Renal Flashcards
Acute kidney injury
A significant deterioration in renal function occurring over hours or days. Severity is defined by 3 stages (1 to 3).
prerenal AKI
decreased perfusion to the kidney– hypoperfusion (sudden/severe drop in BP), atherosclerosis/ischaemia
Prerenal causes of AKI
Renal artery stenosis
Heart failure
Haemorrhage
Renal AKI
(intrinsic renal disease) – direct kidney damage, inflammation, infection, drug, autoimmune disease
4 causes of Renal AKI
Acute tubular injury
Glomerulonephritis
Acute interstitial nephritis
Renal vasculitis
postrenal AKI
obstruction to urine flow
postrenal causes of AKI
Benign prostatic hyperplasia
Kidney stones
Tumour
Pathology of Prerenal AKI
Low vascular volume
Decreased cardiac output
Systemic vasodilation
Renal vasoconstriction
pathology of renal AKI
Glomerular
Interstitial
Vessels
pathology of post renal AKI
Extrinsic compression
3 clinical manifestations of AKI
Oliguria (passing small volumes of urine)
Fatigue or tiredness
Shortness of breath
4 complications of severe AKI
pulmonary oedema, encephalopathy and pericarditis
hyperkalaemia
differential diagnoses for AKI
Chronic kidney disease
Hyperkalaemia/ hypernatremia
Acute tubular necrosis
First line investigations for AKI
Rise in creatinine of >26 micromol/L in 48 hours
Rise in creatinine of >50% from baseline in 7 days
Urine output of <0.5ml/kg/hr for >6 hours
Determine cause: urea:creatinine ratio – pre-renal (>100:1), intrarenal (<40:1), post-renal (40-100:1)
Metabolic panel and urine output monitoring: raised serum creatinine, low urine output, raised potassium, metabolic acidosis (raised H+)
Urinalysis: leucocytes and nitrates (infection), proteinuria and haematuria (acute nephritis)
Gold standard investigations for AKI
Metabolic profile: U&E (GFR) and creatinine – raised serum creatinine, reduced urine output
management of AKI
Identification of risk factors
Dialysis may be needed whilst renal function improves
Manage complications
Dependent on the underlying aetiology
Management of Hypovolaemic AKI
fluid resuscitation;
Renal perfusion will improve with volume replacement
Give crystalloid
management of hypervolaemic AKI
Oxygen supplementation if required
Fluid restriction. Consider oral and IV volumes.
Diuretics – only in symptomatic fluid overload
Renal replacement therapy
Chronic kidney disease
abnormalities of kidney structure or function, present for >3 months, with implications for health. Irreversible loss of nephrons.
4 abnormalities of kidney function
Decreased glomerular filtration rate (GFR)
Increased albuminuria
Urinary sediment abnormalities
Electrolyte and other abnormalities due to tubular disorders
4 main causes of CKD
Acute renal failure, hypertension, diabetes, kidney disease e.g. polycystic kidney disease
4 rarer causes of CKD
Dysplastic kidneys
Reflux nephropathy
Obstructive nephropathy
Infections/ drugs/ systemic diseases that affect the kidney
pathology of CKD
Injury may primarily affect glomeruli, vessels, or the tubulo-interstitium, but eventually it leads to reduction in nephron mass with reduction in renal function.
The reduction in nephron mass may then cause haemodynamic stress in remaining nephrons, leading to further nephron loss.
Manifestation of early CKD
asymptomatic and can only be picked up if GFR is measured in at-risk patients e.g. diabetics, hypertensives
Why do progressed CKD patients have bone pain
Bone decalcification due to metabolic acidosis
What is metabolic derangement
Increased sodium and water retention due to decreased GFR – vomiting and diarrhoea
differential diagnoses for CKD
Acute kidney injury
Diabetic nephropathy
Chronic glomerulonephritis
First line investigations for CKD
FBC (anaemia of CKD), U&E (raised creatinine, phosphate, potassium. Decreased eGFR), urinalysis (haematuria, proteinuria), raised urine albumin (albumin:creatinine >3mg/mmol), renal USS (bilateral renal atrophy)
Gold standard investigations for CKD
U&E for estimated GFR
(eGFR < 60mL/min/1.73m2 or, eGFR <90mL/min/1.73m2 + signs of renal damage)
5 steps to management of CKD
Appropriate referral to nephrology
Treatment to slow renal disease progression
Treatment of renal complications of CKD
Treatment of other complications of CKD
Preparation for renal replacement therapy (dialysis/ transplant)
treatment to slow renal disease progression
Target to lower blood pressure
Offer treatment with renin-angiotensin system antagonist – ace inhibitors
Treatment of renal complications of CKD
Anaemia: treat underlying cause
Acidosis: consider sodium bicarbonate supplements
Oedema: restrict fluid and sodium intake
CKD bone mineral disorders: give vitamin D supplements
why does CKD increase risk of CVD
due to high blood pressure, vascular stiffness, inflammation, oxidative stress, and abnormal endothelial function.
