE
Deposition of antibody complexes leading to inflammation and tissue damage
Tx: immunosuppression
What are the functions of the kidney
A-WET-BED Acid/base balance Water balance Electrolyte balance Toxin removal BP control EPO production vitamin D metabolism (produces a-1-hydroxylase)
What are the 4 classes of diuretics?
SGLT1/2 inhibitors (empagliflozin)
Loop diuretics (furosemide)
Thiazide diuretics (bendroflumethiazide)
K+ sparing diuretics (amiloride/spirololactone)
Describe the difference between eGFR and creatinine clearance
eGFR is calculated using MDRD formula and only calculates an accurate value if GFR is >60
Creatinine clearance is BETTER than eGFR as it takes into account body weight and SA
CC = (140 - age/creatinine) x weight x 1.04/1.23
In rhabdomyolysis, why are there no RBC’s detected in urine microscopy, but the dipstick comes back blood +
This is because the haemoglobin is released causing the positive dipstick test, but there are no actual whole RBC’s in the urine
What is dialysis?
method of removing nitrogenous waste from the body and maintaining extracellular volume, maintaining normal electrolytes and correcting acidosis
Blood filtration
Types: haemodialysis, peritoneal dialysis, transplantation!
Describe haemodialysis and how it works
removes solute by diffusion and fluid by osmosis
Blood passed over a semi-permeable membrane and the dialysis fluid on the other side of the membrane moves in the opposite direction
Dialysate contains electrolytes
Blood volume falls and dialysate can be discarded
Home/hospital based for 4hrs 3x a week
Needs carer, space, and is expensive
Describe peritoneal dialysis and how it works
Catheter inserted into the peritoneum and dialysate inserted
The peritoneal membrane acts as a semi-permeable membrane and solute/waste slowly diffuses from the abdominal capillaries into the peritoneal fluid
Then the peritoneal fluid is emptied and replaced
Needs draining and filling so risk of peritonitis, hernias
Sclerosis and catheter dislodging can occur
Best option for pts with some residual renal function
What are the 5 most common reasons for someone needing a kidney transplant?
CKD (due to DM, HTN, metabolic syndrome...) Chronic infection GN ADPKD Rarer (Allport's syndrome, cancer)
Describe nephrotic syndrome
- non-proliferative, lack of glomeruli cell proliferation
- damaged podocytes lead to proteinuria and low serum albumin
- increased risk of infections, and increased risk of venous thromboembolism due to increased lipidaemia
FEATURES: oedema, low albumin, proteinuria, hyperlipidaemia
Describe nephritic syndrome
- proliferative, increased glomeruli cells, inflammatory damage
- leads to haematuria
- IF SCARRING occurs, also leads to proteinuria
- DANGEROUS as can progress to ESRF
FEATURES: PHHR
- proteinuria
- haematuria
- HTN
- renal impairment
What is the treatment of nephrotic syndrome
- dietary -> restrict Na intake
- diuretics
- avoid bedrest -> as high protein state means the pt is hypercoagulable
Name the 3 nephrotic types of GN
minimal change disease
focal segmental glomerular sclerosis
membranous GN
Name the 3 nephritic types of GN
IgA nephropathy
Post infectious GN
Rapidly progressive GN
Which type of glomerulonephritis is most common in children?
Minimal change disease
Which type of GN is associated with anti-phospholipase A2 receptor antibody?
Membranous GN (this antibody is seen in 70% cases)
Which type of GN is the commonest in adults?
IgA nephropathy (also called Berger’s disease)
How does IgA nephropathy present?
Synpharyngeal presentation (sore throat and haematuria (usually macroscopic)) usually presents 24-48hrs post GI infection/UTI
What type of infection normally causes post-infectious GN?
Usually a UTI (group A strep) and the GN presents weeks after the UTI
Describe rapidly progressive GN
Nephritic type
Breaks in the GBM allow inflammatory cells to enter the glomeruli and infiltrate bowmans capsule
Type 1 -> anti-GBM disease (Goodpasture’s syndrome), autoantibody made against type 4 collagen
Type 2 (vascuitics) a ->microscopic polyangitis b -> granulomatosis w. polyangitis
How is GN investigated and generally treated?
Inv.
- bloods (check BM, ANCA, ANA, anti-phospholipid-A2R-Ab, bence jones protein)
- biopsy (allows histological examination)
- > light and electron microscopy and immunoflourescence!
General treatment: steroids/immunosuppression
Name the 4 congenital abnormalities of the kidneys and urinary tract (CAKUT)
- VUR (vesico-ureteric reflux) = retrograde flow of urine from bladder -> ureters
- VUJO (vesico-ureteric junction obstruction) = obstruction where ureters meet bladder
- PUJO (pelvic-ureteric junction obstruction) = obstruction where ureters enter kidneys
- BOU = bladder outlet obstruction = bladder outlet obstruction, due to BPH/neurogenic bladder
Describe ADPKD (autosomal dominant polycystic kidney disease)
AD (PKD1/2)
Increased cyst growth, reduced kidney functional volume and reduced eGFR
Normal kidney function until ~40yrs
Presents as loin pain, haematuria, high BP, investigate with USS/CT/MRI
Mainly supportive management, RRT or tolvaptan (ADH antagonist to prevent fluid reabsorption and reduce the stress on the kidneys)
What is VHL
Von hippel lindau disease
AD
Multiple benign cysts and malignancy neoplasms
Annual screening for phaeochromocytomas/renal tumours/brain tumours
Describe tuberous sclerosis
AD
Benign hamartoma formation of multiple systems (brain, heart, eyes, lungs…)
CNS involvement associated with epilepsy/CNS involvement
Describe medullary cystic kidney disease
AD
cysts form at the cortico-medullary junction
presents with gout and hyperuricaemia
Describe Alports syndrome
X linked (F carriers, M affected)
collagen mutations mean GMB does not regenerate properly
microscopic protenuria/haematuria
May need dialysis/transplant
Describe Fabry’s disease
X-linked storage disorder
a-galactosidase deficiency, resulting in accumulation of Gb3 protein in glomeruli = proteinuria and ESRF
Patients also get cardiac neuropathy and angiokeratomas
Treat with enzyme replacement!
Describe renal artery stenosis
Part of systemic atheromatous disease
Progressing narrowing of the renal arteries with atheroma
Reduced eGFR
Irreversible kidney damage develops as cortical hypoxia leads to fibrosis of parenchyma
Treat:
BP control, statins, lifestyle, angioplasty
Describe kidney amyloidosis
extracellular protein deposition, due to pathological misfolding of proteins
proteins can deposit in: - kidneys, liver, heart, gut
2 types:
- AA (systemic amyloidosis)
- AL (light chain amyloidosis)
Protein causes mesangial expansion
