Renal Flashcards

(55 cards)

1
Q

AKI

A

Sudden decline in renal function over hours or days

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2
Q

AKI aetiology

A

1) pre-renal - renal hypoperfusion
-Reduced circulating volume
-Reduced CO
-Systemic vasodilation
-Arteriolar changes (eg. ACEi/NSAID use)
2) intrinsic renal - structural damage
-Vasculature - atherosclerosis, thromboembolic disease, renal artery stenosis
-Glomerular
-Tubulointerstitial - damage to renal parenchyma that can lead to scarring and fibrosis
–ATN
3) post-renal - results from obstruction (obstructive uropathy)
-Urinary stones
-Malignancy
-Strictures
-BPH

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3
Q

AKI pathophysiology (ATN)

A

Failure of adequate renal perfusion results in ischaemia
Causes a pro-inflammatory response with the release of cytokines, oxygen free radicals, activations of leucocytes & coagulation pathways (at this point if renal perfusion is not restored, it can lead to cellular injury)
Tubular cells are susceptible due to limited blood supply & high metabolic demand - damaged TCs slough off into the lumen as obstructive casts
Following restoring of normal GFR - kidneys may recover & tubulointerstitial cells regenerate - polyuric phase due to failure of adequate reabsorption by recovering tubules

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4
Q

AKI pre-renal clinical features

A

Reduced CRT
Dry mucous membranes
Reduced skin turgor
Thirst
Dizziness
Reduced urine output
Orthostatic hypotension

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5
Q

AKI intrinsic renal clinical features

A

Features of nephritic syndrome - hematuria, proteinuria, oliguria & hypertension
Features of nephrotic syndrome - heavy proteinuria, hypoalbuminaemia & oedema
Tubulointerstitial disease - arthralgia, rashes & fever

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6
Q

AKI post-renal clinical features

A

Urinary stones - loin to groin pain, haematuria, nausea & vomiting
Prostatic problems - dysuria, frequency, terminal dribbling, hesitancy
Obstruction at bladder neck - palpable bladder, tender suprapubic area

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7
Q

AKI investigations

A

Assess current fluid status - urine output chart
Bedside - urine dipstick, urine microscopy, urine osmolality & electrolytes, ECG
Bloods - FBC, U&Es, bone profile, blood gas (others can be completed to look for cause of AKI)
Imaging - kidney USS, CXR, renal dopplers, MRA (magnetic resonance angiography)

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8
Q

AKI diagnostic criteria

A

Serum creatinine
-Stage 1: >/= 26.5 umol/L OR >/= 1.5-1.9 times baseline
-Stage 2: >/= 2.0-2.9 times baseline
-Stage 3: >/= 353 umol/L OR 3 times baseline OR on RRT
Urine output
-Stage 1: <0.5ml/kg/hr for 6-12 hours
-Stage 2: <0.5ml/kg/hr for >/= 12 hours
-Stage 3: <0.3ml/kg/hr for >/= 24 hours OR anuria for >/= 12 hours

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9
Q

AKI management

A

Guided by the underlying cause
Regular assessment and monitoring
-Monitoring of urine output
-Baseline creatinine & serial U&Es taken daily
-Nephrotoxic drugs should be stopped
Volume dysregulation
-Hypovolaemic - IV fluids
-Hypervolaemic - fluid restriction +/- diuretics
Hyperkalaemia - 10ml of 10% calcium gluconate, insulin and beta agonists
Metabolic acidosis - use of sodium bicarbonate/dialysis

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10
Q

AKI complications

A

Hyperkalaemia
Fluid overload
Metabolic acidosis
Uraemia

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11
Q

CKD

A

The presence of kidney damage/reduced kidney function for three or more months

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12
Q

CKD aetiology

A

Hypertensive nephropathy
Diabetic nephropathy
Glomerulopathies
Inherited kidney disorders
Ischaemic nephropathy
Obstructive uropathy
Tubulointerstitial diseases
Medications

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13
Q

CKD pathophysiology

A

Renal disease leads to a progressive loss of nephrons and subsequent reduction in GFR
As disease progresses, structural abnormalities may occur leading to kidney damage
Eventually, the kidneys start to lose their ability to carry out normal functions

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14
Q

CKD symptoms

A

Anorexia & nausea
Fatigue & weakness
Muscle cramps
Pruritus
Dyspnoea
Oedema

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15
Q

CKD signs

A

Pallor
Hypertension
Fluid overload
Skin pigmentation
Excoriation marks
Peripheral neuropathy

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16
Q

CKD investigations

A

Urine - urine dipstick, microscopy, ACR (spot & 24-hour collection), electrophoresis
Bloods - FBC, U&Es, bone profile, PTH, bicarbonate, LFTs, lipid profile, autoimmune screen, myeloma screen
Imaging - renal USS, MRA, echo, ECG
Renal biopsy