treatment of CVD caused by CKD
Antiplatelets for CKD at risk of atherosclerotic events
Atorvastatin for primary and secondary prevention of CVD
Preparation for renal replacement therapy
Should begin in progressive CKD when the risk of renal failure is 10-20% within a year.
All suitable patients should be listed for a deceased donor transplant 6 months before the anticipated start of RRT.
main complication of CKD
High incidence of cardiovascular disease due to a combination of hypertension, vascular calcification, and hyperlipidaemia
Patients are much more likely to die of CVD than to need renal replacement therapy.
complications of calcium and phosphate metabolism derangement by CKD
leads to renal bone disease, which is a complex mixture of hyper-parathyroid bone disease, Osteomalacia and osteoporosis.
7 Symptoms of renal failure that lead to RRT being needed
Inability to control volume status, including pulmonary oedema
Inability to control blood pressure
Serositis
Acid-base or electrolyte abnormalities
Pruritus
Nausea/ vomiting/ deterioration in nutritional status
Cognitive impairment
Features of Haemodialysis
Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction.
A hydrostatic gradient is used to clear excess fluid as required (ultrafiltration).
Access is preferentially via an arteriovenous fistula which provides increased blood flow and longevity.
Haemodialysis is needed 3 times/week or more.
features of Peritoneal dialysis
Uses the peritoneum as a semi-permeable membrane.
Catheter is inserted into the peritoneal cavity and fluid infused. Solutes diffuse slowly across.
Ultrafiltration is achieved by adding osmotic agents to the fluid.
It is a continuous process with intermittent drainage and refilling of the peritoneal cavity, performed at home.
features of Haemofiltration
Water cleared by positive pressure, dragging solutes into the waste by convention.
The ultrafiltrate (waste) is replaced with an appropriate volume of clean fluid.
Low haemodynamic instability so used in critical care when HD not possible due to low BP.
3 complications of RRT
Cardiovascular disease: increased BP, calcium/phosphate dysregulation, inflammation
Renal bone disease: high bone turnover, renal osteodystrophy
Infection: uraemia causes granulocyte and T-cell dysfunction with increased sepsis-related mortality.
2 types of renal transplants
Living donor: best graft function and survival, especially if HLA matched.
Deceased donor
3 types of deceased donor renal transplant
Donor after brain death
Expanded criteria donor (an older kidney or from a patient with a history of CVA, BP or CKD)
Donor after cardiac death
types of immunosuppressants
Monoclonal antibodies used at time of transplant e.g. daclizumab
Calcineurin inhibitors to inhibit T-cell activation and proliferation e.g. ciclosporin
Antimetabolites to prevent acute rejection and increase graft survival e.g. azathioprine
Glucorticosteroids to decrease transcription of inflammatory cytokines.
surgical complications of renal transplant
bleed, thrombosis, infection, urinary leaks, lymphocele, hernia
4 non-surgical complications of renal transplant
Delayed graft function
Rejection
Infection: increased risk of all infections
Malignancy: immunosuppression increases the risk of cancer
Glomerulonephritis
GN is characterised by inflammation and damage to the glomeruli. This allows protein (+/- blood) to leak out into the urine.
which conditions does the term glomerulonephritis encompass
Are caused by pathology in the glomerulus
Present with proteinuria, haematuria, or both
Are diagnosed on a renal biopsy
Cause CKD
Can progress to kidney failure (except minimal change disease)
5 causes of Glomerulonephritis
IgA nephropathy
Systemic lupus erythematous nephropathy
Post-streptococcal glomerulonephritis
Goodpasture’s syndrome (rapidly progressing glomerulonephritis)
Haemolytic uraemic syndrome
pathology of Glomerulonephritis
Damage to the glomerulus with leakage of protein and blood into the urine. There may be rupture of the glomerular basement membrane, with a cellular reaction in the Bowman’s space.
What can Glomerulonephritis cause
Damage to the filtration mechanism resulting in haematuria and proteinuria
Damage to the glomerulus restricts blood flow, leading to compensatory hypertension
Loss of the usual filtration capacity leads to acute kidney injury
key presentations of Glomerulonephritis
Visible haematuria, proteinuria, hypertension, oedema (peripheral, pulmonary), oliguria (low urine output), uraemic signs
symptoms of IgA nephropathy
visible haematuria, 1-2 days after viral infection
symptoms of post-strep GN
visible haematuria, 2 weeks after strep infection
Symptoms of Rapidly progressing GN (Goodpasture’s, Wegener’s)
Fatigue, SOB, cough, haemoptysis, acute kidney failure.
first line investigations for GN
Urinalysis and microscopy (haematuria, proteinuria, dysmorphic RBCs), 24hr urine protein collection, bloods (anaemia, elevated liver enzymes, elevated creatinine)
Serology: anti-GBM (Goodpasture’s), anti-double-stranded DNA (SLE), antinuclear antibody (SLE), ANCA (Wegener’s vasculitis)
IgA: microscopy shows IgA complex deposition
Rapidly progressive GN: microscopy shows crescentic glomerulonephritis
gold standard investigation for GN
Renal biopsy (crescent shaped glomeruli, Ig deposits, glomerulosclerosis)
cause of Acute nephritic syndrome
Caused by an immune response triggered by an infection or other disease
Most common primary cause is IgA nephropathy
pathology of Acute nephritic syndrome
Kidney leaks blood from its basement membrane – podocytes develop large pores which allows blood and protein to escape into the urine.
Distinguishing histological feature of Acute nephritic syndrome
Red cell casts are the distinguishing feature – formed in the nephrons and indicate glomerular damage
symptoms of Acute nephritic syndrome
Haematuria – visible or non-visible
Proteinuria
Hypertension and oedema
Low volume of urine <300ml/day due to decreased renal function
IgA nephropathy
Immune complex GN related to glomerular deposition of immune complexes containing IgA.
primary causes of IgA nephropathy
incompletely understood; an abnormal mucosal immune system and the production of abnormally glycosylated IgA molecules play a role
secondary causes of IgA nephropathy
IgA can be deposited in glomeruli, in association with liver disease, bowel disease and dermatitis herpetiformis
pathological features of IgA nephropathy
IgA can cause a number of changes in the glomeruli, ranging from mild mesangial hypercellularity only to glocal glomerular hypercellularity.
Crescents may be seen in the most severe cases
presentation of IgA nephropathy
Asymptomatic non-visible haematuria
Episodic visible haematuria
High BP
investigation for IgA nephropathy
Renal biopsy: IgA deposition in mesangium.
treatment of IgA nephropathy
ACE inhibitors – reduce BP and protein in the urine
What is nephrotic syndrome
Proteinuria due to basement membrane pathology. Kidney leaks protein from its basement membrane
triad of symptoms for Nephrotic syndrome
Proteinuria >3.5g/24 hours
Hypoalbuminemia
Oedema (oncotic pressure decreases due to hypoalbuminemia, meaning fluid moves out to surrounding tissues)
What is a common complication of Nephrotic syndrome
Severe hyperlipidaemia is often present: liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots and produces raised cholesterol.
primary renal causes of Nephrotic syndrome
minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, membranoproliferative GN
Secondary causes of Nephrotic syndrome
DM, lupus nephritis, myeloma, amyloid, pre-eclampsia.
pathophysiology of Nephrotic syndrome
The filtration barrier of the kidney is formed by podocytes, the glomerular basement membrane (GBM), and endothelial cells.