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17
Q

CKD diagnostic criteria

A

G1 = GFR > 90
G2 = GFR 60-89
G3 = GFR 45-59 (A), GFR 30-44 (B)
G4 = GFR 15-29
G5 = GFR < 15
A1 = ACR < 3
A2 = ACR 3-30
A3 = ACR > 30

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18
Q

CKD management

A

Renoprotective therapy - centred around BP control and reducing proteinuria
-Standard BP target for patient with CKD is < 140/90 mmHg
-Pharmacological - ACEi/ARB, SGLT-2 inhibitor, statin therapy, antiplatelets for secondary prevention of CVS disease
Treating complications
-Anaemia - erythropoietin stimulating agents (not recommended until iron-deficiency has been managed)
-Hyperkalaemia - low potassium diets, potassium-binding resins and correction of acidosis
-Mineral and bone disorders
–Hypocalcaemia - dietary supplements and calcitriol
–Hyperphosphataemia - dietary restriction & phosphate binders
–Hyperparathyroidism - calcimimetics/surgery
-Fluid overload - fluid restriction, reduced sodium intake, oral diuretics
-Acidosis - oral sodium bicarbonate therapy

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19
Q

CKD complications

A

Anaemia
Mineral and bone disorders
Hyperkalaemia
Fluid overload
Acidosis

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20
Q

CKD RRT

A

Haemodialysis - removal of waste products and other substances by passing blood through a dialysis machine
Peritoneal dialysis - using the peritoneal cavity as the primary site of ultrafiltration
Renal transplant - gold standard for RRT, requires the use of long-term immunosuppressive therapy

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21
Q

Diabetic nephropathy pathophysiology

A

Chronic high level of glucose passing through the glomerulus causes scarring

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22
Q

Diabetic nephropathy management

A

Optimising blood sugar levels and BP
ACEi should be started in patients with diabetic nephropathy even if they have a normal BP

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23
Q

Nephrotic syndrome

A

Triad of heavy proteinuria > 3.5g/day, hypoalbuminaemia & oedema

24
Q

Nephrotic syndrome aetiology

A

Divided into primary or secondary
Primary
-Minimal change disease
-Focal segmental glomerulosclerosis
-Membranous nephropathy
Secondary
-Diabetes mellitus
-Amyloidosis
-HIV