Proteinuria results from podocyte pathology; abnormal function in minimal change disease or immune-mediated damage in membranous nephropathy.
presentations of Nephrotic syndrome
Generalised, pitting oedema of ankles, genital, abdominal wall which can be rapid and severe
Hypoalbuminemia
Frothy urine (due to the protein)
Systemic symptoms e.g. joint, skin
Consider malignancy and chronic infection
differential diagnoses of nephrotic syndrome
Congestive heart failure
Where there is oedema and raised jugular venous pressure
Cirrhosis
Where there is oedema and hypoalbuminemia
investigations for nephrotic syndrome
Establish cause via renal biopsy
Urine dipstick shows very high protein
Serum albumin is low
management of nephrotic syndrome
Reduce oedema
Fluid and salt restriction. Diuretics with loops diuretics
Treat underlying cause
Adults need a renal biopsy to discover cause
Reduce proteinuria
ACEi/ ARB reduce proteinuria
complications of nephrotic syndrome
Thromboembolism
Infection
Hyperlipidaemia
pathology of minimal change disease
loss of podocyte foot processes, vacuolation and appearance of microvilli in the glomerulus = three hallmarks
Podocyte losses may account for proteinuria
diagnosis of minimal change disease
biopsy, electron microscope of biopsy shows abnormal podocytes
clinical presentation of minimal change disease
like nephrotic syndrome
natural history of MCD
has a relapsing – remitting course
Does MCD progress to renal failure
NO
treatment of MCD
steroids (prednisolone). For frequent relapses or steroid dependent cases second line treatment is with cyclophosphamide or cyclosporine
presentation of focal segmental glomerulosclerosis
Presents as nephrotic syndrome
causes of FSGS
Can either be primary (genetic mutations) or secondary (HIV/ reflux nephropathy)
investigations for FSGS
Specific segments of certain glomeruli develop sclerosed lesions
Antibody tests are all negative
treatment of FSGS
Salt restriction and diuretics – reduce oedema
Antihypertensives
Statins – treat hyperlipidaemia
Transplant
presentation of Membranous glomerulonephritis
Presents with nephrotic syndrome
Slowly progressive
cause of Membranous glomerulonephritis
Usually idiopathic but can be associated with Hepatitis B/ Malaria/ Penicillamine/ SLE
Caused by immune complex deposition, which results in complement activation against glomerular basement membrane proteins.
investigations for membranous glomerulonephritis
Microscopic analysis shows thickened glomerular basement membrane
Immunofluorescence shows diffuse uptake of IgG
treatment of Membranous glomerulonephritis
Steroids if disease begins to progress
prognosis of Membranous glomerulonephritis
: 1/3 have chronic membranous glomerulonephritis, 1/3 go into remission, 1/3 progress to end-stage renal failure.
What is Polycystic kidney disease
An inherited disorder in which clusters of cysts develop primarily within your kidneys, causing your kidneys to enlarge and lose function over time.
cause of Adult PKD
an inherited mutation in the PKD1 gene on chromosome 16
pathology of Adult PKD
Defects in the function of the PKD1 protein lead to cystic change in renal tubules and loss of normal renal tissue
presentation of adult PKD
May be clinically silent unless cysts become symptomatic due to size/haemorrhage.
Loin pain
Visible haematuria
Cyst infection
Renal calculi
High BP
Progressive renal failure
Extra renal manifestations of adult PKD
liver cysts and berry aneurysms.
First line and gold standard investigations for PKD
Kidney ultrasound (enlarged bilateral kidneys with multiple cysts). Age 15-39 (at least 3 cysts unilateral or bilateral), 40-59 (at least 2 in each kidney), 60+ (at least 4 in each kidney)
treatment of PKD
Water intake 3-4L/day may suppress cyst growth
High BP should be treated to target <130/80mmHg
1st line ACE-i/ ARB
2nd line thiazide-like
3rd line β-blocker
Treat infection
Persistent/ severe pain may need cyst decompression
Infantile PKD
A rare, inherited condition causing bilateral polycystic kidneys and congenital hepatic fibrosis.
Cause of infantile PKD
mutations in the PKHD1 on chromosome 6p which encodes a component of the cilia on collecting duct epithelial cells
complications of infantile PKD
Severe cases cause neonatal death from pulmonary hypoplasia.
Children with less severe renal disease who survive, suffer from;
Congenital hepatic fibrosis
Complications of portal hypertension
treatment of infantile PKD
Poor prognosis if neonatal respiratory distress. No specific therapy.
Continuous renal replacement therapy needed
Renal colic
a type of pain you get when urinary stones block part of your urinary tract
features of Renal colic
Rapid onset – woken from sleep
Pain that results from upper urinary tract obstruction
Excruciating ureteric spasms – patient is writhing in pain
Pain is from loin to groin
Associated with nausea and vomiting
Worse with fluid loading
Radiates to groin and ipsilateral testis/labia
Often cannot lie still