25
Minimal change disease pathophysiology
Minimal change disease - fusion of podocyte foot processes under electron microscopy Suspected to be immune dysfunction that leads to production of a permeability factor that disrupts the filtration barrier
26
Nephrotic syndrome symptoms
Shortness of breath Foamy urine - excess protein loss Fatigue Poor appetite Peripheral oedema Periorbital oedema
27
Nephrotic syndrome signs
Oedema Ascites Effusions
28
Nephrotic syndrome investigations
Bloods - FBCs, U&Es, LFTs, CRP, lipid profile, clotting profile Urine - dipstick, microscopy Imaging - renal USS, CXR Renal biopsy
29
Nephrotic syndrome management (MC, FSGS, MN)
Minimal change disease - systemic glucocorticoids (eg. prednisolone) FSGS - primary = immunosuppressive medications, secondary = treat underlying cause Membranous nephropathy - primary = immunosuppressive medications, secondary = targets the underlying cause
30
Nephrotic syndrome complications
Thrombosis - DVT and PE are particularly common Hyperlipidaemia Recurrent infections Acute kidney injury
31
FSGS pathophysiology
-Primary - circulating factor that damages podocytes leading to foot process effacement (loss of structure -> causing them to spread out & reduce effectiveness of filtration barrier) -Secondary - adaptive response to renal injury (combination of glomerular hypertrophy & hyperfiltration)
32
Membranous nephropathy pathophysiology
-Primary - autoimmune reaction against important antigens in the filtration barrier -> development of autoantibodies (against phospholipase A2 receptor) -Secondary - SLE, viral hepatitis, prostate cancer, NSAID use
33
Urgent dialysis indications
Uraemic encephalopathy Hyperkalaemia resistant to medical treatment Metabolic acidosis uncontrolled by medical treatment Pulmonary oedema with oliguria
34
Dialysis
Method for performing the filtration tasks of the kidneys artificially in patients with end stage renal failure or complications of renal failure Involves removing excess fluid, solutes and waste products
35
Long term dialysis indications
End stage renal failure (CKD stage 5) Any of the acute indications continuing long term
36
Peritoneal dialysis
Uses the peritoneal membrane as the filtration membrane Special dialysis solution containing dextrose is added to the peritoneal cavity Ultrafiltration occurs from the blood, across the peritoneal membrane, in to the dialysis solution Dialysis solution is then replaced, taking away the waste products that have filtered out of the blood into the solution Tenckhoff catheter – plastic tube that is inserted into the peritoneal cavity with one end on the outside (allows access to the peritoneal cavity, used for inserting and removing the dialysis solution)
37
Peritoneal dialysis complications
Bacterial peritonitis – infusions of glucose solution make the peritoneum a good place for bacteria to grow Peritoneal sclerosis – thickening and scarring of the peritoneal membrane Ultrafiltration failure – occurs when the patients starts to absorb the dextrose in the filtration solution, reduces the filtration gradient making ultrafiltration less effective, becomes more prominent over time Weight gain – absorb the carbohydrates in the dextrose solution Psychosocial effects – having to change dialysis solution and sleep with a machine every night
38
Haemodialysis
Patients have their blood filtered by a haemodialysis machine Regimes can vary but a typical regime might be 4 hours a day for 3 days a week Need good access to an abundant blood supply, options are: 1) Tunnelled cuffed catheter 2) Arterio-venous fistula
39
Tunnelled cuffed catheter
Tube inserted into the subclavian/jugular vein with a tip that sits in the SVC/right atrium Two lumens – one for blood exiting and one where blood enters Dacron cuff – surrounds the catheter, promotes healing and adhesion of tissue to the cuff, making it more permanent and providing a barrier to bacterial infection, can stay long term Main complications – infection and blood clots
40
A-V fistula
Artificial connection between an artery to a vein (surgical operation and a 4 week to 4 month maturation period without use) Provides a permanent, large, easy access blood vessel with high pressure arterial blood flow Typically in patient’s forearm – radio-cephalic, brachio-cephalic, brachio-basilic
41
A-V fistula examination
Skin integrity Aneurysms Palpable thrill (fine vibration felt over the anastomosis) Stereotypical machinery murmur on auscultation
42
A-V fistula complications
Aneurysm Infection Thrombosis Stenosis STEAL syndrome High output heart failure
43
STEAL syndrome
Inadequate blood flow to the limb distal to the AV fistula AV fistula steals blood from the distal limb Blood is diverted away from where it was supposed to supply and slows straight into the venous system Causes distal ischaemia
44
High output heart failure (AV fistula complications)
AV fistula blood is flowing very quickly from the arterial to the venous system through the fistula Means there is rapid return of blood to the heart -> increases the pre-load in the heart -> hypertrophy of the heart muscle and heart failure
45
Polycystic kidney disease
Genetic condition where the kidney develop multiple fluid-filled cysts Kidney function is impaired Palpable, enlarged kidneys may be felt on examination Autosomal dominant and recessive type (dominant is more common) Diagnosis – kidney USS and genetic testing
46
ADPKD genes
PKD-1 (chromosome 1) is majority PKD-2 (chromosome 4)
47
ADPKD extra-renal manifestations
Cerebral aneurysms Hepatic, splenic, pancreatic, ovarian and prostatic cysts Cardiac valve disease (MR) Colonic diverticula Aortic root dilatation
48
ADPKD complications
Chronic loin pain Hypertension CVD Gross haematuria Renal stones End stage renal failure
49
ARPKD
Gene on chromosome 6 Rarer and more severe Often presents in pregnancy with oligohydramnios (fetus does not produce enough urine)
50
ARPKD features
Oligohydramnios leads to underdevelopment of the lungs resulting in respiratory failure shortly after birth Patients may require dialysis within the first few days of life Can have dysmorphic features – underdeveloped ear cartilage, low set ears & flat nasal bridge Usually have end-stage renal failure before reaching adulthood
51
PKD management
Tolvaptan (vasopressin receptor antagonist) – can slow development of cysts & progression of renal failure in ADPKD - Should be initiated and monitored by a specialist Mainly supportive of complications: anti-hypertensives, analgesia, abx, dialysis, renal transplant Other: genetic counselling, avoid contact sports, avoid NSAIDs & anticoagulants, regular USS to monitor cysts, regular BP, MR angiogram can be used to diagnose intracranial aneurysms
52
Donor matching for renal transplant
Matched based on HLA type A, B & C on chromosome 6 Recipients can receive treatment to desensitised them to donor HLA when there is a living donor Less they match, the more likely the transplant is to fail
53
Renal transplant procedure
Patient’s own kidneys are left in place Donor kidney’s blood vessels are connected with the patient’s pelvic vessels, usually the external iliac vessels Donor kidney’s ureter is anastomosed directly with the patient’s bladder Placed anterior in the abdomen and can usually be palpated in the iliac fossa area Typically hockey stick scar
54
Post renal transplant
New kidney will start functioning immediately Patients will require life long immunosuppression to reduce the risk of transplant rejection Usual regime: tacrolimus, mycophenolate, prednisolone Others: cyclosporine, sirolimus, azathioprine
55
Renal transplant complications
Relating to transplant – transplant rejection (hyperacute, acute & chronic), transplant failure, electrolyte imbalances Relating to immunosuppressants – ischaemic heart disease, T2DM, infections more likely & more severe, unusual infections (PCP, CMV, PJP & TB), non-Hodgkin lymphoma, skin cancer (particularly SCC)